Printable list of all cardiac arrest and resuscitation SAQs

College Answer

A case of near electromechanical dissociation  in a 58 year old man. This could be caused by hypovolaemic shock. anaphylaxis or cardiogenic shock etc. Therefore the candidate should have started with a comprehensive approach and be directed to specific problems.

(a) An outline is requested but it should contain some rationale. eg:

•  A/B if the patient is breathing and talking apply a 100% oxygen mask. If not. bag with face mask and high·flow (h.   LOC may improve rapidly with BP restoration, but if not, intubation and ventilation will be necessary.

•  Quickly assess the patient's volume status (JVP visible?, veins engorged). Establish best venous access  possible (peripheral IV. external jugular, femoral). If the patient appears hypovolaemic. commence bolus of fluid. Continue fluid boluses until filling  pressures appear adequate as judged by rise in NP, CVP (or PAOP) or occurrence of worsening respiratory distress(? pulmonary.oedema).

•  If the patient is not hypovolaemic on arrival or remains hypotensive despite achieving adequate filling pressures give 1mg increments of araminc and commence an inoconstrictor infusion.

•     As soon as possible insert an intra·arterial cannula. It is possible that the central BP is adequate.

Meanwhile, a primary survey should be undertaken to determine the cause and a detailed history sought. Life-threatening injuries arc excluded. The patient is quickly examined from head to foot for signs of anaphylaxis (erythema, wheals etc), cardiac failure or tamponade (venous congestion, raised JVP). Tension pneumothorax or sepsis (hot. flushed, local signs) etc.

Investigations and initial treatments should be guided by the history and signs eg. intercostal catheter.pericardio--centesis.·

Discussion

This 58 year old gentleman is about to have a PEA arrest. Perhaps "moribund" is probably not a very precise medical term, but according to the all-knowing oracle of Wikipedia it refers to a "literal or figurative state of near death", which is appropriate to describe a man with a barely palpable rapid pulse.

However difficult to palpate, the pulse is still palpable.

The patient has not yet arrested.

One's priorities, then, are to assess this patient, rapidly determine the cause of his hemodynamic instability, and reverse the immediately reversible factors.

Perhaps he has not arrested yet. Still, the 4 Hs and 4Ts apply:

• Hypoxia
• Hypovolemia
• Hyper/hypokalemia
• Hyper/hypothermia
• Tension pneumothorax
• Tamponade (i.e. cardiac tamponade)
• Toxins (eg. anaphylactic reaction or intoxication)
• Thrombus (eg. a PE or MI)

Thus, a stepwise approach to this problem would be something resembling the following:

1) Ensure personal safety

2) Perform a basic peri-arrest primary survey

• Immediate assessment to diagnose cardiac arrest
  • Are they awake?
  • If they appear unconscious, shake them and ask "Are you alright?"
  • If they are unresponsive, look listen and feel for respiratory effort.
  • If the patient is unconscious, unresponsive, and is not breathing, call for help and start CPR.
    Otherwise, move on with the structured approach to prevent cardiac arrest
• Airway:
  • Assess patency: best done by interrogating the patient. If he provides coherent answers to your questions, his ABCs are unlikely to be desperately compromised. If he does not, one should secure his airway - initially usig unsophisticated techniques (jaw thrush, chin lift), progressing through airway adjuncts to intubation as needed.
  • Look for presence of vomit or foreign body
  • Prepare to progress to intubation
• Breathing
  • Observe respiratory rate
  • maintain oxygenationintially with high flow oxygen via tight-fitting reservoir mask. A high flow nonrebreather mask not only delivers around 75% FiO₂, it also allows one to assess respiratory function by observing the expiratory fogging of the clear plastic, and one can hook up an end-tidal capnometer to it to detect expired CO₂.
  • progress to bag-mask ventilation if respiratory arrest occurs
  • Auscultate the chest, percuss it, palpate for surgical emphysema
  • Investigate with ABG and urgent CXR
  • Specific differentials to consider before moving on with the survey:
    • Massive PE (distended neck veins, cyanosis, tachycardia and hypotension)
    • Acute severe asthma (silent hyperexpanded chest, the hint of wheeze)
    • Tension pneumothorax (unequal air entry, deviated trachea, hyper-resonant chest)
    • Massive haemothorax or effusion (unequal air entry, deviated trachea, dull percussion note over the hemithorax)
    • Pulmonary oedema (pink frothy sputum, coarse gurling creps)
• Circulation
  • Ensure large-bore IV access
  • Measure the blood pressure non-invasively and attach ECG leads for monitoring
  • administer IV fluids as bolus
  • administer readily available vasopressors, eg. metaraminol in order to maintain cerebral perfusion
  • assess for sources of bleeding
  • ABG or FBC to assess Hb, and need for transfusion
  • rapid bedside TTE to assess cardiac chamber volume and contractility
  • Specific differentials to consider before moving on with the survey:
    • Extremes of hypovolemia (collapsed veins, empty chambers, slow capillary refill, dry mucosae, cool extremities, weak rapid pulse)
    • Haemorrhagic shock ( exactly as above but also deathly pallor)
    • Cardiac tamponade (distended neck veins, muffled heart sounds, electrical alternans on ECG)
    • Peri-arrest arrhythmia (eg. VT or SVT)
    • Severe sepsis (mottled skin, fever, hyperdynamic circulation with hypotension)
  • A fluid bolus would be an appropriate reaction in any case. A hand-operated pump giving set with a litre of crystalloid should be set up. Ideally, one should prepare for invasive arterial blood pressure monitoring.
• Disability/neurology
  • Assess for signs of intracranial catastrophe by performing a brief neurological examination, including pupils and muscle tone/reflexes
  • Test BSL: ensure normoglycaemia
  • Specific differentials to consider before moving on with the survey:
    • Intracranial catastrophe (pupils, focal signs)
    • Seizure (increased tone, exaggerated reflexes, gaze deviation, clonus)
    • Extreme hypoglycaemia
    • Hyperglycaemic coma
    • Extremes of electrolyte derangement (eg. a sodium of 90 or 190)
    • Hepatic encephalopathy
• Exposure/examination
  • Assess for sources of bleeding
  • Examine for features of anaphylaxis
  • Check temperature; ensure normothermia

References

ARC Guideline 11.2: Protocols for Advanced Life Support

Additionally, the ARC ALS2 manual contains several chapters dealing with pre-arrest scenarios such as this one.

College Answer

(b) This provides some help.but is not definitive. Possible causes still include pulmonary embolus. hypovolaemia from bleeding DU. myocardial infarction etc. A progression from simple/quick investigations to more complex but specific/diagnostic investigations should be outlined. There should have beeo a sense of appropriate priorities.

If there are signs of GIT bleed with hypovolaemia, then fluid resuscitation, NG tube insertion, endoscopy, FBC and coag screen will be indicated  along with anti-ulcer therapy and perhaps surgery.

If there are signs of acute myocardial infarction. in the setting of recent DU, angiogram and angioplasty would be a preferable course perhaps after urgent echo.

If there are signs of massive pulmonary embolus (right  heart failure), and initial tests are supportive (right heart strain on ECG, oligaemic lung on CXR, distended RV on echo), a spiral CT would be indicated with commencement of IV heparin

Discussion

This part of this multi-part question offers some explanation as why the patient is "moribund". In essence, it narrows the differentials generated by the "4 Hs and 4 Ts" approach, which one can use to systematically organise one's diagnostic approach to this peri-arrest scenario in the first part of this question.

In detail:

• Hypoxia is possible due to pulmonary oedema or atelectasis
• Hypovolemia is a differential, given the history of GI bleeding
• Hyper/hypokalemia is now less likely
• Hyper/hypothermia is also less likely
• Tension pneumothorax is unlikely given the history
• Tamponade (i.e. cardiac tamponade) cannot be excluded but again, does not fit the history
• Toxins (eg. anaphylactic reaction or intoxication) cannot be ruled out, especially given the recent surgery and thus the potential oral antibiotic therapy
• Thrombus (eg. a PE or MI) is a definite possibility - particularly the PE - given the recent history of orthopaedic surgery

Thus, one would organise the following investigations:

• Routine bloods to measure urea and haemoglobin, to investigate the possibility of a GI bleed
• CXR to exclude pneumothorax, atelectasis and APO, as well as to look for subdiaphragmatic gas associated with a perforated duodenal ulcer
• TTE to investigate myocardial contractility and to look for regional wall motion abnormalities associated with MI. Even a low-skilled interpreter will also be able to rapidly rule out cardiac tamponade and right ventricular dilatatation associated with massive PE.
• CTPA to exclude massive PE; the CT will also capture a portion of the upper GI tract giving more information regarding the state of affairs in the duodenum.
• Upper GI endoscopy would be the gold standard to investigate and manage duodenal bleeding, and one should contact a gastroenterologist to organise this.

The following specific management could be commenced while awaiting results:

• High flow oxygen therapy
• Volume resuscitation
• PPI infusion

Seeing as both bleeding and thrombosis are a part of the differentials, anticoagulation/thrombolysis should be thought about but left until investigations reveal more about the cause of this shock state.

References

College Answer

{d) Ideally, intubate and ventilate with 100%  02, turn  up the noradrenaline, repeat fluid bolus, commence CPR if indicated and transfer immediately to the OT for surgery. In the absence of cardiac surgery 'facilities, one is left with a Trendelenberg operation by a general surgeon or continued medical therapy or risk lysis.

Discussion

This is a question regarding the management of a PEA arrest.

Another question - Question 15 from the first paper of 2011 - discusses the management steps, but with a different history of presentation. The steps are generic, and I will reproduce them here to simplify revision. Additionally, PEA is discussed in greater detail in the answer to Question 8 from the second paper of 2004.

Thus:

1) Confirm cardiac arrest

2) Call for help

3) Commence BSL (CPR) until help arrives;

• 100 compressions per minute
• Compression to a depth of 1/3rd of the anterior-posterior chest diamweter
• Asynchronous ventilation of 8-10 breaths per minute if intubated, otherwise 30 compressions to 2 breaths.
• Ensure the ETT is not malpositioned (chest examination, end tidal CO₂ or calorimetry)

4) With help arriving, follow the non-shockable pathway of the ALS algorithm, which consists of CPR and 1mg adrenaline every 2nd cycle.

4) Work on resolving the cause of the arrest, using the "four Hs and four Ts" as a general guide.

References

The index of ARC guidelines is available from the ARC website.

It contains the relevant algorithm for managing a non-shockable rhythm.

College Answer

Efficient support of the potential organ donor is an integral part of IC practice. Since we know nothing of this patient's story a back to basics detailed approach to the patient should have included:
(a) Check airway patency, tube position. 
(b) Ensure adequate ventilation: 
•  Examination, ABG, CXR (to exclude pneumothorax/lung injury, hypoxialhypercarbia) (c) Restore circulation with fluid challenge. Assess filling pressures and response to challenge. 
•  If diabetes insipidus is apparent (eg. urine output >300mlslhr, serum osmolality >300, urine osmolality <300 in the absence of diuretics) give lug ofDDAVP lV or SC 
•  If restoration of  fluid status does not  restore BP and organ  perfusion, commence vasoconstrictor infusion (aramine or noradrenaline) 
•  Moderate hypothermia (35°C} may be well tolerated and require no specific therapy 

•  Persistent hypotension in the presence of impaired pituitary functiODt as evidenced by DI.  It may be an indication for intravenous corticosteroids and T3. There usually is no time for a random cortisol level 
•  Maintain fluid and electrolyte homeostasis eg. replacing urine output ml for ml

Discussion

This question discussess the generic principles of care for the brain-dead organ donor. This issue is explored in great depth in the answer to Question 1 from the first paper of 2012: 

"Outline the Intensive Care management of a 25-year-old male who has fulfilled brain death criteria and is awaiting surgery for organ donation."

Non-clinical issues: (presumably, these have been dealt with now that the patient is "awaiting surgery for organ donation"

• Early involvement of the transplant coordinator
• Non-coercive sensitive family discussion re opportunity for donation
• Tissue typing, viral screen, further organ function tests
• Facilitate family time at bedside
• Ensure aftercare of donor family

1. The circuit should be humidified.
2. Normoxia and normocapnea must be maintained.
   There will be periodic requests for ABGs on 100% FiO₂ from the donor coordinator, but afterwards the FiO₂  must be minimised to prevent oxidative stress damage to the lungs.
3. Haemodynamic instability is to be expected:
   - The initial autonomic storm should be managed with nitroprusside and esmolol
   - The subsequent collapse should be treated with noradrenaline and/or vasopressin
   - Bradycardia will be resistant to atropine (no vagus to block); catecholamines or pacing will be required
   -Though they do not make a direct statement to this effect, ANZICS tacitly support CPR in the brain-dead organ donor; "cardiopulmonary resuscitation may result in recovery of cardiac function and successful transplantation".
4. Normoglycaemia must be maintained.
5. Normothermia must be maintained by warming externally, and by using warmed fluids.
   Electrolytes need to be maintained within normal laboratory ranges;
   particular attention needs to be paid to the sodium.
   DDAVP may be required as a hormone replacement.
   Other "endocrine support" (T3, hydrocortisone) should be considered in the following circumstances:
   - haemodynamic instability
   - an ejection fraction of less than 45%
   - heart donation is being considered
6. Fluid resuscitation should be conservative if you plant to donate lungs,  aggressive if you plan to donate kidneys, and an intelligent compromise if both organs are being considered.
7. Nutrition must continue.
   Good nutrition (or rather, the absence of malnutrition) has been associated with improved raft function (Singer et al, 2005)
8. Coagulopathy must be observed and corrected; if worsening coagulopathy or DIC develop, organ retrieval should be expedited.

References

Summarized from the ANZIC statement on Brain Death and Organ Donation, Version 3.2

Dujardin, Karl S., et al. "Myocardial dysfunction associated with brain death: clinical, echocardiographic, and pathologic features." The Journal of heart and lung transplantation 20.3 (2001): 350-357.

Totsuka, Eishi, et al. "Influence of high donor serum sodium levels on early postoperative graft function in human liver transplantation: effect of correction of donor hypernatremia." Liver Transplantation and Surgery 5.5 (1999): 421-428.

Novitzky, D., D. K. C. Cooper, and B. Reichart. "Hemodynamic and metabolic responses to hormonal therapy in brain-dead potential organ donors." Transplantation 43.6 (1987): 852-854.

Phongsamran, Paula. "Critical care pharmacy in donor management." Progress in Transplantation 14.2 (2004): 105-113.

RANDELL, TARJA T., and KRISTER AV HöCKERSTEDT. "TRIIODOTHYRONINE TREATMENT IN BRAIN-DEAD MULTIORGAN DONORS-A CONTROLLED STUDY." Transplantation 54.4 (1992): 736-737.

Goarin, Jean-Pierre, et al. "The effects of triiodothyronine on hemodynamic status and cardiac function in potential heart donors." Anesthesia & Analgesia 83.1 (1996): 41-47.

Follette, David M., Steven M. Rudich, and Wayne D. Babcock. "Improved oxygenation and increased lung donor recovery with high-dose steroid administration after brain death." The Journal of heart and lung transplantation: the official publication of the International Society for Heart Transplantation 17.4 (1998): 423-429.

Lisman, T., et al. "Activation of hemostasis in brain dead organ donors: an observational study." Journal of Thrombosis and Haemostasis 9.10 (2011): 1959-1965.

Lim, H. B., and M. Smith. "Systemic complications after head injury: a clinical review." Anaesthesia 62.5 (2007): 474-482.

Dalle Ave, Anne L., Dale Gardiner, and David M. Shaw. "Cardio‐pulmonary resuscitation of brain‐dead organ donors: a literature review and suggestions for practice." Transplant International (2015).

Singer, Pierre, Haim Shapiro, and Jonathan Cohen. "Brain death and organ damage: the modulating effects of nutrition." Transplantation 80.10 (2005): 1363-1368.

College Answer

Pulseless VT: managed as per cardiac arrest protocol (immediate unsyncbronised defibrillation [up to 3 sequential  shocks  if  necessary],  followed  by CPR  intubation/IV/oxygen, consider antiarrhythmics  (lignocaine, amiodarone, potassium and magnesium], administer  adrenaline 1 mg every 3 minutes, exclude reversible causes [5Hs and 5Ts].

VT with a pulse: if deteriorates or unstable haemodynamically manage as for pulseless VT.If stable administer  oxygen/obtain  IV  access  and  rapidly  exclude  reversible  factors  (including   wire catheter in RV, hypokalaemia,  hypomagnesaemia, others  as indicated  by a systematic  review to exclude  other  reversible  causes.  Drug  therapy  according  to  scenario  but  useful  drugs include lignocaine (for ischaemia/post  cardiac surgery: 1-1.5  mg/kg IV then infusion), procainamide  (50 mglmin to max of 17 mglk.g),sotalol (l mglkg) or amiodarone (5 mg/kg over 20 minutes).

Discussion

The question draws on the candidate's knowledge of recent resuscitation guidelines.

The ARC has a pretty straightforward view of these sort of tachyarrhythmias. If it is hemodynamically usntable, you shock it. If it is haemodynamically stable, you can afford to think about drugs. If it is without pulse, the patient is dead and you should proceed according to the ALS algorithm for shockable rhythms (nowadays we dont do those three shocks anymore).

Thus:

• Acute management:
  • VT with pulse:
    • haemodynamically stable:
      • control arrhythmia with antiarrhytmic medications
      • Amiodarone is now the preferred agent (ARC guideline 11.9, 2009)
      • 300mg amiodarone over 20-60 minutes, followed by an infusion of 900mg over 24 hrs
      • Class 1a agents like lignocaine are a reasonable alternative, particularly if the QT interval is prolonged.
    • Haemodynamically unstable:
      • Synchronised cardioversion
      • If this does not work, give 300mg amidoarone over 10-20min, and then attempt cardioversion again
      • Follow this with 900mg amiodarone over 24 hours.
  • Pulseless VT:
    • consider a praecordial thump
    • commence CPR
    • progress according to ILCOR ALS algorithm for shockable rhythms
• Prevention of recurrence:
  • correct electrolyte disturbance
  • rule out cardiac ischaemia as cause
  • cease arrhythmogenic medications
  • address mechanical causes of VT: for example, PA catheter or very low CVC tips

References

Pellegrini, Cara N., and Melvin M. Scheinman. "Clinical management of ventricular tachycardia." Current problems in cardiology 35.9 (2010): 453-504.

Hazinski, Mary Fran, et al. "Part 1: Executive Summary 2010 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations." Circulation 122.16 suppl 2 (2010): S250-S275.

College Answer

a)         The roles of the team leader include:

1)   Ensure  that  the  priorities  of  management  are  carried  out  effectively  and  efficiently.

Coordinate defibrillation, intubation cannulation and drug administration

2)   Help  establish  a  diagnosis  by  ECG  and  physical  examination  and  by  obtaining  all available history from hospital notes and bystanders.

3)   Check resuscitation status ( ?DNR) and prognosis

4)   Order investigations

5)   Reassess response to treatment

6)   Communicate with admitting consultant

7)   Ensure family is notified

8)   Organise post resuscitation care

b)         Priorities of cardiac arrest management may be best listed by drawing a sensible algorithm

(preferably AHA 2000 0r ILCOR 1999). The list should include

-     immediate basic life support

-     rapid rhythm diagnosis

-     defibrillation for VF, intubation/adrenaline for asystole or PEA

-     continued drug and defibrillation management

-     effective post –resuscitation care

Discussion

According to the ARC statement, the team leader is responsible for: 

• Directing and co-ordinating the resuscitation attempt 
• The safety of the resuscitation team at the cardiopulmonary arrest
• Ending the resuscitation attempt when indicated, often in consultation with other resuscitation team members and medical staff otherwise in charge of the patient
• Documentation (including audit forms) and for communication with the relatives and other healthcare professionals involved in the patient's management 
• Organising resuscitation team debriefing.

To this, one might add the following responsibilities:

• Assessing the rhythm and evaluating the need for defibrillation
• Ensuring the correct application of ALS and BLS
• Establishing a diagnosis for the cause of the arrest
• Ordering the appropriate investigations
• Ensuring minimal interruptions to CPR
• Allocating roles to the rescuers, and coordinating their efforts.
• Recruiting external resources (eg. cardiologists, ICU staff, cardiothoracic surgeons) into the resuascitation effort
• Communicating with family and the primary admitting consultant

References

ARC statement: Standards for Resuscitation: Clinical Practice and 
Education

Hunziker, Sabina, et al. "Teamwork and leadership in cardiopulmonary resuscitation." Journal of the American College of Cardiology 57.24 (2011): 2381-2388.

College Answer

Rapidly expanding area, answer needs covering of various areas.

Evidence to support use: comatose survivors after cardiac arrest had improved neurological survival (recent PRCT NEJM X 2); controversial/equivocal for severe head injuries (GCS 3-8), certainly demonstrated to decrease ICP; early evidence to support use in stroke and perhaps myocardial infarction; anecdotal evidence to support cooling to at least normothermia (eg. management of malignant hyperpyrexia); experimental for ARDS; use as adjuvant to minimise cerebral insult (prophylaxis) in the operating theatre during cardiac surgery (deep hypothermic circulatory arrest) and some neurosurgical procedures.

Technique: need to define temperature (eg. 32-33 degrees C), method to cool (blankets, surface cooling, intravenous device), and duration of therapy (eg. 12-24 hours or days).

Potential problems: immune suppression (increased infections), risks bleeding, vasoconstriction, shivering (necessitating neuromuscular paralysis and adverse effects of immobility).

Discussion

This question is identical to Question 20 from the second paper of 2006.

References

College Answer

The major determinants of survival after a cardiac arrest are cardiac (arrhythymias and myocardial function) and neurological. Accuracy of assessment of prognosis of both factors increases with time. No techniques have 100% positive predictive value, or more importantly 100% negative predictive value.

•    Cardiovascular techniques of most value are the response to therapy (including thrombolysis or angioplasty) and echocardiography.
•    Neurological survival is best predicted by neurologic examination (again increasing certainty with time). Early poor prognostic signs (eg at 24 hours post-arrest) are fixed,unreactive pupils and extensor or absent motor response to painful stimuli (if not paralysed or deeply sedated). Brain death criteria are rarely met. Further refinement of prognosis may be achieved with investigations such as Somato-Sensory Evoked Potentials or EEG. CT is notoriously unreliable. MRI will detect more abnormalities, as it is a more sensitive test (though studies relating appearance to outcome are lacking).

Discussion

This question closely resembles Question 4 from the second paper of 2013: "Describe the clinical signs and investigations available to predict poor neurological outcome in comatose survivors of cardiac arrest. Include in your answer the factors that may confound the interpretation of these signs and investigations."

References

College Answer

Obvious initial priorities are airway, breathing and circulation, but aware of the fact that there may be some limitations placed on the resuscitative efforts. If no formal documentation is immediately available, it is appropriate to aggressively resuscitate (as usual, without delay) until appropriate information is obtained.

Endotracheal intubation is almost certainly indicated (immediately if unable to protect airway, or after a short period of cardiovascular resuscitation). Rhythm assessment is required to rapidly exclude reversible rhythm disorder. Fluids should be administered (type and amount over time should be discussed), and a vasopressor (bolus ± infusion) may be appropriate when hypovolaemia has been excluded.

Major differential to be considered includes hypovolaemia and sepsis (abdominal, respiratory) but other causes must be considered (including pulmonary embolus, myocardial infarction, anaphylaxis, adrenal insufficiency etc.).

Early administration of broad spectrum antibiotics &/or corticosteroids should be considered.

Discussion

...Should this patient even come to ICU?

Oh well, you can work that out after you have violently resuscitated her, amiright?

Initial assessment, with attention to ABCs with simultaneous brief history and rapid focused examination

• 1) Ensure personal safety

  2) Perform a basic peri-arrest primary survey

• Immediate assessment to diagnose cardiac arrest
  • Are they awake?
  • If they appear unconscious, shake them and ask "Are you alright?"
  • If they are unresponsive, look listen and feel for respiratory effort.
  • If the patient is unconscious, unresponsive, and is not breathing, call for help and start CPR.
    Otherwise, move on with the structured approach to prevent cardiac arrest
• Airway:
  • Assess patency: best done by interrogating the patient. If he provides coherent answers to your questions, his ABCs are unlikely to be desperately compromised. If he does not, one should secure his airway - initially usig unsophisticated techniques (jaw thrush, chin lift), progressing through airway adjuncts to intubation as needed.
  • Look for presence of vomit or foreign body
  • Prepare to progress to intubation
• Breathing
  • Observe respiratory rate
  • maintain oxygenationintially with high flow oxygen via tight-fitting reservoir mask. A high flow nonrebreather mask not only delivers around 75% FiO₂, it also allows one to assess respiratory function by observing the expiratory fogging of the clear plastic, and one can hook up an end-tidal capnometer to it to detect expired CO₂.
  • progress to bag-mask ventilation if respiratory arrest occurs
  • Auscultate the chest, percuss it, palpate for surgical emphysema
  • Investigate with ABG and urgent CXR
  • Specific differentials to consider before moving on with the survey:
    • Massive PE (distended neck veins, cyanosis, tachycardia and hypotension)
    • Acute severe asthma (silent hyperexpanded chest, the hint of wheeze)
    • Tension pneumothorax (unequal air entry, deviated trachea, hyper-resonant chest)
    • Massive haemothorax or effusion (unequal air entry, deviated trachea, dull percussion note over the hemithorax)
    • Pulmonary oedema (pink frothy sputum, coarse gurling creps)
• Circulation
  • Ensure large-bore IV access
  • Measure the blood pressure non-invasively and attach ECG leads for monitoring
  • administer IV fluids as bolus
  • administer readily available vasopressors, eg. metaraminol in order to maintain cerebral perfusion
  • assess for sources of bleeding
  • ABG or FBC to assess Hb, and need for transfusion
  • rapid bedside TTE to assess cardiac chamber volume and contractility
  • Specific differentials to consider before moving on with the survey:
    • Extremes of hypovolemia (collapsed veins, empty chambers, slow capillary refill, dry mucosae, cool extremities, weak rapid pulse)
    • Haemorrhagic shock ( exactly as above but also deathly pallor)
    • Cardiac tamponade (distended neck veins, muffled heart sounds, electrical alternans on ECG)
    • Peri-arrest arrhythmia (eg. VT or SVT)
    • Severe sepsis (mottled skin, fever, hyperdynamic circulation with hypotension)
  • A fluid bolus would be an appropriate reaction in any case. A hand-operated pump giving set with a litre of crystalloid should be set up. Ideally, one should prepare for invasive arterial blood pressure monitoring.
• Disability/neurology
  • Assess for signs of intracranial catastrophe by performing a brief neurological examination, including pupils and muscle tone/reflexes
  • Test BSL: ensure normoglycaemia
  • Specific differentials to consider before moving on with the survey:
    • Intracranial catastrophe (pupils, focal signs)
    • Seizure (increased tone, exaggerated reflexes, gaze deviation, clonus)
    • Extreme hypoglycaemia
    • Hyperglycaemic coma
    • Extremes of electrolyte derangement (eg. a sodium of 90 or 190)
    • Hepatic encephalopathy
• Exposure/examination
  • Assess for sources of bleeding
  • Examine for features of anaphylaxis
  • Check temperature; ensure normothermia

References

College Answer

Timing and the information expected is required. Immediate investigations should include ECG monitoring (for rhythm and ST segment assessment), arterial blood gases (oxygenation, carbon dioxide and acid base status), full blood examination (Hb, WCC) and electrolytes (including renal function and lactate). Blood cultures should be taken as soon as possible. Less urgent (minutes) investigations include chest and abdominal radiographs, ECG, and consideration of further abdominal investigations (eg. CT scan).

More specific investigations may be indicated according to the clinical suspicion. Consider exclusion of pulmonary embolus (CT angiogram, transoesophageal echo), severe myocardial dysfunction (PA catheter, echocardiography), baseline cortisol (before administer corticosteroids).

Discussion

Immediate investigations

• ABG
• CXR
• FBC, EUC, CMP, LFT, group and screen, blood cultures (as well as any other relevant body fluid)
• ECG

Investigations in the short-medium term

• CTPA and CT abdomen (to look for major postoperative bleeding, as well as rule out PE)
• Formal TTE to assess cardiac function in detail
• random cortisol level

References

College Answer

Immediate management should be according to an appropriate ACLS protocol (including confirmation of  lack  of  central  pulse,  management  according  to  rhythm,  vasoconstrictor and external cardiac compression as appropriate, confirm placement of ETT [check position and ETCO2]; search for and correct reversible factors especially vasodilatation, profound hypoxaemia, excessive ventilation and hyperkalaemia [suxamethonium plus chronic muscle wasting).  Other management includes ongoing supportive care of ICU patient (eg. further communication and discussion with family, pressure care, DVT and stress ulcer prophylaxis, cultures and antibiotics if appropriate, etc.)

Discussion

This question consolidates within itself the answers to Question 6 from the first paper of 2006,Question 8 from the second paper of 2004 and Question 14 from the second paper of 2003, which ask about the management of PEA and VF.

Also, this scenario closely resembles Question 18.1 from the first paper of 2010, which asks the candidate for causes of cardiac arrest in a recently intubated tetraplegic patient.

The question states that the patient becomes pulseless, meaning that cardiac output is lost, but it mentions nothing about the underlying rhythm. Thus, the answer should focus on the systematic application of BLS and ALS, as well as the generation of differential diagnoses for the causes of such an arrest.

Thus:

Firstly, one assumes that cardiac arrest has been confirmed as "the cessation of cardiac mechanical activity as confirmed by the absence of signs of circulation".

Thus, first one should commence CPR, with the registrar asynchonously ventilating the patient via the newly inserted ETT.

Then, one should get more help by pressing the alarm button.

When help arrives, one should immediately call for defibrillator pads to be applied. As soon as possible, the underlying rhythm should be assessed, with the defibrillator charging while CPR is in progress.

While waiting for this rhythm check, one should systematically evaluate the situation:

A) - endotracheal position of the ETT should be confirmed by end-tidal capnography

B) - bag ventilation should continue at a CPR-asynchronous rate of 8-10 breaths per minute with 100% FiO₂, using conservative tidal volumes.

C) - CPR should continue at a rate of 100 compressions per minute, ideally with a rotating queu of staff ready to take over from fatigued rescuers. IV access should be expanded upon (I am assuming a cannula at least was available, if thio/fentanyl/sux were used to induce the patient). Through this line, a fluid bolus should be administered via a hand-pumped giving set.The patient must have been monitored while intubation was taking place, and the monitor should offer a log of periarrest rhythm changes one could peruse to determine the pre-arrest rhythm.

D) A BSL should be collected to rule out hypoglycaemia.

E) An ABG should be collected, to rule out hyperkalemia due to suxamethonium, or hypokalemia due to other causes.

The drug chart and obs chart should be quickly reviewed, and a quick examination should be performed, to excluded hypothermia and anaphylaxis as causes of the arrest.

Once the underlying rhythm is established, one can determine whether to defibrillate (for a shockable rhythm) or to give adrenaline (for a non-shockable rhythm, which in this scenario is more likely).

The 4 Hs and 4 Ts should be considered:

• Hypoxia (thus, oesophageal intubation or delayed oxygenation)
• Hypovolemia (thus, cardiovascular collapse due to vasodilation by an induction agent like propofol, or due to the autonomic dysfunction of spinal cord injury)
• Hyper/hypokalemia (thus, the effects of suxamethonium)
• Hyper/hypothermia (probably irrelevant in this case)
• Tension pneumothorax (due to overvigorous bag-mask ventilation, or due to tracheobronchial disruption by violent use of the bougie)
• Tamponade (unlikely in this setting)
• Toxins (eg. anaphylactic reaction to induction agents)
• Thrombus (eg. PE or MI)

References

ARC Guideline 11.2: Protocols for Adult Advanced Life Support

College Answer

Ventricular fibrillation requires an initiating stimulus in a susceptible myocardium. VF can be induced in a previously normal myocardium as a result of electrical stimulation (electrocution, lightning) or by trauma (commotio cordis).  The myocardium can be made more susceptible by the presence of hypoxaemia (e.g. respiratory arrest), electrolyte disturbances (low K and Mg), altered autonomic and vagal inputs, and mechanical stimuli (e.g. wire or catheter in RV).  The myocardium may be abnormally susceptible due to congenital (e.g. conduction abnormalities) or acquired disorders (including ischaemia, hypertrophy, myocarditis, pro-arrhythmic drugs, etc).

Principle of management include early defibrillation, but in concert with correction of any correctible cause (e.g. wire, electrolytes, hypoxaemia etc), support of the cardio-respiratory state with adequate basic life support, and restoration of an appropriate metabolic milieu to support a normal rhythm.  This latter approach may require performance of cardiopulmonary resuscitation, and administration of specific anti-arrhythmic drugs.   Defibrillation is performed with either monophasic (200/200/360J) or biphasic (150/150/150J) defibrillator waveforms in a series of up to three sequential shocks. Subsequent monophasic shocks should be administered at maximal dose.

Discussion

This question is identical to Question 6 from the first paper of 2006.

References

College Answer

Electro-mechanical dissociation refers to a clinical state in which the patient has an ECG compatible with a normal output but has no palpable pulse. Various ways have been proposed to assist practitioners to remember the sort of conditions that could be responsible for EMD (eg. 10 step zigzag sequence [Kloeck 1995], 4Hs and 4Ts [ILCOR 2000]). Specific conditions that should be considered (history, examination, and investigation, with specific management) include:
·           Hypoxia (ensure 100% oxygen),
·           Hypovolaemia (administer fluids, stop haemorrage, clamp bleeding vessels),
·           Hypo/hyperthermia (ensure adequately warmed if severely hypothermic, or cooled
[eg. with dantrolene for malignant hyperpyrexia])
·           Hypo/hyper-kalemia and other metabolic disorders (exclude abnormalities in K [low:
give K; high: give Ca, HCO3, consider insulin/glucose], Mg [low: give Mg;
high:give Ca], Ca [low: give Ca]; severe acidosis: consider HCO3)
·           Tamponade (drain pericardial collection, release ventilation induced intra-thoracic pressure)
·           Tension Pneumothorax (needle thoracostomy then chest tube),
·           Toxins/Poisons/Drugs (consider all recently administered drugs for allergy and/or anaphylaxis [adrenaline, fluids, oxygen, remove hapten], excessive vasodilatation or cardiac depression [consider antidotes: isoprenaline {betablockers}, Ca {Ca channel blockers}, HCO3 for Na channel blockers {especially tricyclic anti-depressants}) ·           Thrombosis Pulmonary/Coronary (consider thrombolytics, urgent surgery)

Discussion

PEA is a situation where one is presented with organised electrical activity (i.e. a potetially perfusing rhythm) in the absence of cardiac output. The old term (electro-mechanical dissociation) is no longer in use.

A good systematic framework for this is the "Four Hs and four Ts" mnemonic:

• Hypoxia
• Hypovolemia (or distributive shock)
• Hyper/hypokalemia
• Hyper/hypothermia
• Tension pneumothorax
• Tamponade
• Toxins
• Thrombus

Thus, one may start by saying that the management of such a situation, whatever the cause, should begin with cardiopulmonary resuscitation.

Specific management then depends on the cause.

Thus:

• Hypoxia in an arrest is usually well-managed with adequate bag-mask ventilation and high concentration of supplied oxygen
• Hypovolemia and distributive shock can be ameliorated by the administration of fluids
• Potassium disturbances will be discovered whent he first ABG returns from the blood gas machine, and these can be managed routinely
• Tension pneumothorax can be suspected from history, and confirmed by examination. Management consists of decompression.
• Cardiac tamponade is also suggested by history and examination findings. Management consist of emergency pericardicentesis
• Toxins are suggested by history and characteristic examination findings, eg. pinpoint pupils, the rashj of anaphylaxis, etc. Management consists of administering an antidote, if it is available.
• Thrombosis - in the context of arrest-inducing massive PE - can be suspected from history; confirmation relies on the presence of an ultrasound machine and a skilled operator. Management consists of intra-arrest thrombolysis. For coronary thrombosis, this may not be a viable option.

Everyone has heard of the 4Hs and 4 Ts, but what the hell is this 10-step zigzag sequence? Apparently, it was described by Walter J.G. Kloeck in 1995. The article is not available to me, and the abstract is uninformative, but this entry in JournalGems confirms that this 10-step mnemonic is in fact the same 4 Hs and 4 Ts with an extra H (hypoglycaemia) and an extra T (separating PE and MI). One could also argue that we could extend the mnemonic further, and end up with 20 Hs and 20Ts, but one ought to remember that these mnemonics are used by critical care staff who have brief two minute breaks between rhythm checks to diagnose the cause of the arrest while running the show. Any complex memory device used to recall causes of arrest is only adding to their already massive cognitive load.

References

The index of ARC guidelines is available from the ARC website.

Kloeck, Walter GJ. "A practical approach to the aetiology of pulseless electrical activity. A simple 10-step training mnemonic." Resuscitation 30.2 (1995): 157-159.

College Answer

Principles include:

Early identification

Discuss with transplant coordinator

Establish  family rapport early

Diagnose brain death correctly

Establish presence of condition causing brain death. Exclude confounders (sedation, paralysis, endocrine, metabolic, temperature) - use vascular imaging if necessary. Satisfy legal criteria for organ donors relevant to the jurisdiction

Non-coercive sensitive family discussion re opportunity for donation

High availability. Answer questions

Initiate  tissue typing, viral screen, further organ function tests

Maintain extra-cerebral physiological stability

Ventilatory - oxygenation, normocapnia, lung protective strategies. Circulatory - monitoring, filling,

noradrenaline, vasopressin. Normothermia. Diagnose and treat diabetes insipidus

(DDAVP/vasopressin, free water). Steroid and T3 replacement

Facilitate family time at bedside

Ensure aftercare of donor family

Transplant co-ordinator. Limited anonymous information available. Further family meeting offered

Few candidates considered that the donor could be either living related, or a non-beating heart donor.

Discussion

This question closely resembles Question 1 from the second paper of 2012.

Non-clinical issues: (presumably, these have been dealt with now that the patient is "awaiting surgery for organ donation"

• Early involvement of the transplant coordinator
• Non-coercive sensitive family discussion re opportunity for donation
• Tissue typing, viral screen, further organ function tests
• Facilitate family time at bedside
• Ensure aftercare of donor family

1. The circuit should be humidified.
2. Normoxia and normocapnea must be maintained.
   There will be periodic requests for ABGs on 100% FiO₂ from the donor coordinator, but afterwards the FiO₂  must be minimised to prevent oxidative stress damage to the lungs.
3. Haemodynamic instability is to be expected:
   - The initial autonomic storm should be managed with nitroprusside and esmolol
   - The subsequent collapse should be treated with noradrenaline and/or vasopressin
   - Bradycardia will be resistant to atropine (no vagus to block); catecholamines or pacing will be required
   -Though they do not make a direct statement to this effect, ANZICS tacitly support CPR in the brain-dead organ donor; "cardiopulmonary resuscitation may result in recovery of cardiac function and successful transplantation".
4. Normoglycaemia must be maintained.
5. Normothermia must be maintained by warming externally, and by using warmed fluids.
   Electrolytes need to be maintained within normal laboratory ranges;
   particular attention needs to be paid to the sodium.
   DDAVP may be required as a hormone replacement.
   Other "endocrine support" (T3, hydrocortisone) should be considered in the following circumstances:
   - haemodynamic instability
   - an ejection fraction of less than 45%
   - heart donation is being considered
6. Fluid resuscitation should be conservative if you plant to donate lungs,  aggressive if you plan to donate kidneys, and an intelligent compromise if both organs are being considered.
7. Nutrition must continue.
   Good nutrition (or rather, the absence of malnutrition) has been associated with improved raft function (Singer et al, 2005)
8. Coagulopathy must be observed and corrected; if worsening coagulopathy or DIC develop, organ retrieval should be expedited.

References

Summarized from the ANZIC statement on Brain Death and Organ Donation, Version 3.2

Dujardin, Karl S., et al. "Myocardial dysfunction associated with brain death: clinical, echocardiographic, and pathologic features." The Journal of heart and lung transplantation 20.3 (2001): 350-357.

Totsuka, Eishi, et al. "Influence of high donor serum sodium levels on early postoperative graft function in human liver transplantation: effect of correction of donor hypernatremia." Liver Transplantation and Surgery 5.5 (1999): 421-428.

Novitzky, D., D. K. C. Cooper, and B. Reichart. "Hemodynamic and metabolic responses to hormonal therapy in brain-dead potential organ donors." Transplantation 43.6 (1987): 852-854.

Phongsamran, Paula. "Critical care pharmacy in donor management." Progress in Transplantation 14.2 (2004): 105-113.

RANDELL, TARJA T., and KRISTER AV HöCKERSTEDT. "TRIIODOTHYRONINE TREATMENT IN BRAIN-DEAD MULTIORGAN DONORS-A CONTROLLED STUDY." Transplantation 54.4 (1992): 736-737.

Goarin, Jean-Pierre, et al. "The effects of triiodothyronine on hemodynamic status and cardiac function in potential heart donors." Anesthesia & Analgesia 83.1 (1996): 41-47.

Follette, David M., Steven M. Rudich, and Wayne D. Babcock. "Improved oxygenation and increased lung donor recovery with high-dose steroid administration after brain death." The Journal of heart and lung transplantation: the official publication of the International Society for Heart Transplantation 17.4 (1998): 423-429.

Lisman, T., et al. "Activation of hemostasis in brain dead organ donors: an observational study." Journal of Thrombosis and Haemostasis 9.10 (2011): 1959-1965.

Lim, H. B., and M. Smith. "Systemic complications after head injury: a clinical review." Anaesthesia 62.5 (2007): 474-482.

Dalle Ave, Anne L., Dale Gardiner, and David M. Shaw. "Cardio‐pulmonary resuscitation of brain‐dead organ donors: a literature review and suggestions for practice." Transplant International (2015).

Singer, Pierre, Haim Shapiro, and Jonathan Cohen. "Brain death and organ damage: the modulating effects of nutrition." Transplantation 80.10 (2005): 1363-1368.

College Answer

Several antiarrhythmic drugs are recommended in the ARC guidelines for use in VF/pulseless VT cardiac arrests and for bradycardia/asystole. However no drugs have been shown to improve long- term survival after cardiac arrests. Basic and advanced life support, early access to defibrillation and treatment of reversible causes take priority.

Guideline recommended drugs that should be considered include:

Lignocaine 1-1.5mg/kg, Amiodarone 300mg, Magnesium 5 mmol and atropine (1-3 mg).

Lignocaine is a class 1 antiarrhythmic, sodium channel blocker and has been traditionally used in VF/ pulseless VT cardiac arrest and while it is listed as first line in the ARC guidelines, the evidence for its use is limited. It should be given as a bolus for refractive VF/VT and occasionally can be used when the patient has recurrent VF/VT to prevent recurrence. Prophylactic use in AMI not complicated by arrhythmia is not recommended as there is some evidence that it may worsen overall prognosis.

Amiodarone is a complex antiarrhythmic drug with effects on sodium, potassium and calcium channels and alpha and beta blocking effects. It is an effective antiarrhythmic agent for both supraventricular and ventricular arrhythmias and it also causes less cardiac depression than other antiarrhythmics. It thus has some advantage over lignocaine. It is toxic to the tissues if it extravasates and is recommended for central venous administration but administration into an antecubital vein in the cardiac arrest situation is acceptable. Bolus injection of 300mg can be

followed by 150 mg if no effect and can be followed by infusion. Amiodarone has been shown to be better than placebo and lignocaine in terms of survival to hospital admission after out of hospital cardiac arrest due to refractory VF.

Magnesium is recommended by the ARC particularly for: Torsades de points, digoxin toxicity, and demonstrated hypokalemia/hypomagnesemia. It can be given as a 5mmol bolus which can be repeated and followed by infusion. There are no clinical studies using magnesium in this setting but it has been demonstrated to be a useful antiarrhythmic in postoperative cardiac surgical patients (Level 1 evidence).

Atropine is recommended by the ARC for use in severe bradycardia and in asystole. There are no controlled or randomised studies supporting its use. It can be given in 1 mg boluses up to 3 mg.

Discussion

This question, written in 2005, pre-dates the changes in ARC guidelines which have done away with lignocaine and atropine, leaving behind only amiodarone. This drug now occupies a shaky position after the third cycle of CPR for a shockable rhythm; the objective of using it is really to convert a defibrillation-refractory VF into one which is defibrillation-sensitive.

The evidence for its use is supported by two trials (Dorian et al 2002, and Somberg et al 2002) which found some benefit of amiodarone over lignocaine in the context of shock refractory or recurrent VT and VF. There was no benefit in survival to hospital discharge, but there was some benefit in survival to hospital admission. This better than the evidence for any other anitarrhytmic drug, and thus amiodarone remains in the guidelines ...for now.

All of this information is available in the ARC Guideline 11.5: Medications in Adult Cardiac Arrest. In brief summary, other drugs which are covered by this guidelines statement are as follows:

• Adrenaline: Favoured because retrospective studies have found an improvement in the rates of ROSC with adrenaline; however there has never been any confirmed improvement in survival associated with it.
• Calcium: Not recommended routinely; no benefit in terms of survival (6.8mmol calcium chloride as a bolus)
• Lignocaine: Not as good as amiodarone, and thus recommended only for those situations when amiodarone cannot be used (1mg/kg bolus)
• Magnesium: Recommended for torsades des pointes, but not recommended for any other situation, as there is no survival benefit. (5mmol bolus)
• Potassium: Recommended for hypokalemic arrests only (5mmol bolus)
• Sodium bicarbonate: Not recommended, as it is associated with poor short-term and long-term outcomes.
• Vasopressin: Not recommended as an alternative to adrenaline, as there is insufficient data to support its use.
• Aminophylline: There is no evidence of harm, but there is insufficient evidence to recommend its routine use.
• Thrombolytics: Recommended only in confirmed or strongly suspected massive PE as a cause of cardiac arrest, in which case one is committed to performing CPR for 60-90 minutes.

Rationale for the use of antiarrhythmic drugs in cardiac arrest

• Cardiac arrest is often the consequence of a non-perfusing arrhythmia. Ergo, an antiarrhythmic drug is the correct treatment.
• The energy required to defibrillate is decreased by acute administration of amiodarone (in dogs - Fain et al, 1987)
• The use of anti-arrhythmics may not be guided by any scientific principles, but it appears so deeply ingrained that it has become accepted as standard practice. Therefore to abjure the use of antiarrhythmics would be viewed as a substantial departure from standard practice. What would the coroner say?

Arguments against the use of antiarrhythmic drugs in cardiac arrest

• Pro-arrhythmic properties of antiarrhythmics must be taken into account; even amiodarone can produce QTc prolongation and torsade.
• The addition of extra drugs or steps to the algorithm complicates it, and makes it more difficult to teach (and to follow).
• The improvement of survival to hospital admission may not translate into any improvement in survival (in fact, none of the studies have found any improvement in survival)
• All the trials involving athiarrhythmics have compared one drug to another; there have been no placebo-controlled trials. We do not know what would happen without these drugs. Would survival rates drop sharply?

References

ARC Guideline 11.5: Medications in Adult Cardiac Arrest

Levine, Joseph H., et al. "Intravenous amiodarone for recurrent sustained hypotensive ventricular tachyarrhythmias." Journal of the American College of Cardiology 27.1 (1996): 67-75.

Dorian, Paul, et al. "Amiodarone as compared with lidocaine for shock-resistant ventricular fibrillation." New England Journal of Medicine 346.12 (2002): 884-890.

Skrifvars, M. B., et al. "The use of undiluted amiodarone in the management of out‐of‐hospital cardiac arrest." Acta anaesthesiologica scandinavica 48.5 (2004): 582-587.

Somberg, John C., et al. "Intravenous lidocaine versus intravenous amiodarone (in a new aqueous formulation) for incessant ventricular tachycardia." The American journal of cardiology 90.8 (2002): 853-859.

Kudenchuk, Peter J., et al. "Amiodarone for resuscitation after out-of-hospital cardiac arrest due to ventricular fibrillation." New England Journal of Medicine 341.12 (1999): 871-878.

Ong, Marcus Eng Hock, Tommaso Pellis, and Mark S. Link. "The use of antiarrhythmic drugs for adult cardiac arrest: a systematic review." Resuscitation 82.6 (2011): 665-670.

Huang, Yu, et al. "Antiarrhythmia drugs for cardiac arrest: a systemic review and meta-analysis." Crit Care 17.4 (2013): R173.

Fain, Eric S., John T. Lee, and Roger A. Winkle. "Effects of acute intravenous and chronic oral amiodarone on defibrillation energy requirements." American heart journal 114.1 (1987): 8-17.

College Answer

Causes: Ventricular fibrillation requires an initiating stimulus in a susceptible myocardium. VF can be induced in a previously normal myocardium as a result of electrical stimulation (electrocution, lightning) or by trauma (Commotio cordis). The myocardium can be made more susceptible by the presence of hypoxaemia (e.g. respiratory arrest), electrolyte disturbances (low K and Mg), altered autonomic and vagal inputs, and mechanical stimuli (e.g. wire or catheter in RV). The myocardium may be abnormally susceptible due to congenital (e.g. conduction abnormalities) or acquired disorders (including ischaemia, hypertrophy, myocarditis, pro-arrhythmic drugs, etc).

Principles of management: include early defibrillation, but in concert with correction of any correctible cause (e.g. wire, electrolytes, hypoxaemia etc), support of the cardio-respiratory state with adequate basic life support, and restoration of an appropriate metabolic milieu to support a normal rhythm. This latter approach may require performance of cardiopulmonary resuscitation, and administration of vasoconstrictors and specific anti-arrhythmic drugs, especially in the setting of prolonged VF. According to the ALS guidelines in place when the question was set, defibrillation is performed with an appropriate energy level for either monophasic (eg.

200/200/360J) or biphasic (eg. 150/150/150J) defibrillator waveforms in a series of up to three sequential shocks. Subsequent monophasic shocks should be administered at maximal dose.

The longer-term management, including the use of implantable defibrillators should be considered according to published guidelines.

Candidates were not penalised if they did not discuss the new guidelines (including higher energy levels for monophasic, and a single shock approach).

Discussion

This question is grounded in the ARC guidelines.

Causes of VF:

• Cardiac ischaemia
• Electrical myocardial injury
• Traumatic myocardial injury
• Irritating mechanical stimulus (eg. CVC guidewires, PA catheter)
• Myocarditis

Predisposition to VF:

• Low potassium
• Low magnesium
• Hypoxia
• Arrhythmogenic drugs eg. theophylline, sympathomimetics
• Congential and idopathic predisposition
• Prior cardiac surgery
• Cardiac chamber hypertrophy
• Severe hypothermia

Principles of management of VF:

• Cardiopulmonary resuscitation with an emphasis on uninterrupted chest compressions
• Early defibrillation - single shock
• When it is witnessed in a monitored environment and the defibrillator is readily available, three "stacked" shocks may be used.
• Correction of immediately responsible cause (eg. withdrawal of PA catheter, or immediate angiography for myocardial infarction)
• Correction of predisposing causes (eg. hypoxia, hypokalemia)
• Consideration for an automated implantable defibrilator (AICD).

References

ARC Guideline 11.2: Protocols for Adult Advanced Life Support

Chen, Qiuyun, et al. "Genetic basis and molecular mechanism for idiopathic ventricular fibrillation." Nature 392.6673 (1998): 293-296.

Wiggers, Carl J. "The mechanism and nature of ventricular fibrillation." American Heart Journal 20.4 (1940): 399-412.

Beck, Claude S., Walter H. Pritchard, and Harold S. Feil. "Ventricular fibrillation of long duration abolished by electric shock." Journal of the American Medical Association 135.15 (1947): 985-986.

College Answer

a) Clinical tests cannot be used to confirm brain death in a number of situations, including:
•    No clear cause of coma
•    Possible drug or metabolic effect on coma
•    Cranial nerves cannot be adequately tested
•    Cervical vertebra or cord injury present
•    Cardiorespiratory instability precludes apnoea testing
•    In term infants and up to 1 year of age, on the assumption that the younger brain has a greater potential for recovery, a confirmatory test is usually conducted

b) The two adjunctive tests recognized in the ANZICS guidelines are 3 or 4 vessel angiogram, and nuclear medicine study capable of imaging posterior fossa blood flow, e.g. use of nuclear study with SPECT.

c) Additional tests which may play a role (but have various limitations) are electrophysiological tests (ie. evoked potentials, EEG), transcranial doppler ultrasound, and simpler nuclear medical perfusion scans. The use of Xe-CT and specific MR sequences have been described, but seem to hold no particular advantages. In the future, CT angiogram, or CT perfusion may play a role. Neither has obvious current advantages, but if sufficiently reliable, may be more widely available. Seventeen out of twenty-six candidates passed this question.

Discussion

This question closely resembles the following questions:

a) "Outline the situations  in which clinical tests cannot be used to confirm brain death." - This is really a question about the preconditions for brain death testing. Thus, clinical brain death testing canot be carried out if there is no obvious cause of the coma, when the patient is desperately hypoxic and hemodynamically unstable, and when you have no intact eyes or ears to test, etc etc.

Pre-conditions for brain death testing are discussed in several other fellowship questions:

• Question 17 from the second paper of 2012
• Question 12.1 from the second paper of 2010
• Question 28 from the first paper of 2009.

In order to simplify revision, the list of reasons for not being able to perform clinical brain death testing is replicated here:

• There is no obvious intracranial explanation for the coma
• The patient is not normothermic
• The patient is hemodynamically unstable
• The effect of sedating drugs cannot be excluded
• The effect of metabolic abnormalities cannot be excluded (eg. uremia, hypoglycaemia)
• Neuromuscular function is not intact
• Brainstem reflexes cannot be tested (eg. eyes and ears are not intact)
• Apnoea testing cannot be performed (eg. severe hypoxia or high spinal cord injury)

b) " List 2 adjunctive tests used in Australia and New Zealand  for the confirmation of brain death when clinical tests are unable to be performed." - This is really a question about imaging modalities to confirm brain death. Four-vessel DSA and Tc-99m HMPAO are the better two, followed by CT angiography.

• Question 12.2 from the second paper of 2010 discusses imaging modalities to assess the intracranial blood flow.

Additonal tests to confirm brain death - which are not gold standard material, but which are mentioned by the ANZICS Statement on Death and Organ Donation - include the following:

• EEG (typical finding in brain death is an isoelectric EEG)
• SSEP (somatosensory evoked potentials)
• MRI
• CT brain
• Transcranial doppler

As diagnostic tools for brain death these leave much to be desired (owing to poor sensitivity or specificity), but as predictors of poor neurological outcome they have merit. In this context, these diagnostic modalities are discussed at great length in Question 4 from the second paper of 2013, "Describe the clinical signs and investigations available to predict poor neurological outcome in comatose survivors of cardiac arrest".

References

ANZICS Death and Organ Donation Committee, THE ANZICS STATEMENT ON DEATH AND ORGAN DONATION Edition 3.2 2013

College Answer

History suggestive of anaphylaxis, although diagnosis not certain. Other differentials for bronchospasm such as asthma / foreign body may be considered, however will not cause rash and hypotension. The focus should be on anaphylaxis.

-    Immediate management;
a)  Given that it is 30 min after relaxant, the patient should be intubated. Maintain endotracheal intubation
b)  100% Oxygen
c)  IV adrenaline: bolus and an infusion may be required. Mention of adrenaline is vital.

d)  Stop all current anaesthetic agents. Maintain with volatile agents (eg. sevoflurane) as
they have bronchodilator properties. Do not attempt to extubate until bronchospasm is under control.
e)  Treat hypotension with fluids, colloids preferable although no hard data against crystalloids
f)   If colloids, use albumin rather than synthetic ones to minimize further risk

g)  cease/abandon surgical procedure as soon as practicable’ -
h)  Arrange transfer to ICU
i)    Bronchodilators

j)   Steroids

k)  Anti-histamines
l)    Extubation after resolution of signs of anaphylaxis

Discussion

Management of anaphylaxis is a standard pathway, outlined in the ARC ALS2 manual (2011).

Thus:

Specific management:

• 0.5mg adrenaline, IM.
• 200mg hydroxortisone, IV
• 25mg phenergan, IV

A) - don't extubate!

B) - ventilate with reduced respiratory rate to allow CO2 clearance in the presence of brnchospasm. Administer salbutamol.

C) - Administer a fluid bolus. Adrenaline infusion may be required

D) - maintain sedation, ideally with anaesthetic gases

E) - observe for hypokalemia

F) - Avoid excess fluid resuscitation (capillaries are leaky)

References

ARC: Advanced Life Support Manual, Australian Edition (6th ed) January 2011

College Answer

Proven role:

1)  cardiac arrest – out of hospital VF arrest improved neurological outcome and survival

32-34C

2)  Control of intracranial hypertension – Improves ICP, but no reduction in mortality

Areas under investigation

1)  Stroke patients

2)  Perinatal asphyxia

Practical issues:

a)  difficulty in achieving hypothermia rapidly

b)  shivering and the need for relaxants which can delay neurological assessment c)  Not proven for non-vf arrests

d)  Not proven for in-hospital arrests

e)  Hypothermia can cause diuresis with attendant electrolyte disorders

f)       Risk of arrhythmias

g)  Risk of infection

Discussion

In general, therapeutic hypothermia in cardiac arrest and the physiology of hypothermia overall are discussed elsewhere. This question also asks about the extended indications for therapeutic hypothermia, which are generally not very well known (being exotic and enjoying only very patchy support from the ICU senior medical community).

In late 2015, this question would be interpreted very differently, and would likely attract a slightly different answer from the candidates. A good example might resemble the college answer to Question 9 from the first paper of 2015. The discussion section for that SAQ is reproduced below, as the two questions are virtually identical, and a 2006-specific answer would be of no interest to the modern candidates.

Rationale for therapeutic hypothermia:

• Therapeutic hypothermia has been advanced a a means of improving survival and good neurological outcome following cardiac arrest.
• It has also been offered as a means of controlling intracranial hypertension which is refractory to other modalities.
• Therapeutic hypothermia modulates the activity of body proteins and electrolytes.
• This modulation is thought to have some beneficial effects in scenarios where inflammatory damage is anticipated.
• This also involves the down-modulation of the overall metabolic rate, which decreases the metabolic demands of the organism in situations where supply of metabolic substrate may be compromised.
• Decrease in oxygen consumption matches decreased demand with decreased supply in "penumbra" areas, at the watersheds, where hypoxic injury has caused oedema.\

Advantages of therapeutic hypothermia

• Decreased granulocyte migration into tissue
• Decreased cerebral oedema
• Intrinsic anticonvulsant effects of hypothermia

Well-accepted indications:

• Mild therapeutic hypothermia for survivors of cardiac arrest
• Therapeutic hypothermia for traumatic brain injury

Evidence for use in cardiac arrest:

• Pseudorandomised unblinded trial in 1996 - promising results
• Bernard et al  demonstrated a survival benefit in out of hospital VF arrest survvors
•  A recent Cochrane review supports the use of therapeutic hypothermia, finding a 1.35 risk reduction for mortality.
• The recent TTM trial  has demonstrated non-inferiority of a more conservative hypothermia (36°C) with standard temperature goals, in terms of mortality.

Evidence for use in traumatic brain injury

• EUROTHERM 3235 trial (2015): 387 patients; hypothermia was used as a second-line therapy to reduce ICP.
• No survival benefit was observed.
• Recruitment was suspended early owing to safety concerns.
• ICP control was in fact better in the hypothermia group (they required rescue therapies less frequently)
• The meta-analysis mentioned by the college is possibly  this 2013 review by Georgiou et al; except there was no benefit in mortality when only high quality trial were included.

Extended indications:

Therapeutic hypothermia in cooling of a hyperthermic patient

• Hyperthermia is associated with substantial harm, particularly if the temperature increases beyod 41°C
• Causes of such hyperthermia may be numerous, including sepsis, malignant hyperthermia, anticholinergic drug poisoning, heat stroke, and so on and so forth.
• In brief, these causes all have specific management strategies which may take time to work.
• In the interim, the temperature must be managed, so that organ damage does not occur
• Induction of hypothermia (or maintenance of controlled normothermia) by cooling the patient can be viewed as one of the indications.

Therapeutic hypothermia for subarachnoid haemorrhage

• Theoretically, TH may be protective in SAH in the same way that it is supposed to be protective in traumatic brain injury. Areas affected by ischaemia in the context of vasospasm may benefit from having a lower metabolic rate.
• TH certainly  seems to decrease the flow velocity in the MCA of subarachnoid haemorrhage patients (Seule et al, 2014), suggesting that the metabolic rate is indeed affected enough to influence cerebral blood flow.
• Animal studies have also demonstrated that hypothermia reverses vasospasm (in rats)
• In patients with "poor-grade" SAH, good functional outcome was achieved in 48% with the combination of barbiturate coma and hypothermia to 33-34°C (Gasser et al, 2003)
• A more recent case series (Seule et al, 2010) found good outcomes in 57% of  severe SAH patients who developed vasospasm.
• In contrast, Karnatovskaia et al (2014) found no difference in neurological outcome within their case series.
• No recommendation in favour of this use of TH can be made with a straight face.

Therapeutic hypothermia for super-refractory status epilepticus

• Hypothermia is known to have antiepileptic effects.
• Case series (eg. Corry et al, 2008) have demonstrated its feasibility in humans (target temperature: 31–35°C)
• Neurocritical care society guidelines for status epilepticus (Brophy et al, 2012) identified only 4 articles in the literature, and were unable to make very strong recommendations.
• The HYBERNATUS trial mentioned in the college answer is apparently ongoing, but no longer recruiting participants.

Therapeutic hypothermia for severe sepsis

• Anti-inflammatory effects of hypothermia were studied in an animal model of severe sepsis (Kwang et al, 2012).
• The hypothermic rats (30–32 °C) did better in terms of acute lung and liver injury.
• Human applications of this are limited by concern that ...firstly, a fever is an antibacterial physiological response, and secondly, that the haemodynamic instability of septic shock will be exacerbated by hypothermia.

Therapeutic hypothermia for meningitis

• Evidence of potential harm mentioned by the college in their answer was found by a 2013 RCT (Mourvillier et al). The investigators found a higher mortality in the hypothermia group.

Therapeutic hypothermia for neonatal asphyxia

• Following on from the success of TH in adult cardiac arrest, this modality has been applied to neonatal hypoxic-ischaemic encephalpathy.
• Shankaran et al (2005) performed an RCT; the group of neonates who were cooled 33.5°C for 72 hours; the rate of cerebral palsy was reduced from 19% to 15%, and mortality improved from 37% to 24%. In the long term, there was no increase in disability among hypothermia-exposed survivors when compared to surviving controls (Shankaran et al, 2012)
• TOBY trial (2014) confirmed that both survival and neurological outcome is improved

Therapeutic hypothermia for stroke

• The college answer points out that fever is associated with two-fold risk of death after haemorrhagic or ischaemic stroke. Pharmacologic methods of fever control have not shown improved outcome in stroke.
• In animal models of stroke, , mild or moderate hypothermia has been shown to decrease infarct size and lead to functional improvement when cooling was initiated within a few hours of ischemia onset (Clark et al, 2008). But... These were rats, and they were cooled to 24°C

Therapeutic hypothermia for acute hepatic encephalopathy

• This use of TH is an extension of the observation that TH reduces cerebral oedema in patients with traumatic brain injury.
• Some authors (Stravitz et al, 2008) have suggested that TH may be an effective bridge to liver transplant.
• Human case series support this assertion (Jalan et al, 1999); during their treatment there was no significant relapse of increased intracranial pressure.
• There are no RCTs, but a large-scale retrospective cohort (Karvellas et al, 2014) did not find any survival benefit.

Therapeutic hypothermia in ARDS :

• Recent studies (Zhicheng et al, 2012) have confirmed that mild hypothermia improves gas exchange, lung compliance, duration of ventilation and the levels of IL-6 in local lung tissue.
• Of particular interest is the use of hypothermia to reduce the whole-body oxygen demand in situations where even veno-venous ECMO is powerless to oxygenate the patient (Hayek et al, 2015)

Intraoperative therapeutic hypothermia

• Cardiothoracic surgery, routinely in use (including DHCA).
• Neurosurgery for aneurysm clipping: IHAST trial, 2005; no benefit ("good-grade" SAH patients)
• Vascular surgery, to protect the spinal cord during prolonged aortic cross-clamp

Suspended animation for delayed resuscitation

• In essence, this is a practice of stopping the circulation with deep hypothrmia, so as to buy time to the definitive management of the cause of the cardiac arrest.
• Animal studies have demonstrated success with up to 90 minutes of no-flow (Safar et al, 2002)
• Wu et al (2006) subjected dogs to rapid haemorrhage, and then used a 2°C saline aortic flush to achieve a brain temperature of 10°C. The dogs remained on ice for 2 hours, and were then revived on cardiopulmonary bypass.  Intact neurological outcome was achieved in 4 out of 6 dogs.

References

Polderman, Kees H. "Application of therapeutic hypothermia in the ICU: opportunities and pitfalls of a promising treatment modality. Part 1: Indications and evidence." Intensive care medicine 30.4 (2004): 556-575.

Seule, M., et al. "Therapeutic hypothermia reduces middle cerebral artery flow velocity in patients with severe aneurysmal subarachnoid hemorrhage." Neurocritical care 20.2 (2014): 255-262.

Gasser, Stefan, et al. "Long‐Term Hypothermia in Patients with Severe Brain Edema After Poor‐Grade Subarachnoid Hemorrhage Feasibility and Intensive Care Complications." Journal of neurosurgical anesthesiology 15.3 (2003): 240-248.

Karnatovskaia, Lioudmila V., et al. "Effect of prolonged therapeutic hypothermia on intracranial pressure, organ function, and hospital outcomes among patients with aneurysmal subarachnoid hemorrhage." Neurocritical care 21.3 (2014): 451-461.

Kim, Jong Youl, and Midori A. Yenari. "Hypothermia for treatment of stroke." Brain Circulation 1.1 (2015): 14.

Todd MM, Hindman BJ, Clarke WR, Torner JC; Intraoperative Hypothermia for Aneurysm Surgery Trial (IHAST) Investigators. Mild intraoperative hypothermia during surgery for intracranial aneurysm. N Engl J Med 2005;352:135-45.

Clark, Darren L., et al. "Comparison of 12, 24 and 48 h of systemic hypothermia on outcome after permanent focal ischemia in rat." Experimental neurology 212.2 (2008): 386-392.

Shankaran, Seetha, et al. "Whole-body hypothermia for neonates with hypoxic–ischemic encephalopathy." New England Journal of Medicine 353.15 (2005): 1574-1584.

Shankaran, Seetha, et al. "Childhood outcomes after hypothermia for neonatal encephalopathy." New England Journal of Medicine 366.22 (2012): 2085-2092.

Azzopardi, Denis, et al. "Effects of hypothermia for perinatal asphyxia on childhood outcomes." New England Journal of Medicine 371.2 (2014): 140-149.

Mourvillier, Bruno, et al. "Induced hypothermia in severe bacterial meningitis: a randomized clinical trial." JAMA 310.20 (2013): 2174-2183.

Rim, Kwang Pil, et al. "Effect of therapeutic hypothermia according to severity of sepsis in a septic rat model." Cytokine 60.3 (2012): 755-761.

Corry, Jesse J., et al. "Hypothermia for refractory status epilepticus." Neurocritical care 9.2 (2008): 189-197.

Villar, Jesus, and Arthur S. Slutsky. "Effects of induced hypothermia in patients with septic adult respiratory distress syndrome." Resuscitation 26.2 (1993): 183-192.

White, H. D., C. D. Spradley, and A. Hayek. "Therapeutic Hypothermia For Refractory Hypoxia In Acute Respiratory Distress Syndrome Undergoing Extracorporeal Membrane Oxygenation." Am J Respir Crit Care Med 191 (2015): A4570.

Zhicheng, Fang, et al. "Effect of mild hypothermia treatment on mechanical ventilation of acute respiratory distress syndrome." Modern Journal of Integrated Traditional Chinese and Western Medicine 29 (2012): 002.

Stravitz, R. Todd, et al. "Therapeutic hypothermia for acute liver failure: toward a randomized, controlled trial in patients with advanced hepatic encephalopathy." Neurocritical care 9.1 (2008): 90-96.

Jalan, Rajiv, et al. "Moderate hypothermia for uncontrolled intracranial hypertension in acute liver failure." The Lancet 354.9185 (1999): 1164-1168.

Karvellas, C., et al. "A multicenter retrospective cohort analysis of therapeutic hypothermia in acute liver failure." Critical Care 18.Suppl 1 (2014): P200.

Wu, Xianren, et al. "Induction of profound hypothermia for emergency preservation and resuscitation allows intact survival after cardiac arrest resulting from prolonged lethal hemorrhage and trauma in dogs." Circulation 113.16 (2006): 1974-1982.

College Answer

Basic Life Support

a)  No signs of life equals: unresponsiveness, not breathi.ng, not moviri.g normally.
Pulse check not required to commence CPR.
b)  The term" Rescue Breathing'' has replaced Expired Air resuscitation
c)  Compression ventilation ratio 30:2 for children & adults. d)  Same ratio regardless of number of rescuers
e)  Identifying the lower halfof sternum by visualizing the centre of chest, no
. need  to measure and remeasure                                .
f)  2 initial breaths, not 5.
g)  Chest compressions at 100 Imin

Advanced Life Support

.  a)  Minimise interruptions to chest compressions
b)  If unwitnessed arrest,  VF or pulseless VT,.single shock instead of stacked shocks.

c)  If witnessed arrest-up to 3 shocks may be given at the first attempt.

d)  If monophasic defibrillator-energy level360 J
e)  Ifbiphasic defibrillator-energy level200 J
f)   If unsure of device, use 200

J. After each defibrillation, 2 min of CPR before checking.pulse.

Discussion

Since the 2006 update (and this question), there has been another guideline update.

The below answer will be based on the most recent change, and thus is going to look different to the college answer from early 2007.

In summary:

Changes to BLS:

• "signs of life" changed into "unresponsive and not breathing normally"
• If unwilling to perform conventional CPR, public is encouraged to perform compression-only CPR
• Pulse check has been downgraded - it is now only for health care professionals
• "S" has been added into DRSABC - it stands for "send for help"
• CPR now commences with chest compressions rather than rescue breaths

Changes to ALS:

• Depth of compression increased to > 5 cm
• Now, we charge the defibrillator while chest compressions continue
• No longer are "stacked shocks" recommended (outside of "special circumstances")
• When amiodarone is given after the third shock, the timing is now "at the time of CPR recommencement"
• Atropine has been removed from the guidelines
• Precordial thump is no longer recommended for VF - monitored pulseless VT only
• Hyperoxia after ROSC is emphasised as a bad thing.

References

The ARC has a portion of their website dedicated to the past update information of their guidelines.

Specifically, one can review a summary of BLS changes and a summary of ALS changes.

The index of the new guidelines is available from the ARC website.

College Answer

Indications
1.  Any doubt about the primary diagnosis of the cause of coma.
2.  Possible drug or metabolic cause of coma.
3.  Cranial nerves can not be tested adequately e.g. periorbital oedema, eye injuries, ruptured tympanum
4.  Apnoea test can not be performed e.g. cervical cord injury, cardiorespiratory instability.
5.  confirmation of brain death in some countries (not ANZ)

Advantages
•    Highly specific
•    Does not require preconditions as for clinical testing –ie patient can be cold, hypoxic, sedated, undiagnosed, etc
•    Can be done at the bedside – if portable gamma camera
•    Safe – non-toxic marker (Te99m  HMPAO) can be delivered via peripheral vein
•    Quick – answer can be given within 30 minutes
•    Provides a hard copy – clear permanent documentation of brain death

Disadvantages

•    Requires specialized equipment, marker and staff (nuclear medicine specialist) usually only available in major centres
•    Requires patient transport – if no portable camera
•    Can show minimal flow ( e.g. from meningeal vessels), cannot easily be repeated, and not very soon after first test

Discussion

This question refers specifically to the Tc-99 HMPAO SPECT scan, which (after the four-vessel DSA) is viewed by the ANZICS Statement on Death and Organ Donation as the second best way of confirming that there is no blood flow to the noggin.

The indications for imaging to confirm brain death, broadly, are as follows:

• Inability to perform clinical brain death testing
  • No access to at least one eye and one ear
  • Severe hypoxia
  • Hemodynamic instability
  • High spinal cord injury
• Presence of persisting confounding factors which invalidate the clinical testing for brain death (eg. severe metabolic disturbances, organ system dysfunction)
• Absence of a clear cause for the coma, which - for the puspose of braindeath testing - is defined as "sufficient intracranial pathology" to explain brain death.

The indications for choosing a radionuclide scan, rather than a DSA, may be as follows:

• Allergy to IV contrast
• Injury to the carotids or vertebral arteries, which precluded fluoroscopic access

Advantages of the HMPAO-SPECT:

• Equivalent to DSA in terms of false positive rate (0%)
• Does not require the precodnitions for brain death to be met
• Rapid return of results
• Safe non-toxic contrast agent
• Visually effective representation of absent brain perfusion

Disadvantages of HMPAO-SPECT:

• Expensive
• Requires specialised equipment
• Not available in all but the best-equipped centers
• Portable gamma-cameras are infrequently available, exposing the patient to the risk of transport.
• In very young infants with open cranial sutures, HMPAO-SPECT may return false positive results if used in a single imaging plane.
• In adults, it may return false positives due to minimal flow in meningeal vessels.

References

ANZICS Statement on Death and Organ Donation

Wieler, H., et al. "Tc-99m HMPAO Cerebral Scintigraphy A Reliable, Noninvaslve Method for Determination of Brain Death." Clinical nuclear medicine18.2 (1993): 104-109.

Donohoe, Kevin J., et al. "SNM practice guideline for brain death scintigraphy 2.0." Journal of nuclear medicine technology 40.3 (2012): 198-203.

Munari, Marina, et al. "Confirmatory tests in the diagnosis of brain death: comparison between SPECT and contrast angiography." Critical care medicine33.9 (2005): 2068-2073.

Joffe, Ari R., Laurance Lequier, and Dominic Cave. "Specificity of radionuclide brain blood flow testing in brain death: case report and review." Journal of intensive care medicine 25.1 (2010): 53-64.

Heran, Manraj KS, Navraj S. Heran, and Sam D. Shemie. "A review of ancillary tests in evaluating brain death." The Canadian Journal of Neurological Sciences35.4 (2008): 409-419.

College Answer

With each of these signs, clearly indicate if they are compatible or not with the diagnosis of brain death and provide a brief explanation  for your answer.

a) generalised tonic clonic seizure

the patient must have intact neural connections to have a grand mal fit - brain death can not be present

b) slow drifting of one eye away from the ear in which cold water is injected during caloric testing

any eye movement in response to caloric testing signifies the presence of some reflex arc function. Brain death cannot be diagnosed

c) flexion of the arm at the elbow following imposition of a painful stimulus to the nail bed on that side this may represents a spinal reflex. It does not influence a diagnosis of brain death

d) sitting up during apnoea testing
this represents another spinal reaction to the acidosis which occurs with hypercarbia and is termed the Lazarus sign. It usually really unsettles nursing staff and is inevitably very disturbing to relatives. However it is compatible with a diagnosis of brain death .

e) an increase in pulse from 70 bpm to 110 bpm during apnoea testing Hypercarbia (which occurs during apnoea testing) results in endogenous adrenaline release. An change in pulse rate and blood pressure is common during apnoea resting and is not incompatible with brain death

Discussion

The ANZICS Statement on Death and Organ Donation is again the primary source for this answer. Specifically, I direct the reader to Page 22 of the most recent version, where sections 2.2.3 and 2.2.4 discuss observations which are compatible and incompatible with drain death.

To simplify revision, I will quote some of them here.

Observations compatible with brain death:

• Spinal reflexes in response to noxious stimulus:
  • Extension-pronation movements of the upper limbs
  • Nonspecific flexion of the lower limbs
  • Undulating toe reflex
  • Lazarus sign
  • Deep tendon reflexes
  • Plantar responses (flexor or extensor)
  • "Respiratory-like movements" without much of a tidal volume
  • Head turning
• Sweating
• Blishing
• Tachycardia
• Normal blood pressure in absence of vasopressors
• Absence of diabetes insipidus

Observations incompatible with brain death:

• Extensor posturing (decorticate)
• Flexor posturing (decerebrate)
• True extensor or flexor responses to painful stimuli
• Seizures

For a more comprehensive overview, a good (ancient) article from the Acta Neurochirurgica describes what the authors have quaintly termed "Spinal Man", a species of human bereft of higher cortical function, which is a creature reliant purely on spinal reflexes.

Additionally, a more recent article discusses the various physiological responses to apnoea testing, including all the various cardiovascular derangements which occur.

Thus:

a) - a seizure - rules out brain death

b) - a positive caloric reflex - is a brainstem reflex which is still working, and it rules out brain death

c) - arm flexion to ipsilateral painful stimulus - could be a spinal reflex, and does not rule out brain death. 

d) - a Lazarus sign - does not rule out brain death

e) - a hypercapnea-associated catecholamine surge - can occur with zero cerebral input, and does not rule out brain death.

References

ANZICS Death and Organ Donation Committee, THE ANZICS STATEMENT ON DEATH AND ORGAN DONATION Edition 3.2 2013

McNair, N. L., and K. J. Meador. "The undulating toe flexion sign in brain death." Movement disorders 7.4 (1992): 345-347.

Jørgensen, E. O. "Spinal man after brain death." Acta neurochirurgica 28.4 (1973): 259-273.

Ropper, Allan H. "Unusual spontaneous movements in brain‐dead patients."Neurology 34.8 (1984): 1089-1089.

Heytens, Luc, et al. "Lazarus sign and extensor posturing in a brain-dead patient: case report." Journal of neurosurgery 71.3 (1989): 449-451.

Lang, C. J. G., and J. G. Heckmann. "Apnea testing for the diagnosis of brain death." Acta neurologica scandinavica 112.6 (2005): 358-369.

College Answer

Diagnosis of the underlying cause of the cardiac arrest ...
(eg drug overdose vs cerebral metastatic adencarcinoma) and any serious comorbidites that may be present.
•      Time to ROSC < 10 min
•      Bystander CPR
•      Rhythm VF better than asystole
•  Neurological status (assessed at 24-72 hours)
•   requires absence of sedation or neuromuscular blocking agents
•   Pupillary response to light – absent is poor prognostic sign
•   Best motor response – absent or extensor motor response is a poor prognostic
sign
•  Biochemical evidence of neurological damage
•   Neurone specific enolase
•   S-100 neuroprotein

•  Electrophysiological evidence of neurological damage
•   Somatosensory evoked potentials

•  Cardiac status
•   Sucessful revascularisation if STEMI is underlying cause
•   Ejection fraction on ECHO

Discussion

This question closely resembles several other questions from subsequent papers:

Question 4 from the second paper of 2013: "Describe the clinical signs and investigations available to predict poor neurological outcome in comatose survivors of cardiac arrest. Include in your answer the factors that may confound the interpretation of these signs and investigations. "

Question 14 from the first paper of 2011: "Outline the value of the following in determining prognosis for neurological recovery in an adult patient admitted to ICU, after successful cardiovascular resuscitation from an out-of-hospital cardiac arrest:  Peri-arrest data, Clinical examination, Neuro-imaging, Neurophysiology, Biomarkers"

In the answers to the above questions, elaborate tables display the information which is relevant in post-arrest prognostication, discuss its prognostic value, and digress upon the various confounding factors which might fuddle one's forecasts.

The AAN report referenced below is an excellent resource for all questions of this nature.

References

For data largely from the pre-hypothermia era:

Wijdicks, E. F. M., et al. "Practice Parameter: Prediction of outcome in comatose survivors after cardiopulmonary resuscitation (an evidence-based review) Report of the Quality Standards Subcommittee of the American Academy of Neurology."Neurology 67.2 (2006): 203-210.

For daa including post-hypothermia data:

Sandroni, Claudio, et al. "Prognostication in comatose survivors of cardiac arrest: an advisory statement from the European Resuscitation Council and the European Society of Intensive Care Medicine." Resuscitation 85.12 (2014): 1779-1789.

College Answer

Treatment

1)  Depends on cause
2)  Fluid bolus +/- inotropes – usually norad
3)  Line change if indicated
4)  Broad spectrum Gram positive and gram negative cover if sepsis is deemed likely.
+/- fungal cover
5)  PRBC as required
6)  Targeted therapy for PE /anaphylaxis

Discussion

One can easily see through the thin veneer of this burns history the college gives us. This is really just a boring question about the differential causes of shock.

Thus:

• Artifactual shock
  • Art line inappropriately zeroed
  • Wrong size NIBP cuff
• Technical error
  • CVC is extravasating vasopressors
  • Vasopressor infusion was improperly prepared
• Obstructive shock
  • Cardiac tamponade
  • Tension pneumothorax
  • Pulmonary embolism
• Distributive shock
  • Septic shock - bacterial translocation from infected burns which have been disturbed
  • Anaphylactic shock - a reaction to antibiotics or anaesthetic agents
  • Propofol-related vasoplegia
• Hypovolemic shock
  • Haemorrhage intraoperatively
  • Inadequate fluid resuscitation in theatre
• Cardiogenic shock
  • Intraoperative MI
  • Cardiodepressant effect of drugs

An approach to investigation would thus consist of the following:

• Examination of the cardiorespiratory system to exclude anahylaxis, cardiac tamponade, pneumothorax and obvious haemorrhage
• ABG to assess the severity of the metabolic acidosis
• FBC to look for haemorrhage
• Mast cell tryptase
• Septic screen
• ECG to exclude perioperative MI
• CXR to look for features of cardiac failure
• TTE to exclude tamponade and to look for features of cardiac failure or right heart dilation
• CTPA to exclude PE

References

College Answer

Patient clearly has no evidence of brain stem reflexes, however, can’t be declared brain dead as there is no known cause of coma.

Discussion

As in the above college answer, this patient cannot be declared brain dead.

The preconditions for brain death testing are not met; according to the ANZICS statement (linked below), "Brain death cannot be determined without evidence of sufficient intracranial pathology". In this, Australians differ to the British; in Britain it is sufficient to have a dead brainstem for a diagnosis of brain death, even with ample blood flow to the rest of the cortex.

So at this stage, one could not declare this patient brain dead without imaging which might demonstrate an absence of cerebral perfusion (or without shipping the patient to Britain).

References

ANZICS Death and Organ Donation Committee, THE ANZICS STATEMENT ON DEATH AND ORGAN DONATION Edition 3.2 2013

College Answer

Preconditions

a) A known cause of coma (check terminology in new ANZICS guidelines)
b) Minimum of 4 hour period observation
c) neuro-imaging consistent with acute brain pathology which could result in brain death;

d) temperature > 35C;
e) normotension (as a guide, systolic blood pressure > 90 mmHg, mean arterial pressure (MAP) >
60 mmHg in an adult);
f) exclusion of effects of sedative drugs: the time taken for plasma concentrations of sedative drugs to fall below levels with clinically significant effects depends on
the dose and pharmacokinetics of drugs used, and on hepatic and renal function. If there is any doubt about the persisting effects of opioids or benzodiazepines, an appropriate drug antagonist should be administered;

g) absence of severe electrolyte, metabolic or endocrine disturbances. These include marked derangements in plasma concentrations of glucose, sodium, phosphate or magnesium, liver and renal dysfunction and severe endocrine dysfunction;

h) intact neuromuscular function. If neuromuscular-blocking drugs have been administered, a peripheral nerve stimulator or other recognised method (e.g. electromyography) should always be used to confirm that neuromuscular conduction is normal;

What are the indications for ancillary tests for brain death?

°     Inability to adequately examine the brain-stem reflexes. It must be possible to examine at least one ear and one eye;

°     Inability to perform apnoea testing. This may be precluded by severe hypoxic respiratory failure or a high cervical spinal cord injury.

What are the 2 imaging techniques  currently recommended by ANZICS for determining the absence of intracranial blood flow:

Four vessel intra-arterial catheter angiography, with digital subtraction; Tc-99 HMPAO SPECT radionuclide imaging

CT angio with certain caveats may be acceptable. Do not recommend MR angio

Discussion

This question resembles several other questions in the past papers:

• Question 17 from the second paper of 2012 and Question 12.1 from the second paper of 2010 ask about pre-conditions for brain death testing.
• Question 12.2 from the second paper of 2010 discusses imaging modalities to assess the intracranial blood flow.

The pre-conditions for clinical brain death testing are:

• Normothermia (over 35 degrees)
• Normotension( MAP >60)
• Not sedated
• Not paralyzed
• Not in a state of electrolyte or metabolic derangement (eg. hypoglycaemia)
• Possessing at least one intact eye and one ear (to examine brainstem reflexes)
• Able to breathe (to test for apnoea; i.e. high C-spine injury may disqualify you)
• Unresponsive coma
• A suitable explanation for why the patient is comatose, which would be consistent with the diagnosis of brain death

Otherwise, this current paper asks one original question: when must one resort to imaging?

Well. The ANZICS Statement on Death and Organ Donation suggests several distinct scenarios when one cannot perform clinical brain death testing:

• Inability to adequately examine the brain-stem reflexes:
  • One ear and one eye are not intact
  • Sedation, hypothermia, paralysis
• Inability to perform apnoea testing:
  • Severe hypoxic respiratory failure
  • High cervical spinal cord injury

References

ANZICS Statement on Death and Organ Donation

College Answer

Apnoea test (as peak pressure has dropped to zero and there is no recordable TV. Not likely to be bronchoscopy as peak pressures are high during bronchoscopy

Discussion

This patient is not breathing, and is demonstrating no respiratory drive in spite of a ridiculously high CO₂. The 100% FiO₂ suggests that an apnoea test for brain death is in progress.

References

Ropper, Allan H., Sean K. Kennedy, and Lisa Russell. "Apnea testing in the diagnosis of brain death: clinical and physiological observations." Journal of neurosurgery 55.6 (1981): 942-946.

College Answer

Reasons supporting the statement

Physiological:
a) In cardiac arrest heart dilates acutely. Decompression  of the heart occurs with good compressions
b) Ventilation can lead to decreased venous return
c) Passive ventilation still occurs with compression only CPR
d)  Gasping  can  provide  adequate  ventilation  and  in  presence  of  a  partial  airway obstruction may lead to increased venous return

Logistic reasons:

a) Reluctance  to perform  mouth  to mouth  by rescuers  therefore  some  people  do not attempt CPR.
b) Interruption to compressions therefore limiting their effectiveness

c) Easier to teach compression only CPR.
d) Out of hospital arrests it will minimise time to hospital.

e) Useful particularly in the setting of a single rescuer

Studies:

Mostly observational or animal. Some RCT
No difference in outcome using compression only versus standard CPRs in most studies
Evidence of value of good compressions

Against:

Most studies are observational.
Reported survival is no better with compression only therefore why change.
Data for most studies are prior to the change in recommendation   to 30:2 RATIO Ventilation is important for many arrests EG drowning/children/in hospital arrests ARC not recommend as standard practice

Present position: 
Not standard currently. Wait further studies. It can be used if rescuer is reluctant to use mouth to mouth

Discussion

This discussion is written in late 2014, with the benefit of four ensuing years of research and policy change.

Introduction

• Compression-only CPR dispenses with recommendation to interrupt CPR for breaths.

Rationale

• In cardiac arrest, ardiac output is the rate-limiting step of oxygen delivery
• Compressions create enough passive circulation for adequate gas mixing to occur
• Breath pauses in compressions may be counterproductive (as they allow cardiac output to decrease)
• Reluctance to provide mouth-to-mouth may discourage all CPR attempts in lay rescuers

Advantages

• Easier to teach
• Easier to perform as a single rescuer
• Definitely better than no CPR
• May encourage grossed-out lay rescuers to provide some CPR, rather than no CPR
• Uninterrupted compressions may be of better quality

Disadvantages

• Supporting data is mainly from animal studies
• Positive pressure ventilation may be essential in drowning, pulmonary oedema, airway obstruction, etc.

Evidence

• In 2007, two observational studies published in Circulation (Iwami, Taku, et al. and Bohm, Katarina, et al.) did not find any survival benefit (or if you rather, confirmed equivalent efficacy) for compression-only CPR.
• A 2010 RCT from NEJM compared the two strategies and again found no mortality difference.
• A larger observational study published in 2011 found some difference, favouring conventional CPR.
• A 2014 meta-analysis confirmed that there is no difference in mortality between conventional and compression-only CPR, but admitted that the issue "is unclear for the patients with noncardiac cause of arrest and with long periods of untreated arrest."

Current status of recommendations

• The ARC still recommends a 30:2 compression-ventilation ratio. "The ARC has extensively reviewed the recently published evidence and does not consider it to be of sufficient magnitude to warrant a change in the current guidelines"
• The ARC also recommends you provide compression-only CPR if you are for some reason unwilling to provide proper CPR.

References

The ARC have a brief FAQ on this issue, as well as a more comprehensive advisory statement.

Iwami, Taku, et al. "Effectiveness of bystander-initiated cardiac-only resuscitation for patients with out-of-hospital cardiac arrest." Circulation 116.25 (2007): 2900-2907.

Bohm, Katarina, et al. "Survival is similar after standard treatment and chest compression only in out-of-hospital bystander cardiopulmonary resuscitation." Circulation 116.25 (2007): 2908-2912.

Svensson, Leif, et al. "Compression-only CPR or standard CPR in out-of-hospital cardiac arrest." New England Journal of Medicine 363.5 (2010): 434-442.

Ogawa, Toshio, et al. "Outcomes of chest compression only CPR versus conventional CPR conducted by lay people in patients with out of hospital cardiopulmonary arrest witnessed by bystanders: nationwide population based observational study." BMJ 342 (2011).

Yao, Lan, et al. "Compression-only cardiopulmonary resuscitation vs standard cardiopulmonary resuscitation: an updated meta-analysis of observational studies." The American journal of emergency medicine 32.6 (2014): 517-523.

College Answer

Primary problem not fixed 
•    Untreated focus of infection/ inadequate  primary source control eg pancreatic abscess, infected pseudocyst
•    New  sepstic  site  eg  central  line/  hospital  acquired  pneumonia  /cholecystitis, urinary tract

Systematic Approach 
“hypovolaemic/ obstructive/ cardiac/ distributive +/- endocrine

•    Hypovolaemia  or hidden  bleeding     eg. From surgical  site/ peptic ulcer, “third space” losses (eg ascites from peritonitis)

•    Undiagnosed  or new     “obstructive  shock” :Tension pneumothorax/  Pericardial effusion/gas trapping (auto PEEP)/ pleural effusions/ pulmonary emboli

•    Severe Intra abdominal hypertension

•    Dysrhythmia eg SVT, junctional rhythm etc
•    New myocardial ischaemia
•    New/ undiagnosed cardiac valve pathology

•    Severe adrenal/ pituitary/thyroid dysfunction.
•    Drug reaction/ anaphylaxis
•    Vitamin deficiency (B1)
•    Electrolyte abnormalities such as hypophosphataemia  and hypocalcaemia (the latter particularly with pancreatitis)

Technical

•    CVL fallen out or not in a central vein / no pressors in the infusion bag
•    Measurement   error  –  eg  arterial  line  not  zeroed/under   or  over  damped, transducer height, wrong NIBP cuff size  etc

Miscellaneous

•    Radial/ central arterial monitoring discrepancy with severe vasoconstriction
•    Upper limb vascular disease (radial arterial line) or obstruction (eg dissection or aorto-occlusive disease: femoral arterial line)
•    Anti hypertensive drugs taken as part of patients usual medications

Discussion

This question is identical to Question 17 from the second paper of 2013.

References

College Answer

•    Oesophageal intubation
•    Hypoxic cardiac arrest (unrelated to oesophageal intubation due to delayed or unanticipated difficulty with intubation)
•    Suxamethonium induced hyperkalemia
•    Incidental PE
•    Autonomic dysfunction from the spinal injury.
•    Tension pneumothorax
•     Anaphylaxis

Discussion

This question relies on the candidate being able to generate a list of differential causes for cardiac arrest.

A good systematic framework for this is the "Four Hs and four Ts" mnemonic:

• Hypoxia (thus, oesophageal intubation or delayed oxygenation)
• Hypovolemia (thus, cardiovascular collapse due to vasodilation by an induction agent like propofol, or due to the autonomic dysfunction of spinal cord injury)
• Hyper/hypokalemia (thus, the effects of suxamethonium)
• Hyper/hypothermia (probably irrelevant in this case)
• Tension pneumothorax (due to overvigorous bag-mask ventilation, or due to tracheobronchial disruption by violent use of the bougie)
• Tamponade (unlikely in this setting)
• Toxins (eg. anaphylactic reaction to induction agents)
• Thrombus (eg. the PE which the college for some reason offer as a valid differential)

References

ARC Guideline 11.2: Protocols for Advanced Life Support

College Answer

•     Capnograph to check tube position and reintubate if not in the right position
•     Urgent serum K
•      ECG
•      CTPA
•      Echo
•     CXray

Discussion

A systematic approach to this question would resemble the following:

A) confirm ETT position with capnography

B) ABG to assess adequacy of oxygenation

...and CXR to rule out pneumothorax

C) ECG to assess cardiac causes (eg. STEMI)

... and TTE to assess for presence of cardiac tamponade, and to evaluate chamber filling (thus investigating hypovolemia)

D) BSL to assess blood glucose

E) ABG to assess serum potassium levels

CTPA is mentioned because PE is considered as a differential for this cardiac arrest in the college answer to the first part of this three-part question.

References

ARC Guideline 11.2: Protocols for Advanced Life Support

College Answer

This is PEA
•    Tension pneumothorax
•     Tamponade
•    PE
•     Hypovolemia
•     Hypothermia

Discussion

It is difficult to justify a prolonged discussion for something like this.

The image I have provided is from LITFL, and demonstrates hypothermia with a slow junctional rhythm, but really any sort of organised electrical activity would have sufficed.

References

College Answer

•    Evidence of sufficient intracranial pathology or a known cause of coma e.g.; traumatic brain injury, intracerebral haemorrhage, hypoxic-ischaemic encephaloopathy
•    normothermia (temperature > 35°C);
•    normotension (as a guide, systolic blood pressure > 90 mmHg, mean arterial pressure (MAP> 60 mmHg in an adult);
•    exclusion of effects of sedative drugs (self-administered or otherwise) — the time taken for plasma  concentrations of sedative drugs to fall below levels with clinically significant effects depends on the dose and pharmacokinetics of drugs used, and on hepatic and renal function. If there is any doubt about the persisting effects of opioids or benzodiazepines, an appropriate drug antagonist should be administered;
•    absence of severe electrolyte, metabolic or endocrine disturbances— these include: marked derangements in plasma concentrations of glucose, sodium, phosphate or magnesium; liver and renal dysfunction; and severe endocrine dysfunction;
•    intact neuromuscular function— if neuromuscular-blocking  drugs have been administered, a peripheral nerve stimulator or other recognised method (e.g. electromyography) should always be used to confirm that neuromuscular conduction is normal;
•    ability to adequately examine the brain-stem reflexes— it must be possible to examine at least one ear and one eye; and
•    ability to perform apnoea testing— this may be precluded by severe hypoxic respiratory failure or a high cervical spinal cord injury.

Discussion

The answer above is lifted straight from the ANZICS Statement on Death and Organ Donation (I have linked to Version 3.2, from 2013).

In brief, the preconditions are:

• Pathology sufficient to explain brain death
• Normothermia
• Normotension
• Exclusion of the effects of sedating drugs
• Absence of severe electrolyte, metabolic or endocrine disturbance:
  • Glucose <3 or > 25 mmol/L
  • Sodium <125 or >160 mmol/L
  • phosphate <0.5 mmol/L
  • magnesium <0.5 mmol/L
  • urea > 40 mmol/L
  • "untreated severe hypothyroidism or severe hypoadrenalism"
• Intact neuromuscular function
• Ability to adequately examine brainstem reflexes
• Ability to perform apnoea testing

References

ANZICS Death and Organ Donation Committee, THE ANZICS STATEMENT ON DEATH AND ORGAN DONATION Edition 3.2 2013

College Answer

Discussion

The answer above borrows heavily from the ANZICS Statement on Death and Organ Donation (I have linked to Version 3.2, from 2013).

In brief, the investigations and expected findings are as follows:

Four-vessel arterial digotal subtraction angiography:

• blood flow should not be demonstrated above the level of the carotid 
  siphon in the anterior circulation, or above the foramen magnum in the posterior circulation

Tc-99m HMPAO radionuclide (SPECT) scan

• Absent intracranial parenchymal Tc-99m HMPAO uptake

CT angiography

• Absent contrast enhancement, at 60 seconds following bolus injection, bilaterally and of all of the following vessels:
  • MCA branches beyond the Sylvian branches
  • P2 segment of the PCA
  • pericallosal arteries
  • internal cerebral veins
• Adequate contrast enhancement of the external carotid artery branches to confirm a technically adequate study.

References

ANZICS Statement on Death and Organ Donation

College Answer

Consider mixed aetiology for shock
•    Cardiogenic (cardiac history, severe sepsis, rhythm)
•    Distributive shock (sepsis)
•    Obstructive  shock (PE, tamponade)  – less likely but will probably  get mentioned.
Maybe give less marks for this than the other causes

Establishing relative contribution of each to the hypotension
•    Clinical Signs
•    Distributive;  warm  and  dilated  (if  adequate  filling),  temperature,  potential  source sepsis

•     Cardiogenic
•    LVF; tachycardia, bibasal crepitations, gallop
•    RVF; JVP, hepatomegaly, oedema
•    Escalating monitoring
•    Minimal: ECG, NIBP, SpO2
•    ABP, CVP progressing to Central Venous O2 Sat / TTE / PICCO / PAC as indicated

•    Laboratory Investigations directed at cause
•    Lactate, Troponin, ECG, CXR, Sepsis screen, UA
•    Collateral history

Interventions
•    Optimise preload
•     Cardiogenic
•    Optimize preload (low from redistribution
•    Optimize contractility
•    Rhythm; rate control / normalization (cardioversion?)
•    Inotropic support
•    Dobutamine / Milrone / Levosimenden / Adrenaline / Nor Ad (increases coronary art perfusion pressure) Caution with inodilators while still hypotensive

•     IABP
•    CPAP
•    Reversible / Specific factors

•    Exclude / treat ischaemia (heparin / angio , revascularisation etc.)
•     Distributive
•    Optimize preload
•    Vasopressor support
•     Noradrenaline
•    Adjuncts: Vasopressin / Steroid (infusion or bolus)
•    Mixed pathology issues
•    Risk of Noradrenaline  alone is an increased  afterload  with worsening  cardiogenic shock / peripheral perfusion

•    Start with inotrope and then add vasopressor; dobutamine / norad combination

•    Adrenaline may a safer choice (inotrope + vasoconstriction)

Discussion

This is a question about undifferentiated shock. The question really should read "how do you assess a patient in a non-specific shock state, and maintain their organ perfusion while looking for a cause?" It would probably be useful to mention a rapid focused bedside echo. Obvious hints in terms of fever and a history of crusty coronaries have been given. The examiners would mainly be looking for a systematic approach to diagnosis and treatment, without overcommitment to any specific diagnosis.

The following is really just a rearrangement of the college answer. A standard template of shock assessment should exist; it can be applied here with minimal variation.

Immediate management:

• Attention to airway and breathing
• Establish secure venous access
• Introduce invasive monitoring tools - arterial/central line

Rapid assessment:

• Focused history to differentiate a source of sepsis, and to assess the contribution of cardiac ischaemia
• Physical examination to assess adequacy of peripheral perfusion
• ABG, ECG, CXR, cardiac enzymes, blood and urine cultures
• Rapid bedside TTE to rule out cardiac tamponade and to assess contractility
• Fluid challenge 20-40ml/kg of crystalloid, to assess fluid responsiveness - plus/minus dynamic bedside manoeuvres
• Consider advanced hemodynamic monitoring, eg. SvO2 PAC or PiCCO

Decisive management for this mixed shock state:

• Control sepsis
  • Broad spectrum antibiotics, given early
  • Consider "stress dose" steroids
• Optimise preload
  • Fluid boluses to continue, as permitted by measures of fluid responsiveness
• Optimise afterload
  • Maintain organ perfusion and coronary filling by maintaining a MAP > 65 and a reasonable diastolic pressure, using vasopressors such as noradrenaline and vasopressin
• Optimise rhythm
  • Consider early DC cardioversion if the rhythm is atrial fibrillation, to recover the "atrial kick"
• Optimise contractility
  • If there is concern regarding contractility, consider inotropes eg. dobutamine milrinone or levosimendan
• Use adjuncts to resuscitation
  • Consider IV thiamine, perticularly if there is lactic acidosis
• Reverse any reversible factors
  • Early angiography or thrombolysis
  • Surgical source control for septic foci

References

Jones, Alan E., et al. "Randomized, controlled trial of immediate versus delayed goal-directed ultrasound to identify the cause of nontraumatic hypotension in emergency department patients*." Critical care medicine 32.8 (2004): 1703-1708.

College Answer

a. Peri-arrest data:

Initial rhythm, bystander CPR, time to ROSC intuitively helpful and commonly considered, but have not been shown to correlate  with individual  outcome.   Co-morbidities  and pre- arrest performance status may determine overall survival.

b. Clinical Examination:

Unreliable  and of no predictive  value before 24 hours, clinical assessment  at ≥ 72 hours conventional
•    Appropriate     pre-conditions:    absence     of    sedation/relaxants,     adequate     CVS
resuscitation, normothermia, corrected biochemistry etc.
•    All data pertains to studies before the common use of therapeutic hypothermia, and the effect of this intervention  unknown.   May need longer than 72 hours to obtain reliable data from CNS examination in patients treated with induced hypothermia
•    GCS < 4, absent corneal response, absent pupillary response to light indicative of poor prognosis
•    myoclonus not sufficiently predictive to be reliable in isolation but myoclonic status epilepticus is a poor prognostic feature

c. Neuro-imaging:

•    CT may be performed early to exclude a CNS cause of arrest
•    CT  signs  of  poor  prognosis   include  qualitative   assessment,   and  quantitative assessment of white matter Houndsfield unit ratio.  Optimum timing not clear
•    MRI demonstration  of diffuse cortical lesions  or sub-cortical  lesions  is associated with poor outcome

d. Neurophysiology:

•    No neurophysiology study reliably predicts outcome at < 24 hours
•    EEG findings  of: diffuse suppression  to < 20 mV, burst suppression,  generalised seizures, diffuse periodic complexes indicate poor prognosis
•    EEG  shown  to  have  increased  false  positive  prediction  for  poor  outcome  after induced hypothermia
•    SSEP:  bilaterally  absent  cortical  responses  to  median  nerve  stimulation  seems highly accurate (0% False Positive Rate), not studied after induced hypothermia

e. Biomarkers:

•    Neurone specific enolase (NSE) most studied, some studies show 0% FPR for poor outcome, but cut-off levels vary, studies small

Discussion

With the exception of the "peri-arrest data" section, this question closely resembles Question 4 from the second paper of 2013.

The table from Question 4 is thus reproduced below, with the peri-arrest data section added, sans the confounding factors column. The whole peri-arrest data issue is better discussed in the chapter on prognostication of neurological recovery following a cardiac arrest.

Peri-arrest data:

• VF arrest has the best prognosis: 40% survive until discharge from hospital.
• PEA has a poor prognosis. 11% survive until discharge from hospital.
• Asystole has the poorest prognosis. 2% survive until discharge from hospital.
• CPR lasting >20 minutes has a poorer prognosis
• A witnessed arrest followed by bystander CPR has a better prognosis
• Increasing age of the patient and presence of comorbidities have a negative influence on prognosis.

The key features of the college answer one would be wise to remember include the following:

• Arrest characteristics (eg. time to ROSC) do not correlate with individual outcome.
• Clinical findings are unreliable within the first 24 hours.

References

Engdahl, Johan, et al. "Can we define patients with no and those with some chance of survival when found in asystole out of hospital?." The American journal of cardiology 86.6 (2000): 610-614.

Bunch, T. Jared, et al. "Outcomes and in-hospital treatment of out-of-hospital cardiac arrest patients resuscitated from ventricular fibrillation by early defibrillation." Mayo Clinic Proceedings. Vol. 79. No. 5. Elsevier, 2004.

Levine, Robert L., Marvin A. Wayne, and Charles C. Miller. "End-tidal carbon dioxide and outcome of out-of-hospital cardiac arrest." New England Journal of Medicine 337.5 (1997): 301-306.

Rea, Thomas D., et al. "Temporal Trends in Sudden Cardiac Arrest A 25-Year Emergency Medical Services Perspective." Circulation 107.22 (2003): 2780-2785.

Carew, Heather T., Weiya Zhang, and Thomas D. Rea. "Chronic health conditions and survival after out-of-hospital ventricular fibrillation cardiac arrest." Heart 93.6 (2007): 728-731.

Goldberger, Zachary D., et al. "Duration of resuscitation efforts and survival after in-hospital cardiac arrest: an observational study." The Lancet (2012).

Wijdicks, E. F. M., et al. "Practice Parameter: Prediction of outcome in comatose survivors after cardiopulmonary resuscitation (an evidence-based review) Report of the Quality Standards Subcommittee of the American Academy of Neurology."Neurology 67.2 (2006): 203-210.

Rogove, Herbert J., et al. "Old age does not negate good cerebral outcome after cardiopulmonary resuscitation: analyses from the brain resuscitation clinical trials."Critical care medicine 23.1 (1995): 18-25.

Levy, David E., et al. "Predicting outcome from hypoxic-ischemic coma." Jama253.10 (1985): 1420-1426.

Zandbergen, E. G. J., et al. "Prediction of poor outcome within the first 3 days of postanoxic coma." Neurology 66.1 (2006): 62-68.

Tapia, F. J., et al. "Neuron-specific enolase is produced by neuroendocrine tumours." The Lancet 317.8224 (1981): 808-811.

Torbey, Michel T., et al. "Quantitative analysis of the loss of distinction between gray and white matter in comatose patients after cardiac arrest." Stroke 31.9 (2000): 2163-2167.

College Answer

a)  How will you respond to this crisis?

•    Confirm cardiac arrest
•    Good BLS i.e.:
•    Check  ETT  position  (pull  back  to  22cm),  listen  to  chest  and  confirm  ETCO2 trace(10)
Check adequate  CPR: correct  position  (lower half of sternum),  correct rate/depth
and  technique  (depress  4-5cm  at  100/min  and  asynchronous   ventilation  with respiratory  rate 8-10)

Call for additional help
•    Confirm IV access
•    Continue CPR for 2 min
•     Adrenaline

b)  You suspect  cardiac tamponade.  Describe  how you would perform blind pericardiocentesis.

•    Some asepsis
•    Identify  landmarks:  Left  paraxiphoid  (traditional)  Left  parasternal  (4th   intercostal space left parasternal)
•    For a left paraxiphoid approach 45° to the abdominal wall, head for the left shoulder, aspirate as you go
•    Could connect  a V lead to the base of the needle  and watch ECG to look for a change  in  the  QRS  morphology,   or  ST  elevation  if  the  needle  contacts  the myocardium
•    Aspirate fluid/blood
•    Consider placing a catheter/pigtail
•    Blood stained pericardial fluid will not clot whereas intraventricular blood will

c)  What  clinical  signs  might  have  indicated  pericardial  tamponade  as  the cause prior to the arrest?

Distended neck veins

Muffled heart sounds

Hypotension

Tachycardia
Pulsus paradoxus

Absent apex beat

ECG findings – low voltage complexes and electrical alternans

Discussion

The scenario presented to us is that of a PEA arrest. In questions which ask "how would YOU respond to this crisis" the college is probably looking for a systematic approach.

Thus:

1) Confirm cardiac arrest

2) Call for help

3) Commence BSL (CPR) until help arrives;

• 100 compressions per minute
• Compression to a depth of 1/3rd of the anterior-posterior chest diamweter
• Asynchronois ventilation of 8-10 breaths per minute
• Ensure the ETT is not malpositioned (chest examination, end tidal CO₂ or calorimetry)

4) With help arriving, follow the non-shockable pathway of the ALS algorithm, which consists of CPR and 1mg adrenaline every 2nd cycle.

4) Work on resolving the cause of the arrest, using the "four Hs and four Ts" as a general guide

Confirm cardiac arrest? According to the AHA, "Cardiac arrest is the cessation of cardiac mechanical activity as confirmed by the absence of signs of circulation". One might struggle looking for signs of circulation. The Australian Resuscitation Council recognises the fact that people are unequal in their ability to detect a pulse, and recommends that "if the victim is not responsive, the airway should be cleared and breathing assessed, and if the victim is not breathing normally, CPR should be commenced..." According to them, "it is reasonable that [rescuers] use the combination of unresponsiveness and absent or abnormal breathing to identify cardiac arrest".

Blind emergency pericardiocentesis is probably an artefact of a bygone era, and many would argue that these days it is not defensible, given the time it takes to find and set up the kit is probably enough time for a runner to return with an ultrasound machine.

However, if caught in such a situation, one would perform the following steps:

• Raise the head of the bed 45° if the situation permits (this one does not)
• Antibacterial prep and drape
• Palpate the xiphisternum and ribs: that is your landmark.
• There are three main approaches:
  • Subxiphoid approach: Insert needle just under the xiphoid, and advance in the direction of the left shoulder while aspirating.
  • Parasternal approach: Insert the needle perpendicular to the chest wall in the fifth intercostal space, just lateral to the sternum.
  • Apical approach: insert the needle in the intercostal space below and 1 cm lateral to the apex beat, aimed toward the right shoulder. One can easily skewer the ventricles in this way. It is not for the faint of heart (pun).
• Withdraw fluid until cardiac output improves
• Advance guidewire and dilate over it.
• Advance pigtail catheter over guidewire, and suture in place

Other methods are available (ultrasound-guided and ECG-guided approaches) but these are not strictly speaking "blind".

As for the signs of cardiac tamponade - these are universally recognised as "Beck's Triad":

• Raised JVP / distended neck veins
• Muffled heart sounds
• Hypotension

It is also universally acknowledged that these features are observed only in a minority of patients. Other, more common features include the following:

• Pulsus paradoxus
• Increased stroke volume variation (art line "swing")
• Decreased QRS amplitude
• Electrical alternans (alternating variation in the QRS amplitude)
• Absent apex beat

References

Jacobs, Ian, et al. "Cardiac arrest and cardiopulmonary resuscitation outcome reports: update and simplification of the Utstein templates for resuscitation registries.: A statement for healthcare professionals from a task force of the international liaison committee on resuscitation (American Heart Association, European Resuscitation Council, Australian Resuscitation Council, New Zealand Resuscitation Council, Heart and Stroke Foundation of Canada, InterAmerican Heart Foundation, Resuscitation Council of Southern Africa)."Resuscitation 63.3 (2004): 233-249.

Cikes, I. "A new millennium without blind pericardiocentesis?." European Journal of Echocardiography 1.1 (2000): 5-7.

Fitch, Michael T., et al. "Emergency pericardiocentesis." New England Journal of Medicine 366.12 (2012).

Sternbach, George. "Claude Beck: cardiac compression triads." The Journal of emergency medicine 6.5 (1988): 417-419.

Spodick, David H. "Acute cardiac tamponade." New England Journal of Medicine 349.7 (2003): 684-690.

Reddy, P. SUDHAKAR, et al. "Cardiac tamponade: hemodynamic observations in man." Circulation 58.2 (1978): 265-272.

College Answer

Post-resuscitation care has an impact on overall outcome and consists of ongoing resuscitation and organ support, neuroprotection, treatment of the cause of the cardiac arrest and management of underlying co-morbidities.

• Check adequacy of airway, ETT position, ventilation and circulatory status
• Appropriate monitoring and intravenous access
• Ventilation:
  • Control CO2
  • Avoid hypoxia and hyperoxia
• Circulation:
  • Stabilise circulation with fluid therapy and vasoactive drugs
  • Consider early echo
  • Diagnosis / treatment of acute coronary syndrome with angiography/PTCA or thrombolysis
  • Evaluation for pacemaker or ICD if primary dysrhythmia
  • Mechanical support - use of IABP for cardiogenic shock in acute MI has recently been questioned.
  • Some centres may consider use of ECMO
• Neurological:
  • Therapeutic hypothermia at 32-34oC for 12-24 hr appears to be neuroprotective with improved neurological outcome although the optimal method and timing of cooling is still to be determined.
  • Treatment of seizures
• Diagnosis and management of precipitating event

Discussion

Let us deconstruct this answer. This question interrogates the candidate's ability to approach a post-arrest patient in a systematic manner. Of course, the natural tendency of any ICU trainee would be to immediately start ranting about therapeutic hypothermia (hard to blame them, of course - it is indeed an exciting topic). And then to strat ranting about family discussions. The savvy candidate will note that there is no mention of family discussions in the model answer.

The answer is organised in a familiar A-B-C-D of resuscitation. I have both a brief summary of post-resuscitation care, and a prolonged elaboration of this topic. In brief, a structured answer would resemble the following:

Airway support:

• The comatose patient should be intubated, and the ETT secured.

Breathing:

• Mechanical ventilation (mandatory mode) should be commenced
• No unique recommendation - standard ventilation
• Aim for normoxia and normocapnea.
• Avoid hyperoxia.
• Anticipate aspiration pneumonia, pneumothorax, pulmonary oedema, pulmonary contusions, and ARDS.

Circulation

• Anticipate distributive shock, potentially with cardiogenic shock
• Vasopressor support, inotropes and fluids as required to maintain a MAP >65
• Urgent coronary angiogram, if there is no obvious non-cardiac cause of arrest.
• Urgent TTE
• Watch for QTc prolongation

Disability (.. or prevention thereof)

• Therapeutic hypothermia to 32-24° if the patient remains comatose;
• Targeted temperature management is a valid alternative, and may be preferred
• Avoid hyperthermia
• Sedation and neuromuscular blockade; avoid benzodiazepines.
• EEG

Electrolytes

• Watch for hypokalemia
• Replace electrolytes to prevent arrhythmias

Fluids and renal function

• Renal function may deteriorate due to hypoxic injury
• Hypothermia may result in hyperviscosity; use crystalloid
• Anticipate a vigorous diuresis with hypothermia

Gastrointestinal and nutritional support

• Normoglycaemia maintained with an insulin-dextrose infusion
• No need to start feeds until after rewarming

Haematological issues

• Avoid invasive procedures while hypothermic
• Platelet dysfunction coagulopathy and thrombocytopenia of hypothermia are reversible.
• If the patient has ongoing uncontrolled bleeding, therapeutic hypothermia is contraindicated.

Infectious complications

• Most common complication is pneumonia (staphylococcal)
• Most common bacteraemia is gram negative (bacterial translocation from the gut)
• In hypothermia, leucocyte migration and phagocytosis are impaired, predisposing to infection.

First, the college wants you to acknowledge that the patient is intubated, and that you are concerned about their ETT position. This, as a matter of general principle, is never wrong.

Secondly, the college wants you to acknowledge that you would pursue normoxia and normocapnea.

TTE, angiography, fluids and vasopressors are mentioned - again, this is consistent with the AHA guidelines.

Therapeutic hypothermia is mentioned, and it would be amiss to write an answer to this question without discussing this.

Overall, the model answer expects nothing suprising or inventive from the candidate. The only unusual feature is the mention of ECMO, which (unlike the rest of the answer) does not have strong evidence behind it in post-resuscitation care.

References

Kilgannon, J. Hope, et al. "Association between arterial hyperoxia following resuscitation from cardiac arrest and in-hospital mortality." JAMA: The Journal of the American Medical Association 303.21 (2010): 2165-2171.

Peberdy, Mary Ann, et al. "Part 9: Post–Cardiac Arrest Care 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care." Circulation 122.18 suppl 3 (2010): S768-S786.

Stub, Dion, et al. "Post Cardiac Arrest Syndrome A Review of Therapeutic Strategies." Circulation 123.13 (2011): 1428-1435.

College Answer

Temperature Maintenance:

• Hypothermia is common due to: cold fluids, heat loss through exposure, inability to vasoconstrict or shiver, reduced metabolic rate.

• Maintain normal core temperature
  • Cover patient
  • Warm room
  • Warming blanket
  • Warm fluids especially high volume
  • Humidification

Respiratory support:

• Aim to avoid fluid overload

• Aim for adequate Sp02 and normocarbia with lowest Fi02 and limit tidal volumes

• Bronchoscopy for persisting collapse

• Chest physiotherapy may be helpful

Circulatory Support:

Immediately prior to brain death there is often a period of sympathetic hyperactivity with associated tachycardia and hypertension. This is lost following brain death commonly resulting in vasodilation and hypotension

• Maintain adequate mean arterial pressure. Use judicious volume expansion and low dose inotropes (usually noradrenaline)

• Monitor peripheral perfusion and urine output regularly

• Continue maintenance fluids

Metabolic haematology and biochemistry:

Diabetes insipidus is common and if not recognized and treated can quickly lead to hypernatraemia and hyperosmolality

• Measure electrolytes and creatinine regularly and treat as appropriate to maintain normal ranges

• Treat Diabetes insipidus with desmopressin (DDAVP) 4-8µgrams intravenously and repeat if necessary, or low dose vasopressin

• Start low dose insulin infusion if blood glucose persistently above 12mmol/L

• Stop bleeding, correct coaguloapthy, thrombocytopaenia and anaemia

• Avoid hypernatraemia

• Other electrolyte abnormalities – K, PO4, Ca, Mg
• Consider thyroxine replacement

Communication:

• Family - counsel, explain, keep updated

• Liaison with donor coordinator and surgical retrieval teams

Discussion

This is a straightforward question about the care of the brain-dead organ donor. A summary exists on this site, which was derived directly from the recent ANZICS guidelines. If one were to rearrange the answer to fit some sort of primitive alphabetical template, it could resemble this:

Non-clinical issues: (presumably, these have been dealt with now that the patient is "awaiting surgery for organ donation"

• Early involvement of the transplant coordinator
• Non-coercive sensitive family discussion re opportunity for donation
• Tissue typing, viral screen, further organ function tests
• Facilitate family time at bedside
• Ensure aftercare of donor family

1. The circuit should be humidified.
2. Normoxia and normocapnea must be maintained.
   There will be periodic requests for ABGs on 100% FiO₂ from the donor coordinator, but afterwards the FiO₂  must be minimised to prevent oxidative stress damage to the lungs.
3. Haemodynamic instability is to be expected:
   - The initial autonomic storm should be managed with nitroprusside and esmolol
   - The subsequent collapse should be treated with noradrenaline and/or vasopressin
   - Bradycardia will be resistant to atropine (no vagus to block); catecholamines or pacing will be required
   -Though they do not make a direct statement to this effect, ANZICS tacitly support CPR in the brain-dead organ donor; "cardiopulmonary resuscitation may result in recovery of cardiac function and successful transplantation".
4. Normoglycaemia must be maintained.
5. Normothermia must be maintained by warming externally, and by using warmed fluids.
   Electrolytes need to be maintained within normal laboratory ranges;
   particular attention needs to be paid to the sodium.
   DDAVP may be required as a hormone replacement.
   Other "endocrine support" (T3, hydrocortisone) should be considered in the following circumstances:
   - haemodynamic instability
   - an ejection fraction of less than 45%
   - heart donation is being considered
6. Fluid resuscitation should be conservative if you plant to donate lungs,  aggressive if you plan to donate kidneys, and an intelligent compromise if both organs are being considered.
7. Nutrition must continue.
   Good nutrition (or rather, the absence of malnutrition) has been associated with improved raft function (Singer et al, 2005)
8. Coagulopathy must be observed and corrected; if worsening coagulopathy or DIC develop, organ retrieval should be expedited.

References

Summarized from the ANZIC statement on Brain Death and Organ Donation, Version 3.2

Dujardin, Karl S., et al. "Myocardial dysfunction associated with brain death: clinical, echocardiographic, and pathologic features." The Journal of heart and lung transplantation 20.3 (2001): 350-357.

Totsuka, Eishi, et al. "Influence of high donor serum sodium levels on early postoperative graft function in human liver transplantation: effect of correction of donor hypernatremia." Liver Transplantation and Surgery 5.5 (1999): 421-428.

Novitzky, D., D. K. C. Cooper, and B. Reichart. "Hemodynamic and metabolic responses to hormonal therapy in brain-dead potential organ donors." Transplantation 43.6 (1987): 852-854.

Phongsamran, Paula. "Critical care pharmacy in donor management." Progress in Transplantation 14.2 (2004): 105-113.

RANDELL, TARJA T., and KRISTER AV HöCKERSTEDT. "TRIIODOTHYRONINE TREATMENT IN BRAIN-DEAD MULTIORGAN DONORS-A CONTROLLED STUDY." Transplantation 54.4 (1992): 736-737.

Goarin, Jean-Pierre, et al. "The effects of triiodothyronine on hemodynamic status and cardiac function in potential heart donors." Anesthesia & Analgesia 83.1 (1996): 41-47.

Follette, David M., Steven M. Rudich, and Wayne D. Babcock. "Improved oxygenation and increased lung donor recovery with high-dose steroid administration after brain death." The Journal of heart and lung transplantation: the official publication of the International Society for Heart Transplantation 17.4 (1998): 423-429.

Lisman, T., et al. "Activation of hemostasis in brain dead organ donors: an observational study." Journal of Thrombosis and Haemostasis 9.10 (2011): 1959-1965.

Lim, H. B., and M. Smith. "Systemic complications after head injury: a clinical review." Anaesthesia 62.5 (2007): 474-482.

Dalle Ave, Anne L., Dale Gardiner, and David M. Shaw. "Cardio‐pulmonary resuscitation of brain‐dead organ donors: a literature review and suggestions for practice." Transplant International (2015).

Singer, Pierre, Haim Shapiro, and Jonathan Cohen. "Brain death and organ damage: the modulating effects of nutrition." Transplantation 80.10 (2005): 1363-1368.

College Answer

a)

• Minimum period of 4 hours in which the patient is observed to have unresponsive coma, unreactive pupils, absent cough/tracheal reflex and no spontaneous respiratory effort
• Normothermia (temp >35oC)
• Normotension (SBP >90 mmHg, MAP >60 mmHg in adult)
• Exclusion of sedative drugs
• Absence of severe electrolyte, metabolic or endocrine disturbance
• Intact neuromuscular function
• Ability to examine the brainstem reflexes including at least one ear and one eye
• Ability to perform apnoea testing

b)

24 hours

c)

(for each part of this question ALL cranial nerves are required in order to receive the 5 marks, no marks should be given for an incomplete response)

d)

1. 1. • Concomitant high cervical cord injury
      • Severe hypoxaemia
      • Haemodynamic instability

e)

• Four vessel intra-arterial catheter angiography with digital subtraction (preferred)
• Radionuclide imaging with Tc-99m HMPAO and single photon emission computerised tomography (SPECT) (preferred)
• CT angiography (limited experience to date) (acceptable)

Discussion

This question tests the candidate's detailed knowledge of the ANZICS Statement on Death and Organ Donation (I have linked to Version 3.2, from 2013).

a) Apart from identifying evidence of sufficient intracranial pathology, list the preconditions that must be met prior to the determination of brain death by clinical criteria:

The below answer is taken directly from the Statement.

• Normothermia
• Normotension
• Exclusion of the effects of sedating drugs
• Absence of severe electrolyte, metabolic or endocrine disturbance
• Intact neuromuscular function
• Ability to adequately examine brainstem reflexes
• Ability to perform apnoea testing

b)What is the recommended minimum time for observation in cases of hypoxic-ischaemic brain injury, prior to performing clinical testing of brain-stem function?

This is an ambiguously worded question, because one could interpret is as " minimum time from cardiac arrest" or "minimum time of unresponsive coma". Quoting the ANZICS document, "There must be a minimum of four hours observation and mechanical ventilation during which the patient has unresponsive coma" before the brain-stem function can be tested. The timing of the tests following ROSC is 24 hours: "It is ... recommended that, in cases of acute hypoxic-ischaemic brain injury, clinical testing for brain death be delayed for at least 24 hours subsequent to the restoration of spontaneous circulation. "

c)For each of the following brainstem reflexes, list the cranial nerves that are tested:

In this list the college have omitted the test for pain in the trigeminal nerve distribution (CN V and VII)

d) List three contraindications to performing apnoea testing:

• Hemodynamic instability
• Severe hypoxic respiratory failure
• High cervical cord injury

The presence of any brainstem reflexes is also a contraindication. Apnoea testing must be carried out only after the brainstem reflexes have been tested, and if any of them were found to be positive any further braindeath testing cannot continue.

e) List the acceptable imaging techniques that may be used to demonstrate brain death as an alternative to clinical testing as recommended by the ANZICS Statement on Death and Organ Donation.

• Four-vessel digital subtraction arterial angiography
• Tc-99m HMPAO (technetium 99m radiolabelled hexamethyl propylene amine oxime) SPECT
• CT angiography

References

ANZICS Death and Organ Donation Committee, THE ANZICS STATEMENT ON DEATH AND ORGAN DONATION Edition 3.2 2013

College Answer

Observations and Investigations:

Clinical Signs:

• Absent brain stem reflexes.
• Myoclonic status epilepticus within the first 24 hours.

• (Generalised and repetitive myoclonus is strongly associated with poor outcome, with a reported false positive rate of 0%. Conversely, single seizures and sporadic myoclonus, do not accurately predict poor outcome.)

• Absence of pupillary responses – within days 1 to 3 after CPR.
• Absent corneal responses - within days 1 to 3 after CPR.
• Absent or extensor motor responses – after 3 days post CPR.

Electrophysiological:

EEG patterns of generalised suppression, burst suppression, or generalised periodic complexes are strongly associated with poor outcome, but the prognostic accuracy is not considered as high as SSEP.

Bilateral absence of N20 component of SSEP with median nerve stimulation within 1-3 days post CPR is strongly associated with poor outcome.

Biochemical:

Serum neuron-specific enolase levels > 33mg/L at days 1-3 strongly associated with poor outcome.

(S100, CSF CKBB are not considered accurate enough for prognostication.)

Radiological:

Imaging may reveal catastrophic intracerebral cause for the arrest.

(Diffuse swelling on CT scan is common, but predictive power not known, role of MRI/PET also unclear.)

Confounding Factors:

Induced Hypothermia – majority of studies carried out before induced hypothermia widely used. Evidence that cooling may alter interpretation of these results, but to what extent remains unclear

Time of assessment: Period of at least 72 hours post CPR recommended. Unclear how hypothermia effects this.

CT scan done too early may not show changes

Sedatives / neuro- muscular blockers 
Metabolic derangements 
Presence of shock

Organ failure

Role of “self-fulfilling prophecy” in interpreting studies

Salient points

• Absent brainstem reflexes
• Extensor motor response
• EEG
• Myoclonic status epilepticus
• SSEP
• Neuron-specific enolase
• CT brain (oedema)

Discussion

This question would benefit from a tabulated answer.

As far as cardiac arrest goes, a  2006 review of the evidence has been published in Neurology by the American Academy of Neurology. It outlines the main factors which influence neurological outcome after cardiac arrest. This 2006 statement has to some extent been superceded by the most recent ERC/ESICM statement (Sandroni et al, 2014). More detail on this topic has been summarised in the chapter on prognostication of neurological recovery following cardiac arrest.

References

Wijdicks, E. F. M., et al. "Practice Parameter: Prediction of outcome in comatose survivors after cardiopulmonary resuscitation (an evidence-based review) Report of the Quality Standards Subcommittee of the American Academy of Neurology."Neurology 67.2 (2006): 203-210.

Rogove, Herbert J., et al. "Old age does not negate good cerebral outcome after cardiopulmonary resuscitation: analyses from the brain resuscitation clinical trials."Critical care medicine 23.1 (1995): 18-25.

Levy, David E., et al. "Predicting outcome from hypoxic-ischemic coma." Jama253.10 (1985): 1420-1426.

Zandbergen, E. G. J., et al. "Prediction of poor outcome within the first 3 days of postanoxic coma." Neurology 66.1 (2006): 62-68.

Tapia, F. J., et al. "Neuron-specific enolase is produced by neuroendocrine tumours." The Lancet 317.8224 (1981): 808-811.

Torbey, Michel T., et al. "Quantitative analysis of the loss of distinction between gray and white matter in comatose patients after cardiac arrest." Stroke 31.9 (2000): 2163-2167.

College Answer

Primary problem not fixed:

Untreated focus of infection/ inadequate primary source control e.g. pancreatic abscess, infected pseudocyst.

New septic site e.g. central line/ hospital acquired pneumonia / cholecystitis, urinary tract.

Systematic approach i.e. Hypovolaemic / obstructive / cardiogenic / distributive +/- endocrine etc.

• Hypovolaemia or hidden bleeding
• E.g. From surgical site/ peptic ulcer, “third space” losses (e.g. ascites from peritonitis)
• Undiagnosed or new “obstructive shock”:

• Tension pneumothorax / Pericardial effusion / gas trapping (auto PEEP) / pleural effusions / pulmonary emboli
• Severe Intra abdominal hypertension
• Dysrhythmia e.g. SVT, junctional rhythm etc.
• New myocardial ischaemia
• New/ undiagnosed cardiac valve pathology
• Severe adrenal / pituitary / thyroid dysfunction.
• Drug reaction / anaphylaxis

• Electrolyte abnormalities such as hypophosphataemia and hypocalcaemia (the latter particularly with pancreatitis)

Technical:

CVL fallen out or not in a central vein / no pressors in the infusion bag

Measurement error – e.g. arterial line not zeroed/under or over damped, transducer height, wrong NIBP cuff size etc.

Miscellaneous:

Radial / central arterial monitoring discrepancy with severe vasoconstriction

Upper limb vascular disease (radial arterial line) or obstruction (e.g. dissection or aorto-occlusive disease: femoral arterial line)

Anti hypertensive drugs taken as part of patients usual medications

Discussion

This question does not rely on published evidence, but rather tests the candidate's ability to reason through shock in a systematic fashion.

If one were to approach it like a normal list of differentials, it would look like this:

Measurement artifact

• Arterial line is incorrectly zeroed
• Wrong sized cuff being used for NIBP

Vascular causes

• CVC has fallen out or is extravasating
• There is cardiac dysfunction due to MI, i.e. a cardiogenic shock - an ECG and TTE are warranted.
• The patient is hypovolemic, and requires more fluid - bedside static and dynamic methods of fluid responsiveness could be employed to rule this out.
• Air embolism (line-related)

Infectious causes

• A new infection may be brewing. Cultures and a septic work-up are warranted.

Inflammatory causes

• SIRS secondary to pancreatitis
• SIRS secondary to systemic hypoperfusion
• Capillary leak syndrome

Drug-induced causes

• Inappropriate drug administration - is there even any noradrenaline in that infusion bag?
• Anaphylactic drug reaction -review allergy history and examine for a rash; look for eosinophilia and send off a mast cell tryptase level.

Traumatic causes

• CVC insertion has resulted in a retroperitoneal, pleural or mediastinal hematoma
• The pancreatic pseudocysts has eroded into the splenic artery aneurysm, and the patient is exsanguinating into the abdomen
• Either way, an FBC and abdominal ultrasound would rapidly exclude these causes

Endocrine causes

• Untreated hypothyroidism
• Untreated absolute adrenal insufficiency
• Relative adrenal insufficiency
  • One would send TFTs and a random serum cortisol, then start "stress dose" steroids.
• Hypocalcemia may be causing vasoplegia.
• Hypocalcemia and hypophosphataemia may be contributing to poor cardiac contractility.
  • One would send a CMP and replace the relevant electrolytes

If one were to approach it like any shock, it would look like this:

• Artifactual shock
  • Art line inappropriately zeroed
  • Wrong size NIBP cuff
• Technical error
  • CVC is extravasating vasopressors
  • Vasopressor infusion was improperly prepared
• Obstructive shock
  • Cardiac tamponade
  • Tension pneumothorax
• Distributive shock
  • Septic shock
  • Anaphylactic shock
  • Post-bypass vasoplegia
• Hypovolemic shock
  • Haemorrhage
  • Inadequate fluid resuscitation

References

Rivers, Emanuel, et al. "Early goal-directed therapy in the treatment of severe sepsis and septic shock." New England Journal of Medicine 345.19 (2001): 1368-1377.

Jones, Alan E., et al. "The effect of a quantitative resuscitation strategy on mortality in patients with sepsis: a meta-analysis." Critical care medicine 36.10 (2008): 2734.

Kumar, Anand, et al. "Duration of hypotension before initiation of effective antimicrobial therapy is the critical determinant of survival in human septic shock*." Critical care medicine 34.6 (2006): 1589-1596.

Early Goal-Directed Therapy Collaborative Group of Zhejiang Province. "The effect of early goal-directed therapy on treatment of critical patients with severe sepsis/septic shock: A multi-center, prospective, randomized, controlled study." Zhongguo wei zhong bing ji jiu yi xue= Chinese critical care medicine= Zhongguo weizhongbing jijiuyixue 22.6 (2010): 331.

Yealy, Donald M., et al. "A randomized trial of protocol-based care for early septic shock." The New England journal of medicine 370.18 (2014): 1683-1693.

Power, GSarah, et al. "The Protocolised Management in Sepsis (ProMISe) trial statistical analysis plan." Critical Care and Resuscitation 15.4 (2013): 311.

Delaney, Anthony P., et al. "The Australasian Resuscitation in Sepsis Evaluation (ARISE) trial statistical analysis plan." Critical Care and Resuscitation 15.3 (2013): 162.

Marik, Paul E. "Early Management of Severe Sepsis: Concepts and Controversies." CHEST Journal 145.6 (2014): 1407-1418.

Peake, Sandra L., et al. "Goal-directed resuscitation for patients with early septic shock." The New England journal of medicine 371.16 (2014): 1496.

Yealy, Donald M., et al. "A randomized trial of protocol-based care for early septic shock." The New England journal of medicine 370.18 (2014): 1683-1693.

College Answer

a)
 Evoked potentials are the electrical signals generated by the nervous system in response to sensory stimuli.
 Somatosensory evoked potentials (SSEPs) consist of a series of waves that reflect sequential activation of neural structures along the somatosensory pathways.
 Somatosensory evoked potentials are usually derived from the median nerve and the tibial nerve
 SSEP components typically are named by their polarity and typical peak latency in the normalb population. N20 is a negativity that typically peaks at 20 milliseconds after the stimulus.

b)
 SSEP is the most reliable test to predict poor outcome in this patient group.
 SSEP does not predict good outcome.
 Pre-test probability for poor outcome essential: use test only in patients who remain unconscious following hypoxic-ischaemic insult (M score ≤ 3).
 Validated to use as early as 24 hours after cardiac arrest.
 SSEP not influenced by sedatives, analgesics, paralysing agents or metabolic insults.
 Bilaterally absent short latency peaks (N20 peaks) have 100% predictive value for poor outcome
(death or severe disability), with false positive rate nearly 0% and narrow confidence intervals.

c)
 Hypothermia affects SSEP test results: mainly delayed peaks (prolongation conduction times);no consistent effect on voltages (amplitudes).
 After rewarming of the patient SSEPs have comparable test characteristics as compared with studies done before therapeutic hypothermia and as such have been validated for prognostication following hypoxic-ischaemic brain injury after rewarming with similar low false positive rate.

Discussion

Rationale for the use of somatosensory evoked potentials in the comatose survivor of cardiac arrest

• Peripheral nerve stimulation should evoke a central response even in the presence of sedation or hypothermia
• The absence of such a response suggests severe damage to the cortex
• Bilateral absence of response suggests global rather than focal damage
• Ergo, SSEP should act as sensitive diagnostic tool to detect severe brain injury after cardiac arrest

Practice of somatosensory stimulation and evoked potential measurement

• Both median nerves are stimulated at the wrist with a bipolar surface electrode
• Alternative site is the tibial nerve
• Stimulus repeats at 2-5 Hz, with a duration of 0.2msec
• Surface electrodes read cortical activity at the scalp
• Evoked potentials are peaks of electrical activity which follow the peripheral stimulus with a predictable latency.
• The responses are named after their polarity (N for negative, P for positive) and their latency.
• N20 indicates a negative response over primary somatosensory cortex at ∼20 ms post stimulation.

Advantages of somatosensory evoked potentials

• Non-invasive
• Portable
• Less confounded by sedation or hypothermia than EEG (in fact, not influenced by sedatives, analgesics, paralysing agents or metabolic insults)
• Bilaterally absent N20 SSEP during hypothermia is a good predictor for absent N20 SSEP after rewarming, which means you can do SSEPs during the period of hypothermia (Bouwes et al, 2010)
• Reproduceable
• Interpretation is guided by specific criteria, rather than subjective expertise.

Evidence supporting the prognostic value of SSEPs

• Bilaterally absent short latency peaks (N20 peaks) have 100% predictive value for poor outcome (death or severe disability), with false positive rate nearly 0% and narrow confidence intervals.
• Recent (2014) consensus statement on prognostication following cardiac arrest suggested that SSEPs are prognostic at > 72 hours in cooled patients and at >24 hours in non-cooled patients
• Among a total 287 patients with bilaterally absent N20 SSEPs, only one was a false positive result (Young et al, 2005)
• Post hoc analysis by independent interpreters has suggested that the false positive was simply interpreted inaccurately in the first instance.

References

Guérit, J-M., et al. "Consensus on the use of neurophysiological tests in the intensive care unit (ICU): electroencephalogram (EEG), evoked potentials (EP), and electroneuromyography (ENMG)." Neurophysiologie Clinique/Clinical Neurophysiology 39.2 (2009): 71-83.

Tjepkema-Cloostermans, Marleen Catharina, J. Horn, and M. J. A. M. Putten. "The SSEP on the ICU: Current applications and pitfalls." Netherlands journal of critical care 17.1 (2013): 5-9.

College Answer

Additional comments:
Candidates  mentioned  detail  that  was  not  requested,  such  as  methods of  cooling.  Candidates also showed poor breadth of knowledge related to the potential use of hypothermia in conditions such as TBI / SAH / CVA.

Discussion

Rationale for therapeutic hypothermia:

• Therapeutic hypothermia has been advanced a a means of improving survival and good neurological outcome following cardiac arrest.
• It has also been offered as a means of controlling intracranial hypertension which is refractory to other modalities.
• Therapeutic hypothermia modulates the activity of body proteins and electrolytes.
• This modulation is thought to have some beneficial effects in scenarios where inflammatory damage is anticipated.
• This also involves the down-modulation of the overall metabolic rate, which decreases the metabolic demands of the organism in situations where supply of metabolic substrate may be compromised.
• Decrease in oxygen consumption matches decreased demand with decreased supply in "penumbra" areas, at the watersheds, where hypoxic injury has caused oedema.\

Advantages of therapeutic hypothermia

• Decreased granulocyte migration into tissue
• Decreased cerebral oedema
• Intrinsic anticonvulsant effects of hypothermia

Well-accepted indications:

• Mild therapeutic hypothermia for survivors of cardiac arrest
• Therapeutic hypothermia for traumatic brain injury (less so post EUROTHERM)

Evidence for use in cardiac arrest: 

• Pseudorandomised unblinded trial in 1996 - promising results
• Bernard et al  demonstrated a survival benefit in out of hospital VF arrest survvors
•  A recent Cochrane review supports the use of therapeutic hypothermia, finding a 1.35 risk reduction for mortality.
• The recent TTM trial  has demonstrated non-inferiority of a more conservative hypothermia (36°C) with standard temperature goals, in terms of mortality.

Evidence for use in traumatic brain injury

• EUROTHERM 3235 trial (2015): 387 patients; hypothermia was used as a second-line therapy to reduce ICP.
• No survival benefit was observed.
• Recruitment was suspended early owing to safety concerns.
• ICP control was in fact better in the hypothermia group (they required rescue therapies less frequently)
• The meta-analysis mentioned by the college is possibly  this 2013 review by Georgiou et al; except there was no benefit in mortality when only high quality trial were included.

Extended indications:

Therapeutic hypothermia in cooling of a hyperthermic patient

• Hyperthermia is associated with substantial harm, particularly if the temperature increases beyod 41°C
• Causes of such hyperthermia may be numerous, including sepsis, malignant hyperthermia, anticholinergic drug poisoning, heat stroke, and so on and so forth.
• In brief, these causes all have specific management strategies which may take time to work.
• In the interim, the temperature must be managed, so that organ damage does not occur
• Induction of hypothermia (or maintenance of controlled normothermia) by cooling the patient can be viewed as one of the indications.

Therapeutic hypothermia for subarachnoid haemorrhage

• Theoretically, TH may be protective in SAH in the same way that it is supposed to be protective in traumatic brain injury. Areas affected by ischaemia in the context of vasospasm may benefit from having a lower metabolic rate.
• TH certainly  seems to decrease the flow velocity in the MCA of subarachnoid haemorrhage patients (Seule et al, 2014), suggesting that the metabolic rate is indeed affected enough to influence cerebral blood flow.
• Animal studies have also demonstrated that hypothermia reverses vasospasm (in rats)
• In patients with "poor-grade" SAH, good functional outcome was achieved in 48% with the combination of barbiturate coma and hypothermia to 33-34°C (Gasser et al, 2003)
• A more recent case series (Seule et al, 2010) found good outcomes in 57% of  severe SAH patients who developed vasospasm.
• In contrast, Karnatovskaia et al (2014) found no difference in neurological outcome within their case series.
• No recommendation in favour of this use of TH can be made with a straight face.

Therapeutic hypothermia for super-refractory status epilepticus

• Hypothermia is known to have antiepileptic effects.
• Case series (eg. Corry et al, 2008) have demonstrated its feasibility in humans (target temperature: 31–35°C)
• Neurocritical care society guidelines for status epilepticus (Brophy et al, 2012) identified only 4 articles in the literature, and were unable to make very strong recommendations.
• The HYBERNATUS trial mentioned in the college answer is apparently ongoing, but no longer recruiting participants.

Therapeutic hypothermia for severe sepsis

• Anti-inflammatory effects of hypothermia were studied in an animal model of severe sepsis (Kwang et al, 2012).
• The hypothermic rats (30–32 °C) did better in terms of acute lung and liver injury.
• Human applications of this are limited by concern that ...firstly, a fever is an antibacterial physiological response, and secondly, that the haemodynamic instability of septic shock will be exacerbated by hypothermia.

Therapeutic hypothermia for meningitis

• Evidence of potential harm mentioned by the college in their answer was found by a 2013 RCT (Mourvillier et al). The investigators found a higher mortality in the hypothermia group.

Therapeutic hypothermia for neonatal asphyxia

• Following on from the success of TH in adult cardiac arrest, this modality has been applied to neonatal hypoxic-ischaemic encephalpathy.
• Shankaran et al (2005) performed an RCT; the group of neonates who were cooled 33.5°C for 72 hours; the rate of cerebral palsy was reduced from 19% to 15%, and mortality improved from 37% to 24%. In the long term, there was no increase in disability among hypothermia-exposed survivors when compared to surviving controls (Shankaran et al, 2012)
• TOBY trial (2014) confirmed that both survival and neurological outcome is improved

Therapeutic hypothermia for stroke

• The college answer points out that fever is associated with two-fold risk of death after haemorrhagic or ischaemic stroke. Pharmacologic methods of fever control have not shown improved outcome in stroke.
• In animal models of stroke, , mild or moderate hypothermia has been shown to decrease infarct size and lead to functional improvement when cooling was initiated within a few hours of ischemia onset (Clark et al, 2008). But... These were rats, and they were cooled to 24°C

Therapeutic hypothermia for acute hepatic encephalopathy

• This use of TH is an extension of the observation that TH reduces cerebral oedema in patients with traumatic brain injury.
• Some authors (Stravitz et al, 2008) have suggested that TH may be an effective bridge to liver transplant.
• Human case series support this assertion (Jalan et al, 1999); during their treatment there was no significant relapse of increased intracranial pressure.
• There are no RCTs, but a large-scale retrospective cohort (Karvellas et al, 2014) did not find any survival benefit.

Therapeutic hypothermia in ARDS :

• Recent studies (Zhicheng et al, 2012) have confirmed that mild hypothermia improves gas exchange, lung compliance, duration of ventilation and the levels of IL-6 in local lung tissue.
• Of particular interest is the use of hypothermia to reduce the whole-body oxygen demand in situations where even veno-venous ECMO is powerless to oxygenate the patient (Hayek et al, 2015)

Intraoperative therapeutic hypothermia

• Cardiothoracic surgery, routinely in use (including DHCA).
• Neurosurgery for aneurysm clipping: IHAST trial, 2005; no benefit ("good-grade" SAH patients)
• Vascular surgery, to protect the spinal cord during prolonged aortic cross-clamp

Suspended animation for delayed resuscitation

• In essence, this is a practice of stopping the circulation with deep hypothrmia, so as to buy time to the definitive management of the cause of the cardiac arrest.
• Animal studies have demonstrated success with up to 90 minutes of no-flow (Safar et al, 2002)
• Wu et al (2006) subjected dogs to rapid haemorrhage, and then used a 2°C saline aortic flush to achieve a brain temperature of 10°C. The dogs remained on ice for 2 hours, and were then revived on cardiopulmonary bypass.  Intact neurological outcome was achieved in 4 out of 6 dogs.

References

Andrews, Peter JD, et al. "Hypothermia for intracranial hypertension after traumatic brain injury." New England Journal of Medicine 373.25 (2015): 2403-2412.

Georgiou, A. P., and A. R. Manara. "Role of therapeutic hypothermia in improving outcome after traumatic brain injury: a systematic review." British journal of anaesthesia (2013): aes500.

College Answer
 

References

Engdahl, Johan, et al. "Can we define patients with no and those with some chance of survival when found in asystole out of hospital?." The American journal of cardiology 86.6 (2000): 610-614.

Bunch, T. Jared, et al. "Outcomes and in-hospital treatment of out-of-hospital cardiac arrest patients resuscitated from ventricular fibrillation by early defibrillation." Mayo Clinic Proceedings. Vol. 79. No. 5. Elsevier, 2004.

Levine, Robert L., Marvin A. Wayne, and Charles C. Miller. "End-tidal carbon dioxide and outcome of out-of-hospital cardiac arrest." New England Journal of Medicine 337.5 (1997): 301-306.

Rea, Thomas D., et al. "Temporal Trends in Sudden Cardiac Arrest A 25-Year Emergency Medical Services Perspective." Circulation 107.22 (2003): 2780-2785.

Carew, Heather T., Weiya Zhang, and Thomas D. Rea. "Chronic health conditions and survival after out-of-hospital ventricular fibrillation cardiac arrest." Heart 93.6 (2007): 728-731.

Goldberger, Zachary D., et al. "Duration of resuscitation efforts and survival after in-hospital cardiac arrest: an observational study." The Lancet (2012).

Wijdicks, E. F. M., et al. "Practice Parameter: Prediction of outcome in comatose survivors after cardiopulmonary resuscitation (an evidence-based review) Report of the Quality Standards Subcommittee of the American Academy of Neurology."Neurology 67.2 (2006): 203-210.

Rogove, Herbert J., et al. "Old age does not negate good cerebral outcome after cardiopulmonary resuscitation: analyses from the brain resuscitation clinical trials."Critical care medicine 23.1 (1995): 18-25.

LEVY, DE, et al. "Predicting Outcome from Hypoxic-Ischemic Coma." Survey of Anesthesiology 30.2 (1986): 93.

Sandroni, Claudio, et al. "Prognostication in comatose survivors of cardiac arrest: an advisory statement from the European Resuscitation Council and the European Society of Intensive Care Medicine." Resuscitation 85.12 (2014): 1779-1789.

College Answer

a)

Pulsus paradoxus is an exaggeration (> 12 mmHg or 10%) of the normal inspiratory decrease in systemic blood pressure.

Decreased intrathoracic pressure with inspiration results in increased venous return to right heart and bulge of IVS to left. Because the ventricle can normally also expand outward, this septal shift is usually small, and the difference in the blood pressure is therefore small between inspiration and expiration (<10 mmHg). With tamponade, the left ventricle cannot expand outward, so the septal shift is exaggerated and the difference in BP is larger. Also, the relatively higher negative pressure in the pulmonary circulation compared to the left atrium in patients with pericardial pathology pooling of blood in pulmonary veins during inspiration resulting in decreased LV stroke volume.

b)

Palpation of pulse- disappears in deep inspiration

Sphygmomanometer- Korotkoffs sounds first heard in expiration only and then in inspiration with progressive deflation

Pulse Oximeter-particularly useful in paediatrics

Arterial pressure trace- exaggerated fall of systolic pressure in inspiration

c)

Hypotension

Elevated JVP (neck vein distension with inspiration- Kussmaul’s sign) Muffled heart sounds

Tachypnoea

Exaggerated drop in diastolic CVP (Friedrich’s sign)

Absent y descent on CVP trace

Clinical signs of shock- decreased peripheral perfusion, slow capillary refill, oliguria, confusion.

d)

Tachycardia

Low QRS voltage trace Electrical alternans

Global concave ST elevation PR depression

e)

Visible pericardial effusion

Diastolic collapse of Right Atrium and Right Ventricle

Respiratory variation in left and right sided volumes. Atrial and ventricular septa move leftward during inspiration and rightward during expiration

Mitral and Tricuspid flow velocities are increased and out of phase. Mitral flow is increased on the first beat of inspiration and tricuspid flow is increased on expiration.

The IVC is distended and does not collapse on inspiration

Discussion

a) The definition of pulsus paradoxus used by the college is from Curtiss et al (1988) who demonstrated that 12 mmHg and 9% systolic variation (not 10%) are the 95% confidence limits for diagnosis of moderate or severe tamponade. Most textbooks instead use 10mmHg as a convenient round number, described by Swami and Spodick (2003) as "a quasi arbitrary but practical level".

b) there are in fact only four methods known:

• Invasive arterial pressure trace: that's the classical ICU technique of demonstrating pulsus paradoxus, and is colloquially described as a "swing" of the arterial line.
• Palpation of the radial pulse:  the disappearance of the radial pulse on inspiration was the original sign described by Kussmaul.
• Sphygmomanometry: with the blood pressure measurement cuff inflated to the level of the systolic blood pressure, one ought to hear Korotkoff sounds.  Because the systolic blood pressure falls during spontaneous inspiration, the Korotkoff sounds disappear during inspiration. 
• Pulse oximetry is "particularly useful in paediatrics" according to the college examiners; they probably said this on the basis of a study by Tamburro et al (2002). The pulse oximeter waveform does something similar to the waveform of an arterial line, i.e "a decrease in the highest value of the upper plethysmographic peak of the pulse-oximetry waveform was observed during inspiration in each patient". Tamburro et al  observed this phenomenon in eight children and adolescents, which might give rise to the impression that this technique is "particularly useful in paediatrics". This might be in reference to the practical difficulties of using invasive blood pressure monitoring in children; otherwise the technique is probably equally useful in adults. 

c) These are the clinical signs of cardiac tamponade (some available mainly via invasive monitoring waveforms)

• Nonspecific findings which include tachycardia and tachypnoea

• Beck's Triad: Muffled heart sounds, hypotension and raised CVP.
• Kussmaul's sign: the neck veins distend with inspiration, instead of collapsing (though not everybody agrees that this is seen in tamponade)
• Friedreich's sign: an exaggerated early drop in diastolic CVP.
• Pulsus paradoxus - an exaggeration of the normal inspiratory fall in blood pressure
• Pericardial rub  if the tamponade is associated with some sort of pericardial inflammation
• Pericardial "knock", first described by Maynard Smith  (consulting surgeon of the British Expeditionary Force, 1918)  as a sound which  "may be compared to that heard in the ear-piece of a telephone when the lever is moved up and down". 
• A third heart sound 
• Displaced apex beat 
• Characteristric CVP findings: classically, a sawtooth "M" or "W"  configuration of a raised CVP.
  
  In summary
  • The CVP is raised
  • All CVP waveform components are elevated
  • a and v waves are tall
  • x descent is steep
  • y descent is (usually) absent

d) Electrocardiograhic features of pericarditis with tamponade are:

• Tachycardia 
• Low QRS voltage trace - which develops as the result of a large volume of fluid in the way between the heart and the electodes, a fluid which has relatively poor conductivity. Not surprisingly, this feature is found more often in patients with large effusions. However,  truly humongous effusions can be present without any tamponade physiology. 
• Electrical alternans  is the presence of alternating high and low QRS complexes. LITFL has a nice example. 
• Global concave ST elevation results from the current of injury which develops from direct pressure on the myocardium. 
• PR depression - this is usually asociated with pericarditis, and because pericarditis is often associated with pericardial effusion the PR segments are often depressed in cardiac tamponade. Obviously, cardiac tamponade which is not due to pericarditis will probably have normal-looking PR segments. 
• T wave inversion may develop as a result of pericardial irritation, but is by no means unique to cardiac tamponade. 

e) Echocardiographic features listed here are from Pérez-Casares et al (2017) 

• A visible pericardial effusion is certainly a helpful finding but is by no means mandatory. Particular examples of tamponade without a significant effusion might include blood clot following cardiac surgery, where the clot does not present as a classical black echolucency you'd normally expect of a pericardial effusion.
• Diastolic collapse of right atrium and right ventricle: this happens when the intra-chamber pressures are at their lowest. In diastole, there will be a timer where the chamber pressures are actually lower than the pericardial fluid pressure. In this situation the chambers will collapse. Atrial collapse is usually seen before ventricular collapse
• Right atrial collapse in systole:  in early systole, atrial cavity pressure  is lower than the pericardial fluid pressure, and there is collapse of the thin free wall. Duration of this phenomenon is important: apparently, collapse for longer than one-third of the cardiac cycle is 100% specific for clinical cardiac tamponade
• Right ventricular collapse in diastole: during the early stages, this is only present in expiration when venous return is at its poorest. Again, the loger the duration of collapse, the more severe the tamponade.
• Diastolic ventricular size variability with respiratory cycle  is visually demonstrated using M-mode. Inspiration brings venous return to the RV and the RV dilates, pushing the septum into the LV. The opposite occurs in expiration. 
• Septal "bounce" is the colloquial-sounding name given to the inspiratory movement of the septum towards the LV. 
• IVC dilatation is seen because all the veins are dilated, and is essentially the echocardiographic equivalent of a raised JVP.
• Mitral flow is decreased on inspiration:  in cardiac tamponade the peak E-wave velocity is decreased by 25% on inspiration.
• Peak E-wave tricuspid valve physiological variation is larger than the mitral valve fluctuations -  in tamponade the peak E-wave velocity will drop by 40% in expiration compared to inspiration.
• RVOT/LVOT flow velocity fluctuation:  during normal respiration the physiologic variation of flow in these regions is less than 10%, but in tamponade the fluctuation is greater. During inspiration the aortic peak velocity will drop by 10%, and a rise of 10% will be seen in the pulmonary trunk.
• Hepatic vein flow reversal: in diastole, before atrial contraction the flow is either slowed or reversed. 
• Pulmonary vein flow reversal: again the flow is either slowed or reversed before the atria contract (usually there would be some flow reversal when the atria contract, which is perfectly normal physiological phenomenon)

References

Beck, Claude S. "Two cardiac compression triads." Journal of the American Medical Association 104.9 (1935): 714-716.

Spodick, David H. "Acute cardiac tamponade." New England Journal of Medicine 349.7 (2003): 684-690.

Ariyarajah, Vignendra, and David H. Spodick. "Cardiac tamponade revisited: a postmortem look at a cautionary case." Texas Heart Institute Journal 34.3 (2007): 347.

Bilchick, Kenneth C., and Robert A. Wise. "Paradoxical physical findings described by Kussmaul: pulsus paradoxus and Kussmaul's sign." The Lancet 359.9321 (2002): 1940-1942.

Lange, Ramon L., et al. "Diagnostic signs in compressive cardiac disorders: constrictive pericarditis, pericardial effusion, and tamponade." Circulation 33.5 (1966): 763-777.

Friedreich, N. "Zur Diagnose der Herzbeutelverwachsungen." Archiv für pathologische Anatomie und Physiologie und für klinische Medicin 29.3-4 (1864): 296-312.

Smith, S. Maynard. "Pericardial knock." British Medical Journal 1.2977 (1918): 78.

Hancock, E. W. "Subacute effusive-constrictive pericarditis." Circulation 43.2 (1971): 183-192.

Shabetai, Ralph, Noble O. Fowler, and Warren G. Guntheroth. "The hemodynamics of cardiac tamponade and constrictive pericarditis." The American journal of cardiology 26.5 (1970): 480-489.

Curtiss, Edward I., et al. "Pulsus paradoxus: definition and relation to the severity of cardiac tamponade." American heart journal 115.2 (1988): 391-398.

Swami, Ashwin, and David H. Spodick. "Pulsus paradoxus in cardiac tamponade: a pathophysiologic continuum." Clinical cardiology 26.5 (2003): 215-217.

Hamzaoui, Olfa, Xavier Monnet, and Jean-Louis Teboul. "Pulsus paradoxus." European Respiratory Journal 2013 42: 1696-1705

Ruskin, Jerome, et al. "Pressure-flow studies in man: effect of respiration on left ventricular stroke volume." Circulation 48.1 (1973): 79-85.

Wong, Frankie WH. "Pulsus paradoxus in ventilated and non-ventilated patients." Dynamics 18.3 (2007): 16-18.

Khasnis, A., and Yash Lokhandwala. "Clinical signs in medicine: pulsus paradoxus." Journal of postgraduate medicine 48.1 (2002): 46.

Möller, C. T., C. G. Schoonbee, and G. ROSENDORFF. "Haemodynamics of cardiac tamponade during various modes of ventilation." British Journal of Anaesthesia 51.5 (1979): 409-415.

Wagner, Henry R. "Paradoxical pulse: 100 years later." American Journal of Cardiology 32.1 (1973): 91-92.

Tamburro, Robert F., John C. Ring, and Kimberly Womback. "Detection of pulsus paradoxus associated with large pericardial effusions in pediatric patients by analysis of the pulse-oximetry waveform." Pediatrics 109.4 (2002): 673-677.

Friedman, Howard S., et al. "The electrocardiographic features of acute cardiac tamponade." Circulation 50.2 (1974): 260-265.

Eisenberg, Mark J., et al. "The diagnosis of pericardial effusion and cardiac tamponade by 12-lead ECG: a technology assessment." Chest 110.2 (1996): 318-324.

Badiger, Sharan, Prema T. Akkasaligar, and M. S. Biradar. "Electrocardiography–pericarditis, pericardial effusion and cardiac tamponade." International Journal of Internal Medicine1.4 (2012): 37-41.

Pérez-Casares, Alejandro, et al. "Echocardiographic evaluation of Pericardial effusion and Cardiac Tamponade." Frontiers in pediatrics 5 (2017): 79.

College Answer

a)                                                                                                                                     

Guidelines recommend PMCD for pregnant women in cardiac arrest > 24/40 weeks (with fundus height at or above the umbilicus) when ROSC has not been achieved with usual resuscitation measures with manual lateral uterine displacement (LUD). In extreme circumstances may be considered in 20 – 24/40 week pregnancy but evidence for benefit is limited.

Decisions on the optimal timing of a PMCD for both the infant and mother are complex and require consideration of factors such as the cause of the arrest, maternal pathology and cardiac function, foetal gestational age, and resources. Shorter arrest-to-delivery time is associated with better outcome.

PMCD should be strongly considered for every mother in whom ROSC has not been achieved after ≈4 minutes of resuscitative efforts. 

If maternal viability is not possible (through either fatal injury or prolonged pulselessness), the procedure should be started immediately; the team does not have to wait to begin PMCD. 

There is no requirement for transfer to an operating theatre, obstetric/surgical expertise, and equipment beyond a scalpel or lengthy antiseptic procedures

        b)                                                                                                                                            

• Manual lateral uterine displacement +/- left lateral tilt to avoid aorto-caval compression. Early intubation to decrease risk of aspiration – likely to be more difficult in pregnant patient Hand placement for chest compressions may need to be slightly higher.
• Standard pad placement may be difficult because of breast size so consider bilateral (biaxillary) placement.
• Early call for obstetric and paediatric help.

Discussion

a)

"Factors that govern the decision " is a strange thing to ask for, and could have been worded better. Unfortunately, the college could not have directly ased for "indications and contraindications" because no guidelines exist to strictly define them. In the absence of hard evidence, the following expert suggestions act as criteria for perimortem caesarian section:

• Less than 4-5 minutes from arrest
• Without a prolonged period of unwitnessed collapse
• At or after 23 weeks of gestation

If the delivery is being performed with foetal survival as the rationale, further criteria apply:

• Without a prolonged period of maternal haemorrhage or hypoxia
• With foetal heart beat confirmed as present

Other "factors that govern" could be listed. In fact, the whole things could really be interpreted as a "critically evaluate perimortem caesarian" sort of question. In which case, one should offer arguments for and against PMCD, as well as the current evidence. Thus:

Arguments for peri-mortem Caesarian

• Improved venous return to the heart
• Improved efficiency of external cardiac compressions (sans pelvic tilt)
• A chance for foetal survival if the mother is unsalvageable
• Allows transabdominal direct cardiac massage.

Arguments against peri-mortem Caesarian

• Strong evidence is lacking.
• The procedure must occur within 4 minutes of arrest
• Rarely can the procedure be performed that fast. Average time is 16 minutes (Einav et al, 2012).
• Of the infants delivered "late", many will have severe neurological sequelae (Katz et al,  1986)

Theoretical risks of perimortem Caesarian

• Foetal injury during the rushed procedure
• Maternal complications consistent with survival, but resulting in disability.
• Medicolegal risks, eg. patient/spouse/siblings will object in the future.
• One may also be determined negligent for not performing this potentially lifesaving procedure.

Evidence regarding the efficacy and safety of  peri-mortem Caesarian

• Morris, 1996: 75% foetal survival in non-arrest trauma setting.
• Beckett et al (2015): improved maternal survival and increased rates of ROSC

b)

Modifications to standard protocols consist of the following points:

Modifications to diagnostic thinking

• Though pregnant women may die of the same causes as non-pregnant non-women (i.e. the four Hs and four Ts), one needs to keep in mind the following alternative causes of arrest:
  • Amniotic fluid embolism
  • Hypertensive disorder of pregnancy (with ensuing cardiac failure)
  • Seizures (with ensuing hypoxia and arrest)
  • Haemorrhage from liver rupture
  • Haemorrhage from uterine rupture

Issues which complicate the pregnant arrest and peri-arrest scenario

• Difficult intubation
• Increased risk of aspiration (the stomach just doent't empty)
• Venous return is impaired by the gravid uterus
• Systemic oxygen consumption is increased
• Cardiac output and circulating volume are greater; decompensation occurs later.

Modifications to basic life support

• Manually displace the uterus to the left (off the aorta and vena cava)
• Add a left lateral tilt (the ideal angle is unknown, and is thought to be between 15° and 30°).
  • A left lateral tilt may compromise effective CPR, but is still recommended by the ARC Guideline 11.10  (2011) "Special Circumstances". In contrast, ECC and AHA no longer recommend the left lateral tilt (see the 2015 AHA update and the 2015 ECC guidelines). Presumably, once the ARC get around to it, their guidelines will fall in line with international consensus. 
• Prepare for an emergency perimortem caesarian.
• Biaxillary defibrillator pad placement

References

Einav, Sharon, Nechama Kaufman, and Hen Y. Sela. "Maternal cardiac arrest and perimortem caesarean delivery: evidence or expert-based?." Resuscitation 83.10 (2012): 1191-1200.

Morris Jr, John A., et al. "Infant survival after cesarean section for trauma." Annals of surgery 223.5 (1996): 481.

Beckett, V. A., P. Sharpe, and M. Knight. "CAPS—A UKOSS STUDY OF CARDIAC ARREST IN PREGNANCY AND THE USE OF PERI-MORTEM CAESAREAN SECTION. IMPLICATIONS FOR THE EMERGENCY DEPARTMENT." Emergency Medicine Journal 32.12 (2015): 995-995.

Elkady, A. A. "Peri-mortem Caesarean Section Delivery: A Literature Review and Comprehensive Overview." Enliven: Gynecol Obstet 2.3 (2015): 005.

Campbell, Tabitha A., and Tracy G. Sanson. "Cardiac arrest and pregnancy." Journal of emergencies, trauma, and shock 2.1 (2009): 34.

Katz, Vern L., Deborah J. Dotters, and William Droegemueller. "Perimortem cesarean delivery." Obstetrics & Gynecology 68.4 (1986): 571-576.

Manner, Richard L. "Court-Ordered Surgery for the Protection of a Viable Fetus:, 247 6a. 8b, 274 SE 2d 457 (1981)." (1982).

College Answer

a)

Conditions precluding clinical testing brain death                         

• Absence of diagnosis consistent with brain death
• Hypothermia (< 35 degrees)
• Hypotension (< 90 mmHg systolic or < 60 mmHg MAP in adult)
• Recent administration of sedative drugs
• Abnormalities of electrolyte, metabolic or endocrine function
• Recent administration of neuromuscular blocking agents or spinal cord injury
• Inability to adequately examine the brain stem reflexes (surgery to pupils/perforated ear drum)
• Inability to perform apnoea testing (acute lung injury)

b)

Examination components:

Observation

• Minimum of 4 hour period of observation and mechanical ventilation during which patient has unresponsive coma

Clinical test                                                         Cranial Nerve

i. Coma

ii. Pupillary reflex                                                   II, III

iii. Corneal reflex                                                   V, VII

iv. Pain reflex in trigeminal nerve distribution  V, VII

v. Vestibular ocular reflex                                     III, IV, VI, VIII

vi. Gag reflex                                                         IX, X

vii. Cough reflex                                                   X

viii. Breathing effort with apnoea

Imaging techniques                                                                                              

• Four vessel intra-arterial angiography with digital substraction
• Radionucleotide imaging with Tc 99m HMPAO
• CT angiography – may be acceptable

Imaging techniques need to be done in association with exclusion of preconditions and assessment of those cranial nerves that can be assessed and results need to be reviewed by 2 appropriate clinicians excluding the clinician performing the test.

Discussion

a)

The below preconditions are taken directly from the ANZICS Statement.

• "Brain death cannot be determined without evidence of sufficient intracranial pathology". There must be an explanation for the coma which is consistent with the diagnosis of brain death.
• Minimum period of 4 hours in which the patient is observed to have unresponsive coma, unreactive pupils, absent cough/tracheal reflex and no spontaneous respiratory effort
• Normothermia
• Normotension
• Exclusion of the effects of sedating drugs
• Absence of severe electrolyte, metabolic or endocrine disturbance
• Intact neuromuscular function
• Ability to adequately examine brainstem reflexes
• Ability to perform apnoea testing

Four hours of observation during which the patient remains in unresponsive coma

• GCS of 3
• Unresponsive pupils
• Absent cough reflex
• No spontaneous breathing efforts

Preconditions for apnoea testing

• Absence of concomitant high cervical cord injury
• Normoxia; satisfactory gas exchange
• Haemodynamic stability
• Absent brain stem reflexes

b)

Testing for unresponsive coma

• Painful stimulus in cranial nerve distribution, eg. supraorbital nerve pressure
• Painful stimulus in all 4 limbs, eg. nailbed pressure
• There should be no response

Brain Stem  Reflex Testing (these are tested in sequence; all reflexes must be absent)

• Pupil Light Reflex: CN II,  III
• Corneal  Reflex: CN V,  VII
• Trigeminal Pain: CN V, VII
• Vestibulo-ocular reflex: CN II, IV, VI, VIII
• Gag reflex: CN IX, X
• Cough reflex: CN X

Apnoea testing

• Preoxygenate with 100% FiO2 for 5 minutes, and then turn off the ventilator.
• Continue supplying oxygen via T-piece or something similar. Watch for absent breaths.
• After 10 minutes, take an ABG to demonstrate that the CO₂ is rising.
• To qualify for  brain death, apnoea must persist despite adequate respiratory stimulus (PaCO₂ 60mmHg, or a rise by 20mmHg)

c)

Investigations used to demonstrate a lack of intracranial blood flow are slightly different to those which might be used to demonstrate brain death, as the lattercategory may include such things as EEG (isoelectric EEG).

The imaging modalities are discussed in greater detail in the chapter on radiological testing for brain death.

In brief, the ANZICS-recommended modalities are:

• Tc-99 HMPAO SPECT scan
• DSA (Four-vessel Intra-Arterial Angiography)

Modalities which are not recommended as strongly include:

• MRI
• CT angiography
• Transcranial doppler

The ANZICS statement now says CT angio "is acceptable", whereas at the time of this exam paper being written they merely weazeled that it "may be acceptable". The argument againt CT angiography is the gated timing of the scan. Whereas DSA watches contrast wash in over time in a series of still images, the CT offers a momentary snapshot of that contrast in the vessels. One might argue that the CT was mis-timed, and the contrast did not yet have time to move into the brain (in this way, perfectly healthy people could be made to appear brain-dead by adjusting the timing of the scan). Obviously, when one is going to declare brain death, there needs to be no argument about the validity of the confirmatory test. The 2014 Cochrane review (Taylor et al) could not support the use of CTA, but subsequent improvements in technology have improved the level of confidence with this modality. ANZICS now recommends the use of a four-point scale to radiologically confirm absent brain perfusion by CTA, which consists of "absent enhancement of both middle cerebral artery (MCA) cortical branches (i.e. beyond the Sylvian branches); andabsent enhancement of both internal cerebral veins"

References

ANZICS Statement on Death and Organ Donation

Taylor, Tim, et al. "Computed tomography (CT) angiography for confirmation of the clinical diagnosis of brain death." The Cochrane Library (2014).

College Answer

a)

Probably multifactorial but potential causes:

• Distributive shock
  • Septic shock
• Cardiogenic shock/cardiac depression from sepsis/drugs
• Obstructive shock- 
  • pneumothorax
  • High PEEP 
  • Dynamic hyperinflation
  • Tamponade less likely
  • PE unlikely
• Hypovolaemic shock less likely but patient may be fluid responsive
• Drug delivery failure – misplaced CVC / kinked or leaking line
• Administration of drugs causing hypotension e.g. propofol, IV paracetamol

b)

Clinical exam (ABCs) to assess for cause and resuscitate simultaneously

• Rapid check to verify BP – non-invasive, check transducer position, check arterial pressure trace not damped
• Recent CXR / lung U/S for pneumothorax
• Associated oxygen requirements
• CVP – baseline and change with fluid responsiveness
• Evidence of end organ perfusion: lactate, urine output, LFTs
• Response to dynamic manoeuvres (e.g. straight leg raise)

Management options:

• Assess for and treat reversible causes: 
• If possible minimise PEEP and sedation o Check ventilator settings
• Judicious fluid filling but conflicting goals given oxygenation difficulties
• Urgent echocardiogram to exclude cardiac cause and assess fluid responsiveness +/- cardiac output monitor (PAC/PiCCO/Vigileo)
  • If hyperdynamic consider addition of steroid therapy and vasopressin
  • If low cardiac output state consider addition of adrenaline +/- other inotrope e.g. milrinone/dobutamine
  • If hypovolaemic appropriate fluid resus
• Maintain adequate oxygenation, ventilation
• Review micro and check sensitivities
• Broad spectrum antibiotics
• Consider fresh bag of noradrenaline

Discussion

a)

Broadly, differential diagnosis for shock would have to include the following categories:

• Neurogenic: another form of “distributive” shock
• Anaphylactic: also “distributive” shock
• Cardiogenic: pump failure. No pumping = no blood flow
• Hypovolemic: loss of blood or water
• Obstructive: eg. tension pneumothorax or cardiac tamponade
• Septic: “distributive” shock; stagnation of blood flow owing to vasodilation

In the context of the history we are offered, one may need to reframe the answer and order it in reference to the likelihood of each cause. The college love it when you prioritise your answer. Thus:

• Septic shock  is the most likely answer, as the patient already has a diagnosed
• Cardiogenic shock is the next most likely, as the patient is in the right age group for coronary artery disease, is at risk of MI, and may have a degree of septic cardiomyopathy
• Hypovolemic shock is the next most likely, and may represent a sudden GI bleed ( as patients with high PEEP are at greater risk of gastric ulceration) or another
• Obstructive shock is possible, given that the PEEP is very high
• Artifactual shock: the blood pressure is being measured incorrectly, or the noradrenaline line has become accidentally disconnected

b)

This approach assumes that the patient does not have any fancy PiCCO or PA catheter in situ.

• Rule out artifactual and spurious causes
  • Re-zero/recalibrate arteral line
  • Ensure vasopressor infusion line is connected
  • Exclude drug error ("is that really noradrenaline?")
  • Ensure sedation infusion rate is not accidentally excessive
• Assess the airway
  • Rule out airway obstruction
  • Examination of the patient'sface to rule out angioedema and anaphylaxis can take place at this stage, as it would be important to exclude these early.
• Assess the respiratory system
  • Examine chest expansion
  • Auscultate the chest
    • Rule out tension pneumothorax
    • Rule out dynamic hyperinflation
  • End-tidal CO2:
    • Rule out hypercapneic vasodiation
    • Consider massive PE if EtCO₂ is suddenly lower than the last PaCO₂
  • Drop PEEP to 8-10, to exclude the contribution of high PEEP
• Assess the circulation in detail, focusing on the following
  • Capillary refill
  • Tachycardia or bradycardia (i.e. is the rate responsible for the hypotension)
  • Arrhythmia (i.e. AF with loss of atrial kick)
  • Heart sounds and murmurs (new murmur? Did the mitral valve just die on me? Are the heart sounds muffled, suggestive of a pericardial effusion?)
  • CVP and its trend: did the CVP just suddenly drop, or rise?
  • Urine output in the last hour
  • Aspirate the NG tube, to look for blood or coffee grounds
• Assess dynamic predictors of fluid responsiveness
  • Pulse pressure variation, arterial line"swing"
  • Passive leg raise test
• At this stage, one should decide whether one wants to give a fluid bolus of 10ml/kg
• Perform a rapid bedside TTE, looking for:
  • LV contractility (grossly: "good, bad, not too bad")
  • RV dilatation (grossly: is it bigger than the LV on a 4-chamber view?)
  • Pericardial effusion and tamponade
  • IVC diameter (although this resembles black magic, because nobody knows what the normal appearance should be. A dry collapsed IVC is more informative than a vaguely mid-sized one).
• At this stage, one should decide whether one wants to add an inotrope, eg. milrinone or dobutamine
• At this stage one should also have come to the conclusion as to what short of shock state this is.
  • If the shock is of a distributive sort, one should consider adding vasopressin to noradrenaline, and giving the patient a "stress dose" of corticosteroids.
• Investigations:
  • Perform a CXR to ensure the CVC tip is in an appropriate position and that no new pathology has emerged beyond the pneumonia
  • Perform an ECG, looking for new change suspicious of MI
  • Perform an ABG and a set of bloods to look for lactic acidosis and to establish any organ system failures
  • Perform a septic screen, including blood cultures and inflammatory markers
• If the cause of haemodynamic instability is still not apparent form these manoeuvres, or a TTE is not available, one may need to resort to advanced haemodynamic monitoring techniques:
  • PA catherisation
  • PiCCO monitoring
  • ScvO₂ sampling

References

College answer

Confirm cardiac arrest

Good BLS i.e.:

• Check ETT position
• Listen to chest 
• Confirm ETCO₂ trace (may not be reliable in complete arrest with absent pulmonary blood flow) 
•  Check adequate CPR: 
  • Correct position (lower half of sternum)
  • Correct rate/depth and technique (depress 4 – 5 cm at 100 – 120 compressions/min 
  • Asynchronous ventilation with respiratory rate 8 – 10) 

Call for additional help

          Local surgical team may be able to re-open sternotomy

Confirm IV access/intraosseous if needed

Adrenaline 1 mg IV immediately and then with alternate cycles

Bolus i.v. fluid as PEA

Continue CPR for 2 min

Rhythm check at 2 min – continue chest compressions, other responders stand clear, charge defibrillator to 200J, pause compressions, all clear, check rhythm and if non-shockable dump charge Immediately continue CPR for further 2 min

Look for and treat reversible causes (needle thoracostomy / pericardiostomy etc – 4Hs and 4Ts)

b)                                                                                                                                  

• Massive pulmonary emboli                                                                          
• Pneumothorax with tension                                                                         
• Hypovolaemia from bleeding elsewhere                                                   
• Graft occlusion and myocardial infarction                                         
• Septic shock possible (post op pneumonia/empyema/sternal wound infection)                                

c)                                                                                                                                  

• Distended neck veins                                                                                   
• Muffled heart sounds 
• Hypotension & tachycardia
• Pulsus paradoxus (may be seen on oximetry trace) Absent apex beat

d)                                                                                                                                  

• Some asepsis
• Identify landmarks: Left paraxiphoid (traditional) Left parasternal (4^th intercostal space left parasternal) For a left paraxiphoid approach 45° to the abdominal wall, head for the left shoulder, aspirate as the needle is advanced
• Could connect a V lead to the base of the needle and watch ECG to look for a change in the QRS morphology, or ST elevation if the needle contacts the myocardium
• Aspirate fluid/blood
• Consider placing a catheter/pigtail
• Blood stained pericardial fluid will not clot whereas intraventricular blood will

Additional Examiners‟ Comments:

A substantial number of candidates failed to recognise a cardiac arrest. Many of the answers were at a junior level e.g. listing the causes of cardiac arrest (Hs and Ts) without reference to this clinical scenario. The question on the technique of blind pericardiocentesis was also badly answered. 

Discussion

This question is in many ways identical to Question 15 from the first paper of 2011.The discussion section was copy-pasted below to simplify revision. Interestingly, though some of the candidates failed to identify cardiac arrest, the pass rate suggests that this was not essential. 

a)

• 1) Confirm cardiac arrest
• 2) Call for help
• 3) Commence BSL (CPR) until help arrives;
  • 100 compressions per minute
  • Compression to a depth of 1/3rd of the anterior-posterior chest diamweter
  • Asynchronois ventilation of 8-10 breaths per minute
  • Ensure the ETT is not malpositioned (chest examination, end tidal CO₂ or calorimetry)
• 4) With help arriving, follow the non-shockable pathway of the ALS algorithm, which consists of CPR and 1mg adrenaline every 2nd cycle.
• 4) Work on resolving the cause of the arrest, using the "four Hs and four Ts" as a general guide

b)

• Other "four Hs and four Ts" with reference to  this scenario:
  • Hypoxia due to oesophageal intubation
  • Hypovolemia due to dehydration (too short of breath to drink!)
  • Hyper/hypokalemia due to cardiac drug side effects, eg. frusemide or spironolactone
  • Hyper/hypothermia is unlikely, but cannot be ruled out without actually measuring the temperature
  • Tension pneumothorax this late is unlikely, but could be the result of a ruptured emphysematous bull
  • Tamponade is already mentioned, and isthe  most likely
  • Toxins eg. drug intoxication
  • Thrombus i.e. PE or MI - PE coudl easily give rise to PEA of this sort, and intracardiac thrombus could be the consequences of cardiac surgery

c)

As for the signs of cardiac tamponade - these are universally recognised as "Beck's Triad":

• Raised JVP / distended neck veins
• Muffled heart sounds
• Hypotension

It is universally acknowledged that these features are observed only in a minority of patients. Other, more common features include the following:

• Pulsus paradoxus
• Increased stroke volume variation (art line "swing")
• Decreased QRS amplitude
• Electrical alternans (alternating variation in the QRS amplitude)
• Absent apex beat

d)

The approach is as follows:

• Raise the head of the bed 45° if the situation permits
• Antibacterial prep and drape
• Palpate the xiphisternum and ribs: that is your landmark.
• There are three main approaches:
  • Subxiphoid approach: Insert needle just under the xiphoid, and advance in the direction of the left shoulder while aspirating.
  • Parasternal approach: Insert the needle perpendicular to the chest wall in the fifth intercostal space, just lateral to the sternum.
  • Apical approach: insert the needle in the intercostal space below and 1 cm lateral to the apex beat, aimed toward the right shoulder.
• Withdraw fluid until cardiac output improves
• Advance guidewire and dilate over it.
• Advance pigtail catheter over guidewire, and suture in place

The college answer also suggests one connect  an ECG lead (one of the chest leads) to the base of the needle  and watch the ECG to look for a change  in  the  QRS  morphology,   or  ST  elevation  if  the  needle  contacts  the myocardium.

References

Jacobs, Ian, et al. "Cardiac arrest and cardiopulmonary resuscitation outcome reports: update and simplification of the Utstein templates for resuscitation registries.: A statement for healthcare professionals from a task force of the international liaison committee on resuscitation (American Heart Association, European Resuscitation Council, Australian Resuscitation Council, New Zealand Resuscitation Council, Heart and Stroke Foundation of Canada, InterAmerican Heart Foundation, Resuscitation Council of Southern Africa)."Resuscitation 63.3 (2004): 233-249.

Cikes, I. "A new millennium without blind pericardiocentesis?." European Journal of Echocardiography 1.1 (2000): 5-7.

Fitch, Michael T., et al. "Emergency pericardiocentesis." New England Journal of Medicine 366.12 (2012).

Sternbach, George. "Claude Beck: cardiac compression triads." The Journal of emergency medicine 6.5 (1988): 417-419.

Spodick, David H. "Acute cardiac tamponade." New England Journal of Medicine 349.7 (2003): 684-690.

Reddy, P. SUDHAKAR, et al. "Cardiac tamponade: hemodynamic observations in man." Circulation 58.2 (1978): 265-272.

College answer

c)                                                          
•    Immediate VF or pacing (if indicated) before external cardiac massage – can delay ECM up to one minute to administer shock/pace 
•    No need for pulse check – observe monitored waveforms/ECG sufficient for diagnosis • Avoid adrenaline/vasopressin bolus 
•    Cease all infusions until reviewed 
•    If IABP in situ set to pressure trigger 
•    If PEA and paced, turn off pacemaker to exclude underlying VF 
•    Plan for emergency re-sternotomy, ideally within five minutes. 
 

Discussion

For a definitive resource, one should read the 2015 or 2009 ERC guidelines (they did not change much).

In short, the basic differences are:

• You do not use full dose adrenaline (rather, give smaller doses)
• You do three "stacked shocks"
• You try pacing in asystole if pacing wires are available; if they are already paced and in PEA, you turn off the pacing to "unmask" VF.
• These shocks and attempted pacing are all measures you take before  starting CPR, which is a departure from the ACLS norms.
• If you can't control a shockable rhythm with three stacked shocks, you give amiodarone immediately rather than after three cycles.
• CPR is something you do while waiting to re-open the chest. After five minutes of unsuccessful resuscitation the chest should be re-opened.
• Non-surgical staff are encouraged to re-open the chest in an emergency

References

College answer

a)                                                         
•    Capture beats: VT 
•    Fusion beats: VT 
•    Concordance in chest leads (or absence of RS complex): VT 
•    Typical RBBB or LBBB morphology: SVT 
•    R to S interval >100ms: VT 
 
(Note: there are some more specific criteria from diagnostic algorithms – if correct these should receive credit.) 
b)                                                          
•    Correction of electrolyte abnormalities or hypothermia 
•    Magnesium 
•    Isoprenaline 
•    Phenytoin 
•    Sodium Bicarbonate 
•    Lignocaine 
•    Electrical cardioversion 
•    Atrial overdrive pacing 
•    Cessation of provoking drugs 
 

Discussion

Some of the criteria are somewhat duplicated because the features are listed according to the society guideline being quoted. It makes sense that most of the guideline-makers would agree on such obvious things as "wide QRS" and "regular", etc.

Management of torsades is somewhat less complex. Thomas and Behr (2015) have published a good article which describes the management strategies for torsades:

• Preventative strategies
  • Stop the QT-prolonging drugs
  • Keep the serum K⁺ around 4.7 - 5.2 mmol/L
• Immediate treatment
  • IV magnesium sulfate
  • Isoprenaline (to increase heart rate to 100-110)
  • Overdrive pacing
  • Lignocaine
• Experimental treatments and last resort measures
  • Clonidine
  • Ranolazine

References

College answer

General 

• Testing too early (esp. before 72 hrs) is unreliable
• Hypothermia and sedative/ relaxants confound most tests
• Associated organ impairments (renal, hepatic) may delay sedative drug clearance and cause encephalopathy
• Seizures (convulsive or non-convulsive)
• Many studies done were not blinded – risk of self-fulfilling prophesy

Clinical: 

• Pupil responses may be underestimated cf. pupilometer
• Pre-existing ocular pathology – e.g. cataracts, blindness
• Recent use of high dose adrenaline, eye drops 
• Corneal reflex- Less specific than pupil response
• Motor responses before 72 hrs unreliable
• Status myoclonus is poorly defined
• Lance-Adams syndrome of awake myoclonus not predictive
• Pre-existing weakness or other pathologies

Electrophysiological: 

• Background signal noise may cause false positives.
• Lack of standardisation in measurement
• Electrode placement may be inconsistent
• Poorly defined endpoints

Radiology

• Brain imaging studies are substantially effected by timing of the study as changes evolve over time. All imaging studies limited by small sample size and selection bias.

Biomarkers: 

• Threshold values for and timing not well established
• Measurement and other tissue confounders not well established e.g. in haemolysis. Poorly defined endpoints

Minimising the confounders

• Define the context/ exclude other causes of unconsciousness
• Caution with renal or hepatic impairment
• Knowledge of any pre-existing pathologies from history
• Waiting at least 72 hrs longer before testing if hypothermia/ sedation/ relaxant
• Multiple modality testing is more reliable than single tests
• Repeated observation especially when patient is hypothermic/ recent sedation or there is doubt Most unconscious patients will recover within 5 days and nearly all by 8 days.
• Skill in interpretation is required for most test especially electrophysiology and imaging
• Use of TOF to exclude paralysis
• Be aware of the risk of self-fulfilling prophesy.

Examiners Comments:

Overall poorly answered with limited detail and little attention paid to the factors which confound prognostication.

Discussion

This question has apppeared many times before in varying forms. This incarnation most closely resembles Question 4 from the second paper of 2014. This time, of the confounding factors,  the college also asked "and how they can be minimised". The table below was plagiarised from the chapter on prognostication after cardiac arrest, with little modification

References

College answer

a) 
Torsade de pointes/ VT triggered by a R on T phenomenon 
 
b) 
Congenital Long QT syndromes 
Acquired long QT 
     Drugs 
     Hypokalemia, hypomagnesemia 
     MI, Takotsubo cardiomyopathy 
     SAH 
     Female gender 
     Bradycardia 
 
c) 
Assess ABC, ALS algorithm, unsynchronized defibrillation. Magnesium. Prevent recurrence by pacing or isoprenaline to increase the heart rate to a level that prevents further torsade. 
 

Discussion

The official college ECG image is of course not available, and in most such cases the reader needs to acknowledge the possibility that the author has substituted something completely different to the official college paper. Fortunately, this time examiners made the mistake of leaving a faint "e-cardiogram.com" watermark on their paper, which makes it possible for track down their source to this page, where a detailed exploration of "tachycardie ventriculaire polymorphe" takes place. This file (torsades-de-pointes-web-free.jpg) has been reproduced multiple times, and appears to be something of a classic.

a) What is your diagnosis?   To be perfectly precise, that would have to be "Polymorphic VT". If the complexes clearly demonstrated a rotation around an isoelectric point "Torsades des Pointes" would also be reasonable, especially given the file name, and the fact that the one visible normal-looking QRS complex appears to have a relatively long-looking QT interval. The fact that the VT begins during the T-wave suggests that the R-on-T phenomenon is responsible. For 10% of the total SAQ marks, no more detail would be expected. Given that the patient has lost consciousness, "cardiac arrest" is another potentially valid way to describe the situation.

b) is also a 10% question. "What risk factors could precipitate this arrhythmia?" Generally speaking, non-Torsades VT is associated with organic and structural heart disease, whereas Torsades tends to be related to molecular and channel related problems.

• Acute coronary ischaemia
• Long QT (congenital or acquired)
• Brugada syndrome
• Catecholaminergic polymorphic VT
• Arrhythmogenic right ventricular dysplasia (ARVD)
• Cardiomyopathy of any cause
• Hypokalemia
• Hypomagnesemia

c) How will you manage the patient? 

Thomas and Behr (2015) have published a good article which describes the management strategies for Torsades, which is also helpful for people trying to answer part (b) of Question 30.1 from the second paper of 2017. In short:

• Preventative strategies
  • Stop the QT-prolonging drugs
  • Keep the serum K⁺ around 4.7 - 5.2 mmol/L
• Immediate treatment
  • IV magnesium sulfate
  • Isoprenaline (to increase heart rate to 100-110)
  • Overdrive pacing
  • Lignocaine
• Experimental treatments and last resort measures
  • Clonidine
  • Ranolazine

References

College answer

Pros 
a.    In the presence of ST elevation post OHCA (Out of Hospital Cardiac Arrest) all patients without absolute contra-indications should go to cath lab 
b.    Patients without clear symptoms or signs of ischaemia may still have had an ischaemic cause for arrest. Case series and registries of OHCA have suggested that 1/4 cases taken to cab lab with no ECG evidence of ischemia will have lesions requiring treatment. Treatment in these patients will lead to a 60% survival improvement with a 90% chance of good neurological recovery. Most studies have published a number needed to treat of 4 to prevent one death with a 90% chance of good neurological recovery. 
c.    Current recommendations from the American Heart Association suggest that any OHCA with 
ROSC should go to cath lab if ischemia is suspected 
d.    Transfer to cath lab with treatment may prevent further cardiac arrests 
e.    Professional (American Heart Association and European Resuscitation council) bodies who have made recommendations say there is no role in waiting to assess neurological recovery 

Cons 
a.    These may be unstable patients  
b.    The cath lab maybe isolated from other emergency services and take staff away from ED or ICU 
c.    Transfer to another centre may be required 
d.    Experienced staff are required to anaesthetize a patient undergoing coronary angioplasty or stenting. 
e.    Taking all comers to cath lab may lead to many poor outcomes due to high pre OHCA morbidities. 
f.    Many patients may be taken after prolonged cardiac arrest who may go onto survive with poor neurological recovery 
g.    There are financial consequences to running a 24-hour cath lab service 
h.    If there is another explanation for the cardiac arrest the time in the catheter lab maybe detrimental to the patient 
i.    Anti-coagulation and anti-platelet medications may increase the risk of haemorrhage  
j.    Difficulty with targeted temperature management in cath lab environment 
 
Examiner Comments: 
 
Overall reasonable answers. Not a great deal of reference to guidelines, and the “pro” side was not as well answered as the “con”. 
 

Discussion

The excellent powerpoint presentation by Georg Furnau Luebeck for the European Society of Cardiology is a good starting point to look for references. Some of the best review of the most important arguments for and against angiography in unselected cardiac arrest patients can be found in the paper on the study design of the COACT trial by Lemkes et al (2016).

Pros:

• Angiography for all would pick up coronary artery disease which would otherwise be missed:
  • ST changes in the ECG post arrest are difficult to interpret 
  • History of chest pain may not be available
  • There is often coronary disease without ECG changes: of the patients who had no ECG changes, Hollenbeck et al (2014) found an acute thrombotic coronary occlusion in 26%.
• To exclude coronary artery disease is an important step in the process of determining the causes of the cardiac arrest
• Patients undergoing angiography receive a "greater intensity of care" (Lemkes et al, 2016) - they are resuscitated more aggressively, get seen by more doctors, receive early anticoagulation and have more mechanical / pharmacological support, which could translate into better outcomes.
• Multiple studies have demonstrated improved outcomes in patients who had no ST changes and who ended up having a PCI for a clinically significant stenosis (Spaulding et al, 1997; Dumas et al, 2010)
• There is society support for this practice (AHA/ACC, ESC/ERC)

Cons

• Cardiac arrest is not uniformly a phenomenon of coronary artery disease, i.e. there are many noncardiac causes, of which several (eg. SAH) would surely not benefit from the obligatory loading doses of dual antiplatelets. This is an argument against immediately rushing to the cath lab.
• Angiography may exacerbate the acute kidney injury which often accompanies the post-resuscitation syndrome, mainly by means of a contrast load.
• Even where there is coronary artery disease, not all patients can be stented, and the survival benefit of angiography seems to be limited to those patients in whom stenting was successful. In about 25% of patients undergoing PCI, there is either no lesion or a non-stentable lesion, even when there are ST changes (and if there aren't, that proportion rises to 75%) according to Dumas et al (2010)
• Even where there is stentable disease, there may be no mortality benefit to stenting it, because outcome depends more on the global ischaemic damage from "down-time" than the events in local coronary territories. SWEDEHEART study (Wester et al, 2018) certainly did not find any mortality difference between patients who had early PCI versus those who did not, even though 43% of the patients were found to have 90% stenosis in one of their vessels.
• If stenting is so good for outcomes, then stenting all the lesions should give maximal benefit - but in fact it seems the fewer stents you do, the better. The CULPRIT-SHOCK trial (Thiele et al, 2017) found improvement in mortality if the angiographer limited their post-arrest intervention to just the culprit lesion, with both mortality and risk of AKI
• Even when there is coronary artery disease, and where you end up stenting it immediately, there does not appear to be a substantial survival benefit. The COACT trial from the Netherlands (Lemkes et al, 2019) found that immediate angiography following cardiac arrest without ST elevation did not improve survival at 90 days. Unlike the PROCAT registry, only 20% of the COACT patients had an acute coronary lesion (33% in the "immediate angiography" group).   

What's happened since the last time this appeared in 2018?

• Jentzer et al published a trial in (2018), specifically in February of 2018 (i.e. long after the examiners would have stopped thinking about this question paper, but before was inflicted on the trainees in March). Survival was much better in the angio group (56.2% vs 31%) as was the neurological outcome (28% vs 11%). However, 
• Verma (2020) performed a meta-analysis of about 3500 patients, and found little difference in mortality or outcome; rather, the 30-day mortality was more related to the presentation comorbidities 
• Song et al (2021) used the GRACE risk score and found that patients with a high score (i.e. old age, history of CCf or MI, tachycardia or hypotensive, with ST-segment depression, AKI, raise cardiac enzymes) seem to have some survival benefit from early angiography

References

College answer

)

Pulmonary Embolism (must state this to gain any marks in this section)

Severe Hypoxaemia (airway obstruction/lung collapse/aspiration/AFE [see below])

Amniotic Fluid Embolism 

Coronary ischaemia 

Tension pneumothorax / Tamponade (potentially post CVC etc., spontaneous unlikely)

 ‘Iatrogenic’ catastrophe/other: air embolism, drug error, anaphylaxis etc.

Hypovolemia (unlikely unless massive concealed bleed but possible), placental abruption

b)

Factors relate to the underlying cause of arrest, the woman’s state pre-arrest, the physiological changes of pregnancy and the presence of a gravid uterus/unborn fetus.

Underlying cause of arrest

Lack of a rapidly reversible cause such as pneumothorax /airway obstruction.

Woman’s state pre-arrest

Severe pre-existing/worsening hypoxaemia

Physiological Changes of Pregnancy

Airway oedema and increased incidence of difficult airway and airway bleeding, high oxygen consumption and increased minute ventilation, reduced FRC, increased risk of aspiration, supine hypotensive syndrome [aortocaval syndrome], procoagulant state, chest compressions may be challenging with obesity/breast enlargement

Presence of gravid uterus/unborn fetus

Prevention of supine hypotensive syndrome [aortocaval syndrome] requires lateral tilt but chest compressions should be performed supine with manual displacement of uterus [AHA rec: see below], reduced diaphragmatic excursion due to presence of uterus with reduced FRC, poor ECHO windows especially subcostal, need for resuscitative hysterotomy and potential simultaneous neonatal resuscitation, potential for delay/hesitation in delivering indicated treatment e.g. antiarrhythmics, thrombolysis, extracorporeal support due to concerns regarding pregnancy.

c)

Main differences are

10-15 degrees of lateral tilt during chest compressions to avoid aortocaval compression or continuous lateral uterine displacement (LUD).

Early perimortem caesarean section

Early intubation

Examiners Comments:

Candidates often gave a routine list for cardiac arrest causes (Hs and Ts) without much specific consideration of situation. Almost no consideration given to underlying cause and pre-arrest condition of patient as factors making successful resuscitation challenging. Often no justification given for alterations to ALS algorithm

Discussion

a)

To counter the examiners' comments, one might present them with a "routine list of cardiac arrest causes" which relates the 4 Hs and 4 Ts to the specific scenario. Thus:

• Hypoxia  due to
  • Aspiration
  • Community-acquired pneumonia (it's what the patient presented with)
  • Airway loss during seizures (eclampsia)
  • Pulmonary oedema due to peripartum cardiomyopathy or preeclampsia
• Hypovolemia (or distributive shock, or cardiogenic shock )
  • Purpueral sepsis
  • Septic abortion
  • Haemorrhage (eg placental abruption or liver rupture)
  • Takotsubo cardiomyopathy
  • Peripartum cardiomyopathy
  • Exacerbation of pre-existing cardiac disease (eg. mitral stenosis)
• Tension pneumothorax 
  • due to positive pressure ventilation or CVC insertion
• Tamponade
  • due to pericardial fluid collection
• Toxins,  including
  • intentional overdose
  • Iatrogenic overdose (eg. accidental bolus infusion of magnesium sulfate)
• Thrombus which includes all embolic phenomena:
  • Pulmonary embolism (which we must mention)
  • Amniotic fluid embolism 
  • Air embolism

b) 

The "factors that may make successful resuscitation of this woman more challenging" is a strangely worded question, as it could be interpreted as almost anything. The examiner's comments about how disappointing it was that the trainees didn't give enough attention to "underlying cause and pre-arrest condition of patient" are rendered all the more bizarre given that the presented pre-arrest history of the scenario was hardly sufficient to make any judgments about the challenging aspects of the specific situation. We know that she is very pregnant, hypoxic, and previously healthy. Almost everything else is left up to the imagination  (eg. are we resuscitating her in a narrow corridor? Has the registrar had enough sleep? Is this a small regional hospital with a single GP anaesthetist? Are you the baby's father?). As such, one must reinterpret the question as "what features of third trimester pregnancy make it more difficult to successfully resuscitate a pregnant patient from cardiac arrest?"

These features can be separated into categories:

Airway issues

• Difficult intubation (for various reasons)
• Increased risk of aspiration
• Decreased FRC makes respiratory decompensation more rapid, and makes airway access more urgent (though, some might say, the patient has arrested - how much more urgent could it get)

Breathing issues

• On the list of differentials are amniotic fluid embolism and pulmonary embolism, which are problems with no real immediate reversible solution in the arrest scenario.
• Oxygen consumption increased
• Foetal oxygenation needs to be considered
• If tension pneumothorax is for some reason a serious differential, the chest drains need to be placed higher because of the displacement of the diaphragm by the gravid uterus

Circulatory issues

• Venous return impaired by gravid uterus
• Placental arteries are more sensitive to catecholamines, and will constrict when you start giving large boluses of adrenaline
• Trans-thoracic echocardiography during CPR will be difficult if not impossible, because of the problematic subcostal view

Disability issues

• If the patient had eclampsia-related seizures and has arrested because of this, it will not be immediately apparent to the rescuers (i.e. the clues may not be obvious, eg. incontinence and a bitten tongue may go unnoticed in the melee of resuscitation)

Performance issues

• Though it seems an unusual thing to mention specifically as a hindrance to the normal process of resuscitation, the college in their answer mention "potential for delay/hesitation in delivering indicated treatment e.g. antiarrhythmics, thrombolysis, extracorporeal support due to concerns regarding pregnancy",  which implies that a necessary consideration in resuscitating a pregnant arrest patient is the possibility that your team will refuse to carry out your order to give adrenaline or amiodarone. If your grasp of the reigns of leadership is indeed so tenuous in this arrest, it is unclear why this comment is limited to antiarrhythmics, thrombolysis and ECMO, as the staff would probably not follow any of your other orders either.

c)

The main differences to the ALS algorithm are:

• Manually displace the uterus to the left (off the aorta and vena cava)
• Add a left lateral tilt (the ideal angle is unknown, and is thought to be between 15° and 30°)
  • A left lateral tilt may compromise effective CPR, but is still recommended by the ARC Guideline 11.10  (2011) "Special Circumstances". In contrast, ECC and AHA no longer recommend the left lateral tilt (see the 2015 AHA update and the 2015 ECC guidelines). 
• Biaxillary defibrillator pad placement may be considered. Anterolateral pad placement requires the lateral pad to go under the breast rather than over it. 
• Early intubation is mentioned in the college answer, and is therefore the definitive opinion of the examiners, but it does not appear in any of the guidelines. Jeejeebhoy et al (2015), in the AHA scientific statement on this issue, did not mention anything about early intubation, though airway management is otherwise made much of. 
• Prepare for an emergency perimortem caesarian.

References

College answer

1. Ensure severity of brain injury is compatible with brain death (i.e. sufficient intracranial pathology) by reviewing relevant imaging.

   Confirm that there has been a minimum of four hours observation and mechanical ventilation during which the patient has had unresponsive coma (GCS-3), no spontaneous breathing effort, absent cough/tracheal reflex. 

   Complete brainstem reflexes cannot be performed in this case and therefore brain death cannot be certified by clinical testing alone and will have to be determined by demonstrating absence of intracranial blood flow. However, the part of the clinical examination that can be undertaken should be performed.

   Ensure that the following pre-conditions have been met in order to do limited brain death testing-

   1. Normothermia (temperature > 35C); 

   2. Normotension (as a guide, systolic blood pressure > 90 mmHg, mean arterial pressure (MAP) > 60 mmHg in an adult); 

   3. Exclusion of effects of sedative drugs  

   4. Absence of severe electrolyte, metabolic or endocrine disturbances 

   5. Intact neuromuscular function   

   6. Ability to perform apnoea testing 

2. Undertake the clinical tests that can be done

   1. Response to painful stimulus to four limbs and trunk.

   2. Response to pain in trigeminal nerve distribution          

   3. Gag reflex

   4. Cough reflex

   5. Apnoea testing
      
      * Pupillary, corneal and cold caloric reflexes cannot be tested.

3. If all above reflexes absent, proceed to 4-vessel intra-arterial catheter angiography. Blood flow should not be demonstrable above the level of the carotid siphon in the anterior circulation, or above the foramen magnum in the posterior circulation 

   Alternatives- 

   Radionuclide imaging with Technetium -99m radiolabelled hexamethyl propylene amine oxime. (Tc-99mHMPAO)

   Contrast CT or CT-angiography subject to specific radiologic diagnostic guidelines. (Absent enhancement bilaterally of all of the following are likely to be the most reliable early CT indicators of brain death:  middle cerebral artery cortical branches — that is beyond the Sylvian branches; P2 segment of the posterior cerebral arteries; pericallosal arteries; and internal cerebral veins) 

   Brain death can then be certified by 2 medical practitioners (not including the practitioner who performed the imaging investigation) who have examined the patient and have knowledge of the circumstances of the coma

   Important points in the answer:

   Confirmation of a diagnosis compatible with brain death 

   Why clinical testing will not be sufficient 

   Preconditions satisfied 

   List of clinical tests that can be performed 

   Details of imaging test of choice + list of 2 alternatives 

   Detailed radiologic features required for diagnosis on contrast CT was not required, but an indication that specific radiologic criteria exist was expected.

   Confirmation with clinical testing alone was considered a fatal error.

Discussion

The diagnosis of brain death should be the bread and butter of an ICU specialist (as it is the thing that we do which is sufficiently unique to be the domain of intensivists alone). It is therefore surprising that only 43% of the candidates scored a passing mark. The college answer is remarkable in that it offers us a glimpse of the normally hidden marking rubric for an SAQ.

To break down this rubric into answerable components:

Confirmation of a diagnosis compatible with brain death 

• "Brain death cannot be determined without evidence of sufficient intracranial pathology". There must be an explanation for the coma which is consistent with the diagnosis of brain death.

Why clinical testing will not be sufficient 

• The patient has "significant bilateral ocular injuries resulting in a ruptured globe on the right and traumatic third nerve palsy on the left". This prevents one from performing clinical testing, which requires an opportunity to adequately examine brainstem reflexes.

Preconditions satisfied 

• A minimum period of 4 hours in which the patient is observed to have unresponsive coma, unreactive pupils, absent cough/tracheal reflex and no spontaneous respiratory effort
• Normothermia
• Normotension
• Exclusion of the effects of sedating drugs
• Absence of severe electrolyte, metabolic or endocrine disturbance
• Intact neuromuscular function
• Ability to perform apnoea testing

List of clinical tests that can be performed 

One needs to be reminded that the ANZICS statement recommends clinical testing should still be attempted: "If a complete examination is not possible (e.g. eye or ear trauma) or apnoea testing precluded (e.g. severe lung injury or high cervical trauma), then that part of the clinical examination that can be performed, should be undertaken".

• Painful stimulus in cranial nerve distribution, eg. supraorbital nerve pressure
• Painful stimulus in all 4 limbs, eg. nailbed pressure
• Painful stimulus over the supraorbital nerve. (CN V, VII)
• Gag reflex
• Cough reflex
• Apnoea testing

Details of imaging test of choice + list of 2 alternatives 

• Four-vessel intra-arterial angiography is the gold standard
• Tc-99 HMPAO SPECT scan is the next best option
• CT angiography is an "acceptable choice" but has significant limitations. Provided it fits the criteria of a technically adequate study ( contrast enhancement of external carotid artery branches). The college model answer offers a cut-and-pasted list of features from the ANZICS statement (p. 23); "Absent enhancement bilaterally of all of the following are likely to be the most reliable early CT indicators of brain death:
  •  middle cerebral artery cortical branches — that is beyond the Sylvian branches;
  • P2 segment of the posterior cerebral arteries;
  • pericallosal arteries; and
  • internal cerebral veins."

References

College answer

a) 
Although the CO2 has risen to above 60 mmHg, the pH remains above 7.3, and so brain death cannot be diagnosed. The Na of 152 does not preclude the diagnosis of brain death. 
       

Discussion

This question is straight from the CICM ANZICS statement (version 3.2) which reads:

"At the end of the period without mechanical ventilation, apnoea must persist in the presence of an adequate stimulus to spontaneous ventilation, i.e. an arterial PaCO2 > 60 mmHg (8 kPa) and an arterial pH < 7.30"

The key point there is an arterial PaCO2 > 60 mmHg (8 kPa) and an arterial pH < 7.30. Both must be demonstrated in order for the clinical diagnosis of brain death to be valid.  As to why and how this was decided, the ANZICS statement is silent. The American guidelines do not contain this rule.

Interestingly, as a reader had pointed out, there is more material in this blood gas result to discredit the apnoea test result. Consider the pre-test bicarbonate value, which is 31 mmol/L. The PaCO₂ is only 49 at this stage, but surely the high baseline bicarbonate means there must be some sort of chronic CO₂ retention here. And if so, you'd want the PaCO₂ to rise by at least 20 mmHg (i.e. up to 69 mmHg) in order to be able to declare the apnoea test as failed, considering that the ANZICS statement clearly says:

"In patients with pre-existing hypercapnia, it is recommended to wait for a PaCO₂ rise of >20 mmHg (2.7 Kpa) above the chronic level, with a pH <7.30."

This did not happen in the example, and the high initial bicarbonate may also to some extent account for the pH being higher than 7.30 at the end of the test.

 As for the sodium level, the old  ANZICS statement was not prescriptive; "marked derangements" were disqualifying, but there no was mention as to how marked these must be. The new Version 4 of the statement gives the following ranges:

• Glucose <3 or > 25 mmol/L
• Sodium <125 or >160 mmol/L
• phosphate <0.5 mmol/L
• magnesium <0.5 mmol/L
• urea > 40 mmol/L
• "untreated severe hypothyroidism or severe hypoadrenalism"

Other Intensive Care Societies differ slightly;  for example the Irish ICSI guidelines recommend 125-155mmol/L as the acceptable range for clinical testing.  

References

College answer

• Left or Right ventricular failure
• Severe mitral regurgitation
• Septal rupture
• Cardiac tamponade/ventricular free wall rupture
• Arrhythmia (brady or tachy)
• Drug induced

Discussion

This is an exercise in generating differentials for causes of shock which are applicable to the post-MI period. Thus:

References

College answer

Neuro: Loss of cerebrovascular regulation, coma, loss of ocular reflexes
CVS: Decline in BP and cardiac output, VF (<28°C) bradycardia and asystole (<20°C)
Respiratory: Pulmonary oedema, apnoea
Renal: Oliguria
Musculoskeletal: Pseudo-rigor mortis (may appear dead)
Metabolic: Decreased metabolic rate, hyper or hypoglycaemia

Considerations in providing ACLS
Decision to start

May commence cardiac life support in an apparently “dead” hypothermic patient. Beware that very slow, irregular small volume pulse may be present and an unrecordable blood pressure. The brain can tolerate cardiac arrest for long periods at 18°C.

Rewarming

Patients need to be actively rewarmed while resuscitation is being continued.
Extra-corporeal support, not mandated, but can be mentioned
More emphasis on the continuing re-warming, an issue of priority, should state early
Temperature should be measured centrally
 
Physical difficulties

Hypothermia can cause stiffness of chest wall making ventilation and chest compression difficult – early use of mechanical devices as resuscitation attempts are likely to be prolonged.
Be aware that interventions (e.g. CPR, central line placement, endotracheal intubation) may precipitate arrhythmias

Medications

Consider withholding drugs (e.g. Adrenaline) until core temp > 30°C and then double the interval between giving the drugs (i.e. give adrenaline every 4th cycle compared with every 2nd cycle) until temperature 35°C
The hypothermic heart may be unresponsive to cardioactive drugs, electrical pacing and defibrillation. Arrhythmias
Arrhythmias other than VF tend to revert spontaneously as temperature rises. Bradycardia does not usually need treatment as it is physiological in severe hypothermia
VF therapy: unclear at which temp shocking should be first attempted. After 3 shocks if no response, consider delaying further attempts at defibrillation until temperature > 28-30°C

Examiners Comments:

In part a), candidates listed things that were not clinical signs e.g. ECG changes and ETCO2, and there was also a focus on the CVS aspect which showed a limited breadth of clinical signs, and hence limited marks. In part b), many candidates did not show a breadth of considerations, and focussed mainly on the rewarming in great depth, hence did not score well on this section. Also, candidates often listed their management rather than outline their considerations, so the aspects they discussed also often lacked depth.
 

Discussion

The cranky CICM examiners complained that, when asked for clinical signs, many of the candidates "listed things that were not clinical signs e.g. ECG changes and ETCO₂" And then they themselves had listed "loss of cerebrovascular regulation", "decline in ... cardiac output" and "decreased metabolic rate" in their model answer. Looking at their list, one might come to the conclusion that the question asked for the physiological consequences of hypothermia.

Anyway, the clinical signs are:

• Observation
  • Mottled appearance
  • Cyanosis
  • Pallor
  • No shivering
  • Cold oedematous skin
• Respiratory findings
  • Apnoea, hypoventilation or Cheyne-Stokes respiration
  • Creps on auscultation, suggestive of pulmonary oedema
• Cardiovascular findings
  • Sinus bradycardia, AF or asystole
  • Hypotension
  • Weak thready pulse, or altogther impalpable peripheral pulses
  • Poor capillary refill
• Neurological findings
  • Coma (unresponsiveness below 32°C)
  • Increased muscle tone
  • Sluggish deep tendon reflexes
  • Extensor plantar responses
  • Loss of cranial nerve reflexes (with fixed mid-dilated pupils)
• Gastrointestinal findings
  • Absent bowel sounds
  • Abdominal tenderness (hypothermia-induced pancreatitis)
• Renal findings
  • Decreased urine output

All of this comes from excellent reviews by Rosin et al (1964) and Aslam et al (2006). 

Now, as for the management of cardiac arrest in hypothermia. "Outline the considerations", judging by the wording of the model answer, appears to mean "discuss all the ways hypothermic arrest is different". Though the college question asks specifically about ACLS, the college answer also discusses some BLS material. The ideal reference for this would probably have to be the AHA "Special Circumstances" section from the 2015 cardiac arrest guidelines. Following the AHA's own structure:

• Prognostic implications of cardiac arrest with severe hypothermia:
  • Prognosis may be better than expected given the usually prolonged duration of CPR
  • A large percentage of survivors (~ 40%) have a good neurological outcome
• Changes to basic life support:
  • It may take longer than normal to detect signs of life (up to 1 minute)
  • CPR should ideally be performed mechanically (prolonged CPR is to be expected)
  • Intermittent CPR (stopping for 5 minutes every 5 minutes) is reasonable for prehospital and retrieval staff, particularly when interruption facilitates retrieval
  • Manual or mechanical ventilation may encounter poor lung compliance
• Changes to advanced life support
  • Do not defibrillate until core temperature is over 30°C.
  • If you decide to defibrillate and after three shocks the rhythm remains VF, withhold further attempts until core temperature is over 30°C.
  • Do not give adrenaline until core temperature is over 30°C.
  • After 30°C is achieved, double the interval between adrenaline doses until 35°C
  • Use a low-reading thermometer to record core body temperature
• Rewarming techniques
  • Rewarming is central to the success of resuscitation
  • Extracorporeal circuit rewarming is the ideal
  • Warmed fluids and peritoneal lavage is the next best option
  • External warming is least effective
  • Remember that intubation will produce a increase in the rate of cooling by interruption of shivering though paralysis and anaesthesia.
• Supportive post-arrest management
  • The temperature of approximately 32° to 34°C can be maintained after rewarming, according to standard post-cardiac arrest guidelines.
  • The AHA recommend that we "do not delay urgent interventions such as airway management and insertion of vascular catheters regardless of evidence of cardiac irritability"

References

Lexow, Kristian. "Severe accidental hypothermia: survival after 6 hours 30 minutes of cardiopulmonary resuscitation." Arctic medical research 50 (1991): 112-114.

Meyer, Marie, et al. "Sequela-free long-term survival of a 65-year-old woman after 8 hours and 40 minutes of cardiac arrest from deep accidental hypothermia." The Journal of thoracic and cardiovascular surgery 147.1 (2014): e1-e2.

Saczkowski, Richard S., et al. "Prediction and risk stratification of survival in accidental hypothermia requiring extracorporeal life support: An individual patient data meta-analysis." Resuscitation 127 (2018): 51-57.

Danzl, Daniel F., et al. "Multicenter hypothermia survey." Annals of emergency medicine 16.9 (1987): 1042-1055.

Fell, R. H., et al. "Severe hypothermia as a result of barbiturate overdose complicated by cardiac arrest." The Lancet 291.7539 (1968): 392-394.

Lee, H. A., and A. C. Ames. "Haemodialysis in severe barbiturate poisoning." British medical journal 1.5444 (1965): 1217.

Paal, Peter, et al. "Accidental hypothermia–an update." Scandinavian journal of trauma, resuscitation and emergency medicine 24.1 (2016): 111.

Gordon, Les, et al. "Delayed and intermittent CPR for severe accidental hypothermia." Resuscitation 90 (2015): 46-49.

Oberhammer, Rosmarie, et al. "Full recovery of an avalanche victim with profound hypothermia and prolonged cardiac arrest treated by extracorporeal re-warming." Resuscitation 76.3 (2008): 474-480.

Lee, Christopher H., et al. "Advanced cardiac life support and defibrillation in severe hypothermic cardiac arrest." Prehospital Emergency Care 13.1 (2009): 85-89.

Mortensen, Elin, et al. "Changes in ventricular fibrillation threshold during acute hypothermia. A model for future studies." Journal of basic and clinical physiology and pharmacology 4.4 (1993): 313-320.

Kornberger, Elisabeth, et al. "Effects of epinephrine in a pig model of hypothermic cardiac arrest and closed-chest cardiopulmonary resuscitation combined with active rewarming." Resuscitation 50.3 (2001): 301-308.

Ujhelyi, Michael R., et al. "Defibrillation energy requirements and electrical heterogeneity during total body hypothermia." Critical care medicine 29.5 (2001): 1006-1011.

Stoner, Jason, et al. "Amiodarone and bretylium in the treatment of hypothermic ventricular fibrillation in a canine model." Academic emergency medicine 10.3 (2003): 187-191.

College answer

References

Muth, Claus M., and Erik S. Shank. "Gas embolism." New England Journal of Medicine 342.7 (2000): 476-482.

Palmon, Sally C., et al. "Venous air embolism: a review." Journal of clinical anesthesia 9.3 (1997): 251-257.

Oh's Intensive Care manual: Chapter 34   (pp. 392) Pulmonary  embolism by Andrew  R  Davies  and  David  V  Pilcher

Anderson, Frederick A., and Frederick A. Spencer. "Risk factors for venous thromboembolism." Circulation 107.23 suppl 1 (2003): I-9.

Konstantinides, Stavros V., et al. "2014 ESC Guidelines on the diagnosis and management of acute pulmonary embolism." European Heart Journal (2014): ehu283.

College answer

The rhythm strip shows polymorphic ventricular tachycardia, and it looks like torsades de pointes. TdP is caused by QT prolongation and is often precipitated by bradycardia.

Management Plan
ECG to establish QT interval. Stop amiodarone
IV Magnesium infusion (to keep Mg around 1.5-2 mmol/L)
Avoid/stop any other medications that prolong the QTc e.g. haloperidol / erythromycin / quinolones / methadone etc.
Exclude hypokalaemia / hypocalcaemia and treat as appropriate
Consider using lignocaine if recurrent episodes.

Institute temporary pacing (or could use epicardial wires if in place) or may use positive chronotrope, e.g. judicious isoprenaline infusion.
Overdrive pacing may be useful in recurrent episodes.
Exclude ischaemia as a precipitant (most likely if normal QT): ECG / Troponin / ECHO / angiography of grafts. If ischemia is the cause and the QTc is normal, amiodarone and beta blockade are useful.

Urgent echocardiography is reasonable to help exclude ischemia and also in the setting of CPR post sternotomy/cardiac surgery to exclude structural problems/pericardial effusion etc.
Further follow up :Cardiology opinion (electrophysiology) regarding need for further EP studies, PPM/AICD and ongoing maintenance medication choices.
Recurrent episodes may require short term mechanical circulatory support.

Discussion

State what the rhythm strip shows

Yup, that's polymorphic VT, straight from the polymorphic VT page in LITFL. It could also be torsades des pointes but for that diagnosis one would need a 12-lead ECG which demonstrates a long QT interval. 

outline your management plan for this patient

• Immediately lifesaving steps
  • Stop the amiodarone (that will only prolong the QT even further)
  • IV magnesium sulfate, aiming ffor a higher than normal serum level
  • Isoprenaline (to increase heart rate to 100-110)
  • Pacing (day 3 post CABG, they may still have wires in)
  • Lignocaine infusion
• Investigations
  • ECG to confirm long QT interval
    • if QT is normal, amiodarone may be recommenced, provide the heart rate permits
  • Bloods to look for electrolyte derangement
  • Troponin to exclude graft failure/occlusion
  • TTE to look for regional wall motion abnormalities
  • Graft angiography
• Preventative strategies
  • Stop the other QT-prolonging drugs
  • Keep the serum K⁺ around 4.7 - 5.2 mmol/L
• Experimental treatments and last resort measures
  • Clonidine
  • Ranolazine
• Specific definitive management
  • EPS and catheter ablation

References

Roberts-Thomson, Kurt C., Dennis H. Lau, and Prashanthan Sanders. "The diagnosis and management of ventricular arrhythmias." Nature Reviews Cardiology 8.6 (2011): 311.

ARC Guideline 11.2: Protocols for Adult Advanced Life Support

Aronow, Wilbert S. "Treatment of Ventricular Arrhythmias." (2014).

John, Roy M., et al. "Ventricular arrhythmias and sudden cardiac death." The Lancet 380.9852 (2012): 1520-1529.

College answer

References

Einav, Sharon, Nechama Kaufman, and Hen Y. Sela. "Maternal cardiac arrest and perimortem caesarean delivery: evidence or expert-based?." Resuscitation 83.10 (2012): 1191-1200.

Morris Jr, John A., et al. "Infant survival after cesarean section for trauma." Annals of surgery 223.5 (1996): 481.

Beckett, V. A., P. Sharpe, and M. Knight. "CAPS—A UKOSS STUDY OF CARDIAC ARREST IN PREGNANCY AND THE USE OF PERI-MORTEM CAESAREAN SECTION. IMPLICATIONS FOR THE EMERGENCY DEPARTMENT." Emergency Medicine Journal 32.12 (2015): 995-995.

Elkady, A. A. "Peri-mortem Caesarean Section Delivery: A Literature Review and Comprehensive Overview." Enliven: Gynecol Obstet 2.3 (2015): 005.

Campbell, Tabitha A., and Tracy G. Sanson. "Cardiac arrest and pregnancy." Journal of emergencies, trauma, and shock 2.1 (2009): 34.

Katz, Vern L., Deborah J. Dotters, and William Droegemueller. "Perimortem cesarean delivery." Obstetrics & Gynecology 68.4 (1986): 571-576.

Manner, Richard L. "Court-Ordered Surgery for the Protection of a Viable Fetus:, 247 6a. 8b, 274 SE 2d 457 (1981)." (1982).

College answer

a)    72-year-old female ventilated in ICU 4 hours post cardiac surgery

References

College answer

Not available.

Discussion

This question is essentially the same as Question 18 from the first paper of 2018, except that this time the examiners asked for "advantages and disadvantages" instead of "pros and cons".  Sensitive readers may find themselves awake at night, wondering what sort of hidden meaning might be lurking in these seemingly random changes. On one hand, this certainly does not look like a deliberate creative decision; on the other hand, surely every inch of this exam paper must be lovingly crafted by experts in medical education? To believe otherwise would be to go mad. Before the reader loses all hope, here are the advantages and disadvantages of urgent post-cardiac-arrest angiography:

Pros Advantages:

• Angiography for all would pick up coronary artery disease which would otherwise be missed:
  • ST changes in the ECG post arrest are difficult to interpret 
  • History of chest pain may not be available
  • There is often coronary disease without ECG changes: of the patients who had no ECG changes, Hollenbeck et al (2014) found an acute thrombotic coronary occlusion in 26%.
• To exclude coronary artery disease is an important step in the process of determining the causes of the cardiac arrest
• Patients undergoing angiography receive a "greater intensity of care" (Lemkes et al, 2016) - they are resuscitated more aggressively, get seen by more doctors, receive early anticoagulation and have more mechanical / pharmacological support, which could translate into better outcomes.
• Multiple studies have demonstrated improved outcomes in patients who had no ST changes and who ended up having a PCI for a clinically significant stenosis (Spaulding et al, 1997; Dumas et al, 2010)
• There is society support for this practice (AHA/ACC, ESC/ERC)

Cons Disadvantages:

• Cardiac arrest is not uniformly a phenomenon of coronary artery disease, i.e. there are many noncardiac causes, of which several (eg. SAH) would surely not benefit from the obligatory loading doses of dual antiplatelets. This is an argument against immediately rushing to the cath lab.
• Angiography may exacerbate the acute kidney injury which often accompanies the post-resuscitation syndrome, mainly by means of a contrast load.
• Even where there is coronary artery disease, not all patients can be stented, and the survival benefit of angiography seems to be limited to those patients in whom stenting was successful. In about 25% of patients undergoing PCI, there is either no lesion or a non-stentable lesion, even when there are ST changes (and if there aren't, that proportion rises to 75%) according to Dumas et al (2010)
• Even where there is stentable disease, there may be no mortality benefit to stenting it, because outcome depends more on the global ischaemic damage from "down-time" than the events in local coronary territories. SWEDEHEART study (Wester et al, 2018) certainly did not find any mortality difference between patients who had early PCI versus those who did not, even though 43% of the patients were found to have 90% stenosis in one of their vessels.
• If stenting is so good for outcomes, then stenting all the lesions should give maximal benefit - but in fact it seems the fewer stents you do, the better. The CULPRIT-SHOCK trial (Thiele et al, 2017) found improvement in mortality if the angiographer limited their post-arrest intervention to just the culprit lesion, with both mortality and risk of AKI
• Even when there is coronary artery disease, and where you end up stenting it immediately, there does not appear to be a substantial survival benefit. The COACT trial from the Netherlands (Lemkes et al, 2019) found that immediate angiography following cardiac arrest without ST elevation did not improve survival at 90 days. Unlike the PROCAT registry, only 20% of the COACT patients had an acute coronary lesion (33% in the "immediate angiography" group).   

What's happened since the last time this appeared in 2018?

• Jentzer et al published a trial in (2018), specifically in February of 2018 (i.e. long after the examiners would have stopped thinking about this question paper, but before was inflicted on the trainees in March). Survival was much better in the angio group (56.2% vs 31%) as was the neurological outcome (28% vs 11%). However, 
• Verma (2020) performed a meta-analysis of about 3500 patients, and found little difference in mortality or outcome; rather, the 30-day mortality was more related to the presentation comorbidities 
• The TOMAHAWK trial (Desch et al, 2021) looked at a cohort of 554 patients and also did not find any mortality benefit at 30 days.
• Song et al (2021) used the GRACE risk score and found that patients with a high score (i.e. old age, history of CCf or MI, tachycardia or hypotensive, with ST-segment depression, AKI, raise cardiac enzymes) seem to have some survival benefit from early angiography.

References

College answer

Not available.

Discussion

1. The circuit should be humidified.
2. Normoxia and normocapnea must be maintained.
   There will be periodic requests for ABGs on 100% FiO₂ from the donor coordinator, but afterwards the FiO₂  must be minimised to prevent oxidative stress damage to the lungs.
3. Haemodynamic instability is to be expected:
   - The initial autonomic storm should be managed with nitroprusside and esmolol
   - The subsequent collapse should be treated with noradrenaline and/or vasopressin
   - Bradycardia will be resistant to atropine (no vagus to block); catecholamines or pacing will be required
   -Though they do not make a direct statement to this effect, ANZICS tacitly support CPR in the brain-dead organ donor; "cardiopulmonary resuscitation may result in recovery of cardiac function and successful transplantation".
4. Normoglycaemia must be maintained.
5. Normothermia must be maintained by warming externally, and by using warmed fluids.
   Electrolytes need to be maintained within normal laboratory ranges;
   particular attention needs to be paid to the sodium.
   DDAVP may be required as a hormone replacement.
   Other "endocrine support" (T3, hydrocortisone) should be considered in the following circumstances:
   - haemodynamic instability
   - an ejection fraction of less than 45%
   - heart donation is being considered
6. Fluid resuscitation should be conservative if you plant to donate lungs,  aggressive if you plan to donate kidneys, and an intelligent compromise if both organs are being considered.
7. Nutrition must continue.
   Good nutrition (or rather, the absence of malnutrition) has been associated with improved raft function (Singer et al, 2005)
8. Coagulopathy must be observed and corrected; if worsening coagulopathy or DIC develop, organ retrieval should be expedited.

References

College answer

Not available.

Discussion

The question did not ask for "advantages and disadvantages", they only wanted limitations. Thus, a mangled truncated version of summary the table from the neuroprognostication chapter is offered here.

References

College answer

Not available.

Discussion

Rationale:

• Therapeutic hypothermia has been advanced as a means of improving survival and good neurological outcome following cardiac arrest.
• Therapeutic hypothermia modulates the activity of body proteins and electrolytes.
• This modulation is thought to have some beneficial effects in scenarios where inflammatory damage is anticipated.
• This also involves the down-modulation of the overall metabolic rate, which decreases the metabolic demands of the organism in poor cardiac output states
• Decrease in oxygen consumption matches decreased demand with decreased supply in "penumbra" areas, at the watersheds, where hypoxic injury has caused oedema

Advantages:

• Decreased granulocyte migration into the brain tissue.
• Decreased cerebral oedema
• Intrinsic anticonvulsant effects of hypothermia

Disadvantages:

• Decreased rate of drug metabolism
• Impaired immunity
• Decreased cardiac output and bradycardia
• Prolongation of QT
• Risk of arrhythmias
• Increased haematocrit and blood viscosity
• Hyperglycaemia
• Counterproductive energy expenditure via shivering

Evidence:

• Pseudorandomised unblinded trial in 1996 showed promising results
• Bernard et al (2002), in a small study (n=77) demonstrated a marked difference in survival (26% vs 49%) in out of hospital VF arrest survivors using 33°C.
• HACA trial (2002) in a small study (n=134) demonstrated good neurological outcomes in 55% of cooled patients, vs. 39% of non-cooled patients.
• TTM trial (2013) in a larger and more methodologically robust study (n=950) had demonstrated non-inferiority of a more conservative hypothermia (36°C), in terms of mortality.
• HYPERION trial (2019), specifically among patients with nonshockable rhythm (n=584) , found a benefit to good neurological outcome (10.2% vs 5.7%) using 33°C.
• TTM2 trial (2021), the largest so far (n=1861) had further demonstrated that merely maintaining normothermia (under 37.8°C) was also non-inferior to using  33°C (54% vs 54% mortality).

Society recommendations

• ESC (2021) recommend 32 and 36 °C for at least 24 hours
• AHA (2020) recommend TTM 
• AHA (2015) had specifically recommended 32-36° C
• ARC recommended 32-36° C in 2016 (and that was their last update)

Own practice:

• Any reasonable response, so long as it incorporates the avoidance of fever, eg. "In my practice, I cool patients to keep their temperature in the normal range, under 37.8° C"

References

College answer

Not available.

Discussion

ECPR has never been seen in the CICM exams until this paper.

Rationale

• Survival from cardiac arrest remains poor even in well-resourced urban medical systems where bystander CPR is common.
• This is partly because conventional CPR yields a meagre 50% of normal cardiac output at best
• This poor cardiac output results in a low flow state which progressively diminishes the chances of a successful resuscitation
• Many causes of cardiac arrest (MI, massive PE, overdose, primary arrhythmia) are amenable to intervention, if only the patient could be sustained for long enough to benefit from it
• From this, it follows that mortality from cardiac arrest could be improved by the early use of VA ECMO to support the circulation while the cause of cardiac arrest is being found and reversed. 

Advantages

• Rapid restoration of circulation on ECMO should protect from organ system damage
• Facilitates coronary and endovascular interventions
• Carefully selected patients have had good outcomes:
  • 22% survival at 180 days for Belohlavek et al, 2022
  • 43% for Yannopoulos et al, 2020
  • 44% for Dennis et al, 2020
  • 54% for Stub et al, 2015
  • This is compared to 3-10% survival for conventional CPR
• The cost of the program is comparatively lower than the cost of similarly low-yield interventions which still associate with high mortality (eg. radiation therapy and chemotherapy).

Disadvantages

• Expensive, mainly in terms of staff (in the sense that not everybody is trained in VA ECMO cannulation, and not everybody trained in it is willing to go on a 24/7 roster)
• May facilitate the survival of patients with profound neurological disabilities
• May prolong the dying process in some patients, preventing the "good death".
• Though ethically withdrawal of ECMO support is equivalent to the decision to stop CPR when the patient is not expected to make any recovery, practically it may be difficult to contemplate discontinuing ECMO support from the viewpoint of the family.
• The availability of this technique in only dense urban areas may increase the inequality in healthcare availability between metropolitan and rural populations

Patient selection

• ELSO criteria:
  • Age < 70 years
  • Witnessed cardiac arrest
  • Initial cardiac rhythm of VT/VF (PEA)
  • Low flow (cardiac arrest to initiation of full ECMO flow) of <60 minutes
  • EtCO₂ > 10mmHg
• 2CHEER criteria:

  • age 12-70 years

    AND meets ALL of the following criteria:

    • the cardiac arrest is likely to be of primary cardiac or respiratory cause

    • the cardiac arrest was witnessed by a bystander or paramedic or hospital staff member

    • chest compressions commenced within 10 minutes

    • initial cardiac rhythm of ventricular fibrillation (VF)

    • immediate availability of a mechanical CPR device with paramedic staff

    • the cardiac arrest duration (collapse to arrival at ED) has been < 60minutes

  • OR meets ONE of the following criteria:

    • Severe hypothermia (<32°C) due to accidental exposure

    •  Severe overdose with β-blockers, tricyclic antidepressants, digoxin or other agents causing profound reversible myocardial depression and/or cardiac rhythm disturbance

    • Any other cause where there is likely to be reversibility of the cardiac arrest if an artificial circulation can be provided (e.g. massive pulmonary embolism)

References

College answer

Not available.

Discussion

This is a lot like Question 3 from the first paper of 2020, except that time the examiners called them "modifications". "Outline the modifications to the standard adult ALS algorithm", thy asked. This time they wanted to "discuss the key differences". It would no doubt be highly instructive to learn, what possible key differences (or modifications?) could distinguish "outline" from "discuss" enough for the examiners to change the wording, but their minds are alien and inscrutable. 

Anyway. The following "differences" can be identified:

• Differences in diagnostic thinking:
  • Hypovolemia, tension pneumothorax and cardiac tamponade are among the most common causes of cardiac arrest following cardiac surgery.
• Differences in ALS algorithm:
  • You do not use full dose adrenaline (rather, give smaller doses)
  • You do three "stacked shocks"
  • You try pacing (rate of 90, DDD) in asystole if pacing wires are available
  • If they are already paced and in PEA, you turn off the pacing to "unmask" VF.
  • These shocks and attempted pacing are all measures you take before  starting CPR, which is a departure from the ACLS norms.
  • If you can't control a shockable rhythm with three stacked shocks, you give amiodarone immediately rather than after three cycles.
  • Amiodarone is the only drug in the protocol, which makes it easy to remember. Atropine is mentioned in the college answer but it is not a part of the 2017 consensus statement recommendations.
  • The college suggests you grab the knife after one minute, but the official guidelines makers say "we recommend this within 5 minutes". In short, after five minutes of unsuccessful resuscitation the chest should be re-opened.  External CPR is pointless in all of the common causes of arrest in this scenario. Therefore, CPR is something you do while waiting to re-open the chest. 
• Differences in logistics
  • Non-surgical staff are encouraged to re-open the chest in an emergency. However:
  • Operating theatres, cardiac surgeon and cardiac anaesthetist need to be notified
  • Blood bank need to be notified to be ready for a massive transfusion
• Additional steps which are not a part of the normal adult algorithm:
  • Take the patient off the ventilator and manually ventilated them
  • Drop the PEEP to zero, to optimise preload
  • Stop the sedating infusions. With diminished cerebral perfusion, the chances of awareness are pretty minimal.  In fact, stop all the infusion (to prevent drug errors). 
  • Switch the IABP to pressure trigger mode (that way it assists CPR)

References

Dunning, Joel, et al. "The Society of Thoracic Surgeons Expert Consensus for the Resuscitation of Patients Who Arrest After Cardiac Surgery." The Annals of Thoracic Surgery103.3 (2017): 1005-1020.

Dunning, Joel, et al. "Guideline for resuscitation in cardiac arrest after cardiac surgery." European Journal of Cardio-Thoracic Surgery 36.1 (2009): 3-28.