In general, an assessment of the peri-arrest patient closely resembles the primary survey in trauma, in particular in terms of the "find the bleeding, fix the bleeding" approach to immediately lifethreatening problems. As one progresses from airway to breathing to circulation, one addressess the immediately lifethreatening issues first, and only then moves on with the survey.

Beyond rehearsing this stereotypical approach to assessment, in the CICM fellowship exam the candidates are frequently asked to generate a list of reasons as to why a person has suddenly arrested. The scenarios are usually fairly straightforward, and require little deviation from the 4 Hs and 4 Ts.

Previous such questions included the following:

  • Question 5 from the second paper of 2016 (cardiac tamponade)
  • Question 15 from the first paper of 2011 (cardiac tamponade)
  • Question 8.1 from the second paper of 2010 (PEA: list 5 causes)
  • Question 18.1 from the first paper of 2010 (arrest in general: list 5 causes)
  • Question 18.2 from the first paper of 2010 (investigations to discriminate among the 4Hs and 4Ts)
  • Question 1b from the first paper of 2003 (causes of arrest during intubation)
  • Question 1a from the second paper of 2002 (peri-arrest; initial management)
  • Question 1b from the second paper of 2002 (peri-arrest; initial investigations)
  • Question 2a from the first paper of 2000 (peri-arrest; initial management)
  • Question 2b from the first paper of 2000 (peri-arrest;  initial investigations)

Causes of cardiac arrest

For the majority of situations, being able to reason in terms of Hs and Ts is enough. These are the reversible causes. To repeat them again:

  • Hypoxia 
  • Hypovolemia 
  • Hyper/hypokalemia 
  • Hyper/hypothermia 
  • Tension pneumothorax 
  • Tamponade 
  • Toxins 
  • Thrombus 

According to an audit of in-hospital cardiac arrest by Bergum et al (2015), in 66% of cases the cause of cardiac arrest is determined correctly by the rescuers. In the majority of cases (60%) cardiac problems were to blame; in a minority (20%) hypoxia was to blame. The other Hs and Ts among them covered only 20% of the cardiac arrest spectrum. It is therefore safe to bet on a cardiac aetiology. One might expect all these cardiac causes to have generated a preponderance of VF/VT, but in fact almost half (48%) of the arrests were PEA, and shockable rhythms represented only 27%.

A stereotyped approach to the peri-arrest patient

This approach is extracted from the ARC ALS II course manual, of which I have the 2011 copy. There was no specific section which might have been of greatest use for answering the peri-arrest scenario questions. "Chapter 3:  Recognition of the Deteriorating Patient and Prevention of Cardiorespiratory Arrest" (page 11) was probably the most helpful. From this section, the following generic approach was synthesised. As in trauma, the problems are addressed as they are discovered, without moving on with the survey.

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

Immediate investigations for the peri-arrest patient

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
  • CT of any specific suspicious cavity (abdomen, chest, brain)
  • TTE
  • random cortisol level, TFTs, etc (to exclude exotic causes of haemodynamic instability)

Causes of peri-arrest deterioration which can be identified by rapid bedside TTE

This list of easily echo-able causes of peri-arrest deterioration comes from one of those all-important Blue Boxes in Oh's Manual. The specific box is Box 21.2 (page 196) from Peter T Morley's chapter ("Adult cardiopulmonary resuscitation"). He references his own 2007 article as the main source of this list.

  • Hypovolaemia
  • Tamponade  (pericardial)
  • Tension pneumothorax
  • Thrombosis – pulmonary (thromboembolism)
  • Thrombosis – coronary (regional or global wall motion
  • abnormalities, including lack of cardiac motion)
  • Pacemaker capture
  • Unexpected VF
  • Acute valvular insufficiency (e.g. papillary muscle rupture)
  • Ventricular rupture
  • Aortic dissection
  • Massive pleural effusion

A stereotyped approach to the patient in cardiac arrest

This is not some sort of prescriptive guide to what you should do in a cardiac arrest situation.Rather, this is a stereotyped answer to all those CICM SAQs.

Thus:

1) Confirm cardiac arrest

2) Call for help

3) Commence BSL (CPR) as a sole responder until help arrives

  • 100 compressions per minute
  • Compression to a depth of 1/3rd of the anterior-posterior chest diameter
  • If airway is unprotected, 30:2 ratio of compressions to breaths
  • If intubated, asynchronous ventilation of 8-10 breaths per minute
  • Ensure the ETT is not malpositioned (chest examination, end tidal CO2 or calorimetry)

4) Once help arrives, commence ALS arrest algorithm

  • Apply defibrillator pads and charge defibrillator with CPR in progress
  • Perform a rhythm check, minimising interruption of compressions
  • If shockable rhythm, administer shock:
    • Then, adrenaline every 2nd rhythm check
    • Amiodarone after the 3rd shock (300mg)
  • If non-shockable rhythm, administer adrenaline 1mg.

5) Exclude treatable causes of cardiac arrest (4 Hs and 4 Ts).

References

Neumar, Robert W., et al. "Part 1: Executive Summary 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care." Circulation 132.18 suppl 2 (2015): S315-S367.

Bergum, Daniel, et al. "Causes of in-hospital cardiac arrest–Incidences and rate of recognition." Resuscitation 87 (2015): 63-68.

Morley, Peter T. "Monitoring the quality of cardiopulmonary resuscitation." Current opinion in critical care 13.3 (2007): 261-267.