Printable list of all equipment and procedure SAQs

College Answer

Lists were acceptable.

(a) Indications:
•  Venous access in collapsed. hypovolaemic or hypcrvolaemic child with DO other venous
access after several attempts
• Child up to 6 years of age
•  Administration of drugs or fluids

(b) Contraindications:
•  Age> 7years (relative contraindication. bone difficult to penetrate)
•  Other access available
•  No experience of technique

(c) Risks:
•  Osteomyelitis
•  Compartment syndrome from fluid extravasation
•  Bone marrow embolism

(d) Minimising risks:      .
•  Training and practice
•  Sterile technique
•  Establish conventional venous access ASAP and remove needle
•  Limb observation

Discussion

This question is very similar to Question 15.1 from the first paper of 2012.

In the interest of revision, and because this question is worded slightly differently, the answer to Question 15.1 is modified and presented below.

Thus:

Indications

• Cardiac arrest
• Need for immediate IV access, when it is difficult to establish by conventional methods

Contraindications

• Underlying fracture
• Underlying prosthesis
• Severe osteoporosis
• Contaminated site
• Inability to identify landmarks
• Insertion at a site of recently attempted IO access
• Unfamiliarity with the device (you might hurt yourself)

Age is no longer a contraindication; IO access has become very popular in adults since this 2000 paper.

Complications

• Osteomyelitis
• Fracture
• "through and through" penetration
• Extravasation
• Compartment syndrome due to extravasation
• Injury to staff (slipped needle)
• Damage to surrounding structures
• Microscopic fat emboli

With sternal approach:

• Mediastinal injury
• pneumothorax
• Greater vessel injury

References

Probably the best single reference for this:

Day, Michael W. "Intraosseous devices for intravascular access in adult trauma patients." Critical care nurse 31.2 (2011): 76-90.

Dev, Shelly P., et al. "Insertion of an Intraosseous Needle in Adults." New England Journal of Medicine 370.24 (2014).

James Cheung, Warren, Hans Rosenberg, and Christian Vaillancourt. "Barriers and Facilitators to Intraosseous Access in Adult Resuscitations When Peripheral Intravenous Access Is Not Achievable." Academic Emergency Medicine 21.3 (2014): 250-256.

College Answer

(a) The candidate should have been aware of the basic principles of pulse oximetry. 
Pulse oximetry is based on the Beer-Lambert Law which states that. the concentration of an absorbing substance in solution can be determined from the intensity of light transmitted through the solution, given the intensity and wavelength of incident light, the transmission path length and the characteristic absorbency at a specific wavelength. 
To   arrive  at   oxygen  saturation,  the   relative   concentrations  of   reduced  Hb   and oxyhaemoglobin must  be  calculated. At  wavelengths of  660nm and  940nm  there is 
.maximum separation·of absorption. These wavelengths also penetrate tissue and LEDs emitting these wavelengths are readily available.                                                . 
The pulse oximeter thus has two LEDs emitting light  of  these wavelengths through a vascular bed. A photodiode detector detects the intensity of transmitted light. It rejects the absorption from tissue and venous blood by sensing the pulsatile or AC components and 
rejecting the fixed or DC component. 
Factory calibration is based on nomograms·from young normals.

{b) False readings may be caused by: 
• Optical interference eg. abnormal haemoglobin, dye 
•  Signal artefact eg. fluorescent light 
•  False assumptions/calibration eg. inaccurate saturation's below 90%

Pulse Oximetry: principles and limitations. American J ofEmerg Med 17,1;59-67.

Discussion

Physical principles of pulse oximetry:

• Oxygen saturation is the ratio of reduced haemoglobin to oxyhaemoglobin
• Reduced haemoglobin and oxyhaemoglobin absorb different wavelengths;
  • Reduced Hb absorbs red light (660nm)
  • Oxygenated Hb absorbs infra-red light (940nm)
• When fingertip blood is exposed to these two wavelengths, one can measure the absorption of red and infra-red light, and from this infer the concentration of the two types of haemoglobin.
• Tissue and venous absorption is eliminated by processing the signal and rejecting non-pulsatile components

Causes for false readings of the pulse oximeter:

• Technical problems
  • Poor calibration
  • Damage to sensor or leads
• Interference
  • Ambient lighting
  • Patient movement
• Poor signal quality due to decreased access to blood
  • Poor perfusion
  • Nail polish
• Abnormal blood contents:
  • Carboxyhaemoglobin
  • Methaemoglobin
  • Methylene blue dye
  • Indocyanine blue dye

References

Tremper, Kevin K. "Pulse oximetry." CHEST Journal 95.4 (1989): 713-715.

Sinex, James E. "Pulse oximetry: principles and limitations." The American journal of emergency medicine 17.1 (1999): 59-66.

Ralston, A. C., R. K. Webb, and W. B. Runciman. "Potential errors in pulse oximetry III: Effects of interference, dyes, dyshaemoglobins and other pigments*." Anaesthesia 46.4 (1991): 291-295.

College Answer

A rapid response in this setting of severe haemoptysis is expected but if there is time an angiogram or bronchoscopy may help to isolate the pulmonary vessel involved.  Immediate management  may be simple. For example: 

(a} Withdraw catheter 2-3cm and then refloat PA catheter with balloon inflated to occlude the pulmonary artery. 

(b) Insert double lumen ETT to secure the airway and attempt to isolate the affected lung. A single lumen tube advanced into the unaffected side may be a quicker and easier option.

(c) Transfer to OR for immediate lobectomy if bleeding does not settle. The application of PEEP has also been reported to stem the bleeding.

Discussion

You have just caused a pulmonary artery rupture with your PA catheter. What do you do?

The savvy candidate will form a structured approach.

A)

Isolate the affected lung.

• Either insert a dual-lumen tube to isolate the affected lung, or advance the existing tube into the right main bronchus (if this is an option).This should protect the unaffected lung from contamination with blood and clots.

B)

If the lung is not isolated:

• crank up the PEEP. This may decrease the rate of haemorrhage by putting up a resistance to pulmonary blood flow.
• Position the patient affected-side down. This way, only one lung fills up with blood.

If the lung is isolated:

• Increase the FiO2. If a DLT is in position, the pulmonary vasodilation should encourage blood flow into the good lung.
• Position the patient affected-side up. This way, the affected lung will have decreased blood flow.

C)

Attempt temporary haemostasis.

• One may try to wedge the balloon in the affected pulmonary artery, thereby preventing further blood loss.

Establish definitive haemostasis

• Cardiothoracic surgical repair will be the only way this situation can be salvaged.
• Case reports have demonstrated that angioembolisation is also a viable option if urgent surgery is impossible or undesirable.

Lastly;

Family conference and full disclosure.

The historical mortality rate from these is about 70% according to Kearney & Shabot (1995)

References

Kearney, Thomas J., and M. Michael Shabot. "Pulmonary artery rupture associated with the Swan-Ganz catheter." CHEST Journal 108.5 (1995): 1349-1352.

Bossert, Torsten, et al. "Swan‐Ganz Catheter‐Induced Severe Complications in Cardiac Surgery: Right Ventricular Perforation, Knotting, and Rupture of a Pulmonary Artery." Journal of cardiac surgery 21.3 (2006): 292-295.

Bussières, Jean S. "Iatrogenic pulmonary artery rupture." Current Opinion in Anesthesiology 20.1 (2007): 48-52.

College Answer

The determinants of cardiac output are many  and  varied. A good understanding  is required. The standard four factors usually considered to control cardiac output are: heart rate (and rhythm), myocardial contractility, preload  and afterload. Many  interactions  between  these factors  may be present at one time. (Also could think of in terms of Cardiac Output= Heart Rate • Stroke Volume). Heart rate: loss of atrial kick (AF, nodal rhythms etc.), tachycardias, bradycardias, ectopic beats all may significantly decrease stroke volume and cardiac output.

Myocardial contractility  :generally consider: 
neurally mediated (sympathetic activity [increases], parasympathetic activity [decreases]), hormonally  mediated (adrenal medulla [adrenaline, noradrenaline], adrenal cortex [corticosteroids increase],  thyroid   hormone   (increase),  insulin  increase],  other                                                 [growth   hormone,  glucagon, endothelins  increase;  circulation  myocardial  depressants  including  some  cytokines,  nitric  oxide etc.]) 
oxygen (hypoxia: moderate stimulates, severe depresses),  carbon dioxide (direct: lower increases, 
higher decreases) 
drugs (beta-agonistslblockers, calcium agonistslblockers, inodilators, etc.) 
electrolytes (especially calcium, magnesium, phosphate)

Preload:                                                               . 
decreased   preload   with   normal  left  ventricular   compliance:  absolute   hypovolaemia,   relative 
hypovolaemia  (venodilatation; increased  resistance  to  venous  return:  including  increased intrathoracic  pressure  with IPPV/PEEP; right  heart dysfunction  including  AMI, pulmonary hypertension eg. pulmonary emboli) 
decreased preload with decreased LV compliance: LV hypertrophy, ischaemia, beta-agonists

Afterload: 
changes in  intrathoracic  pressure, sympathetic  tone (inhibition/paralysis etc),  vasodilatation  ( . 
direct effects of drugs, anaphylaxis etc).

Discussion

This is not as complicated as the college answer would have you think.

Cardiac output = heart rate x stroke volume.

• Determinants of heart rate:
  • Sympathetic tone
  • Exogenous sympathomimetics
  • Exogenous rhythm device (pacemakers)
  • Arrhytmias
• Determinants of stroke volume:
  • Preload
    • Volume status
    • Intrathoracic pressure eg PEEP
    • Pulmonary arterial flow (eg. obstructed by PE)
    • Atrial arrhythmias (loss of atrial kick)
    • Ventricular rate (allowing for diastolic filling)
    • Ventricular compliance
  • Afterload
    • Outflow tract resistance
    • Aortic/pulmonic valve resistance
    • peripheral vascular resistance
    • Haematocrit (as component of cardiac wotrkload)
  • Contractility
    • exogenous sympathomimetics
    • electrolyte balance
    • cardiac conduction system, presence of resynchronisation therapy eg. biventricular pacemaker

Jean-Louis Vincent has published a delightful commentary on this topic. It has a cute cartoon of a bicycle rider, in whom the gravelly pavement is the afterload, and the wind to his back the preload. One boggles how this representation might incorporate levosimendan.

References

Vincent, Jean-Louis. "Understanding cardiac output." Crit Care 12.4 (2008): 174.

College Answer

The role of cardiac output measurement  depends  largely on local practice. Units will vary in both aggressiveness of determination of cardiac output (PA catheter, echocardiography etc.), and in the way that the information is used (targeting particular goals, having monitoring protocols). Much of our haemodynamic and respiratory management can be done without regular assessment of cardiac output.  The levels  of  evidence  to  support  roles, indications  and  changes  in  therapy  should  be provided

Discussion

This complicated question did not merit a very detailed college answer, forcing me to elaborate upon this by myself.

One must be aware that the question refers to the role of cardiac output measurement in the ICU - not the merits of each specific method, or the risks vs benefits of cardiac output monitoring techniques.

Of course, how the hell do you provide levels of evidence for that?

Here is a table instead.

References

Mathews, Lailu, and Kalyan RK Singh. "Cardiac output monitoring." Annals of cardiac anaesthesia 11.1 (2008).

de Waal, Eric EC, Frank Wappler, and Wolfgang F. Buhre. "Cardiac output monitoring." Current Opinion in Anesthesiology 22.1 (2009): 71-77.

Pinsky, Michael R. "Hemodynamic evaluation and monitoring in the ICU."CHEST Journal 132.6 (2007): 2020-2029.

College Answer

Commonly used* techniques to measure cardiac output are few. Many techniques can be used, 
these include: intermittent thermodilution (inject cold fluid•), "continuous" thermodilution 
(heated*), use of doppler ( echocardiograhic probes• : transthoracic, trans-oesophageal. suprasternal, 
oesophageal), transthoracic bioimpedance•, and calculated using the Fick equation• (intermittent 
mixed venous oxygen, continuous SVO2 catheter), and variations on arterial waveform analysis. 
Appropriate critical analysis will include balances between advantages and disadvantages 
(mcluding invasiveness, insertion, limitations, misinterpretation, other data obtained etc.), and detail 
of accuracy (bias and precision) as well as indicator of reproducibility ( eg .. coefficient of variation).

Discussion

Again, a question which would be well suited to a tabulated answer.

References

Mathews, Lailu, and Kalyan RK Singh. "Cardiac output monitoring." Annals of cardiac anaesthesia 11.1 (2008).

de Waal, Eric EC, Frank Wappler, and Wolfgang F. Buhre. "Cardiac output monitoring." Current Opinion in Anesthesiology 22.1 (2009): 71-77.

Pinsky, Michael R. "Hemodynamic evaluation and monitoring in the ICU."CHEST Journal 132.6 (2007): 2020-2029.

College Answer

The difference in pressures may be caused by:

(a)  error in intra arterial measurement due to

- zero error (poor calibration, drift, wrong height)

-poor system (long tubing, soft wall, narrow bore)

-local arterial stenosis, spasm, hypothermia, intense vasoconstriction, subclavian stenosis etc

(b) error in NIBP measurement

- wrong size cuff

- irregular pulse, AF (consecutive pulses required)

- subclavian stenosis

(c) lack of correlation because measures are from different sites and use different principles.

The candidate might have explained the oscillotonometric and invasive pressure recording principles to elucidate the problem.

The choice of reading for clinical use depends on the above factors. Mean arterial pressure from the arterial lime in the absence of hypothermia, subclavian stenosis etc may be the most reliable. If there is doubt about this reading then a more proximal recording (eg femoral catheter or long brachial catheter or implantable transducer) may be necessary. In a vasculopath it would seem wise to trust the higher pressure.

Discussion

This is a practical question.

The discrapancy can arise as a result of device factors, or patient factors.

I.e either the measurements are wrong, or the patient genuinely has different blood pressure in different limbs.

One can approach this systematically:

Device factors

• Non-invasive measurement error
  • The cuff is the wrong size
  • The oscillometric measurement is confused by an arrhythmia
  • The patient is moving around too much
• Invasive measurement error
  • The transducer is zeroed incorrectly
  • The zero level is incorrectly selected
  • The transducer system is incorrectly set up

Patient factors

• The artery being measured is in spasm
• There is peripheral vascular disease, which is unequally distributed
• The patient has subclavian artery stenosis
• There is aortic pathology which influences flow into the limbs (eg. aneurysm)

Which measurement would you choose? This is a judgement call.

One might wish to exclude all device-related problems before making a decision. Ultimately, one may wish to measure the NIBP manually on the same arm as the arterial line, noting the cuff pressure at the point at which the arterial trace goes flat.

References

Crul, J. F. "Measurement of arterial pressure." Acta Anaesthesiologica Scandinavica 6.s11 (1962): 135-169.

Beevers, Gareth, Gregory YH Lip, and Eoin O'Brien. "Blood pressure measurement." Bmj 322.7293 (2001): 1043-1047.

Ward, Matthew, and Jeremy A. Langton. "Blood pressure measurement."Continuing Education in Anaesthesia, Critical Care & Pain 7.4 (2007): 122-126.

Pickering, Thomas G., et al. "Recommendations for blood pressure measurement in humans and experimental animals part 1: blood pressure measurement in humans: a statement for professionals from the Subcommittee of Professional and Public Education of the American Heart Association Council on High Blood Pressure Research." Hypertension 45.1 (2005): 142-161.

College Answer

Central venous pressure (CVP) is dependent on intravascular fluid volume, right ventricular function, pulmonary vascular resistance, venous capacitance, intrathoracic pressure, ventricular compliance and viz a tergo (arterial pressure).

Measurement of CVP is used as an indirect guide of right ventricular filling but any absolute measure has a complex relationship with right ventricular preload. If other conditions are constant, trends in CVP may reflect vascular compliance and changes in volume status.

Absolute measures along with pulmonary wedge pressure may help in the diagnosis of:

-    right ventricular infarction

-     pulmonary embolus

-     ARDS severity

-     Cor pulmonale

-     tamponade

CVP waveforms may indicate nodal rhythm, tricuspid incompetence etc

Discussion

This question closely resembles Question 8 from the first paper of 2014.

However, the college answer for the 2014 version is a massive improvement on this 2001 version.

Factors which determine CVP:

• Reference level of the transducer
• Intravasculr volume
  • and the distribution of this volume between the venous and arterial compartment
• Central venous compliance
• Right ventricular compliance
  • myocardial or pericardial disease; tamponade
• Right ventricular systolic function
• Cardiac rhythm (i.e. AF vs. sinus rhythm)
• Tricuspid valve disease
• Pulmonary vascular resistance
• Intrathoracic pressure

Influence of central venous pressure on patient management

The relationship of CVP to preload and fluid responsiveness is discussed in greater detail elsewhere.

In general, one can divide this answer into two components:

Pressure analysis

• Assists the diagnosis of cardiac failure
• Assists decisionmaking regarding fluid resuscitation (though this is not supported by evidence)
• Informs hemodynamic management in situations where CVP is surgically important (eg. in hepatic resection or transplant)

Waveform analysis

• Informative regarding tricuspid disease
• Informative regarding atrial contractility

References

Most of this material can be found in Bersten and Soni’s” Oh's Intensive Care Manual”, 6th Edition, as well as the CVC section from The ICU Book by Paul L Merino (3rd edition, 2007)

Marik, Paul E., and Rodrigo Cavallazzi. "Does the central venous pressure predict fluid responsiveness? An updated meta-analysis and a plea for some common sense*." Critical care medicine 41.7 (2013): 1774-1781.

College Answer

Consideration  should  be  given  to  pharmacodynamics  (dose  requirements,  side  effect  profile, effectiveness),  as  well  as  cost  and  other  interrelated  effects.     Methods  of  delivery  include intravenous, sub-cutaneous, via metered dose inhaler and via nebuliser.

Intravenous: excellent systemic delivery assured, but to areas that are perfused.  Systemic effects maximal so side effects are more pronounced.

Sub-cutaneous: easy to administer, but less predictable effects as delayed peak effect and lower bioavailability.  Systemic side effects still prominent.

Metered dose inhaler: easy to administer via adapter; many multiples of non-

intubated dose are required [eg. 10 puffs per treatment]; does not require breaking of ventilatory circuit; very low bioavailability, optimal via inline spacer (but adds cost, breaks circuit at least once, may become reservoir for infection); minimal systemic side effects.

Nebuliser:  can  be  given  continuously;   maximises  local  delivery  while  minimising  systemic absorption; easy to administer but requires specific equipment; requires break in circuit for each treatment; variable interaction with ventilator [some cannot compensate for flow].

Discussion

Prior to reading this question, I was not aware that beta-2 agonists could be given subcutaneously.Turns out, people have done this to infants, and "no local or general adverse reactions were observed".

References

Brémont F, Moisan V, Dutau G.Continuous subcutaneous infusion of beta 2-agonists in infantile asthma. Pediatr Pulmonol. 1992 Feb;12(2):81-3.

College Answer

The use of a pulmonary artery catheter in critically ill patients  remains controversial.

(a)        What potential  benefits are associated with its use?
Potential benefits relate to the information that is provided. These include:
•    Estimates of left-heart filling pressures. Clinical assessment is notoriously unreliable.
Allows better assessment of true filling pressures, in particular in the presence of pulmonary or right heart dysfunction.
•    Measurement of pulmonary arterial pressures. Clinical assessment is unreliable. Allow titration of therapies to improve right heart function (nitric oxide, GTN, oxygenation, ventilation etc).
•    Measurement of core temperature. Useful assessment of true core temperature.
•    Measurement of cardiac output. Gold standard for measurement (more accurate than clinical assessment).
•    Measurement of mixed venous oxygen saturation. Allows assessment of global oxygen extraction, and facilitates management directed towards this endpoint (eg. fluids, inotropes, sedation etc.)
•    Measurement of right heart pressures. Allows titration of specific management.
•    Calculation of derived variables (eg. SV, SVR) which may provide further direction for management.
•    Some extra features may be available. Consider ability to calculate right ventricular ejection fraction, and to measure cardiac output and mixed venous oxygen saturation continuously.

(b)        What potential  complications are associated with its use?

Potential complications are multiple, some of which are rare and life threatening, others are more subtle, may affect morbidity, and are far more common. Some reference to magnitude of importance of various potential complications should be made. Consider:
•    Additional cost of catheter and flush lines, exposure to heparinised (usually) catheter, ±
requirement for additional staff and/or monitoring equipment
•    Problems associated with delays in instituting management while awaiting completion of insertion

•    Problems associated with the venepuncture (including damage to surrounding structure at risk [dependent on site] eg. nerves, arteries, veins, lung etc).
•    Problems associated with the passage [insertion or removal] (including malposition, arrhythmias)
•    Problems associated with the catheter in situ (including trauma to valves, infection, air embolus)
•    Problems predominantly associated with balloon inflation (including pulmonary artery rupture, air embolus)
•    Problems associated with the information obtained or its interpretation (including limitations of various assumptions relating pressure [eg. PAOP] and preload [eg. LVEDV], errors in calculating derived indices, treatment based on erroneous information)

(c)        In what groups of patients  do you think that it should be used?

The answer should represent a combination of the candidate’s knowledge of the literature, and their experience/expertise. There is very little data to support the routine use of PA catheters in any particular group of patients. Specific reference to situations where it has not been proven to be of benefit may be of value, but has not been asked for specifically. Some justification (eg. risk benefit analysis) for the groups of patients is required.
Expected groups of patients may include:

•    those with combination organ dysfunction (eg. cardiac and lung), with conflicting priorities
•    those who are not responsive (or respond abnormally) to small amounts of inotropic/vasopressor support
•    those where additional information may not be readily obtainable (eg. no echocardiography service)
•    those undergoing cardiac surgery (often restricted to those with impaired LV function)
•    those requiring cardiovascular optimisation for high risk non-cardiac surgery.

Discussion

With this question, one could become overexcited, and write extensively about the various possible minute details of PA catheter use, its various merits and demerits, recruting massive amounts of literature as references.

However, one only has 10 minutes.

(a) What potential  benefits are associated with its use?

• Direct measurement of several variables with one device:
  • RA pressure
  • PA pressure
  • PA wedge pressure
  • Core temperature
  • Mixed venous saturation
• Measurement of cardiac output, and mathematical derivation of other variables from thermodilution
• Titration of therapies to these measurements

(b)What potential  complications are associated with its use?

• Same as CVC:
  • Perforation of SVC
  • Hemothorax, pneumothorax
  • Atrial fibrillation
• Unique to PA catheter
  • Ventricular Arrhythmia
  • Thromboembolic events (the catheter is a nidus for clot formation)
  • Mural thrombi in the right heart (up to 30%)
  • Air embolism from ruptured balloon
  • Pulmonary infarction
  • Endocarditis of the pulmonary valve ( 2%)
• Right bundle branch block
  • If you already have LBBB, this causes complete heart block
  • If you are lucky, it is a transient phenomenon and you only need to pace them transcutaneously for a brief period. If you are unlucky, you have injured the AV node, and the patient needs prolonged transvenous pacing
• Knotting on structures or on itself ( ~ 1%)
  • If it has gone into the right ventricle by 25-30cm and its still not in the pulmonary artery, you start to worry
• Damage to the valves
  •  Never pull the catheter back with the balloon inflated! You could tear the valve leaflets
• Pulmonary artery rupture: 0.2% risk,  70% mortality (The historical mortality rate from Kearney & Shabot, 1995)
  • Risk factors: pulmonary hypertension, mitral valve disease, anticoagulants and age over 60

(c)In what groups of patients  do you think that it should be used?

• Patients who require the titration of multiple simultanous resuscitation strategies (inotropes, vasopressors and fluid resuscitation)
• Situations where non-invasive assessment of hemodynamic parameters and cardiovascular funtion is not available, or impossible (eg. where there is no TTE service, or where TTE or TOE is impossible, for instance in patients with oesophagectomy or an open mediastinum)
• Situations where therapy is titrated to pulmonary artery pressure (eg. inhaled pulmonary vasodilators), and more generally situations when therapy is titrated to any of the directly measured variables
• Situations where the risk of PA catheter insertion is outweiged by the benefit, and where less invasive methods of monitoring are considered inferior, or are impossible (eg. when PiCCO pulse contour analysis is invalidated by arrhythmia)

The awesomeness of the PA catheter is discussed in greater detail elsewehere.

References

This a full-text version of the seminal paper from 1970:

Swan HJ, Ganz W, Forrester J, Marcus H, Diamond G, Chonette D (August 1970). "Catheterization of the heart in man with use of a flow-directed balloon-tipped catheter". N. Engl. J. Med. 283 (9): 447–51.

A manufacturer (Edwards) offers some free information about the PA catheter on their product page.

The PA catheter section from The ICU Book by Paul L Marino (3rd edition, 2007) is a valuable read.

Armstrong, Ehrin J., James M. McCabe, and Melvin D. Cheitlin. "Pulmonary artery catheterization in the intensive care unit: just numbers floating by?."Archives of internal medicine 171.12 (2011): 1110-1111.

Kearney, Thomas J., and M. Michael Shabot. "Pulmonary artery rupture associated with the Swan-Ganz catheter." CHEST Journal 108.5 (1995): 1349-1352.

Additionally, UpToDate has an article on PA catheter complications

College Answer

Measurement of ETCO2  implies the use of a quantitative device, and usually this is one which allows assessment of waveform morphology (ETCO2 vs time).  Specific roles include: confirmation of tracheal placement of artificial airway, pattern recognition of ETCO2 waveform, use of value of ETCO2 during cardiac arrest or hypotensive states, prediction of arterial PaCO2.

Confirmation of tracheal placement is highly sensitive and specific in the presence of pulmonary blood flow.  False negative values may occur with minimal pulmonary blood flow, but should not usually occur with adequate CPR.  False positives are very uncommon and short lived (eg. CO2 in stomach).

Waveform pattern can assist in the diagnosis in particular of expiratory flow obstruction (and gas trapping) and attempts at spontaneous breathing.

During cardiac arrest, the absolute level of ETCO2  is proportional to pulmonary blood flow (and hence cardiac output). It may be used to guide cardiac compression, but apart from this it adds little to prognostication (ie. confirms that patient is likely to die).  Sudden decreases in ETCO2 may be indicative of the decrease in pulmonary blood flow associated with pulmonary emboli.

Prediction of PaCO2 from ETCO2 is fraught with difficulty.   The major limiting factors are pulmonary blood flow and V/Q balance.  Unless these factors are unchanging, even the trending of the relationship of between PaCO2 and ETCO2 unreliable.  Unfortunately if the PaCO2 is important (eg. major head injuries), it must be measured.

Discussion

This question is identical to Question 6 from the second paper of 2005.

References

College Answer

The PA catheter provides access to pulmonary and central venous circulations, at a relatively low incremental cost.   The main information obtained is from measurement of pressures (eg. within right atrium or pulmonary arteries), but additional information includes core temperature, pressure waveforms,  occlusion  pressure,  cardiac  output  (thermodilution  or  continuous),  mixed  venous oxygen saturation (intermittent [including from sites other than PA] or continuous).  Standard limitations include the variable relationship between pressure and volume, and the risks of using derived variable.   Other risks can be categorised into those associated with central venous catheterisation (e.g. arterial puncture, air embolus, infection), floating of the catheter (e.g. arrhythmias), and balloon inflation (e.g. PA rupture).   Some information can be continuously monitored (e.g. pulmonary arterial pressures); other is intermittently sampled (e.g. occlusion pressure, thermodilution cardiac output), but without the risks of reinsertion.

Transoesophageal echocardiography requires additional very expensive monitoring equipment, and an expensive (but re-usable) probe. The TOE allows visualisation of cardiac (and surrounding) structures, and measurement/estimation of a number of haemodynamic parameters.   A visual estimate is obtained of various parameters: including volume status (pre-load), contractility (left and right sided systolic and diastolic function), regional wall motion, abnormal masses (eg. vegetations) and peri-cardial/pleural/peri-aortic collections. Using Doppler, assessment of valvular function, and estimate of pressures and cardiac output is also possible.   This is an intermittent technique (not usually left in situ for more than a few hours), which is highly operator dependent, where most risks associated with insertion and manipulation (eg. gastrointestinal bleeding/rupture).   Insertion and manipulation usually requires some degree of sedation.

Indications depend on specific information desired, and the local expertise.   The potential information obtained with either technique must be weighed against the risks in any given clinical scenario.  If standard precautions are used, mortality or major morbidity with either technique is thankfully rare.

Discussion

This question lends itself well to a table format.

References

This is an article on how one might measure PAC-style chamber pressures using the TOE and the Bernoulli equation.

Chassot, P. G. "[Hemodynamic surveillance: transesophageal echocardiography or Swan-Ganz catheter?]." Revue medicale de la Suisse romande 121.9 (2001): 667-675.

College Answer

Accuracy of central venous pressure measurements depend on a number of factors. These include placement of device (tip in RA, RV, femoral vein etc), levelling (usually to phlebostatic axis), zeroing (zero means atmospheric pressure), calibration (measurement above zero is accurate when compared with gold standard [was mercury sphygmomanometer]), damping (not over or under, assessed by square wave or balloon bursting, prefer coefficient approximately 0.7). Frequency response of the system (intrinsic plus additional tubing) may significantly impact on damping (prefer shorter and stiffer tubing). Running averages also significantly alter ability to interpret spontaneous readings or variability associated with intra-thoracic pressure (better with printed waveform). Water column measurement is rarely done.

Discussion

The topic of CVP measurement is discussed in greater detail elsewhere.

In brief, the following factors influence the accuracy of CVP measurement:

Device factors

• Zeroing
• Calibration of the transducer
• Selection of zero level
• Dynamic response of the circuit

Artifact

• Transducer drift
• Infusions running through the monitored lumen
• Damping in the system (eg. the presence of air bubbles)

Patient factors

• CVC position (femoral vs. IJ, SVC)
• Tricuspid regurgitation

Note that the question asked about accuracy. We were not expected to produce a list of different factors which influence the CVP, for instance PEEP, intravascular volume, etc. This was purely a device-oriented measurement question.

References

Alzeer A et al. Central venous pressure from common iliac vein reflects right atrial pressure. Can J Anaesth 1998 Aug 45 798-801.

Most of this material can be found in From and Soni’s” Oh's Intensive Care Manual”, 6th Edition, as well as the CVC section from The ICU Book by Paul L Merino (3rd edition, 2007)

Additionally, I have made use of the amazing Essentials of Critical Care, 8th ed.(ch.3 - Monitoring in the ICU)

Marik, Paul E., and Rodrigo Cavallazzi. "Does the central venous pressure predict fluid responsiveness? An updated meta-analysis and a plea for some common sense*." Critical care medicine 41.7 (2013): 1774-1781.

College Answer

Arterial puncture is a well recognised but uncommon complication of central venous catheter insertion. The potential complications include all those associated with venous/arterial puncture, as well as specific ones associated with the large hole in the artery. Damage to associated structures (nerves [eg. vagus], pleura, oesophagus and trachea!) can result in specific problems (either directly or indirectly from compression [eg. haematoma]). A large bore catheter in a blood vessel can result in air embolus (worse if arterial) or even embolus of atheromatous material (stroke risk). Specific problems related to the arterial site include: toxicity of inadvertently administered drugs (before actual position recognised), higher risk of significant haematoma and blood loss (augmented by coagulopathy especially if removed/dislodged). Referral to surgeons with vascular experience is essential to facilitate definitive management because of the size of the hole in the artery (suture repair, patch
repair etc). If surgical repair is not considered indicated, prolonged pressure for haemostasis has associated potential problems (carotid body, distal flow), and haematoma formation likely.

Discussion

This question is identical to Question 23 from the first paper of 2008.

References

Nair, Sanil, et al. "A case of accidental carotid artery cannulation in a patient for hemofilter: complication and management." British Journal of Medical Practitioners 2.3 (2009): 57-58.

College Answer

The femoral vein lies in the intermediate compartment of the femoral sheath.  It is usually accessed just inferior to the inguinal ligament.  The inguinal ligament can be defined by the surface anatomy of a line between the pubic tubercule and the anterior superior iliac spine. The mid point of the inguinal ligament is the site of the internal ring.   A needle inserted through the skin will pass through subcutaneous tissue, and the fascia of the femoral sheath before entering the femoral vein.  Posterior to the femoral vein is the posterior fascia of the femoral sheath, and the pectineus.   Lateral to the femoral vein is the fibrous septum separating the intermediate compartment of the femoral sheath from the lateral compartment (containing the femoral artery).  Further lateral to this is the femoral nerve.  Medial to the femoral vein is the medial compartment of the femoral sheath (femoral canal), which contains lymph vessels, nodes and fatty tissue.

Discussion

Judging by the collge answer,  "outline the anatomical structures relevant to the insertion of a femoral venous catheter" probably means "discuss the relations of the femoral vein in the usual site of femoral venous cannulation". In other words, the femoral triangle.

Basic points:

• The femoral vein lies within the femoral triangle:
  • The superior border is formed by the inguinal ligament.
  • The medial border is formed by the adductor longus.
  • The lateral border by the sartorius muscle.
  • The apex is formed by the sartorius crossing the adductor longus muscle.
  • The roof is composed of the skin, subcutaneous tissue, the cribriform fascia, and the fascia lata.
  • The floor is formed of underlying adductor longus, adductor brevis, pectineus, and iliopsoas muscles.
  • Lateral to the femoral vein is the femoral artery in a fibrous sheath
  • Medial to the femoral vein is the fatty lymphatic contents of the femoral sheath

Anatomical landmarks for localisation of the femoral vein:

• The inguinal ligament runs from the pubic tubercle medially to the anterior superior iliac spine laterally.
• The femoral artery pulse is roughly at the midpoint of the inguinal ligament
• The femoral vein is medial to the femoral pulse
• The puncture of the vessel should be approximately 1-1.5cm medially to the maximal femoral pulse, and approximately 1cm inferior to the inguinal ligament (thus the skin puncture should be slightly more inferior than this)

References

Tsui, Janet Y., et al. "Placement of a femoral venous catheter." New England Journal of Medicine 358.26 (2008).

Bannon, Michael P., Stephanie F. Heller, and Mariela Rivera. "Anatomic considerations for central venous cannulation." Risk management and healthcare policy 4 (2011): 27.

College Answer

Wet ventilator circuits require power for heating, a chamber for water to be heated, and temperature sensors to feedback appropriate temperature within chamber and ideally to within circuit.  Benefits include potential for optimal efficiency (under all circumstances), reliability, ability to warm patient, and proven track record of safety.  Disadvantages include potential for condensation (rain-out) with excessive (potentially hot) fluid delivery to airways, microbiological colonisation, lack of transportability, and increased cost.

Heat and moisture exchangers come in a variety of types (with more emphasis on humidification and/or microbiological filter).  Benefits include ease of use (including during transport),  lower  staff  workload,  lower  costs  and  potential  for  decreased  ventilator associated pneumonia [Kola, Intensive Care Med (2005) 31:5-11].  Disadvantages include inability to use with all patients (eg. those haemoptysis, tenacious secretions, increased airway resistance, ARDS), problems with increased dead space and resistive load, and potential for airway occlusion.

Discussion

The various features of the HME are discussed in greater and more general detail elsewhere. A good article which is both recent and detailed is this 2014 piece from BioMed Research International.

This question would benefit from a tabulated answer.

References

Martin, Claude, et al. "Comparing two heat and moisture exchangers with one vaporizing humidifier in patients with minute ventilation greater than 10 L/min."CHEST Journal 107.5 (1995): 1411-1415.

Kirton, Orlando C., et al. "A Prospective, Randomized Comparison of an In-Line Heat Moisture Exchange Filter and Heated Wire Humidifiers Rates of Ventilator-Associated Early-Onset (Community-Acquired) or Late-Onset (Hospital-Acquired) Pneumonia and Incidence of Endotracheal Tube Occlusion." CHEST Journal 112.4 (1997): 1055-1059.

Kollef, Marin H., et al. "A randomized clinical trial comparing an extended-use hygroscopic condenser humidifier with heated-water humidification in mechanically ventilated patients." CHEST Journal 113.3 (1998): 759-767.

Siempos, Ilias I., et al. "Impact of passive humidification on clinical outcomes of mechanically ventilated patients: A meta-analysis of randomized controlled trials*." Critical care medicine 35.12 (2007): 2843-2851.

Al Ashry, Haitham S., and Ariel M. Modrykamien. "Humidification during Mechanical Ventilation in the Adult Patient." BioMed research international2014 (2014).

College Answer

Zeroing: is a process which confirms that atmospheric pressure results in a zero reading by the measurement system. Intermittent confirmation ensures the absence of baseline drift (relatively common with disposable transducers), where atmospheric pressure no longer reads zero, resulting in aberrant results.

Levelling (or establishing the “zero reference point”): is a process which determines the position on the patient you wish to be considered to be your zero.  Transducers are placed at a point level with this point (often utilising fluid filled tubing).  Usually this is chosen as the midaxillary line (in a supine patient) or it could be the phlebostatic axis.  Significant errors in measurement may occur if readings using different zero reference points are used (eg. Cerebral Perfusion Pressure).

Calibration: is a process of adjusting the output of a device to match a known input value. Verification of calibration requires using a gold standard (eg. mercury or water manometer), and usually a simple two-step procedure (eg. confirming that zero = zero and 100mmHg =

100mmHg),  which  assesses  linearity  of  the  system.  The  calibration  of  disposable transducers is preset, and cannot be altered.

Discussion

This question relies on the candidate's ability to generate definitions for terms which are in ubiquitous use. Unfortunately, this also means that their definition is frequently grasped intuitively, and never formally taught. LITFL have a good page on this material.

One can come up with a variety of definitions for these terms. Below, one can find a few non-canonical definitions. However, if this question appears again, one would be strongly advised to quote the college definition verbatim. The examiners wrote them in this way for a reason.

Alternatives?

"Zeroing"can also be defined as "the use of atmospheric pressure as a reference standard against which all other pressures are measured".

"Levelling"can be defined as "the selection of a position of interest at which the reference standard (zero ) is set".

"Calibration"can be defined as "an adjustment of system gain to ensure the proper response to a known reference value".

References

McCann, Ulysse G., et al. "Invasive arterial bp monitoring in trauma and critical care: Effect of variable transducer level, catheter access, and patient position." CHEST Journal 120.4 (2001): 1322-1326.

Thomas, E., M. Czosnyka, and P. Hutchinson. "Calculation of cerebral perfusion pressure in the management of traumatic brain injury: joint position statement by the councils of the Neuroanaesthesia and Critical Care Society of Great Britain and Ireland (NACCS) and the Society of British Neurological Surgeons (SBNS)." British journal of anaesthesia (2015): aev233.

Gondringer, N., and J. D. Cuddeford. "Monitoring in anesthesia: clinical application of monitoring central venous and pulmonary artery pressure (continuing education credit)." AANA journal 54.1 (1986): 43-56.

Abby Jones, Oliver Pratt; PHYSICAL PRINCIPLES OF INTRA-ARTERIAL  BLOOD PRESSURE MEASUREMENT - ANAESTHESIA TUTORIAL OF THE WEEK 137 8TH JUNE 2009

College Answer

Testing should involve

a) Confirmation that the appropriate outlets are at each bed space, with correct labelling, colour coding, and sleeve index system. Bed spaces in a level three ICU are supplied with at least three O2, two air, and three suction outlets.

b) Testing that the correct gas is supplied, and that the gas is pure. Oxygen concentrations should be measured at all gas outlets. This will distinguish between oxygen, air, and another gas such as nitrous oxide or nitrogen. A sniff test assessing for objectionable odours should be performed at medical air outlets only. If a non-respirable gas is present, this testing must be performed by an anaesthetist.

c) Tests for flow rate and pressure. Tested using a device that fits the outlet, and incorporates a pressure manometer, a variable flow restrictor, and a flow meter. Static pressure is measured and should be 415 kPa (60 psi) on O2 and air outlets, and -60 kPa at suction outlets. The flow rate is then set to 40 L/min, and the change in pressure measured. The change in pressure should be <
10 kPa for air and O2, and < 15 kPa for suction.

d) Testing of alarms. Tested by turning off the isolating valve for each supplied gas in turn, and
ensuring that visible and audible alarms activate.

References: JFICM policy document IC-1; Australian Standard 2896 1998, Medical gas systems –
installation and testing of non-flammable medical gas pipeline systems.
Four out of forty-one candidates passed this question.

Discussion

Four out of forty-one candidates passed this question; this is a testament not to the quality of the candidates, but to the obscurity of the question.

The document referenced by the college answer is the Australian Standard 2896 1998, Medical gas systems – installation and testing of non-flammable medical gas pipeline systems. Its is not available online except for the steep price of $200 or so. The free sample of it looks like this.

The CICM policy document IC-1 (Minimum Standards for Intensive Care Units) is available for free, however. The following point from that document is relevant to this question:

• There must be piped gas supply failure alarms.

The rest must come from the inaccesible Australian Standard. However, a helpful summary is available from this copper tubing company. Their document adds the following points:

• The nominal design working pressure shall be 415 kPa for medical gas supply,
  -60 kPa for medical suction, and 1400 kPa for surgical tool gas supply.

Nowhere are there online guidelines as to how one must perform a sniff test assessing for objectionable odours.

In short, it is difficult to determine where the four passing candidates got their information from.

Presumably, these people had an intimate familiarity with Dorsch and Dorsch's Understanding Anaesthesia Equipment; specifically, Chapters 1 to 4 are dedicated exclusively to medical gas supply and distribution systems. Of course it is a textbooks which one has to pay for. For the freegan, the best I could come up with is this article from the Indian Journal of Anaesthesia.

In brief summary;

• Make sure all the outlets have the right gases in them
• Make sure the gases are at the correct static pressure (~ 400kPa)
• Make sure the gas pressure does not drop when the flow is turned up
• Make sure the low pressure alarms are working.

A more detailed Dorsch-and-Dorschian list of tests can be found in my brief point-form summary of medical gas supply and distribution system testing.

References

Das, Sabyasachi, Subhrajyoti Chattopadhyay, and Payel Bose. "The anaesthesia gas supply system." Indian journal of anaesthesia 57.5 (2013): 489.

Love-Jones, Sarah, and Patrick Magee. "Medical gases, their storage and delivery." Anaesthesia & Intensive Care Medicine 8.1 (2007): 2-6.

Westwood, Mei-Mei, and William Rieley. "Medical gases, their storage and delivery." Anaesthesia & Intensive Care Medicine 13.11 (2012): 533-538.

College Answer

Measurement of ETCO2 implies the use of a quantitative device, and usually this is one which allows assessment of waveform morphology (ETCO2 vs time). Specific roles include: confirmation of tracheal placement of artificial airway, pattern recognition of ETCO2 waveform, use of value of ETCO2 during cardiac arrest or hypotensive states, prediction of arterial PaCO2.
Confirmation of tracheal placement is highly sensitive and specific in the presence of pulmonary blood flow. False negative values may occur with minimal pulmonary blood flow, but should not usually occur with adequate CPR. False positives are very uncommon and short lived (eg. CO2 in stomach).
Waveform pattern can assist in the diagnosis in particular of expiratory flow obstruction (and gas trapping) and attempts at spontaneous breathing particularly during apnoea testing.
During cardiac arrest, the absolute level of ETCO2 is proportional to pulmonary blood flow (and hence cardiac output). It may be used to guide cardiac compression, but apart from this it adds little to prognostication (ie. confirms patient that patient likely to die is likely to die). Sudden decreases
in ETCO2 may be indicative of the decrease in pulmonary blood flow associated with pulmonary emboli.
Prediction of PaCO2 from ETCO2 is fraught with difficulty. Very few candidates demonstrated an understanding of this area. The major limiting factors are pulmonary blood flow and V/Q balance. Unless these factors are constant, even the trending of the relationship of between PaCO2 and ETCO2 unreliable. Unfortunately if the PaCO2 is important (eg. major head injuries), it must be measured.
Utility in neonates and children may be impaired by small tidal volumes.

Discussion

Though EtCO₂ has been discussed in Question 9.2 from the second paper of 2008, it was not a "critically evaluate" style of question.

A systematic "critical evaluation" should resemble the following:

Rationale

• CO₂ elimination is an important component of gas echange
• This can be assessed indirectly by serial measurements of arterial PaCO₂; however ideally the measurement should be performed continuously.
• Trends in gas exchange are an important parameter to observe in patients whose respiratory function is compromised
• CO₂ monitoring is also of critical importance in patients with increased intracranial pressure

Applications in ICU

• Confirmation of ETT placement
• Airway disconnection alarm
• Monitoring during transport
• During CPR to assess adequacy of cardiac compression
• Recognition of spontaneous breath during apnoea test
• Neurosurgical patient to provide protection against unexpected hypercapnia
• Quick bedside assessment of bronchospasm
• Alert of sudden changes in pulmonary perfusion (eg. PE)
• Early alert of PEA in the absence of continuous BP monitoring
• More accurate monitoring of respiratory rate

Advantages

• Continuous monitoring
• Immediate feedback regarding cardiac output and ETT position
• Waveform analysis is possible
• Cheap
• Increased safety; decreased risk of undetected airway circuit disconnection

Disadvantages

• Produces vigilance-impairing false alarms
• EtCO₂ values may not correlate with PaCO₂ values and the two may be substantially different
• The monitor in-line connector creates a small amount of apparatus dead space
• The adaptor fitted to the end of the ETT may be heavy, and may increase the risk of accidental extubation, particularly in children and neonates
• The gas sampling models of EtCO₂ monitors can diminish the delivered minute volume, as they access the circuit gas at a rate of about 200ml/min.
• Nitrous oxide can confuse some capnometers (i.e. be mistaken for CO₂)
• The presence of helium can cause the EtCO₂ measurement to be incorrectly elevated in some capnometers (i.e. those which use a reporting algorithm that assumes that the only gases present in the sample are those that the device is capable of measuring)

Evidence and Guidelines

• EtCO₂ rapidly detects lifethreatening complications in transported patients.
• American Heart Association Guidelines for Cardiopulmonary Resuscitation make the following recommendations
  • Use EtCO₂ to assess ETT position
  • Use EtCO₂ to assess efficacy of CPR
  • Use EtCO₂ to confirm the return of spontaneous circulation

Capnography is discussed in greater detail elsewhere:

• The normal capnometry waveform
• The relatioship of abnormal capnograph waveforms to lung pathology

There is also an excellent site by Prasanna Tilakaratna which explains infra-red absorption spectrophotometry using vividly colourful diagrams.

References

The best, most detailed review:

Walsh, Brian K., David N. Crotwell, and Ruben D. Restrepo. "Capnography/Capnometry during mechanical ventilation: 2011." Respiratory care 56.4 (2011): 503-509.

Whitaker, D. K. "Time for capnography–everywhere." Anaesthesia 66.7 (2011): 544-549.

Kodali, Bhavani Shankar. "Capnography outside the operating rooms." Anesthesiology 118.1 (2013): 192-201.

Yamauchi, H., et al. "Dependence of the gradient between arterial and end-tidal PCO2 on the fraction of inspired oxygen." British journal of anaesthesia (2011): aer171.

Razi, Ebrahim, et al. "Correlation of End-Tidal Carbon Dioxide with Arterial Carbon Dioxide in Mechanically Ventilated Patients." Archives of trauma research 1.2 (2012): 58.

Ahrens, Tom, Helen Wijeweera, and Shawn Ray. "Capnography. A key underutilized technology." Critical care nursing clinics of North America 11.1 (1999): 49-62.

Kingston, E. V., and N. H. Loh. "Use of capnography may cause airway complications in intensive care." British journal of anaesthesia 112.2 (2014): 388-389.

Ortega, Rafael, et al. "Monitoring ventilation with capnography." New England Journal of Medicine 367.19 (2012).

Rückoldt, H., et al. "[Pulse oximetry and capnography in intensive care transportation: combined use reduces transportation risks]." Anasthesiologie, Intensivmedizin, Notfallmedizin, Schmerztherapie: AINS 33.1 (1998): 32-36.

College Answer

As the bronchoscope exits the endotracheal tube, the tracheal rings are seen anteriorly. They are deficient posteriorly, where the trachealis muscle runs longitudinally. As the bronchoscope is advanced a narrow antero-posterior ridge (the carina) is seen, where the trachea divides into the right and left main bronchi. The right main bronchus is relatively in line with the trachea, while the left comes off at a greater angle. Advancing down the right main bronchus; the right upper lobe bronchus comes off laterally (3 o’clock) approximately 2 cm past the carina, and divides into the branches to the apical, anterior and posterior segments; the middle lobe bronchus is seen anteriorly (12 o’clock) and divides into the branches to the medial and lateral segments; soon after the apical segment of the lower lobe is seen posteriorly (6 o’clock); then the four basal segments are seen (medial, lateral, anterior and posterior). Pulling back to the trachea, then advancing down the left main bronchus; at approximately 5 cm the left main bronchus divides into the left upper lobe bronchus which is seen laterally (9 o’clock) and the left lower lobe bronchus. The upper lobe bronchus divides into the superior division and the lingular division. The superior division gives rise to two branches, the apicoposterior and anterior segments. The lingula gives rise to the superior and inferior segments. The lower lobe bronchus gives rise to the apical segment of the lower lobe seen posteriorly (6 o’clock), then the three basal segments (lateral, anterior, and posterior).

Fourteen out of forty-one candidates passed this question.

Discussion

A picture is worth a thousand words. However, there is no concise graphical summary of this, and one can really go berzerk with bronchial nomenclature.

The low pass rate for this question demonstrates the lack of access to quality bronchoscopy teaching in our specialty.

Additonally, the college answer seems to fail to acknowledge the need to change the orientation of the bronchoscope when advancing it. Thus, instead of coming off at 3o'clock, the right main bronchus is actually seen at 12 o'clock (because you have turned the bronchoscope in order to guide the flexible tip into the right main bronchus).

In short, these are the landmarks one encounters when performing a bronchoscopy.

• Right main bronchus
  • right upper lobe bronchus at 12 o'clock
    • branches to the apical, anterior and posterior segments
  • right bronchus intermedius
    • right middle lobe bronchus
      • 3 branches: to the right middle medial and lateral segments
    • right lower lobe bronchus
      • apical segment of the lower lobe
      • four basal segments: medial, lateral, anterior and posterior
• Left main bronchus
  • left upper lobe bronchus
    • superior division
      • apicoposterior and anterior segments
    • lingular division
      • superior and anterior segments
  • left lower lobe bronchus
    • apical segment of the lower lobe
    • three basal segments: lateral, anterior, and posterior.

References

LITFL have some excellent bronchoscopy videos.

Educational resources for bronchoscopy are available from the wonderful website of the American Thoracic Society.

Additionally, ThoracicAnaesthesia.com has a full-on virtual bronchoscopy simulator which is essentially a Flash-based game, and which is disturbingly fun to play with.

Lastly, bronchoscopy.org is probably the definitive resource for all this, and represents the pinnacle of bronchoscopic excellence. Their bronchoscopic anatomy poster is the best thing ever.

College Answer

The abnormalities present include:
Sinus tachycardia, Pulsus Alternans, pulmonary hypertension, systolic hypotension, tricuspid regurgitation (large v waves), low calculated Systemic Vascular Resistance (about 500-600; though the estimate of cardiac output may be artificially elevated by the TR).
The specific pathophysiological disturbances revealed are:
Severe LV dysfunction and tricuspid regurgitation. The low SVR at this stage is most likely to be due to a systemic inflammatory response rather than sepsis.
Common problems related to lack of relevant detailed knowledge.

Discussion

This question is identical to Question 3.3 of the second 2009 paper.

However, the college answer here is more detailed, and comments are more snarky.

Not only that, but the examiners actually calculated the SVR ( 80 x (mean arterial pressure - mean right atrial pressure) / cardiac output) - that would be 80 x (63-23) / 5.7, or 561.4 dynes.s.cm^-5

That would indeed be low. Normal is 700-1600.

References

College Answer

Definition: Oxygen delivery is the total amount of oxygen delivered to the tissues by the cardiac
output and is calculated as the product of blood flow (QT) and arterial oxygen content (CaO2). The normal global oxygen delivery is approximately 1000 ml/min.
The adequacy of oxygen delivery can assessed by various means including:
•    Clinical examination: (ie signs of inadequate oxygen delivery) can result from hypovolemia, sepsis, myocardial dysfunction or severe hypoxemia in the face of a normal circulation. Clinical features include shock, cyanosis, Kussmaul respiration, pallor, raised or lowered JVP, bounding pulses if sepsis, gallop rhythm.
•    Monitoring:     pulse  oximetry, Hb,  PaO2,  cardiac output,  MV  oximetry,  ABGs,  serum lactate and creatinine, central venous oxygen saturation, tonometry, sublingual capnometry.
•    Absolute value: No precise data exist for what is adequate in critical illness. There was a vogue for achieving supranormal oxygen delivery in sepsis and ARDS in the early 1990s, but this approach has been shown to result in excess mortality in the critically ill.

Discussion

Oxygen delivery? Surely they must mean DO₂.

One might vaguely recall this equation:

And indeed, with a cardiac output of about 5L/min and a oxygen carrying capacity of 1.39ml O₂ per 1g Hb, at a Hb of 150, and at a saturation of 100%, one can calculate that the DO₂ is around 1042.5ml of O2 per minute.

But ... is that adequate?

The adequacy of oxygen delivery can  be determined by a variety of ways. Instead of listing various methods of assessment in a disorganised fashion, I expect the college would have preferred to see a systematic approach.

Thus:

Methods of assessing adequacy of DO₂

• Adequacy of oxygen delivery into the organism
  • FiO₂
• Adequacy of oxygen transport into the bloodstream
  • A-a gradient
  • SaO₂, SpO₂
  • Hb concentration
  • Proportion of ineffective haemoglobin (eg. methaemoglobin, carboxyhaemoglobin)
• Adequacy of macrocirculation
  • Mean arterial pressure
  • Cardiac output indices, including advanced haemodynamic data eg. CI derived from PAC or PiCCO
• Adequacy of microcirculation
  • Physical examination, particularly
    • Capillary refill
    • Mottling
    • Temperature of the extremities
• Adequacy of oxygen utilisation at the cellular level
  • mixed or central venous oxygen saturation (thus allowing the calculation of the oxygen extraction ratio)
  • arteriovenous CO₂ gradient
  • arterial lactate

References

This old article is the result of a meeting where several luminaries put their heads together about what the best method is for assessing tissue oxygenation:
Haglund, U., and R. G. Fiddian-Green. "Assessment of adequate tissue oxygenation in shock and critical illness: oxygen transport in sepsis, Bermuda, April 1+ 2, 1989." Intensive care medicine 15.7 (1989): 475-477.

Gutierrez, Juan A., and Andreas A. Theodorou. "Oxygen Delivery and Oxygen Consumption in Pediatric Critical Care." Pediatric Critical Care Study Guide. Springer London, 2012. 19-38.

College Answer

Discussion

The disparity between central venous and mixed venous saturation measurements is discussed in greater detail in the chapter on ScVO₂ physiology.  These measurements are means of assessment of the adequacy of oxygen delivery.

A slight adjustment to the college answer is probably called for.

References

Chawla, Lakhmir S., et al. "Lack of equivalence between central and mixed venous oxygen saturation." CHEST Journal 126.6 (2004): 1891-1896.

College Answer

Pulsus paradoxus

•           The systolic blood pressure fluctuates with breathing (note that this is different than pulsus altemans, where the rhythm is regular but the systolic pressure alternates between one strong and one weak stroke volume).
•            There is a difference of greater than 15 mmHg between inspiratory and expiratory systolic pressures.
•         R- R interval on ECG is regular, ruling out arrhythmia as the cause for the fluctuating systolic pressure.

causes:

1) Pericardial effusion

2)Asthma

3) Hypovolemia in a mechanically ventilated patient

Discussion

In the grainy mobile-phone-snapped image above, the patient has a significant pulse pressure variation. In fact the picture was taken around the time we inserted a PiCCO. The SVV as measured by that device was 28% at that stage. The cause was "hypovolemia in a mechanically ventilated patient".

Apart from true hypovolemia, one can generate a whole list of causes for why this sort of picture might develop:

• Loss of RV compliance:
  • Pericardial effusion
  • Mediastinal haemorrhage
• Increased intrathoracic pressure
  • High positive pressure of mechanical ventilation, high PEEP
  • High AutoPEEP:
    • Asthma
    • COPD
    • Anaphylaxis
  • Tension pneumothorax
• Decreased preload
  • Decreased intravascular volume
  • Increased central venous compliance (eg. in sepsis)

More on this topic is available in a through discussion of the hemodynamic effects of a mechanical breath, as well as in this excellent aticle

The hemodynamic changes in cardiac tamponade and pericarditis are also discussed here.

References

Toska, K., and M. Eriksen. "Respiration-synchronous fluctuations in stroke volume, heart rate and arterial pressure in humans." The Journal of physiology472.1 (1993): 501-512.

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.

College Answer

Following insertion of a pulmonary artery catheter

a)  list 3 tests which suggest appropriate Zone 3 positioning
PAWP < PADP
PAWP alters by < 50% of applied PEEP
PAWP increases by < 50% of changes in alveolar pressure
O2 satn in the wedged position greater than unwedged position
On the CXR, tip of catheter below level of LA.

b)  list 2 conditions where PAWP will read higher than LVEDP
Mitral stenosis
Atrial myxoma
Pulm venous obstruction – fibrosis, vasculitis
MR

non-zone 3 catheter placement

L to R shunt

COPD

IPPV+/-PEEP

c)  list 3 causes of inaccurate cold thermodilution cardiac output  measurements
1)  catheter malposition,
2)  injection mistakes (volume, injection speed, injectate temperature)
3)  inaccurate thermistor
4)  Tricuspid regurgitation
5)  Intra-cardiac shunts
6)  Wrong computation constant

d)  Is the pulmonary capillary hydrostatic pressure normally higher or lower than the pulmonary artery wedge pressure ?

Higher

Discussion

The PA catheter receives a thorough treatment in a series of chapters dedicated all to itself, somewhere deep in the Haemodynamic Monitoring section. . Appropriate zone positioning is also discussed.

The tip should be in West's 3rd Zone.

The following features confirm this position:

• On lateral CXR, the tip of the catheter is at or below the left atrium
• Respiratory variation of PAOP is < 50% of the static airway pressure (peak – plateau)
• Change the PEEP: PAOP changes by 50% of the change in PEEP
• The PAWP is less than the PA diastolic pressure
• The PAWP contour has recognizable a and v waves; in Zones 1 and 2 it is unnaturally smooth.
• Wedge PO2 minus Arterial PO2 = 19mmHg
• Arterial PCO2 minus Wedge PCO2 = 11mmHg
• Wedge pH minus Arterial pH = 0.008

Situations where the wedge pressure is higher than the LV end-diastolic pressure:

• Mitral stenosis (gradient across the mitral valve is high, LA pressure is increased)
• Atrial myxoma (same reason)
• Mitral regurgitation (large v waves interfere with wedge measurement, and LA pressure is high)
• Pulmonary fibrosis (obstruction to venous flow)
• Inappropriate placement (eg. into a high Wests zone)
• High PEEP
• High Auto-PEEP

Causes of inaccurate cold thermodilution cardiac output  measurements:

• Catheter is in the wrong position
• The thermistor tip is up against the wall
• The respiration is erratic
• There is an intracardiac shunt
• Tricuspid regurgitation
• Cardiac arrhythmia
• Rapid infusion happening via the IJ line
• Abnormal hematocrit
• Slow injectate delivery
• Injectate not cold enough, or not enough of it

Finally, pulmonary capillary hydrostatic pressure is usually higher than the wedge pressure. Normally, because of the venous resistance, Pcap will be higher than PAWP; in situations when this resistance is zero (i.e never) the two values might be equal.

References

An excellent online resource is available, which treats this subject with a massive amount of detail.

Also, the PA catheter section from The ICU Book by Paul L Marino (3rd edition, 2007) is a good source for most of this information.

Finally, Edwards Life Sciences has a booklet on invasive haemodynamic monitoring, which is a good solid overview.

College Answer

a) What gas is delivered through this cylinder shown in the photograph?
Oxygen

b)  When  this  gas  is  delivered  in  the  ICU  through the  wall  outlet,  what  is  the pressure at the wall outlet?
The Australian Standards are 415 kPa static pressure in pipeline, which is allowed to fall to by a maximum of 50 kPa under some conditions. Therefor any answer between 365 and 415 kPa was acceptable.

c) What is the pressure of the gas in a full cylinder?
Whilst it varies from cylinder to cylinder, any answer between 12 to 17 megapascals (12000-17000kPa) , is acceptable.

Discussion

Yes, even though that says "N", it is in fact an oxygen cylinder, ready to be transported to a CT scan. And the porter was taking so long that I started taking pictures of the scenery.

The standard (mandatory) wall gas pressure is indeed 415 kPa (about 4 atmospheres). For the gas which powers surgical tools, the pressure is 1400 kPa.

The cylinders, according to a reputable source, can withstand a pressure of 24,000 kPa, but normally rest at around 12,000-17,000 (that is the "green zone" on the gauge).

References

This excellent lecture from the University of Sydney has a vast amount of obscure information (did you know oxygen tanks are aged at 175°C for 8 hours, and that their walls are only 3mm thick?)

Medical Gas Standard AS 2896-2011 is available online, but you have to pay over $200 to purchase it.

Dorsch and Dorsch have a chapter dedicated to medical gas supply and suction equipment, which can be accessed by Google Books.

College Answer

A photograph of a cuffed endotracheal tube with a connector was shown.

a) What is the diameter of the connector (shown by the arrow)?
15 mm

b) List 2 factors which predispose to obstruction of this tube in intensive care?

Lack of humidification
Infrequent physio/suctioning
Patients with large volumes of secretions

c) List 3 design features of this device which improve its safety.

i.  Clear non-toxic plastic
ii.  Low profile, high volume low pressure cuff
iii.  Radio-opaque line for identification of tip on xray iv.  Murphy’s eye
v.  Left bevelled atraumatic tip

d) Write down the formula to determine the size of the endotracheal tube required in children 1-10 yrs of age?

(Age in yrs/4) + 4        (Some use 4.25 or even 4.5 in the denominator and they are acceptable.

Discussion

The ETT and its various bits is discussed in greater detail elsewhere.

The connector pointed to is a 15mm connector, and there is a certain body which determines the size of connectors for airway equipment. The connectors are 15 and 22mm (internal diameters), conforming to ISO5356-1.

There are numerous factors which predispose the tubes to obstruction. The college has discussed the inspissation of secretions, and infrequent physiotherapy, but there are many other possibilities, such as clots due to pulmonary haemorrhage, or kinking because of patient chewing on the tube.

Safety features of the ETT are familiar. Question 30.1 from the second paper of 2013 asks this exact same thing. In summary:

• Single use item, no risk of cross-infection
• Standardised 15mm connector to fit all airway devices
• Low-allergen PVC construction, free of latex
• Transparent body,to see blood or vomit
• Markings to indicate depth of insertion
• Black line to guide insertion to appropriate depth
• High volume low pressure cuff to seal the trachea
• Size labelling on pilot balloon
• Pilot cuff to gauge cuff pressure
• Rounded atraumatic edges
• Murphy's eye to protect against occlusion
• Bevelled tip to assist insertion
• Radio-opaque line to help gauge position on chest X-rays

There are actually several methods to guide ETT selection in children:

• diameter of the pinky finger
• (Age in years + 16)/4
• The Khine formula: (Age /4) + 3
• Broselow paediatric tape

The formula quoted by the college is also the one they teach you in the APLS course, so perhaps it has been locally accepted as the right formula for any young Australian larynx.

References

King, Brent R., et al. "Endotracheal tube selection in children: a comparison of four methods." Annals of emergency medicine 22.3 (1993): 530-534.

Duracher, Caroline, et al. "Evaluation of cuffed tracheal tube size predicted using the Khine formula in children." Pediatric Anesthesia 18.2 (2008): 113-118.

Davis, D. I. A. N. E., L. Barbee, and D. Ririe. "Pediatric endotracheal tube selection: a comparison of age-based and height-based criteria." AANA journal66 (1998): 299-303.

College Answer

A photograph of a Sengstaken-Blakemore tube was shown.

a.   Identify this piece of equipment

i.    SBT

b.  List one indication for its use

i.         Variceal bleed

c.   List 3 contraindications to the use of this device

i.  Known Oesophageal stricture
ii.      Unidentified source of bleeding

iii.           Unprotected airway

d.  List 3 complications associated with its use

i.          Aspiration pneumonia
ii.      Cardiac arythmias
iii.      Oesophageal perforation
iv.      Acute upper airway obstruction

Discussion

This question closely resembles Question 30 from the first paper of 2013.

References

King, Brent R., et al. "Endotracheal tube selection in children: a comparison of four methods." Annals of emergency medicine 22.3 (1993): 530-534.

Duracher, Caroline, et al. "Evaluation of cuffed tracheal tube size predicted using the Khine formula in children." Pediatric Anesthesia 18.2 (2008): 113-118.

Davis, D. I. A. N. E., L. Barbee, and D. Ririe. "Pediatric endotracheal tube selection: a comparison of age-based and height-based criteria." AANA journal66 (1998): 299-303.

College Answer

Arterial puncture is a well recognised but uncommon complication of central venous catheter insertion. The potential complications include all those associated with venous/arterial puncture, as well as specific ones associated with the large hole in the artery. Damage to associated structures (nerves [eg. vagus], pleura, oesophagus and trachea!) can result in specific problems (either directly or indirectly from compression [eg. haematoma]). A large bore catheter in a blood vessel can result in air embolus (worse if arterial) or even embolus of atheromatous material (stroke risk). Specific problems related to the arterial site include: toxicity of inadvertently administered drugs (before actual position recognised), higher risk of significant haematoma and blood loss (augmented by coagulopathy especially if removed/dislodged). Referral to surgeons
with vascular experience is essential to facilitate definitive management because of the size of the hole in the artery (suture repair, patch repair etc). If surgical repair is not considered indicated, prolonged pressure for haemostasis has associated potential problems (carotid body, distal flow), and haematoma formation likely.

Discussion

Well, this is embarrassing.

LITFL have a nice page on this topic.

Additonally, the BJMP has an article with a case report of precisely this sort of complication. The author has done a literature search, and presents a list of complications which have been reported in the papers in association with this problem:

• Haematoma formation
  • Airway obstruction; plus the airway will be difficult with the larynx displaced off midline 
  • Cerebral venous outflow obstruction
  • Jugular venous thrombosis due to stasis
  • Haemomediastinum
  • Compromised cardiac function due to RV compression by down-tracking haematoma
• Vascular injury
  • Pseudoaneurysm
  • Carotid dissection
  • Retrograde aortic dissection
  • Aortic valve damage 
  • Arteriovenous fistula
  • Occlusion by flap, catheter or thrombus
• Cerebral injury
  • Ischaemic stroke
  • Atheroembolic stroke
  • Thromboembolic stroke
  • Air embolism
• Peripheral neurological injury
  • Compression damage to the vagus nerve
  • Compression damage to the phrenic nerve
  • Damage to the brachial plexus roots

Interestingly, having spoken to some of the vascular surgeons about such complications, the general opinion seems to be that if you have already dilated the artery and inserted the vas cath, the best thing you can do is suture it in position and leave it there until they arrive. Apparently that is somehow better than taking it out and then putting pressure on a carotid with a vas-cath-sized hole in it.

​​​​​​​How to deal with this problem:

• Prevent further complications
  • ​​​​​​​Keep the catheter in situ
  • Clamp the lumens
  • Label it clearly as "not for use"
  • Assess the urgency of removal and repair, i.e ischaemic stroke symptoms, ongoing bleeding, aortic dissection, known high grade carotid stenosis on the contralateral side, etc
  • Assess the extent of haematoma with imaging: ideally CT, but ultrasound may be enough
  • Correct any coagulopathy
• Deal with the need for vas cath
  • ​​​​​​​Consider the placement of another vas cath into a venous structure at a different site, depending on the urgency for CRRT in this patient
  • Amend the CRRT protocol accordingly to expose this patient to minimal or no anticoagulation (i.e. use pre-dilution or citrate only)
• Deal with the need to remove the vas cath
  • ​​​​​​​Determine the extent of the damage by combination of ultrasound, CT imaging and CXR (eg. to define the tip position)
  • Consult vascular surgeon to repair the carotid puncture, if that's all there is
  • Consult cardiac surgeon to repair any aortic arch damage
• Deal with the consequences for staff and family
  • Debrief with the staff member who inserted the vas cath
  • Offer education and discussion to cover any knowledge gaps
  • Notify appropriate incident management body regarding the insertion
  • Commence the open disclosure process with the patient and family

References

Nair, Sanil, et al. "A case of accidental carotid artery cannulation in a patient for hemofilter: complication and management." British Journal of Medical Practitioners 2.3 (2009): 57-58.

College Answer

1.  Left ventricular failure/cardiogenic shock

2.  Mitral regurgitation

3.  Acute aortic incompetence

Discussion

What would give you hypotension, tachycardia and a murmur? What could compel the Australian College of Intensive Care Medicine to use the American spelling of "haemodynamic"?

The abnormalities are:

• Hypotension
• Dyspnoea and tachypnoea
• Tachycardia
• Raised JVP/CVP
• Raised PA pressure
• Raised PAWP
• A murmur of some sort

With the raised PAWP and CVP, one starts thinking about cardiac causes. Certainly such a presentation might result from the sudden failure of the aortic or mitral valves (with ensuing pulmonary oedema). With a major pulmonary embolus, the PAWP should actually be low (though it generally does not have much of a relationship with the LVEDP in that setting). The college include cardiogenic shock in their answer, which one one hand is reasonable because it certainly describes "the above clinical and hemodynamic presentation". However on the other hand, cardiogenic shock is what you get as the result of any number of possible pathologies, i.e. it describes a constellation of clinical features rather than any specific aetiology. One might argue that the question is worded in a way which requires a list of such aetiologies.  One possible list could include:

• Dilated cardiomyopathy  (explains everything, including the murmur -as the mitral annulus would be stretched the valve would become regurgitant)
• Mitral regurgitation (acute, eg. prolapse) - which explains everything, including the respiratory symptoms which are presumably due to pulmonary oedema. The PAWP would be raised, which it is. 
• Aortic regurgitation (acute, eg. aortic dissection or root dilatation) which explains everything
• Cardiac tamponade (which explains everything except for the murmur, which might be confused with a pericardial rub)
• Aortic stenosis (which, if severe enough, could give rise to this picture)
• Hypertrophic obstructive cardiomyopathy (which explains all of the findings)

References

Quintana, E., et al. "Erroneous interpretation of pulmonary capillary wedge pressure in massive pulmonary embolism." Critical care medicine 11.12 (1983): 933-935.

College Answer

60% = pulmonary artery catheter       - pooled blood from SVC and IVC

67% = subclavian vein (superior vena cava) - in sepsis, cerebral blood flow relatively maintained initially

50% = femoral vein (inferior vena cava) - in sepsis, regional O2 consumption and extraction in gut/splanchnic circulation increases

Discussion

Central venous saturation measurements are discussed in greater detail elsewhere. These measurements are a means of assessment of the adequacy of oxygen delivery.

In brief summary, the further up you move away from the pulmonary artery, the greater your SvO₂becomes; whereas if you go further down, the very hypoxic splanchnic venous blood will decrease the SvO₂.

References

Chawla, Lakhmir S., et al. "Lack of equivalence between central and mixed venous oxygen saturation." CHEST Journal 126.6 (2004): 1891-1896.

College Answer

a)  What dominant abnormality is indicated by the right heart catheter data?
Pressure gradient between the RV and PA

b)  List two (2) likely causes of the abnormality

pulmonary valve stenosis supravalvular or RVOT stenosis

Discussion

This question - with identical wording - was used again in 2012, paper 2 - Question 30.2

The gentle reader is redirected there, in order to avoid SEO-impairing text duplication.

References

College Answer

Septic shock
Left to right shunt
High FIO2
Hyperbaric oxygenation
Measurement error (poor calibration)
Reduced oxygen consumption – Hypothermia, NM blockade, hypothyroidism, general anaesthesia

Discussion

This question tests the candidate's appreciation for the relevance of an abnormally high SvO₂ (or low tissue oxygen extraction ratio). It is a means of assessing the adequacy of oxygen delivery.

One can usually group these "data interpretation" answers into a series of subcategories:

Measurement error

• bubble of gas in the sample
• poorly calibrated ABG machine

Anatomical error

• Left to right shunt
• Microvascular shunt (eg. in sepsis)

Increased supply

• Hyperbaric oxygen therapy
• High FiO2
• Hyperdynamic circulation, eg. phaeochromocytoma or ECMO

Reduced demand

• Neuromuscular blockade
• Deep sedation / anaesthesia
• Hypothermia
• Hypothyroidsm
• Failure of mitochondrial oxygen use (eg. cyanide poisoning, sepsis)

A general overview of mixed and central venous saturation can be found elsewhere.

There is also an excellent article with satisfying explanations of the physiology behind oxygen delivery and extraction.

References

Walley, Keith R. "Use of central venous oxygen saturation to guide therapy."American journal of respiratory and critical care medicine 184.5 (2011): 514-520.

College Answer

This area remains controversial with, in reality, no single correct answer. Examiners expected and were prepared to accept a range of approaches (if reasonable)

a)  The type of fluid – crystalloid/colloid . No ideal fluid in all clinical settings.

In general no differences in mortality in critically ill patients, between crystalloids and colloids (SAFE study). However in subgroups, albumin may be useful (sepsis) whilst in neurotrauma, crystalloids may be preferable.

b)  Rate of fluid administration (250-500 ml of colloid /500-1000 ml of crystalloid or
20 ml/kg of crystalloid over 30 min.)
Again, no hard data exist to support either regime, but these are rules of thumb and recommended in the Surviving Sepsis Campaign Guidelines.

c)  A clear defined goal such as a MAP/Urine output or resolution of tachycardia –
commonly used goals in clinical practice.

d)  Defining safety limits – such as an upper limit or an increment of CVP/ PAWP Although no criteria for the above end points exist, an increment in CVP 2-5 mm Hg and PCWP 3-7 mm Hg in 30 min or earlier should be used as an indication to cease fluid challenge. In the absence of invasive monitoring, measurement of JVP and signs of pulmonary oedema should be looked for.

Parameters predicting fluid responsiveness

1)  Clinical endpoints such as collapsed veins and state of peripheral circulation not sensitive.
2)  CVP / PCWP changes poor predictors
Other end points have been proposed:
a)  Systolic pressure variation with respiration b)  Pulse pressure variation with respiration
c)  Stroke volume variation with respiration
d)  Aortic blood velocity variation with respiration e)  Intra-thoracic blood volume
f)   Respiratory variation in SVC / IVC diameter
g)  Haemodynamic responses to passive leg raising.

None of the above has been shown to be a reliable predictor, although the haemodynamic response to passive leg raising is thought to be more sensitive than the rest.  The reliability of some of these end points are also influenced by the presence of positive pressure ventilation

Discussion

There are no set guidelines for fluid administration. It sounds like the examiners were prepared to tolerate a range of wacky responses to this. A 2006 article by JL Vincent attempts to bring some sort of order into the lawless Mad Max wasteland of fluid resuscitation practice; another attempt was made in 2011 by Cecconi et al. I will use his suggestions in this answer.

In summary:

• Which fluid?
  • Colloid and crystalloid are equivalent in terms of mortality (SAFE study)
  • Of the colloids, there is insufficient evidence to recommend one over another in terms of mortality (though albumin may have non-oncotic ancillary effects which may be beneficial in sepsis)
  • Of the crystalloids, "balanced" fluids eg. Plasmalyte-148 are associated with improved mortality (at least in sepsis) when compared to isotonic saline.
• How much fluid?
  • At least in sepsis, perhaps less fluid is better (FEAST study).
  • Conventional teaching recommends 500-1000ml of crystalloid, or (in other sources) 10-20ml/kg. This convention may be closely related to the usual fluid bag content.
• How fast?
  • Rate of administration may be more important than the amount and type of fluid.
  • There is no scientific consensus as to how fast is fas enough.
  • Surviving Sepsis people recommend the fluids be given over 30 minutes.
  • Another technique is SV maximisation - a process where 250ml boluses are given over 5-10 minutes until stroke volume (as measured by invasive hemodynamic monitoring) stops increasing by 10-15% with each bolus
• When to stop?
  • Though not based in any firm evidence, resuscitation endpoints have historically included the following parameter theresholds:
    • MAP > 65mmHg
    • CVP >8mmHg, or a change of over 7mmHg in response to the bolus
    • PAOP change of over 5mmHg in response to the bolus
    • Normal lactate (<2.0mmol/L)
    • Urine output >0.5ml/kg/hr
    • ScvO₂~ 75mmHg
    • Resolution of clinical features of hypovolemia which had given rise to the decision to administer the fluid bolus.

As for the assessment of fluid responsiveness - it is a vast topic, and is dealt with in a chapter dedicated to its bewildering detail.

In brief summary:

• Dynamic manoeuvres are better than static measurements.
• Among dynamic manoeuvres:
  • Expiratory hold manoeuvre (the change in pulse pressure with a 15 second expiratory hold) is the most sensitive and specific manoeuvre, but is limited to mechanically ventilated patients in sinus rhythm.
  • Stroke Volume Variation (SVV) is a good predictor of fluid responsiveness under perfect circumstances, when the hypotensive patient has virtually nothing else wrong with them.
  • Passive leg raise autotransfusion (over 1 minute) is the next most sensitive and specific manoeuvre, and it can be perfomed on patients with arrhythmia and breathing spontaneously
  • Inferior Vena Cava ultrasonography is not an accurate method of assessment.
• Among static measurements,
  • Clinical signs are poor at predicting fluid responsiveness
  • Central venous pressure (CVP) and Pulmonary Artery Wedge Pressure (PAWP)have no correlation whatsoever with preload and cannot be used to assess fluid responsiveness
  • GEDVI or GEDI derived from PiCCO correlate well with preload but do not predict fluid responsiveness.

References

Finfer, Simon, et al. "A comparison of albumin and saline for fluid resuscitation in the intensive care unit." N Engl j Med 350.22 (2004): 2247-2256.

Bunn, Frances, Daksha Trivedi, and S. Ashraf. "Colloid solutions for fluid resuscitation." Cochrane Database Syst Rev 7 (2012).

Raghunathan, Karthik, et al. "Association Between the Choice of IV Crystalloid and In-Hospital Mortality Among Critically Ill Adults With Sepsis." Critical care medicine (2014).

Maitland, Kathryn, et al. "Mortality after fluid bolus in African children with severe infection." New England Journal of Medicine 364.26 (2011): 2483-2495.

Vincent, Jean-Louis, and Max Harry Weil. "Fluid challenge revisited." Critical care medicine 34.5 (2006): 1333-1337.

Cecconi, Maurizio, B. Singer, and Andrew Rhodes. "The Fluid Challenge."Annual Update in Intensive Care and Emergency Medicine 2011. Springer Berlin Heidelberg, 2011. 332-339.

Gan, Tong J., et al. "Goal-directed intraoperative fluid administration reduces length of hospital stay after major surgery." Anesthesiology 97.4 (2002): 820-826.

College Answer

Patient A – 90%

Patient B -  90%

Pulse oximetry only uses 2 wavelengths  and COHb  is measured as OxyHb.

Discussion

Well, this is a flaw of pulse oximetry. Both the oxygenated hemoglobin and the "carboxygenated" COHb will be measured as 100% saturated. Thus, in both patients, the oxygen saturation will read 90%.

References

Pulse oximetry is discussed at lengths in a fine article:

Mendelson, Yitzhak. "Pulse oximetry: theory and applications for noninvasive monitoring." Clinical chemistry 38.9 (1992): 1601-1607.

Co-oximetry is a fine thing indeed. LITFL has a nice summary.

College Answer

Discussion

The answer table from the college is a comprehensive response, and it is difficult to improve upon it without a swamp of useless detail.

The key point is that the PA catheter is the gold standard, and everything else is measured against it. The general trend can be described thus: the closer your probe gets to the heart, the more accurate your measurement to the temperature of intracardiac blood.

It would make sense that intracardiac blood should be a good measure of body temperature, as the blood has been circulating all around the body, exchanging heat everywhere. However, not all agree that this is a valid viewpoint. Some have suggested that the better temperature to be guided by is the temperature of the hypothalamus, because it is the organ which is responsible for regulating temperature.

References

Giuliano, Karen K., et al. "Temperature measurement in critically ill orally intubated adults: a comparison of pulmonary artery core, tympanic, and oral methods." Critical care medicine 27.10 (1999): 2188-2193.

Lefrant, J-Y., et al. "Temperature measurement in intensive care patients: comparison of urinary bladder, oesophageal, rectal, axillary, and inguinal methods versus pulmonary artery core method." Intensive care medicine 29.3 (2003): 414-418.

NIERMAN, DAVID M. "Core temperature measurement in the intensive care unit." Critical care medicine 19.6 (1991): 818-823.

WEBB, GEORGE E. "Comparison of esophageal and tympanic temperature monitoring during cardiopulmonary bypass." Anesthesia & Analgesia 52.5 (1973): 729-733.

College Answer

a) What technology is used for the detection  of CO2  in expired breath in the
ICU?

Infra-red absorption spectrophotometry

b) List 3 uses for capnography in intensive care

Airway disconnection alarm
Confirmation of ET tube placement in airway
During CPR to assess adequacy of cardiac compression
Recognition of spontaneous breath during apnoea test
Neurosurgical patient to provide protection against unexpected hypercapnia

c) List 3 conditions  which may increase the gradient between end-tidal and arterial PCO2?

Low cardiac output or cardiogenic shock
Pulmonary embolism
Cardiac arrest
Positive pressure ventilation and use of PEEP

High V/Q ratios.
Candidates who mention increased alveolar dead space should also get some credit.

Discussion

Capnography is discussed in greater detail elsewhere:

• The normal capnometry waveform
• The relationship of abnormal capnograph waveforms to lung pathology

There is an excellent site by Prasanna Tilakaratna which explains infra-red absorption spectrophotometry using vividly colourful diagrams (how else?). In brief, CO₂ absorbs infra-red radiation (it being a greenhouse gas and all) and so expired air enriched with CO₂ will absorb more infra-red than CO₂-poor air.

Uses of capnography in the ICU: some from the college, and some endogenously generated uses:

• Confirmation of ETT placement
• Airway disconnection alarm
• Monitoring during transport
• During CPR to assess adequacy of cardiac compression
• Recognition of spontaneous breath during apnoea test
• Neurosurgical patient to provide protection against unexpected hypercapnia
• Quick bedside assessment of bronchospasm
• Alert of sudden changes in pulmonary perfusion (eg. PE)
• Early alert of PEA in the absence of continuous BP monitoring
• More accurate monitoring of respiratory rate

Conditions  which increase the gradient between end-tidal and arterial PCO₂

• Pulmonary perfusion
  • Pulmonary embolism
  • Fat embolism
  • Air embolism
  • Cardiac failure (RHF)
  • Cardiac arrest
• Ventilation
  • Increased V/Q mismatch due to high PEEP
  • Increased alveolar dead space
  • High FiO2 (causing shunt into poorly ventilated alveoli)
• Artifact
  • The presence of helium can cause the EtCO₂ measurement to be incorrectly elevated in some capnometers (i.e. those which use a reporting algorithm that assumes that the only gases present in the sample are those that the device is capable of measuring)
  • The presence of nitrous oxide can confuse some capnograph devices, and the NO₂ may be misinterpreted as CO₂
  • The use of an inline HME filter can reduce the end-tidal CO₂ concentration.

References

The best, most detailed review:

Walsh, Brian K., David N. Crotwell, and Ruben D. Restrepo. "Capnography/Capnometry during mechanical ventilation: 2011." Respiratory care 56.4 (2011): 503-509.

Whitaker, D. K. "Time for capnography–everywhere." Anaesthesia 66.7 (2011): 544-549.

Kodali, Bhavani Shankar. "Capnography outside the operating rooms." Anesthesiology 118.1 (2013): 192-201.

Yamauchi, H., et al. "Dependence of the gradient between arterial and end-tidal PCO2 on the fraction of inspired oxygen." British journal of anaesthesia (2011): aer171.

Razi, Ebrahim, et al. "Correlation of End-Tidal Carbon Dioxide with Arterial Carbon Dioxide in Mechanically Ventilated Patients." Archives of trauma research 1.2 (2012): 58.

College Answer

A drawing & description which identifies the following was required:-

A) A collection chamber which is connected to the intercostal drain and collects pleural fluid. This chamber can be independently emptied and in addition allow for an accurate record of pleural drainage amount.

B) A water seal chamber which ensures that the water seal is maintained at a predetermined level whilst still allowing for drainage of pleural fluid.

C)  A  suction  control  chamber  which  ensures  that  an  accurate  ,  easily  verifiable  and consistent level of suction is being delivered to the pleural cavity as long as wall suction is greater than the required suction pressure.

Discussion

This question closely resembes Question 24.2 from the second paper of 2012.

In any case, here is a diagram:

References

NSW Health: Chest Drain - Set up of Atrium Oasis Dry Suction Under-Water Seal Drainage

Atrium have published their instructions online.

Additionally, they provide this training document which is surprisingly full of useful information.

College Answer

Name: A McCoy Blade laryngoscope (- improved visualization of the cords in the setting of a difficult intubation .   It has a controllable flexible tip which allows for the elevation of distal structures, espec the epiglottis .

Discussion

Yes, this is a McCoy Articulating Tip Laryngoscope, or the levering laryngoscope as McCoy himself called it (he did not name it after himself). Instead of relying on brute force to elevate the epiglottis, the airway enthusiast can squeeze the lever and elevate it gently. It is particularly useful in situations where the larynx is very anterior. The disadvantage is, sometimes the epiglottis can get caught in the hinge.

References

AnaesthesiaUK have a nice page about McCoy blades.

Cook, T. M., and J. P. Tuckey. "A comparison between the Macintosh and the McCoy laryngoscope blades." Anaesthesia 51.10 (1996): 977-980.

Doyle, D. J. "A brief history of clinical airway management." Revista Mexicana de Anestesiologia 32 (2009): S164-S167.

McCoy, E. P., and R. K. Mirakhur. "The levering laryngoscope." Anaesthesia48.6 (1993): 516-519.

College Answer

Name: Glidescope (but mention of a video assisted laryngoscope would be sufficient), used in the setting of a difficult intubation for improved visualization of the cords.

Design features: a specifically angled laryngoscope with an integrated camera allowing direct visualization(via external monitor) of the cords.

Discussion

Though the C-MAC is the local favourite, one should at least be able to recognise the Glidescope. There is no Engadget review for these products, but LITFL do a damn good job.

References

Cooper, Richard M., et al. "Early clinical experience with a new videolaryngoscope (GlideScope®) in 728 patients." Canadian Journal of Anesthesia 52.2 (2005): 191-198.

Cavus, Erol, et al. "The C-MAC videolaryngoscope: first experiences with a new device for videolaryngoscopy-guided intubation." Anesthesia & Analgesia 110.2 (2010): 473-477.

College Answer

When there is a difference in the oxygen saturation between a pulse oximeter reading and a co- oximeter reading, seen with CO poisoning and other drugs which result in a methemoglobinemia.

Discussion

Though not a formally accepted term to describe this phenomenon, the "gap" is a well recognised feature of dyshemoglobinaemia. It develops when the pulse oximeter reads a certain saturation, and the ABG machine or CO-oximeter returns a different reading. The "gap" in saturation readings is vaguely representative of the concentration of the abnormal haemoglobin in the blood.

References

Akhtar, Jawaid, Bradford D. Johnston, and Edward P. Krenzelok. "Mind the gap."The Journal of emergency medicine 33.2 (2007): 131-132.

Mokhlesi, Babak, et al. "Adult Toxicology in Critical CarePart I: General Approach to the Intoxicated Patient." CHEST Journal 123.2 (2003): 577-592.

College Answer

a) What pathophysiological abnormality is illustrated by the arterial waveform?

Systolic pressure variation > 10 mm Hg

Pulse pressure variation

b) What is the clinical significance of the abnormality illustrated above?

Often implies a degree of fluid responsiveness

c) List 3 conditions in which such a scenario can occur.

Hypovolaemia, tamponade, bronchospasm, pneumothorax, raised intra-abdo pressure, raised intra- thoracic pressure, LV dysfunction, Dynamic hyperinflation

Discussion

This is an example of the haemodynamic effects of positive pressure ventilation.

An increase in respiratory pulse pressure variation could be due to any of the following:

• Inadequate right heart filling, for example:
  • Hypovolemia (thus, it can imply a degree of fluid responsiveness)
  • Vasodilated shock state (central venous venodilation)
• Excessive right heart afterload, for example: 
  • Acute severe asthma with gas trapping and hyperinflation
  • Tension pneumothorax
  • Massive pulmonary embolism
• Decreased right ventricular compliance, for example:
  • Cardiac tamponade or large pericardial effusion
  • RV failure due to infarction
  • Post-radiotherapy changes or infiltrative disease, eg. amyloid
  • LV failure with a significant haemodynamic benefit from the afterload reduction associated with positive pressure ventilation
  • LV dilatation causing RV diastolic failure

The degree to which this arterial line "swing" correlates with fluid responsiveness is discussed elsewhere.

The conditions in which PPV can occur are a fairly straightforward bunch, with the exception of LV dysfunction. This one is weird. PPV should predict good LV function rather than bad. Turns out, cardiac resynchonisation therapy has been shown to increase PPV, which leads one to correctly conclude that a ventricle with poor contractility will not be briskly responsive to changes in preload.

However, severe LV failure with LV dilatation can still produce increased pulse pressure variation by two mechanisms:

• LV dysfunction results in an amplification of the afterload-reducing effects of positive pressure ventilation; thus the systolic pressure increases  in early inspiration, giving rise to pulse pressure variation.
• LV dysfunction decreases the compliance of the right heart. This is a purely mechanical effect: the RV cannot fill effectively if the LV is a huge dilated slob, occupying most of the pericardial sack with its bulk.

References

Michard, Frédéric, Marcel R. Lopes, and Jose-Otavio C. Auler. "Pulse pressure variation: beyond the fluid management of patients with shock." Critical Care11.3 (2007): 131.

He, Huai-wu, and Da-wei Liu. "The pitfall of pulse pressure variation in the cardiac dysfunction condition." Critical Care 19.1 (2015): 1-1.

College Answer

The abnormalities are Pulsus Alternans, pulmonary hypertension, systolic hypotension, tricuspid incompetence (large v waves).

Discussion

There seems to be little to discuss. Pulsus alternans is difficult to miss. Similarly, the presence of massive fused cv waves in the CVP trace is a end-of-the-bed diagnosis of tricuspid regurgitation.

Abnormal CVP waveforms are discussed elsewhere.

References

College Answer

•    The patient has smear positive untreated TB and is therefore highly infectious

•    The infection risk is greatly magnified by bronchoscopy which generates aerosols. It is therefore important to review the need for bronchoscopy .

•    Regardless of whether a bronchoscopy is carried out the following precautions should be taken:

•    Nurse in a single room with negative pressure ventilation and 12 air changes per hour
•    Bacterial filter in ventilator circuit and closed suction
•    All staff entering room should take personal respiratory precautions including fit tested N95/100 mask.

•    Infection warning signs
•    If bronchoscopy is undertaken:

•    Minimize generation of aerosols:

Prevent coughing (muscle relaxant)

Consider apnoeic oxygenation during bronchoscopy

•    Consider use of powered air purifying respirator if available and staff have been appropriately trained

Staff screen – In the event of accidental exposure during the procedure, consideration for a CXR, mantoux baseline and at 2 months.

Advice and help of the Occupational Health and Infectious diseases team should also be sought.

Discussion

The college seems to have derived their answer from the ACCP/AAB consensus statement on the prevention of flexible bronchoscopy-associated infections. This document regulates every last detail of bronchoscopy, down to record-keeping and the number of air exchanges in the negative pressure room.

• Maintain standard precautions, including full barrier clothing - gloves, gown and eye protection.
• Indications for the bronchoscopy must be carefully considered (i.e. can it be delayed until after the patient has been treated?) Given the story about haemoptysis, I would say not.
• Fit-tested N95 particulate respirators should be worn at least by the bronchoscopist, and ideally by all staff involved.
  • Fit-testing and familiarity with the equitment is essential for all staff
  • The ideal equipment for this is a power air-purifying respirator (PAPR)
• A procedure log should be maintained which retains in it the names of the staff involved, the patient details, the name of the bronchoscopist, the serial number of the bronchoscope and the details of which automated endoscope reprocessor was used to clean it afterwards.
• The bronchoscopy should be performed in a negative pressure room.
• The negative pressure room should have at least 12 air exchanges per hour (or at least 6 exchanges if the room was constructed before 2001...)
• The air must be discharged outside, or through a HEPA filter.
• A liberal amount of topical anaesthetic should be used to minimise coughing
• Alternatively, one could perform bronchoscopy with apneic oxygenation, using neuromuscular paralysis.
• Mechanical cleaning of the bronchoscope should be scrupulous and should occur immediately after the procedure.

References

Mehta, Atul C., et al. "American College of Chest Physicians and American Association for Bronchology Consensus StatementPrevention of Flexible Bronchoscopy-Associated Infection." CHEST Journal 128.3 (2005): 1742-1755.

Culver, Daniel A., Steven M. Gordon, and Atul C. Mehta. "Infection control in the bronchoscopy suite: a review of outbreaks and guidelines for prevention."American journal of respiratory and critical care medicine 167.8 (2003): 1050-1056.

.Frumin, M. Jack, ROBERT M. EPSTEIN, and GERALD COHEN. "Apneic oxygenation in man." Anesthesiology 20.6 (1959): 789-798.

College Answer

Answer:          Pressure transducer

b)         What is the principle of operation of this device?

Transduces pressure (via strain) to electrical resistance

c)         Name the associated electrical circuit configuration.

Answer:          Wheatstone bridge

Discussion

Yes, this is a Wheatstone bridge pressure transducer. The device works by transducing strain into electrical resistance. Typically, it is an arrangement of resistors where the resistance of all but one is known; the remaining resistor acts as the strain gauge. As pressure on the gauge changes, so does its resistance, and this causes a change in the current which flows though the Wheatstone bridge. Thus, pressure can be inferred from the changes in current.

This device is treated with more respect and admiration in a Required reading summary.

References

For a casual acquaintance with electrical circuits, this Wikipedia entry is enough.

For the masochist, this FRCA study document will fill in all the blanks.

Myers, Kenneth. "The investigation of peripheral arterial disease by strain gauge plethysmography." Angiology 15.7 (1964): 293-304.

Lambert, Edward H., and Earl H. Wood. "The use of a resistance wire, strain gauge manometer to measure intraarterial pressure." Experimental Biology and Medicine 64.2 (1947): 186-190.

College Answer

For haemodynamic measurements?   A, B, or C?

Answer           B

For intracranial pressure measurement?  A, B, or C?

Answer           C

6.2 b)  Assuming the item is correctly set-up and integrated within the appropriate system - how will the displayed value change if the device is raised by 13cm relative to the zero point?

Fall in displayed pressure by 10 mmHg.

Discussion

B vaguely corresponds to the right atrium, and C vaguely corresponds to the circle of Willis.

Generally speaking, the circle of Willis is the appropriate place where one should zero one's transducer for the measurement of cerebral perfusion pressure. However, the Brain Trauma Foundation's guidelines regarding CPP use are all based on studies where the transducer was zeroed at the atrum.  The controversial topic of where to properly  "zero" one's CPP transducer is discussed in the chapter on the utility of the cerebral perfusion pressure as a therapeutic target.

The second part of the question calls upon the candidate to recall the conversion of cmH₂O into mmHg. The conversion is, 1mmHg = 1.36cmH₂O.

Thus, 13cm H₂O = 10mmHg.

References

College Answer

Adjustable flange allows variability of tracheostomy length
Softer tube enables more flexible curvature
Reinforced tubing prevents kinking
High volume, low pressure cuff
Radio-opaque due to reinforced tubing
Able to be inserted via percutaneous technique

Discussion

This is a flanged tracheostomy tube.

John Hopkins have a good basic page about the diffrent types of tracheostomy tubes.

A more detailed look is afforded by this product brochure from Smith.

An insanely detailed review is also available.

Thus :

• The tube has a curved portion and a straight portion, which allows the flange to be adjusted to the appropriate pretracheal tissue thickness.
• Adjustable flange allows adjustment of tracheostomy length to any length of patient neck
• It is suitable for patients with up to 50mm of pretracheal tissue
• Soft tube allows a degree of flexibility, especially when warmed to body temperature.
• The tubing is reinforced, which prevents kinking
• The material is MRI-friendly
• High volume, low pressure cuff
• Radio-opaque tubing allows visualisation of position on CXR (but there is no "blue line" like with ETTs
• Some of these are designed for percutaneous insertion

References

Hess, Dean R. "Tracheostomy tubes and related appliances." Respiratory care50.4 (2005): 497-510.

College Answer

1.  Cardiac output
2.  Central blood temperature
3.  Mixed venous oxygen saturation

Discussion

This question closely resembles Question 28.1 from the first paper of 2011.

References

College Answer

1.  Pulmonary infarction
2.  Pulmonary artery rupture
3.  Right ventricular perforation

Discussion

In brief:

• Same as CVC:
  • Perforation of SVC
  • Hemothorax, pneumothorax
  • Atrial fibrillation
• Unique to PA catheter
  • Ventricular Arrhythmia
  • Thromboembolic events (the catheter is a nidus for clot formation)
  • Mural thrombi in the right heart (up to 30%)
  • Air embolism from ruptured balloon
  • Pulmonary infarction
  • Endocarditis of the pulmonary valve ( 2%)
• Right bundle branch block
  • If you already have LBBB, this causes complete heart block
  • If you are lucky, it is a transient phenomenon and you only need to pace them transcutaneously for a brief period. If you are unlucky, you have injured the AV node, and the patient needs prolonged transvenous pacing
• Knotting on structures or on itself ( ~ 1%)
  • If it has gone into the right ventricle by 25-30cm and its still not in the pulmonary artery, you start to worry
• Damage to the valves
  •  Never pull the catheter back with the balloon inflated! You could tear the valve leaflets
  • The RV can be perforated, particularly a dilated weak-walled RV
  • The RA can be perforated (perhaps even more easily)
• Pulmonary artery rupture: 0.2% risk,  30% mortality
  • Risk factors: pulmonary hypertension, mitral valve disease, anticoagulants and age over 60

References

This a full-text version of the seminal paper from 1970:

Swan HJ, Ganz W, Forrester J, Marcus H, Diamond G, Chonette D (August 1970). "Catheterization of the heart in man with use of a flow-directed balloon-tipped catheter". N. Engl. J. Med. 283 (9): 447–51.

A manufacturer (Edwards) offers some free information about the PA catheter on their product page.

The PA catheter section from The ICU Book by Paul L Marino (3rd edition, 2007) is a valuable read.

Additionally, UpToDate has an article on PA catheter complications.

College Answer

a)  Ventilator disconnection

b)  Esophageal intubation

c)  Cardiac / respiratory arrest

d)  Apnoea test in a brain dead patient

e)  Capnograph obstruction

Discussion

Though abnormal capnography waveforms are discussed in greater detail elsewhere, there is little discuss here. Either the patient is not producing any CO₂, or the CO₂ is not making its way to the capnograph.

Reasons for a flat capnograph trace include:

• Ventilator disconnection
• Airway obstruction (eg. patient suddenly bit down on the tube)
• ETT perforation (the end tidal gas is escaping via the hole before it gets to the capnograph)
• Capnograph disconnection or obstruction
• Water droplet contamination of capnography module
• Cardiac / respiratory arrest
• Apnoea test in a brain dead patient

References

Thompson, John E., and Michael B. Jaffe. "Capnographic waveforms in the mechanically ventilated patient." Respiratory care 50.1 (2005): 100-109.

Babik, Barna, et al. "Effects of respiratory mechanics on the capnogram phases: importance of dynamic compliance of the respiratory system." Crit Care 16 (2012): R177.

Additonally, capnography.com has a series of excellent diagrams and is otherwise an indispenasable resource for this topic.

College Answer

Patient A: 
CoHb 
Met Hb
Radiofrequency interference

Patient B: 
Tricuspid regurgitation
Ambient light
Poor peripheral perfusion Dyes- Methylene blue

Poor probe contact

Discussion

The pulse oximeter is a dumb machine, whereas the co-oximeter will measure lots of different subtypes of haemoglobin simultaneously.

In general terms, the co-oximeter is correct, and the pulse oximeter is frequently confused.

Thus, in Patient A, the co-oximeter reads 85% (the true saturation of haemoglobin) while the pulse oximeter reads 95%. Clearly, there is some haemoglobin here which closely resembles normal oxygenated haemoglobin, but is in fact carrying no oxygen.

The causes of that could be:

• Carboxyhaemoglobin
• Methaemoglobinaemia
• Radiofrequency interference

Interestingly, only mild methaemoglobinaemia should be on that list. Pulse oximetry measurement of mixed normal haemoglobin and methaemoglobin will usually be depressed. When one's methaemoglobin level is in excess of 35%, the pulse oximeter will usually read 85% (Barker et al, 1989). The pulse oximeter will then continue to read this value, whether the oxygenation deteriorates or improves, i.e. at 60% methaemoglobin concentration and a fractional oxygen saturation of 30% or 100%, it will still give you an SpO2 of 85%. This is why highly respected resources report that "methemoglobinemia typically causes the pulse oximeter to report a [pulse oximeter] saturation of ~82-86% (even if the PaO2 is very high)." 

In Patient B, the co-oximeter confirms a normal oxygen saturation of haemoglobin; however, something is confusing the pulse oximeter.

• Poor peripheral perfusion
• Ambient light
• Poor probe contact
• Dyes – methylene blue, indocyanine green
• Tricuspid regurgitation

References

Here is the operations manual for an AVOXimeter 4000.

Barker, Steven J., et al. "Measurement of carboxyhemoglobin and methemoglobin by pulse oximetry: a human volunteer study." Anesthesiology105.5 (2006): 892-897.

Mathews Jr, P. J. "Co-oximetry." Respiratory care clinics of North America 1.1 (1995): 47-68.

Watcha, Mehernoor F., Michael T. Connor, and Anne V. Hing. "Pulse oximetry in methemoglobinemia." American Journal of Diseases of Children 143.7 (1989): 845-847.

Barker, Steven J., Kevin K. Tremper, and John Hyatt. "Effects of methemoglobinemia on pulse oximetry and mixed venous oximetry." The Journal of the American Society of Anesthesiologists 70.1 (1989): 112-117.

College Answer

Non-rebreather or partial rebreather oxygen mask

Reservoir bag attached to FGF
One way valve between reservoir bag and patient which prevent expired gas entering the reservoir bag.
Usual FiO2 reached is between 60-90%. Achieving 100% FiO2 is difficult because of valve inefficiency and lack of a tight fit around the face thus entraining room air.

Discussion

This question closely resembles Question 15.3 from the first paper of 2012.

References

College Answer

1)  Colour coding (oxygen is white, suction is yellow)
2)  A unique sleeve index arrangement for each wall gas

Discussion

"A unique sleeve index arrangement" means "it won't fit there".

That said, people have in the past connected oxygen wall outlets to patient's joint cavities and IV lines, so there is a good reason for this unique sleeve index arrangement.

References

Herod, Ruth, and Rachel Markham. "Suction devices." Anaesthesia & Intensive Care Medicine 13.10 (2012): 459-462.

College Answer

Pressure gradient, radius of the catheter raised to the power of 4 (r4) and length of the catheter. As described by the simplified Poiseuilles formula for laminar flow through tube

Flow α ∆ρ.r4/l

Discussion

Even more simplified, Poiseuilles formula is:

Flow = (π × pressure gradient × radius⁴) / ( 8 × viscosity × length of tubing)

Thus, for every doubling of the radius, the flow rate increases by the fourth power, or by sixteen times. Length of tubing and viscosity matter, but are not as important.

The Rapid Infusion Catheter (RIC) is discussed in some brief detail in one of the Equipment and Procedures "required reading" chapters. It is unlikely to come up again as an examinable topic.

References

Sutera, Salvatore P., and Richard Skalak. "The history of Poiseuille's law."Annual Review of Fluid Mechanics 25.1 (1993): 1-20.

REETER, ALAN K., and KENNETH V. ISERSON. "A New Device For Rapid Fluid Replacement." Journal of Clinical Engineering 9.1 (1984): 37-42.

College Answer

A- central aorta
B- proximal UL
C- Distal UL or LL
D- Proximal LL
E- Distal UL or LL

Discussion

Normal arterial line waveform variations are discussed in greater detail elsewhere.

In brief:

The further you get from the aorta,

• The taller the systolic peak (i.e. a higher systolic pressure)
• The further the dicrotic notch
• The lower the end-diastolic pressure (i.e. the wider the pulse pressure)
• The later the arrival of the pulse (its 60msec delayed in the radial artery)

But, the MAP doesn't change very much.

This is because, from the aorta to the radial artery, there is little change in the resistance to flow.

MAP only really begins to change once you hit the arterioles.

This is called Distal systolic pulse amplification:

The systolic peak is steeper the further down the arterial tree you travel because of “reflected waves”.

References

From Bersten and Soni's" Oh's Intensive Care Manual", 6th Edition; plus McGhee and Bridges Monitoring Arterial Blood Pressure: What You May Not Know (Crit Care Nurse April 1, 2002 vol. 22 no. 2 60-79 )

For those who like hardcore physics, this excellent resource will be an enormous source of amusement. It appears to be a free online textbook of anaesthesia. Nowhere else was this topic covered with a greater depth, or with a greater attention to mathematical detail.

College Answer

What procedure has been performed?

Fast flush test

(b)        What is your impression of the fidelity of the arterial system? Give two (2) reasons.

Underdamped trace – Multiple oscillations and systolic overshoot

Discussion

The dynamic response testing of arterial lines is discussed in greater detail elsewhere.

In brief: the under-damped trace will overestimate the systolic, and there will be many post-flush oscillations.

References

From Bersten and Soni's" Oh's Intensive Care Manual", 6th Edition; plus McGhee and Bridges Monitoring Arterial Blood Pressure: What You May Not Know (Crit Care Nurse April 1, 2002 vol. 22 no. 2 60-79 )

For those who like hardcore physics, this excellent resource will be an enormous source of amusement. It appears to be a free online textbook of anaesthesia. Nowhere else was this topic covered with a greater depth, or with a greater attention to mathematical detail.

College Answer

1)  Systolic, diastolic, mean and pulse pressures
2)  Heart rate and rhythm
3)  Effect of dysrhythmias on pefusion
4)  ECG lead disconnect
5)  Continuous cardiac output using pulse contour analysis
6)  Specific waveform morphologies  might be diagnostic – eg slow rising pulse –AS, pulsus paradoxus in tamponade
7)  Systolic pressure variation or pulse pressure variation may be useful in predicting fluid responsiveness.

Discussion

This question closely resembles Question 30.2 from the second paper of 2013

References

From Bersten and Soni's" Oh's Intensive Care Manual", 6th Edition; plus McGhee and Bridges Monitoring Arterial Blood Pressure: What You May Not Know (Crit Care Nurse April 1, 2002 vol. 22 no. 2 60-79 )

For those who like hardcore physics, this excellent resource will be an enormous source of amusement. It appears to be a free online textbook of anaesthesia. Nowhere else was this topic covered with a greater depth, or with a greater attention to mathematical detail.

College Answer

a) Identify the lumens / lines labelled A, B, C, D, E

A         right atrial lumen
B         thermistor
C         mixed venous oximeter

D         pulmonary artery lumen

E          balloon inflation/deflation

b) List the parameters that can be directly measured using this device.

•    Right atrial pressure
•    Right ventricular systolic and diastolic pressure
•    Pulmonary artery systolic and diastolic pressure
•    Pulmonary artery occlusion pressure
•    Mixed venous saturations
•    Core temperature

Discussion

Here is a diagram of the important ports:

The following "direct" measurements can be made:

• Core temperature
• RA pressure
• PA pressure
• PA wedge pressure
• Mixed venous saturation

With a malpositioned catheter, one could potentially also read the RV pressure, the IVC pressure and the hepatic venous pressure. Anatomy of the PA catheter is discussed elsewhere, as are the directly measured and derived variables.

References

This a full-text version of the seminal paper from 1970:

Swan HJ, Ganz W, Forrester J, Marcus H, Diamond G, Chonette D (August 1970). "Catheterization of the heart in man with use of a flow-directed balloon-tipped catheter". N. Engl. J. Med. 283 (9): 447–51.

A manufacturer (Edwards) offers some free information about the PA catheter on their product page.

The PA catheter section from The ICU Book by Paul L Marino (3rd edition, 2007) is a valuable read.

College Answer

With regards to the endotracheal  tube pictured below, what is the purpose of the lumen labelled A

Suction  port  with  aperture  above  the  cuff  enables   continuous   suction  of  subglottic secretions which and thus may limit nosocomial pneumonia occurring as a consequence of aspiration.

Discussion

 The endotracheal tube is discussed in detail elsewhere.

This added supraglottic port enables the aspiration of secretions which collect above the tube cuff. According to a review of the available evidence in Revista Brasileira de Terapia Intensiva one should not expect very much improvement in mortality or duration of ventilation. The risk of VAP is somewhat reduced.

The disadvantage of suctioning above the cuff is mucosal damage. The sucker applies 100mmHg pressure to the tracheal wall. This sort of pressure- though considered "low wall suction" - can still strip mucosa off the walls of the trachea. This, it seems, is predominantly a risk associated with continuous rather than intermittent subglottic suction.

References

Souza, Carolina Ramos de, and Vivian Taciana Simioni Santana. "Impact of supra-cuff suction on ventilator-associated pneumonia prevention." Revista brasileira de terapia intensiva 24.4 (2012): 401-406.

DePew, Charlotte L., and Mary S. McCarthy. "Subglottic secretion drainage: a literature review." AACN advanced critical care 18.4 (2007): 366-379.

College Answer

a)  Nitric oxide 800ppm and Nitrogen

b)  PO2 pulmonary artery pressure, methaemoglobin and nitrogen dioxide

Discussion

The marvels and wonder of nitric oxide are discussed elsewhere.

The following adverse effects have been reported with its use:

• Methemoglobinaemia, as abundantly discussed already
• Hypotension (maybe some of it does leak into the systemic circulation, or maybe this the effect of depressed LV function
• Rebound hypoxia after abrupt withdrawal
• Thrombocytopenia (in as many as 10% of patients)
• Increased susceptibility to pulmonary infections probably due to NO₂ formation and associated lung injury

The college recommend some monitoring:

• PO₂ and presumably by extension SpO₂, which seems like something standard for a hypoxic patient
• Methaemoglobin levels, which are measured by all good ABG machines - and frequent ABGs appear inevitable in any situation in which nitric oxide therapy is seriously considered
• PA pressure, which implies a PA catheter. This cannot be viewed as a mandatory step in the modern era, but most studies of nitric oxide come from a time when most ICU patients would have had a PA catheter.
• Nitrogen dioxide levels, which seems problematic. The measurement of NO₂ in air by the colorimetric Saltzman method (1960) using a commercially available badge device is possible at 1ppm resolution, but this is usually something done to monitor air pollution. Electrochemical or chemoluminiscent analysers for expired gas do exist (Fox, 2009), but their availability is limited.   In the lung its activity is local and mainly due to its tendency to cause oxidative stress (it produces nitric and nitrous acids upon contact with water), which makes measurement of blood NO₂ levels some combination of difficult and pointless.

There are some official (1997) UK guidelines for the use of nitric oxide, which recommend:

• Monitor for a 20 % rise in PaO₂ as a test of a dose response (20% rise is a minimum response)
• Monitor NO and NO₂ concentration in expired gas using an electrochemical analyser (maximum NO₂ concentration should be no more than 8ppm over an 8 hr period)
• Monitor methaemoglobin levels at 1hr, 6 hrs and thereafter daily or with dose increases

References

Ikaria, the only company which produces this stuff in Australia, has an excellent product information pamphlet.

Barker, Steven J., and John J. Badal. "The measurement of dyshemoglobins and total hemoglobin by pulse oximetry." Current Opinion in Anesthesiology21.6 (2008): 805-810.

Afshari, Arash, et al. "Inhaled nitric oxide for acute respiratory distress syndrome (ARDS) and acute lung injury in children and adults." Cochrane Database Syst Rev 7 (2010).

Cuthbertson, B. H., et al. "UK guidelines for the use of inhaled nitric oxide therapy in adult ICUs." Intensive care medicine23.12 (1997): 1212-1218.

Saltzman, BERNARD E. "Colorimetric microdetermination of nitrogen dioxide in the atmosphere." Anal. Chem 3 (1960): 135-136.

Fox, Terry. "Inspired and Expired Gas Monitoring." Respiratory Disease and its Management. Springer London, 2009. 121-126.

College Answer

Hydrophobic pleated filter for heat and moisture exchange
Bacterial and viral filtration properties
Filter protects against liquid and airborne contamination
Minimal resistance to airflow
Luer lock gas sampling port (connects to ETCO2 monitoring)
15mm/22mm ISO standard connectors
Disposable single patient use

Discussion

Well, no. It really tests the candidates anaesthetic background. The anaesthetic trainee will have a detailed (some may say, intimate) understanding of all their various gadgets.

This thing is a heat and moisture exchanger (HME) and it is discussed in greater detail elsewhere.

There really isnt much to it. Ultimately, its a plastic box with cardboard in it.

The features listed in the college answer will suffice.

Here they are in point form, battered and lightly fried.

• Single use item
• Transparent plastic body
• 30-40ml of apparatus dead space
• Hydrophobic pleated filter
• Antimicrobial filter lining
• ETCO₂ monitoring port with Luer lock connector
• Standardised ISO ventilation equipment connectors

References

College Answer

a) What is the device depicted below?
Double lumen endobronchial tube (right sided)

b) List the indications for its use in the ICU
Anatomical or physiological lung separation
Massive haemoptysis from unilateral lesion
Whole lung lavage eg alveolar proteinosis
Copious infected secretions with risk of soiling unaffected lung eg bronchiectasis, lung abscess
Unilateral parenchymal injury
Aspiration
Pulmonary contusion
Pneumonia
Unilateral pulmonary oedema
Single lung transplant
Bronchopleural fistula
Unilateral bronchospasm

Discussion

Yes, that's a right sided dual lumen tube. You can tell because the blue cuff is eccentric - its unusual shape is owed to need to ventilate the right upper lobe bronchus. A normal-shaped tube would block that lobe, with predictably unhealthy consequences.

The indications for the use of the dual lumen tube are discussed in greater detail in the dual-lumen endotracheal tube chapter from the mechanical ventilation section.  I will not duplicate that content, and I will merely regurgitate the college answer in a slightly adjusted form.

• Prevention of cross-contamination of one lung by the other, eg. in the following cases:
  • Infection (e.g. unilateral pulmonary abscess)
  • Massive pulmonary haemorrhage

• Enable the ventilation of each lung with a different ventilation setting in settings where the each hemithorax is wildly different from the other, for example:
  • Severe chest injury
  • Bronchopleural fistula
  • Open chest (eg. mid thoracic surgery)
  • Giant unilateral lung cyst or bulla
• Bypass a damaged section of the airway
  • Tracheobronchial tree disruption /Major airway trauma
• Permit the lavage of each lung independently - pulmonary alveolar proteinosis is frequently mentioned as an indication, and I suppose if one finds oneself bringing it up during a viva, one should then be prepared to discuss what it is.

References

A detailed autopsy of these devices can be found in the 5th edition of "Understanding Anaesthesia Equipment" By Dorsch and Dorsch. Section III, chapter 20.
This chapter seems to be available for free.

Trapnell, Bruce C., Jeffrey A. Whitsett, and Koh Nakata. "Pulmonary alveolar proteinosis." New England Journal of Medicine 349.26 (2003): 2527-2539.

College Answer

a) What is the device depicted below?

Passy Muir speaking valve

b) List the contra-indications to its use

Unconscious / comatose patient
Inflated tracheostomy tube cuff
Severe upper airway obstruction that may prevent sufficient exhalation
Excessive secretions
Severe COPD with gas trapping
Foam filled cuff tracheostomy tube (eg Bivona)
Endotracheal tube

Discussion

Designed by Patricia Passy and David Muir, this device is more correctly named the Passy-Muir Speaking and Swallowing Valve. David was in fact a tracheostomy patient, and the valve is his idea. This device is discussed in greater detail in the The Passy-Muir Valve chapter.

The company guards its patents jealously, but there are some free educational materials to be found on their site.

I have compiled a list of contraindications which closely mirrors the college answers. Some of the college answers seem bizarre. Would anybody ever really try to attach one of these to an endotracheal tube? Is that really a contraindication?

• Inflated (or foam filled) tracheostomy cuff (you wont be able to exhale)
• Absence of a cuff leak with tracheostomy cuff deflated (you wont be able to exhale)
• Thick uncontrolled tracheal secretions (you will clog the valve)
• Thick uncontrolled oral secretions (you need to be able to swallow those, or they will get inhaled)
• Severe respiratory weakness (you will not be able to overcome the valve resistance to inspiration)
• Unconsciousness (You cant deflate the cuff in these people)
• Gas trapping with autoPEEP (the valve will increase PEEP)

References

College Answer

• Identify the device depicted above
  • Intra-osseous needle

• List the indications for use of this device
  • Difficulty in establishing IV access
  • Need for rapid high-volume fluid infusion eg hypovolaemic shock or burns, and failure to establish IV access
  • Cardio-pulmonary arrest

• List the potential complications associated with the use of this device
  • Infection – cellulitis and osteomyelitis
  • Extravasation of blood / infusion fluid / drugs
  • Compartment syndrome secondary to extravasation
  • Bone fracture or through and through penetration
  • Damage to surrounding structures

Discussion

This question is very similar to Question 10 from the first paper of 2000: "List your indications and contraindications for the use of the lntraosseous needle. What are the risks associated with its use and how can they be minimised? "

The college-specified indications for the use of the intraosseous needle are difficult to expand upon. There is little to say!

• Cardiac arrest
• Need for immediate IV access in the absence of easy IV access

Complications

• Osteomyelitis
• Fracture
• "through and through" penetration
• Extravasation
• Compartment syndrome due to extravasation
• Injury to staff (slipped needle)
• Damage to surrounding structures
• Microscopic fat emboli

With sternal approach:

• Mediastinal injury
• pneumothorax
• Greater vessel injury

References

Luck, Raemma P., Christopher Haines, and Colette C. Mull. "Intraosseous access." The Journal of emergency medicine 39.4 (2010): 468-475.

College Answer

Indications

• • Defibrillation and monitoring in cardiac arrest
  • Continuous heart rhythm monitoring
  • Cardioversion
  • Transcutaneous pacing

Precautions

• • Avoid fluid – water, perspiration etc
  • Avoid excessive hair
  • Avoid metal (metal-backed patches, piercings, jewellery)
  • Do not place over bone
  • Roll on to the skin to avoid air pockets
  • Do not place over implanted pacemakers
  • Avoid wounds / broken skin

Discussion

There aren't many things you could do with the cutaneous defib pads. You can monitor, pace, cardiovert or defibrillate - that is about it. The image of the pads above was stolen from Zoll's UK website - there is quite a variety of electrode pads, for every conceivable use.

The precautions for the use of these pds can be found in the ARC ALS manual (I have the 2011 version).

Avoid the following:

• Water
• Vomit
• Sweat
• Excessive chest hair
• Piercings
• Necklaces
• Bony prominences
• Air pockets (burns may occur)
• Implanted devices
• Subclavian lines
• Wounds

References

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

ARC: Guideline 11.4: Electrical Therapy for Adult Advanced Life Support

College Answer

Reservoir oxygen mask / non-rebreather or partial rebreather oxygen mask

• • Fresh gas flow attached to reservoir bag and adjusted to ensure bag remains 2/3 full at all times
  • One-way valve between reservoir bag and patient preventing expired gas entering reservoir bag
  • One or two valves on side ports in mask close in inspiration reducing entrainment of room air and open in expiration to prevent rebreathing. (The presence of two valves requires close monitoring of the patient to ensure adequate fresh gas flow from the reservoir bag)
  • FiO2 varies from 60-80% depending on presence of valves on side ports and mask fit

Discussion

That image comes from www.acesurgical.com; no permission whatsoever has been granted for its use, and it remains in place only until somebody complains.

Anyway. The basics:

• The reservoir fills with 100% oxygen
• The patient inhales, entraining the reservoir oxygen from the bag
• One-way valves in the mask prevent the entrainment of room air
• The patient exhales, and the one-way valve prevents expired air from entering the reservoir
• The expired air instead escapes through side-vents and around the sides of the mask
• One optimistic article suggests that NRBMs may be capable of 90% FiO₂ at 10L flow rate.

References

Garcia, Juan A., et al. "The oxygen concentrations delivered by different oxygen therapy systems." CHEST Journal 128.4_MeetingAbstracts (2005): 389S-b.

Abe, Yukiko, et al. "The efficacy of an oxygen mask with reservoir bag in patients with respiratory failure." The Tokai journal of experimental and clinical medicine 35.4 (2010): 144-147.

College Answer

Therapeutic hypothermia can be induced by a number of methods. These differ in their ease of use and the rapidity of onset of hypothermia. In all cases, irrespective of the methods used, core temperature should be monitored, as should be invasive arterial pressure, ECG etc. Shivering needs to be suppressed with sedation+/- muscle relaxants.

The various methods are outlined below:

Discussion

The college has presented an excellent tabulated answer.

Following such an effort, one can do little other than provide references.

One such reference is a 2009 article by Kees Polderman and Herold Ingeborg which goes though cooling methods listing their advantages and limitations. In this article, I was surprised to find a table (Table 2) which is almost identical to the college answer - only more detailed. The table is huge, it spans over two pages, and the article as a whole is an amazing resource. This paper, sadly, is not available as a free full text offering. The table below is a stripped-down surrogate.

References

Polderman, Kees H., and Ingeborg Herold. "Therapeutic hypothermia and controlled normothermia in the intensive care unit: Practical considerations, side effects, and cooling methods*." Critical care medicine 37.3 (2009): 1101-1120. This article is ideal, but not available without institutional access.

College Answer

b) Causes 
• Loss of atrial contraction 

c) 
i) Haemodynamic Abnormality 
The important haemodynamic abnormality is pulse pressure variation (systolic pressure variation 
also acceptable). 

ii) Causes 
Causes of this abnormality include: 
• Hypovolaemia (fluid responsiveness acceptable) 
• Acute severe asthma 
• Cardiac tamponade 
• Excessive tidal volume 

 

Discussion

Unfortunately, the college has removed the images, so nobody can recognise the patterns.

It is difficult to make much sense of it, but I can only assume the pattern in (b) was supposed to be an arterial line trace which suddenly dips in pressure and becomes irregular, demonstrating that the patient has gone into rapid AF. This, at  least, is what I have attempted to re-create.

The pattern in (c) probably depicts a respiratory variation in arterial pressure, which can either be caused by inadequate right heart filling (eg. hypovolemia), excessive right heart afterload (eg. acute severe asthma) or decreased right ventricular compliance (cardiac tamponade). I went on and on about it in the stroke volume variation section of my PiCCO rant. The variation in stroke volume (or, more accurately, pulse pressure - because that is all you can measure directly with the arterial line).

But let us not get carried away.

References

College Answer

a) Indications- (any 3 of these)

• To avoid contamination of a non-diseased lung 
• Infection (e.g. unilateral pulmonary abscess)
• Massive pulmonary haemorrhage
• Unilateral pulmonary lavage (pulmonary alveolar proteinosis)
• Control of distribution of ventilation 
• Bronchopleural fistula 
• Giant unilateral lung cyst or bulla 
• Tracheobronchial tree disruption /Major airway trauma
• Severe hypoxaemia due to unilateral lung disease
• During surgical procedures
  • Pneumonectomy, lobectomy
  • Oesophageal resection
  • Lung transplant
  • Thoracic aneurysm surgery
  • Thoracic spine surgery

• Advantages - (any 2)

• • Can be used in patients through existing endotracheal tube (oral or nasal) without requirement to change to a double-lumen tube or back to a single lumen tube after. Therefore useful in patients with difficult airway, cervical spine injury, etc.

• • Can be used in patients with major airway trauma or distorted trachoebronchial anatomy more safely than DLT

• • Can provide selective lobar blockade of a specific lobe- in cases of haemorrhage, air leak, infection in one lobe, thereby allowing ventilation of more lung units.

Limitations - (any 2)

• Do not allow suctioning of deflated lung due to small lumen
• Requires ETT >7.5mm diameter.
• Collapse of desired lung may be slow
• Easily dislodged
• Risk of perforation of bronchus or lung parenchyma
• Difficult to block R upper lobe bronchus due to variable take-off.

Discussion

The image above is a picture of a PRO-Breathe endobronchial blocker, from PROACT Medical. The image was used without any permission from the manufacturer. We can also be grateful to PROACT for this detailed user manual, with diagrams and technical information.

So; what is the indication for its use?

Well.

It is essentially any situation when a double-lumen tube would be ideal, but for some reason you can't (or don't want to) insert it.

For instance:

• nasal intubation
• small patient
• difficult intubation
• patient with a tracheostomy
• subglottic stenosis
• thick and excessive secretions

All the other indications resemble the indications for the insertion of a dual-lumen tube:

• Prevention of cross-contamination of one lung by the other, eg. in the following cases:
  • Infection (e.g. unilateral pulmonary abscess)
  • Massive pulmonary haemorrhage

• Enable the ventilation of each lung with a different ventilation setting in settings where the each hemithorax is wildly different from the other, for example:
  • Severe chest injury
  • Bronchopleural fistula
  • Open chest (eg. mid thoracic surgery)
  • Giant unilateral lung cyst or bulla
• Bypass a damaged section of the airway
  • Tracheobronchial tree disruption /Major airway trauma
• Permit the lavage of each lung independently - pulmonary alveolar proteinosis is frequently mentioned as an indication, and I suppose if one finds oneself bringing it up during a viva, one should then be prepared to discuss what it is.

Advantages for its use:

• Can use the current normal ETT- no need to insert a DLT
• Safer than the DLT in patients with a traumatic airway injury
• Can provide selective lobar blockade of a specific lobe, rather than of the entire lung

• Technically, simpler than DLT isnertion

Disadvantages to its use:

The college suggest the following:

• Do not allow suctioning of deflated lung due to small lumen
• Requires ETT >7.5mm diameter.
• Collapse of desired lung may be slow
• Easily dislodged
• Risk of perforation of bronchus or lung parenchyma
• Difficult to block R upper lobe bronchus due to variable take-off.

To this I would add:

• Surgery on a mainstem bronchus is impossible if the bronchus is blocked
• Bronchoscopy of the blocked lung is impossible

References

Neustein, Steven M. "The use of bronchial blockers for providing one-lung ventilation." Journal of cardiothoracic and vascular anesthesia 23.6 (2009): 860-868.

Campos, Javier H. "An update on bronchial blockers during lung separation techniques in adults." Anesthesia & Analgesia 97.5 (2003): 1266-1274. This excellent article discusses several different styles of EBBs, with commends on the merits and demerits of each.

This article was found at the amazing www.onelung.org.uk, a site dedicated to a thoracic anaesthesia course which teaches anaesthetists to perform lung isolation.

College Answer

A = Trap or Collection Bottle

B = Underwater Seal Bottle

C = Manometer Bottle

D = Distance below water is equal to the negative pressure generated when suction is applied

E = Adjustable Vent tube

In the 1-bottle system the chest drain is connected by collecting tubing to a tube approximately 3 cm under water (the seal) in the underwater-seal bottle while another vent tube is open to atmosphere. In this system pleural pressure greater than + 3 cm water will force air or fluid from the pleural space into the bottle while negative pressure in the pleural space will suck fluid up the tube. As long as the underwater-seal bottle is well below the patient (e.g., on the floor beside the patient), the hydrostatic pressure of the fluid column in the tube will counterbalance the negative pleural pressure and prevent water from being sucked into the pleural space. The hydrostatic pressure is proportional to the height of the fluid column. Therefore a disadvantage of this single bottle system is that, as liquid contents (blood, pus, effusion fluid) is expelled from the pleural space and collects in the underwater-seal bottle, the seal tube becomes immersed deeper under water and the pressure required to force more contents into the bottle increases thus impeding the clearance of the pleural collection.

In a 3-bottle system, a trap or collection bottle is interposed between the drain tube and the underwater-seal bottle and a third bottle, called the manometer bottle, is added after the underwater-seal bottle. This manometer bottle has a vent tube under water to regulate the negative pressure generated by suction. The maximum negative pressure (in cm H2O) generated by suction equals to the distance (in cm) this vent tube is below the water line (represented by D in the figure above).

The negative pressure generated by the vent tube (D) is independent of the amount of pleural drainage that is collected in the trap bottle (A).

Discussion

So, how are the three-bottle systems different to the one-bottle system?

Briefly,

• The single-bottle system is just the underwater seal bottle
• The underwater seal provides counterpressure to pleural pressure
• As long as this bottle remains well below the patient, no fluid will get sucked up into the chest.
• The more fluid drains out of the patient, the deeper the tip of the tube, and the more pressure will be required to force further fluid/gas out of the pleural cavity.
• In contrast, in a three-bottle system the depth of the vent tube determines the negative pressure, and the amount of fluid collecting in the collection bottle does not determine the pressure.

In case there is any interest, here is a diagram of our dearly beloved Atrium system, with labels.

References

NSW Health: Chest Drain - Set up of Atrium Oasis Dry Suction Under-Water Seal Drainage

Atrium have published their instructions online.

Additionally, they provide this training document which is surprisingly full of useful information.

College Answer

a) 
Pressure gradient between RV and PA

Pulmonary valve stenosis

Supravalvular or RVOT stenosis

Discussion

This answer relies on the candidate to have some recollection of normal right heart pressures.

In order to make this analysis easier, I will present the data again, but this time with normal values included.

One immediately notices the massive difference between the pressure in the RV and the pressure in the pulmonary arteries. Surely, at least the systolic should be the same?

And then one's attention is drawn to the monstrously elevated RV pressure.

Thus, one forms the impression that the RV must generate vastly increased pressures in order to generate a relatively normal PA pressure. This is the case in RVOT obstruction or in pulmonic valve stenosis.

References

Normal Hemodynamic Parameters and Laboratory Values pocket card from Edwards Life Sciences, a manufacturer of Swan-Ganz catheters.

College Answer

• Physical examination [warm hands, urine output, mentation]
• Vital signs – heart rate, blood pressure, oxygenation Lactate
• Urine output

• Blood pressure response to passive leg raise or fluid challenge

• Invasive arterial monitoring [Vigileo/LiDCO (cardiac output, stroke volume variation, stroke volume)]

• Central venous pressure measurement, central venous oxygen saturation

• Invasive cardiac monitoring
  • PiCCO measurements [Intra thoracic blood volume, global end diastolic volume, cardiac output, stroke volume variation]
  • Pulmonary Artery Flotation Catheter [pulmonary artery occlusion pressure, cardiac output, mixed venous oxygenation]
• Echocardiogram [cardiac output, left ventricular ejection fraction, IVC collapsibility]

• Transcutaneous Doppler [cardiac output/stroke volume variation]

• Research tools
  • Techniques for measuring microvascular perfusion eg contrast US, SDF Techniques for measuring tissue oxygenation eg, gastric tonometry [D pCO2], sublingual tonometry, microdialysis
  • Impedance cardiography [cardiac output, stroke volume variation, stroke volume]

Discussion

This question is a "list" question, and thus one should resist the temptation to critically evaluate, or to compare and contrast. A list of techniques is reasonably easy to generate. Specifically, techniques to assess volume-responsiveness are extensively discussed in the section concerned with Fluid Resuscitation, Vasopressors and Inotropes. If one needed to generate a dumb noncomparative list for whatever reason, one should do so in a manner which follows a system of some sort.

References

Marik, Paul E. "Hemodynamic parameters to guide fluid therapy." Transfusion Alternatives in Transfusion Medicine 11.3 (2010): 102-112.

College Answer

a)  O2ER = VO₂ / DO₂

b)

• The normal value is around 0.2 – 0.3 and if the value is higher this suggests that the tissues are extracting excessive amounts because oxygen delivery is inadequate due to inadequate cardiac output from either inadequate contractility or inadequate preload and may respond to inotropes and/or fluid resuscitation.
• A low normal OER in this patient suggests failure of the microcirculation with inadequate oxygen uptake due to shunting and microvascular occlusion and resultant tissue ischaemia. This would be confirmed by rising lactate levels.

Discussion

The Oxygen Extraction Ratio is very simply the proportion difference between the oxygen entering your patient and the oxygen exiting your patient.

A professional-sounding equation is what is called for in this scenario, and that equation is O₂ER = VO₂ / DO_2.

Or, 

O₂ER = VO2/DO2 = (CaO2-CvO2)/CaO2

or, as Walley (2010) abbreviates, 

O₂ER = (SaO₂-SvO₂)/SaO₂

One can (and I have) fall tumbling into the rabbit-hole of metabolic physiology when faced with a question like this. One must remember that it is asking "How do you calculate the OER", not "How do you get the objective data which allows you to calculate OER" or "critically evaluate the use of central venous oxygen saturation in the ICU"

An OER of 0.5 suggests that about 50% of arterial oxygen is gone by the time the blood returns to the heart. This corresponds to an ScVO₂ of about 50%, and suggests that something is woring with the circulation, i.e. it may be too sluggish. Similarly, an OER of 20% suggests something is wrong with the circulation (it might be too fast). Unfortunately, there is nothing specific about the OER; it only describes the matching of supply and demand, but it is powerless to identify the cause of a mismatch.

For an example, here is a table listing the causes of an abnormal oxygen extraction ratio:

References

Walley, Keith R. "Use of central venous oxygen saturation to guide therapy."American journal of respiratory and critical care medicine 184.5 (2011): 514-520.

McLellan, S. A., and T. S. Walsh. "Oxygen delivery and haemoglobin." Continuing Education in Anaesthesia, Critical Care & Pain 4.4 (2004): 123-126.

Leach, R. M., and D. F. Treacher. "The pulmonary physician in critical care• 2: Oxygen delivery and consumption in the critically ill." Thorax 57.2 (2002): 170-177.

Ronco, Juan J., et al. "Identification of the critical oxygen delivery for anaerobic metabolism in critically ill septic and nonseptic humans." JAMA: the journal of the American Medical Association 270.14 (1993): 1724-1730.

Orlov, David, et al. "The clinical utility of an index of global oxygenation for guiding red blood cell transfusion in cardiac surgery." Transfusion 49.4 (2009): 682-688.

Bakker, Jan, et al. "Blood lactate levels are superior to oxygen-derived variables in predicting outcome in human septic shock." CHEST Journal 99.4 (1991): 956-962.

College Answer

a)

Sengstaken-Blakemore tube 
(Gastro-oesophageal balloon tamponade device or Minnesota tube acceptable)

b)

• Estimate appropriate length of tube to be inserted for the patient
• Evaluation of compliance curve of gastric balloon pre-insertion by inflation of balloon with incremental 100ml aliquots of air to maximal recommended volume (usually 250 -300ml for SBT, 450-500ml for Minnisota) and notation of corresponding balloon pressure at each step.
• If, post-insertion, balloon pressure on inflation with a given volume is >15 mmHg than the pre-insertion pressure, the balloon may be in the oesophagus and should be deflated and position checked
• iii) Check balloon position with Xray or ultrasound post insertion

OR Any other acceptable technique.

E.g.: inflate gastric balloon with no more than 80 ml of air (or contrast) and confirm position on AXR or via gastroscope then inflate gastric balloon slowly to a volume of 250-300 ml (up to 450 for Minnesota tube) and clamp balloon inlet.

c) 
Aspiration:

• Use only in intubated patient and position patient head-up 30-45o

Oesophageal perforation:

• Ensure both balloons completely deflated prior to insertion
• Avoid inflation of oesophageal balloon
• Ensure gastric balloon is correctly positioned during inflation

Pressure necrosis of gastric mucosa:

• Do not leave SBT in situ for more than 24-36 hr
• Avoid prolonged inflation of gastric balloon – deflate after 12 hr and reinflate if ongoing bleeding

Upper airway obstruction secondary to balloon migration:

• Avoid use in unintubated patient. If SBT in unintubated patient and develops respiratory distress, immediately cut lumens for oesophageal and gastric balloons and remove tube

Discussion

The college had omitted their own image. The picture above was stolen from www.medipicz.com.

The college say "Minnesota tube acceptable". But... is it really? Is there any difference between them?

Well. Yes there is.

The Minnesota tube is actually a modified version of the original Sengstaken-Blakemore device. The modification is an oesophageal suction port, which prevents the pooling of filth in the upper oesophagus. You can tell them apart instantly - the Minnesota tube has four ports at the end, whereas the SB tube has only three. One can also have a Linton-Nachlas tube, which only has two ports, and a single 600ml gastric balloon.

Thus, the device in my picture is properly called a Sengstaken-Blakemore tube, and to call it a Minnesota tube would just be plain wrong.

Now then.

The balloon labelled "A" is the gastric ballon. It inflates to a considerable diameter, and so it is fairly important that you do not inflate it in the oesophagus. Hence the anxiety regarding its position.

One can do this in a number of ways. The college would have accepted "any other acceptable technique".

For instance:

• One can inflate it with a safe 80mls of air, and look for its position on AXR
• One can inflate it with radio-opaque contrast, and look for its position on AXR
• One can position it under direct vision during gastroscopy
• One can compare the balloon pressure pre and post insertion (as suggested by the college), observing a change of 15mmHg as a sign that it is in the oesophagus.

The complications and preventative measures are best presented in the form of a table:

What are the indications for the use of the SB tube? There really is only one. Control of variceal bleeding. However, others have used it to tamponade uterine bleeding, which can possibly extend to rectal bleeding via protocol creep.

What are the contraindications for the use of the SB tube?

Well;

• Unprotected airway
• Oesophageal rupture (eg. Boerhaave syndrome)
• Oesophageal stricture
• Uncertainty regarding the source of bleeding (how do you know it is not duodenal?)

References

Nepean ICU - A McLean, V McCartan - Insertion, care and removal of the Sengstaken Blakemore or Linton tube (2005)

Bennett, Hugh D., Lester Baker, and Lyle A. Baker. "Complications in the use of esophageal compression balloons (Sengstaken tube)." AMA archives of internal medicine 90.2 (1952): 196-200.

Bauer, JOEL J., I. S. A. D. O. R. E. Kreel, and ALLAN E. Kark. "The use of the Sengstaken-Blakemore tube for immediate control of bleeding esophageal varices." Annals of surgery 179.3 (1974): 273.

Seror, J., C. Allouche, and S. Elhaik. "Use of Sengstaken–Blakemore tube in massive postpartum hemorrhage: a series of 17 cases." Acta Obstetricia et Gynecologica Scandinavica 84.7 (2005): 660-664.

College Answer

• Clear non-toxic plastic
• Single use
• Radio-opaque line so visible on CXR
• High volume low pressure cuff with pilot tube
• Murphy’s eye
• Bevelled tip to assist insertion
• Centimetre markings to assess depth of insertion
• Black line to guide insertion to appropriate depth
• Standard 15mm connector
• Size labelling on pilot balloon

Discussion

The college answer represents the bare minimum. More detailed discussions of the ETT are also available:

• Endotracheal tube and intubation (a brief exam-oriented summary)
• The Endotracheal Tube (a digression into apocryphal detail)

In summary, the safety featues are::

• Single use item, no risk of cross-infection
• Standardised 15mm connector to fit all airway devices
• Low-allergen PVC construction, free of latex
• Transparent body,to see blood or vomit
• Markings to indicate depth of insertion
• Black line to guide insertion to appropriate depth
• High volume low pressure cuff to seal the trachea
• Size labelling on pilot balloon
• Pilot cuff to gauge cuff pressure
• Rounded atraumatic edges
• Murphy's eye to protect against occlusion
• Bevelled tip to assist insertion
• Radio-opaque line to help gauge position on chest X-rays

References

​

College Answer

• Systolic, diastolic, mean and pulse pressures
• Heart rate and rhythm
• Effect of dysrhythmias on cardiac output / perfusion
• ECG lead disconnect / problem
• Continuous cardiac output using pulse contour analysis
• Specific diagnostic waveform morphologies eg slow rising pulse in AS, pulsus paradoxus in tamponade, dynamic hyperinflation
• Systolic pressure variation, pulse pressure variation may be useful in predicting fluid responsiveness

Discussion

The section on haemodynamic monitoring contains chapters on arterial line waveform interpretation. Also, Information derived from the arterial pressure waveform contains more detail about the specifics, and has examples of both normal and pathological waveforms.

In brief summary:

Information from amplitude

• Systolic pressure
• Diastolic pressure (coronary filling)
• Mean arterial pressure (systemic perfusion)
• Pulse pressure (high in AR, low in cardiac tamponade or cardiogenic shock)
• Changes in amplitude associated with respiration (pulse pressure variation) as a predictor of fluid responsiveness

Information from frequency

• Heart rate
• Rhythm
• Effect of rhythm on MAP

Waveform shape

• Slope of anacrotic limb represents aortic valve and LVOT flow
• Slurred wave in AS
• Collapsing wave in AS
• Rapid systolic decline in LVOTO
• Bisferiens wave in HOCM
• Low dicrotic notch in states with poor peripheral resistance

References

​

McGhee and Bridges "Monitoring Arterial Blood Pressure: What You May Not Know" (Crit Care Nurse April 1, 2002 vol. 22 no. 2 60-79 )

For those who like hardcore physics, this excellent resource will be an enormous source of amusement. It appears to be a free online textbook of anaesthesia. Nowhere else was this topic covered with a greater depth, or with a greater attention to mathematical detail.

College Answer

a)
Determinants of CVP:
 Intravascular volume status
 Mean systemic filling pressure
 Right and left ventricular status and compliance
 Pulmonary vascular resistance
 Venous capacitance / tone
 Intra-thoracic pressure
 Intra-abdominal pressure

b)
Introductory statement
 For example: CVP is the pressure recorded from the right atrium or superior vena cava and is representative of the filling pressure of the right side of the heart. CVP monitoring in the critically ill is established practice but the traditional belief that CVP reflects ventricular preload and predicts fluid responsiveness has been challenged.
Most critically ill patients have central venous vascular access with multi-lumen catheters, making CVP monitoring easy to do.

Information derived from the waveform and/or measured value assists with / assists the diagnosis of:
 Confirmation of correct line placement.
 Tricuspid regurgitation or stenosis.
 Complete heart block.
 Constrictive pericarditis.
 Tamponade.
 Right ventricular infarction.
 Differential diagnosis of shock state.
 Determining mechanical atrial capture with AV pacing.
 Determining the presence of P waves in cases of SVT.

Traditionally, CVP measurement has been used to assess fluid responsiveness – including assessment of change in CVP after fluid boluses – and the use of target values as resuscitation end-points as recommended in the Surviving Sepsis Guidelines. However increasing evidence including a recent meta-analysis (Marik in Chest) has shown there is no correlation between CVP and fluid status and targeting a certain CVP value can lead to overload in one patient and to another remaining hypovolaemic. Current thinking suggests that interpretation of CVP should be in association with information relating to other haemodynamic variables.
Complications associated with CVC insertion means that CV monitoring is not risk-free. Correct placement, calibration and measurement (at end-expiration) are needed to obtain an accurate recording. Simultaneous fluid administration through the CVC leads to inaccuracies.

Alternative monitoring modalities include devices such as PiCCO and Vigileo analysing stroke volume variation, pulse contour analysis, global end-diastolic blood volume, etc. and bedside echo.

Summary
 For example: CVP monitoring may contribute information relating to the haemodynamic state of a patient but the value must be interpreted in the context of what else is known about that patient's cardiac function. Use of CVP as a measure of fluid responsiveness is flawed. The increasing use of bedside echo in the ICU is decreasing the utility of CVP monitoring.

Discussion

This question is a repeat, closely resembling Question 16 from the first paper of 2001, "What are the determinants of central venous pressure? How may its measurement guide patient management?"

Detailed discussions of this can be found elsewhere:

• Determinants of central venous pressure
• Utility of CVP measurement in the ICU
• Information derived from analysis of the CVP waveform
• Factors which influence the accuracy of CVP measurement

In brief, the answer may resemble this:

Factors which determine CVP:

Measurement technique:

• Transducer position
• Timing of measurement with the cardiac cycle
• Timing of measurement with the respiratory cycle

Central venous blood volume

• Venous return
• Cardiac output (which determines venous return)
• Volume of blood in the central capacitance vessels

Central venous vascular compliance

• Vascular tone of the central venous walls
• Right atrial and right ventricular compliance
  • Pericardial compliance
  • Myocardial compliance
  • Incompressible fluid in the pericardium, eg. tamponade
• Pulmonary arterial compliance
  • Right ventricular outflow tract obstruction
  • Pulmonary hypertension

Tricuspid valve competence

• Tricuspid stenosis will increase the CVP
• Tricuspid regurgitation will also increase the CVP

Cardiac rhythm

• The absence of atrial contraction decreases the CVP (eg. AF)
• Asynchronous atrial contraction (eg. during ventricular pacing) increases the CVP

Compartment pressures in the thorax and abdomen.

• An increase in intrathoracic pressure will increase the CVP:
  • PEEP
  • Intermittent psitive pressure ventilation
  • Tension pneumothorax
• Intrabdominal pressure may increase OR decrease the CVP.

References

College Answer

a)
Intraosseous needle (with insertion driver).

b)
The marrow of long bones has a rich network of vessels that drain into a central venous canal,
emissary veins, and, ultimately, the central circulation. Therefore, the bone marrow functions as a
non-collapsible venous access route when peripheral veins may have collapsed because of
vasoconstriction. This approach is particularly important in patients in shock or cardiac arrest, when
blood is shunted to the core due to compensatory peripheral vasoconstriction. The intraosseous
route allows medications and fluids to enter the central circulation within seconds.

c)

• Proximal tibia
• Femur
• Distal tibia (medial malleolus)
• Proximal humerus
• Manubrium (upper sternum)

The anterior inferior iliac spine, clavicle, and distal radius have also been used successfully for IO
vascular access as have bones without medullary cavities, including the calcaneous and radial
styloid

d)

• Aspiration of bone marrow
• Ability to flush fluid with no evidence of extravasation

e)

• Extravasation of fluid/Compartment syndrome
• Infection/Osteomyelitis/Bacteraemia
• Fracture
• Haematoma
• Growth plate injury (in children)
• Fat embolus

f)

• Proximal ipsilateral fracture
• Ipsilateral vascular injury
• Local cellulitis/infection
• Inability to locate landmarks
• Osteogenesis imperfecta

Discussion

This question is very similar to Question 15.1 from the first paper of 2012, and to Question 8 from the first paper of 2000. The only difference in this version is the addition of the "how would you confirm placement" bit. In brief:

Your IO is in the right place if

• You are able to aspirate bone marrow (which looks a lot like venous blood)
• You are able to flush the line with little resistance, and with no obvious extravasation

Additional methods to confirm placement:

• Ultrasound- colour flow within the intraosseous space (though this is so far experimental)
• Circumferential pressure around to the IO site: if the needle is extravasating into soft tissues, the gravity-fed fluid infusion rate will slow considerably when those soft tissues are compressed by a blood pressure cuff.
• X-rays

References

​Probably the best single reference for this:

Day, Michael W. "Intraosseous devices for intravascular access in adult trauma patients." Critical care nurse 31.2 (2011): 76-90.

Dev, Shelly P., et al. "Insertion of an Intraosseous Needle in Adults." New England Journal of Medicine 370.24 (2014).

James Cheung, Warren, Hans Rosenberg, and Christian Vaillancourt. "Barriers and Facilitators to Intraosseous Access in Adult Resuscitations When Peripheral Intravenous Access Is Not Achievable." Academic Emergency Medicine 21.3 (2014): 250-256.

Luck, Raemma P., Christopher Haines, and Colette C. Mull. "Intraosseous access." The Journal of emergency medicine 39.4 (2010): 468-475.

Stone, Michael B., Nathan A. Teismann, and Ralph Wang. "Ultrasonographic confirmation of intraosseous needle placement in an adult unembalmed cadaver model." Annals of emergency medicine 49.4 (2007): 515-519.

STRAUSBAUGH, STEVEN D., et al. "Circumferential pressure as a rapid method to assess intraosseous needle placement." Pediatric emergency care11.5 (1995): 274-276.

College Answer

References

Stub, Dion, et al. "Refractory cardiac arrest treated with mechanical CPR, hypothermia, ECMO and early reperfusion (the CHEER trial)." Resuscitation 86 (2015): 88-94.

Rubertsson, Sten, et al. "Mechanical chest compressions and simultaneous defibrillation vs conventional cardiopulmonary resuscitation in out-of-hospital cardiac arrest: the LINC randomized trial." Jama 311.1 (2014): 53-61.

Perkins, Gavin D., et al. "Mechanical versus manual chest compression for out-of-hospital cardiac arrest (PARAMEDIC): a pragmatic, cluster randomised controlled trial." The Lancet 385.9972 (2015): 947-955.

Wik, Lars, et al. "Manual vs. integrated automatic load-distributing band CPR with equal survival after out of hospital cardiac arrest. The randomized CIRC trial." Resuscitation 85.6 (2014): 741-748.

Steen, Stig, et al. "The critical importance of minimal delay between chest compressions and subsequent defibrillation: a haemodynamic explanation." Resuscitation 58.3 (2003): 249-258.

Gallagher, E. John, Gary Lombardi, and Paul Gennis. "Effectiveness of bystander cardiopulmonary resuscitation and survival following out-of-hospital cardiac arrest." Jama 274.24 (1995): 1922-1925.

Yu, Ting, et al. "Adverse outcomes of interrupted precordial compression during automated defibrillation." Circulation 106.3 (2002): 368-372.

Ochoa, F. Javier, et al. "The effect of rescuer fatigue on the quality of chest compressions." Resuscitation 37.3 (1998): 149-152.

Hallstrom, Al, et al. "Manual chest compression vs use of an automated chest compression device during resuscitation following out-of-hospital cardiac arrest: a randomized trial." Jama 295.22 (2006): 2620-2628.

Pantazopoulos, C., et al. "1036. Comparison of the hemodynamic parameters of two external chest compression devices (LUCAS versus AUROPULSE) in a swine model of ventricular fibrillation." Intensive Care Medicine Experimental 2.Suppl 1 (2014): P83.

Gates, Simon, et al. "Mechanical chest compression for out of hospital cardiac arrest: Systematic review and meta-analysis." Resuscitation 94 (2015): 91-97.

Carretero Casado, Maria Jose, et al. "RESUSCITATION WITH AUTOMATED DEVICES: HAEMODYNAMIC COMPARISON BETWEEN LUCAS AND AUTOPULSE IN A PORCINE MODEL." Emergencias 26.6 (2014).

Smekal, David, et al. "A pilot study of mechanical chest compressions with the LUCAS™ device in cardiopulmonary resuscitation." Resuscitation 82.6 (2011): 702-706.

College Answer

a)

The IJ vein:

Has an elliptical shape Is larger

More collapsible with modest external surface pressure than the carotid artery (CA), which has rounder shape, thicker wall, and smaller diameter

A Valsalva manoeuvre will further augment their diameter

The IJ vein diameter varies depending on the position and fluid status of the patient and is particularly useful in hypovolemic patients.

Adding Doppler, if available, can further distinguish whether the vessel is a vein or an artery. Colour flow Doppler demonstrates pulsatile blood flow in an artery in either SAX or LAX orientation.

A lower Nyquist scale is typically required to image lower velocity venous blood flows. At these reduced settings, venous blood flow is uniform in colour and present during systole and diastole with laminar flow, whereas arterial blood flow will alias and be detected predominantly during systole (Figure 5) in patients with unidirectional arterial flow (absence of aortic regurgitation).

A small pulsed-wave Doppler sample volume within the vessel lumen displays a characteristic

Veins are thin walled and compressible and may have respiratory-related changes in diameter. In contrast, arteries are thicker walled, not readily compressed by external pressure applied with the ultrasound probe and pulsatile during normal cardiac physiologic conditions.

b)

Pneumothorax Air embolus

Haematoma Haemorrhage Thrombosis Stenosis

Arterial puncture / catheterisation Incorrect catheter tip position

Central vein perforation Tamponade

Cardiac arrhythmia

Embolised, fractured or irretrievable guide wires Infection

Discussion

From the central venous cannulation chapter, the complications of CVC insertion are as follows:

• Immediate
  • Failure of procedure
  • Pneumothorax
  • Haemothorax
  • Retroperitoneal haematoma
  • Arterial puncture
  • Local haematoma
  • Guidewire-induced arrhythmia
  • Thoracic duct injury
  • Guide wire embolism
  • Air embolism
• Early
  • catheter blockage
  • chylothorax
  • catheter knots
• Late
  • Infection : 2.5 infections/ 1000 catheter days
  • catheter fracture
  • vascular erosion
  • vessel stenosis
  • thrombosis
  • osteomyelitis of clavicle (subclavian access)

This is the first time the college have asked about the ultrasound features which help us distinguish between different neck vessels. For most of us, the two are fairly easy to tell apart, but... if one were asked to articulate exactly how they differ, one might come to trouble. "Squishy" and "roundly pulsatey" are probably inappropriately loose terms to use in this context. Instead, please find the table below:

References

Williams, William M. Vascular ultrasound of the neck: an interpretive atlas. Lippincott Williams & Wilkins, 2001.

College Answer

a)

Minnesota tube (Sengstaken-Blakemore or gastro-oesophageal balloon tamponade device acceptable) for balloon tamponade of bleeding oesophageal varices.

b)

Intubate patient to protect airway and simplify insertion. Check balloon for leaks & lubricate tube.

Pass via nares (or mouth if severe coagulopathy present) and guide under laryngoscopic control into oesophagus, until 50cm inserted.

Slowly inflate gastric balloon: 250ml air.

Gently withdraw tube until resistance felt (~30-35cm) as balloon engages with gastro-oesophageal junction.

Aspirate both ports. Check volume of fresh blood: reducing?

If bleeding has ceased (~80%) then leave oesophageal balloon deflated. Apply traction to tubing (as below)

If bleeding from mouth or oesophageal aspiration port continues, then inflate oesophageal balloon with air to 25-30mmHg (max 40).

Deflate oesophageal balloon for 10 min every 2-hrs.

Apply traction to tubing by tying 500ml bag of fluid over pulley.

Check position on CXR: identify gastric balloon below diaphragm & radio-opaque marker along course.

Or any acceptable technique

c)

Oesophageal stricture

Recent oesophageal surgery

Hiatus hernia

Unknown cause of GI bleed

d)

Trauma to nose, pharynx, oesophagus

Incorrect placement or dislodgement of gastric balloon in pharynx or oesophagus (may result in acute upper airway obstruction if airway not secured)

Oesophageal tear or rupture Failure to control bleeding. Aspiration pneumonitis.

Secondary infection: pneumonia, sinus

Nasal or oral mucosal ulceration & necrosis from traction.

Discussion

In order to be specific: that image above is of a Minnesota tube, not  an SB tube (see the number of ports?). This question is essentially identical to Question 30 from the first paper of 2013 and Question 18.3  from the first paper of 2008.

b)

The sequence of insertion should be as follows:

1. Protect the airway.
   Ideally, the patient should be intubated.
   This prevents you from inserting the tube into the trachea accidentally, and prevents aspiration of pooling oesophageal blood or displaced gastric content.
2. Inspect the tube and check the balloons for leaks.
   LITFL also recommend to calculate the compliance of the balloon "by inflating the  balloon with incremental 100ml aliquots of air to maximal recommended volume (usually 250 -300ml for SBT, 450-500ml for Minnesota) and note the corresponding balloon pressure at each step". This is highly appealing to any person who enjoys graphs.
3. Lubricate the tube.
4. Position the patient sitting up to 45°
   This protects them from aspiration
5. Insert the tube into the mouth or nose.
   The college answer offers the nares as an option, but realistically everybody always uses the orogastric route because these patients are always coagulopathic and thrombocytopenic from their chronic liver disease. Moreover, the tube is huge and thick, with big balloons- they will shred the nasal mucosa on the way in regardless of how much lube you cake them in. The insertion should ideally be performed under direct laryngoscopy so that you can be sure you are in the oesophagus.
6. The tube should be advanced to 50cm.
   The college answer prescribes a depth of 50cm, which is consistent with the classical technique for insertion (Bauer et al, 1974). The alternative is to measure from mouth to angle of the jaw, then suprasternal notch and xiphisternum. LITFL authors recommend the latter method, acknowledging that humans vary in the length of their oesophagus.
7. Inflate the gastric balloon. Check position with a chest Xray.
   There seems to be some disagreement as to how much one might inflate. The college recommend 250ml; LITFL mention that the Minnesota tube should take 450-500ml. Locally, we are more cautions: we inflate with about 100ml and then check position with an AXR. If one has produced a compliance curve for their balloon, one may check the balloon pressure against their curve to see whether it has been inflated in the oesophagus (LITFL offer a 15mmHg increase in pressure as a rough guide: if the post-inserion pressure for a given volume is more than 15mmHg higher than the pre-insertion pressure, then the balloon needs to be repositioned as it is likely in the oesophagus. )
8. Withdraw the tube until resistance is felt (at 30-35cm)
   This is usually the depth to the gastro-oesophageal junction. Tension develops, which gives one the impression that the balloon is up against an obstacle of some sort. If one has not inflated with enough air there will be no resistance, and the balloon will come out of the mouth to the embarrassment of the operator. 
9. Aspirate the gastric and oesophageal ports.
   If there was vigorous bleeding, it should have stopped by balloon tension.
10. Decide whether or not to inflate the oesophageal balloon.
    If you already know where the varices are on the basis of a gastroscopy result, you may use your judgment (i.e. there is no point of inflating the oesophageal balloon for gastric varices). Otherwise, one is guided by blood loss.  If bleeding from oesophageal and gastric ports has ceased,  then you may leave oesophageal balloon deflated. Bauer et al (1974) recommend to irrigate the suction ports with warm saline, to assure oneself that the aspirate returns clear and that there is no new bleeding.
11. If appropriate, inflate the oesophageal balloon to 25-30 mmHg pressure.
    The maximum oesophageal pressure is 40mmHg. If the bleeding in the oesophagus has stopped, one should deflate the oesophageal balloon by 10mmHg every 2 hours.
12. Apply traction to the tubing
    The precise amount of traction is uncertain. Some centres specify 1kg, others 2kg. The college answer calls for a 500ml bag of fluid, suspended over a pulley.

Contraindications to SB tube insertion include the following:

• Unprotected airway
• Oesophageal rupture (eg. Boerhaave syndrome)
• Oesophageal stricture
• Uncertainty regarding the source of bleeding (how do you know it is not duodenal?)
• Well-controlled variceal bleeding

Complications of SB tube insertion and measures to prevent them:

References

College Answer

a)

Cardiac protected electrical area:                                                                     

Power reticulation and devices are designed and constructed to minimise unequal electrical potentials between different devices, so that potential current flow between a device and a patient is limited to a defined level.  Class 1c (cardiac protection) ensures leakage currents do not exceed 50 microamps)

b)

Microshock                                                                                                                            

"Micro-shock" is a sub milliamp current applied directly or in very close proximity to the heart muscle of sufficient strength, frequency, and duration to cause disruption of normal cardiac function. There are no incontrovertibly demonstrated fatal cases, but proving causality is difficult.

c)

Microshock Susceptibility:                                                                                                  

• Invasive devices, (CVC, PAC, pacing wires) 
• Altered fibrillation thresholds:
  • Electrolyte abnormality
  • Underlying heart disease

Discussion

Electrical safety in the ICU is discussed at length elsewhere.

a)

A "cardiac protected area" is an area where where microshock is likely, eg. areas where patients have intravascular devices such as central lines or IV infusions. These areas have the following features:

• Equipotential earthing which ensures all equipment is earthed at the same low potential; usually identified by a sign in the room
• Residual current devices  which detect small current leaks and break the circuit if the leak is detected
• Line isolation monitors which monitor escess current and alarm when excess current is detected.

These areas contrast with "body protected electrical areas", where microshock is unlikely (eg. outpatient clinics, anywhere there is ECG monitoring)

b)

A microshock is a small current delivered via electrodes directly into the body, bypassing the resistance of the poorly conductive skin. In the definitive-sounding words of Lester AH Critchley (Oh's Manual, Chapter 83, p. 844- Electrical Safety and Injuries):

"Microshock occurs when there is a direct current path to the heart muscle that bypasses the protective electrical resistance of the skin surface. Such a pathway may be provided by saline-filled arterial or venous-pressure-monitoring catheters or transvenous pacemaker wires. The current required to produce ventricular fibrillation in microshock settings is extremely small, in the order of 60 µA."

The key issue is that a lethal magnitude of current (1-2mA) is not cutaneously detectable by a normal person with dry skin, and yet it can kill an ICU patient if it happens to be conducted to their fluid giving set, for example.

c)

Patient-related factors which increase susceptibility to microshock? As per Walter Olson (1978), "The following clinical devices make patients susceptible to microshock":

1. Epicardial or endocardial electrodes of externalized temporary cardiac pacemakers
2. Electrodes for intracardiac electrogram (EGM) measuring and stimulation devices
3. Liquid-filled catheters placed in the heart to
   1. Measure blood pressure (eg. PA catheter)
   2. Withdraw blood samples
   3. Inject substances such as dye or drugs into the heart

To these, in the modern era we may add:

1. Diathermy
2. Continuous vacuum wound management systems
3. MRI-induced current in implanted conductors

The college also mention altered fibrillation thresholds, which certainly make it more likely that one responds with fibrillation to any irritant, be it microshock, dobutamine infusion, low PICC line tip or a sudden loud noise.

References

O'HARA Jr, JEROME F., and THOMAS L. HIGGINS. "Total electrical power failure in a cardiothoracic intensive care unit." Critical care medicine 20.6 (1992): 840-845.

NASEERUDDIN, ENGR SM. "ELECTRICAL SAFETY IN HEALTHCARE FACITILIES." (2004).

Olson, Walter H. "Electrical safety." Medical instrumentation. Boston: Houghton Mifflin Co (1978): 667-707.

Χριστοδούλου, Χριστόφορος. Recommendations and standards for building and testing an Intensive Care Unit (ICU) electrical installation. Diss. 2011.

Oh's Manual, Chapter 83   (pp. 844)  Electrical  safety  and  injuries by Lester  AH  Critchley. 

College answer

         a) Systems for storage and delivery                                                               

Large supply of oxygen in a remote storage area and piped to the wall outlets Two main types of supply:

Cylinder manifold

Liquid oxygen tank or vacuum insulated evaporator (VIE)

Oxygen may also be supplied by an oxygen concentrator but this is a relatively new technology

Cylinder manifold

Multiple cylinders are arranged in banks with each bank containing enough cylinders to last for 2 days normal use for that hospital. 

Each cylinder is connected to a pipeline which passes to a central control box with   High-pressure gauges indicating the contents of the cylinder banks:

High-pressure reducing valves lowering the cylinder pressure from 137 bar to 10 bar

Changeover valve that switches automatically from the in-use bank to the reserve bank of cylinders when the pressure falls to a certain value. 

At the outlet of the changeover valve is a second-stage pressure-reducing valve to reduce the pipeline pressure from 10 bar to 4.1 bar, the pressure at the wall outlet.

VIE

Main source of supply in large hospitals

Vacuum insulation allows storage of oxygen at or below its critical temperature (-118^oC) in liquid form Normally temperature of around -160^oC with pressure at about 7 bar (vapour pressure of oxygen at this temperature)

Oxygen is taken form top of storage vessel and passed through superheater coil then pressure regulator to keep pipeline pressure at 4.1 bar

The supply usually has a capacity to last for at least 6 days Reserve manifold of cylinders as back-up

b) Safety features for hoses                                                                          

Colour coding: (O₂ white, air black, suction yellow)  Sleeve indexing:

The internal threads are the same for each outlet, but the sleeves are differently configured to prevent placing the wrong hose on the wrong outlet

Pin indexing:

When attaching regulators to cylinders

Schraeder quick release valves (most commonly where gas line attaches to the high pressure inlet of ventilators)

Additional Examiners‟ Comments:

Most candidates had little or no knowledge about oxygen storage and delivery. Some could describe a VIE, but then gave bizarre pressure levels or storage temperatures, which were possibly just guesses. The safety systems aspect of the question highlighted poor learning – candidates frequently realised that a sleeve index system was used, but couldn't name it.

Discussion

I sat this paper. Those are my bizarre pressure levels or storage temperatures they are talking about.

a)

This answer is discussed at greater length in the chapter on the medical gas supply testing and wall oxygen outlets. 

At a basic level, the system consists of:

• A central source
• A vapouriser and pressure regulator
• Pipelines
• Pressure regulators (decreasing presure along the system)
• Manual and service shut-off valves (to isolate whole sections of the system)
• Pressure release valves upstream of any regulators and shut-off valves, to prevent the whole thing from exploding from pressure excess
• Pressure monitors and alarms to detect the fact that you're out of oxygen

Here's an unhelpfully complicated diagram:

For those of us who wish to quote non-bizarre pressure levels and storage temperatures, here they are:

• The VIE is between -150 and -119° C, and at 1000 kPa
• The pressure in the vacuum chamber is 0.3 kPa
• The blow-off valve goes off at 1500 kPa
• The pressure regulator on the supply side downregulates the delivered gas to 415 kPa

The "sleeve index system" is  "a range of male and female components intended to maintain gas-specificity by the allocation of a set of different diameters to the mating connectors for each particular gas" (thank you, ISO/DIS 9170-1(en))

The examiners complained that the candidates knew what this system was, but could not name it. Some might argue that a rose by any other name is still capable of acting as a non-interchangeable gas coupling, but clearly the college are very attached to correct nomenclature.

The information about this can be found in Australian Standard AS 2902-2005, "Medical gas systems—Low pressure flexible hose assemblies". Section 6 ("Connectors and couplers")  speaks about the various hoses and outlets in great detail. Unfortunately, the AS is not free. But: we can borrow this excellent resource from cinder.hk, meant for ANZCA Primary candiates. In short, "the screw threads are the same size for each gas. The fittings are made non interchangeable by the presense of the sleeve". After the sleeve is screwed on to the gas outlet, that outlet becomes gas-specific (and thereafter no "wrong" hose can be coupled to it). 

b)

Michael Richard Cohen's Medication Errors (2006), in the chapter on "Fatal Gas Line Mix-up", makes the following safety recommendations:

• Non-interchangeable connectors (i.e. the air regulator cannot be connected to the oxygen outlet: it is physically impossible). This is called the Diameter Index Safety System (DISS). In Australia we use the sleeve index system (SIS) described above, which does essentially the same thing.
• Standardised flow meters, regulators and connectors (i.e. they all look the same everywhere in the hospital)
• Easily identifiable gas connectors (obvious colour, as well as outlet shape and texture)
• Observable connections (i.e. not hidden under a shelf or table)
• Regular testing and  preventative maintenance of gas supply system (i.e. even if a gas outlet is not in routine us, the engineers need to regularly test it to make sure it still supplies the specified gas)

References

This excellent lecture from the University of Sydney has a vast amount of obscure information (did you know oxygen tanks are aged at 175°C for 8 hours, and that their walls are only 3mm thick?)

Medical Gas Standard AS 2896-2011 is available online, but you have to pay over $200 to purchase it.

Dorsch and Dorsch have a chapter dedicated to medical gas supply and suction equipment, which can be accessed by Google Books.

Das, Sabyasachi, Subhrajyoti Chattopadhyay, and Payel Bose. "The anaesthesia gas supply system." Indian journal of anaesthesia 57.5 (2013): 489.

Westwood, Mei-Mei, and William Rieley. "Medical gases, their storage and delivery." Anaesthesia & Intensive Care Medicine 13.11 (2012): 533-538.

STANDARD, BRITISH, and BSEN ISO. "Medical gas pipeline systems—." (1998).

UK department of health: Department of Health. Health technical memorandum 02-01. Medical Gas Pipeline Systems, (2006) Part A Design, Installation, Validation and Verification; pp. 41–51

College answer

Fluid responsiveness is not synonymous with hypovolaemia and is defined as an increase in stroke volume (or cardiac output/index) by 10 – 15% after fluid administration (volumes vary), depending on technique. The assessment is therefore functional: to induce a change in cardiac preload and observe the effects on cardiac output and arterial pressure. 
 
i. Passive Leg Raise- 
Basis- Involves lifting the legs passively from the horizontal position to 45o with the patient supine. This draws venous blood stored in the lower body veins to the inferior vena cava, increasing the right then the left ventricle pre-load. It represents a „reversible volume challenge‟ which can help to predict the haemodynamic response to real volume challenge.  
 
Limitations- 
Leg movement may be contraindicated in some patients e.g. pelvic trauma, limbs that are not intact, presence of IABP, femoral ECMO, recent angiography etc. 
Unreliable in severely hypovolaemic patients as blood stored in lower body veins may be insufficient to augment stroke volume 
May be unreliable in the presence of intra-abdominal hypertension. 
Should not be performed in the presence of raised ICP 
 
Central Venous Pressure- 
Basis- The CVP is an approximation of right atrial pressure, which is a major determinant of RV filling. It has been assumed that the CVP is a good indicator of RV preload. Furthermore, because RV stroke volume determines LV filling, the CVP is assumed to be an indirect measure of LV preload. A change in the CVP (delta-CVP) with a fluid challenge is thought to be useful in determining fluid management decisions. 
 
Limitations- 
CVP is determined by factors other than intravascular volume –i.e. venous tone, intrathoracic pressures, LV and RV compliance, and geometry that occur in critically ill patients, which results in a poor relationship between the CVP and RV end-diastolic volume.  
The RV end-diastolic volume may not reflect the patients' position on the Frank-Starling curve and therefore the preload reserve. 
 
Pulse Pressure Variation- 
Basis- Pulse pressure variation is derived from the arterial pressure waveform. The reduction in RV preload and increase in RV afterload with positive pressure ventilation both lead to a decrease in RV stroke volume, which is at a minimum at the end of the inspiratory period. The inspiratory reduction in RV ejection leads to a decrease in LV filling after a phase lag of two or three heartbeats because of the long blood pulmonary transit time. Thus, the LV preload reduction may induce a decrease in LV stroke volume, which is at its minimum during the expiratory period when conventional mechanical ventilation is used. The cyclic changes in pulse pressure are greater when the ventricles operate on the steep rather than the flat portion of the Frank-Starling curve. 
 
PPV variation % = (PPmax – PPmin) / PPmean   x 100  
 
The magnitude of the respiratory changes in pulse pressure is an indicator of biventricular preload dependence. A PPV of 10-15% is likely to indicate potential for fluid responsiveness. The higher the PPV the more likely the patient is to be fluid responsive. 
 
Limitations- 
Unable to interpret in the presence of arrhythmias. 
Limited utility in patients ventilated with small tidal volumes (<8 ml/kg) and spontaneously breathing patients 
Cannot be used in patients with an open chest. 
 
Candidates were not expected to provide the same level of detail as is in the template. 
 
Additional Examiners' Comments: 
For a core topic, the overall understanding of the topic was lacking in a significant number of candidates. 

Discussion

a)

There is no agreed-upon definition! Paul Marik  suggests that a response to fluids is "an increase of stroke volume of 10-15% after the patient receives 500 ml of crystalloid over 10-15 minutes". Others have used measures like a 10% increase in cardiac output. Stroke volume seems like the most sensible measure, because stroke volume is the main variable which changes in response to changes in preload.

b)

In brief summary, the measures of fluid responsiveness:

References

An excellent resource for this topic is a paper by Marik, Paul E. "Hemodynamic parameters to guide fluid therapy." Transfusion Alternatives in Transfusion Medicine 11.3 (2010): 102-112.

Zochios, V., and J. Wilkinson. "Assessment of intravascular fluid status and fluid responsiveness during mechanical ventilation in surgical and intensive care patients." (2011).

Marik, Paul E., et al. "Dynamic changes in arterial waveform derived variables and fluid responsiveness in mechanically ventilated patients: a systematic review of the literature*." Critical care medicine 37.9 (2009): 2642-2647.

Marik, Paul E., and Rodrigo Cavallazzi. "Does the central venous pressure predict fluid responsiveness? An updated meta-analysis and a plea for some common sense*." Critical care medicine 41.7 (2013): 1774-1781.

Marik, Paul E. "Noninvasive cardiac output monitors: a state-of the-art review."Journal of cardiothoracic and vascular anesthesia 27.1 (2013): 121-134.

College answer

a)

• Haemoptysis, tenacious secretions
• Patients with large air leaks 
• ARDS where controlling dead space is important
• Large minute ventilation (e.g. > 10L/min)
• Need for frequent nebulised medications
• Long term ventilation (needs changing every 3-4 days)

b)

• Avoid fluid – water, perspiration etc.
• Avoid excessive hair
• Avoid metal (metal-backed patches, piercings, jewellery) 
• Do not place over bone
• Roll on to the skin to avoid air pockets
• Do not place over implanted pacemakers 
• Avoid wounds / broken skin  Ensure oxygen not flowing over pads

c)

• Infection – cellulitis and osteomyelitis
• Extravasation of blood / infusion fluid / drugs
• Compartment syndrome secondary to extravasation
• Bone fracture or through and through penetration
• Damage to surrounding structures 

Discussion

This question is a concatenation of Question 15.1 and Question 15.2 from the first paper of 2012. Apart from this, no previous questions have asked about the contraindications for the use of a HME.

Contraindications to the use of a HME include:

• Conditions which demand minimsation of apparatus dead space
• Large volume of secretions or froth 

• Large minute volume ( over 10L/min) 

• Large air leak, eg. bronchopleural fistula

• Long term ventilation

• Frequent nebulised medications

With the defib pads, avoid the following:

• Water
• Vomit
• Sweat
• Excessive chest hair
• Piercings
• Necklaces
• Bony prominences
• Air pockets (burns may occur)
• Implanted devices
• Subclavian lines
• Wounds

With intraossesous needle devices, the following complications occur:

• Osteomyelitis
• Fracture
• "through and through" penetration
• Extravasation
• Compartment syndrome due to extravasation
• Injury to staff (slipped needle)
• Damage to surrounding structures
• Microscopic fat emboli

With sternal approach:

• Mediastinal injury
• Pneumothorax
• Greater vessel injury

References

College answer

Advantages: 
Simple 
Drain simple pneumothoraces

Disadvantages: 
Cannot drain fluid from pleural cavity safely 
Cannot apply suction safely 
 

Advantages: 
Drain simple pneumothoraces and fluid

Disadvantages: 
Cannot apply suction safely 
 

Advantages: 
Drain simple pneumothoraces and complex fluid collections

Can apply suction

Disadvantages: 
Complexity and cost 
 

Examiners Comments: 
 
Extremely poorly done with many candidates showing a complete lack of even a basic understanding of the set up or physics of pleural drains.   
 

Discussion

The chest drain systems asked about are:

The single chamber system

Advantages

• Simple
• Cheap
• Easily improvised from unrelated equipment
• For simple pneumothorax, there is usually no need for anything more sophisticated
• The fluid level (i.e. valve pressure) is adjustable, though there are few scenarios where one might wish to adjust it. 

Disadvantages

• It is unsuitable for draining pleural fluid.  Air will vent out of the single bottle effortlessly, but any fluid drained will collect in the bottle, increasing the fluid level. As the fluid level rises, the pressure required to force air and fluid out of the chest cavity increases; i.e. the more fluid drains out of the patient, the deeper the tip of the tube, and the more pressure will be required to force further fluid/gas out of the pleural cavity.
• If pleural fluid coes enter the bottle, froth will form. Protein from the pleural space tends to foam due to the bubbling of the drain, which fills the chamber with froth. This makes the level of the fluid difficult to read, and is aesthetically unappealing. 
• Fluid may reflux into the patient's chest cavity. As long as this bottle remains well below the level of the patient's pleural space, no fluid will get sucked up into the chest. If the bottle is held above the level of the chest, everything inside it may regurgitate back into the pleural cavity, with non-hilarious consequences.

The double chamber system

Advantages

• Fixed underwater seal level, therefore consistent (low) resistance to air expulsion
• Pleural fluid and water seal are separate: therefore, no froth will form.
• The collection bottle permits the drainage of pleural fluid, so the case uses of this system are not limited to pneumothoraces.

Disadvantages

• It is less efficient at draining air cavities. The air of the first chamber becomes essentially an extension of the pleural air pocket, a large compressible volume of gas. Air expelled from the pleural cavity must compress this gas volume enough to overcome the underwater seal, which requires more effort than the single chamber drain. In this fashion, the two-chamber system impedes the drainage of pneumothorax and the re-expansion of the lung.
• Without suction, the drainage is less efficient: the pressure difference between the drainage chamber and the underwater seal chamber is fairly low. One can apply a sucking subatmospheric pressure to the seal chamber, thereby increasing that gradient, but this system does not innately offer any mechanism by which one might regulate that pressure.

The three-chamber system

Advantages

• Adjustable pressure of the suction: in a three-bottle system the depth of the vent tube determines the negative pressure. The pressure can be adjusted to the desired level by manipulating the depth of the manometer vent tube in the third bottle. This also protects the pleural cavity from the unmoderated effects of wall suction.
• Effective for both pneumothorax and pleural fluid: There is no loss of drainage efficiency with pleural fluid drainage, i.e. the volume of fluid collecting in the first chamber has no influence on either the suction or the underwater seal.
• No likelihood of fluid refluxing back up the tubing: there is virtually no chance that pleural drain fluid will re-enter the chest cavity with a sudden decrease in intrathoracic pressure.

Disadvantages

• Continuous bubbling: while the drain is on suction, it constantly entrains room air, and bubbles gurgle around in the third chamber. Depending on how much you like this sound, this is either a feature or a bug.
• Complexity is often quoted as a disadvantage, though one must consider that we are usually protected from this complexity by packaged pre-assembled drain systems (i.e. at no stage is one ever expected to actually assemble such a system from glass bottles and rubber stopcocks). 
• No failsafe for suction failure: if the suction line is occluded, one is left with what is essentially a blocked two-chamber system. There will be no way for the pleural pressure to overcome the resistance of the water column in the third chamber, and the air pressure in the chambers will increase to the point of re-expanding the pneumothorax. 

References

College answer

Discussion

Advantages:

• Education and communication
  • Enhances training of junior staff in anatomy
  • Skill set can be transferred to direct laryngoscopy (Low et al, 2008)
  • In reverse, direct laryngoscopy skills transfer well to videolaryngoscopy
  • Communication regarding difficulty is made easier
  • Medical information regarding intubation progress is exchanged more easily
• Intubation success
  • Videolaryngoscopy improves the likelihood of a "successful" intubation in difficult intubation scenarios (Pieters et al, 2017) and unsorted critically ill patients (De Jong et al, 2014) as well as in general ward situations  (Baek et al, 2018).
  • Relatively unskilled staff have comparatively higher rates of success
• Safety
  • Allows intubation in suboptimal position
  • Allows the airway assistant to improve your view in a more guided informed fashion
  • Less fore required for laryngoscopy, which should translate into less injury
•  Convenience and cost
  • It permits a permanent video record of the intubation
  • Cost is relatively low compared to other interventions (hello, eculizumab)

Disadvantages:

• Education and communication
  • The airway anatomy may be different to what is seen on direct laryngoscopy
  • Direct laryngoscopy skills must share training time with videolaryngoscopy skills during medical training, which degrades the former. However, direct laryngoscopy is still the dominant technique used routinely in anaesthesia
  • There are multiple devices each of which is used differently and requires different training
  • The videolaryngoscope screen can act as a distraction to the team
• Intubation success
  • The view is not guaranteed to be good: secretions, blood or mist may cover the camera
  • Even if the view is good, the passage of the tube is not guaranteed to be easy
• Safety
  • Because of the screen taking attention away from the oropharynx, the passage of airway equipment into the mouth and oropharynx is not directly observed. Dental and pharyngeal damage may result. Aziz et al (2008) reported a 1% rate of traumatic laryngoscopy, including vocal cord trauma, one tracheal injury, one trauma to the hypopharynx, one tonsillar perforation, and two dental injuries (21 cases from a series spanning 2 years).
• Convenience and cost
  • Videolaryngoscopy equipment is expensive and will not be available in resource-poor environments
  • Maintenance and disinfection is time consuming, taking the device out of commission for prolonged periods
  • The availability of a video record raises privacy concerns and exposes staff to medicolegal risk

References

Cooper, Richard M., et al. "Early clinical experience with a new videolaryngoscope (GlideScope®) in 728 patients." Canadian Journal of Anesthesia 52.2 (2005): 191-198.

Cavus, Erol, et al. "The C-MAC videolaryngoscope: first experiences with a new device for videolaryngoscopy-guided intubation." Anesthesia & Analgesia 110.2 (2010): 473-477.

AnaesthesiaUK have a nice page about McCoy blades.

Cook, T. M., and J. P. Tuckey. "A comparison between the Macintosh and the McCoy laryngoscope blades." Anaesthesia 51.10 (1996): 977-980.

Doyle, D. J. "A brief history of clinical airway management." Revista Mexicana de Anestesiologia 32 (2009): S164-S167.

McCoy, E. P., and R. K. Mirakhur. "The levering laryngoscope." Anaesthesia48.6 (1993): 516-519.

Chemsian, R. V., S. Bhananker, and R. Ramaiah. "Videolaryngoscopy." International journal of critical illness and injury science 4.1 (2014): 35.

Norris, A., and T. Heidegger. "Limitations of videolaryngoscopy." (2016) BJA: 148-150.

Baek, Moon Seong, et al. "Video laryngoscopy versus direct laryngoscopy for first-attempt tracheal intubation in the general ward." Annals of intensive care 8.1 (2018): 83.

Pieters, B. M. A., et al. "Videolaryngoscopy vs. direct laryngoscopy use by experienced anaesthetists in patients with known difficult airways: a systematic review and meta‐analysis." Anaesthesia 72.12 (2017): 1532-1541.

De Jong, Audrey, et al. "Video laryngoscopy versus direct laryngoscopy for orotracheal intubation in the intensive care unit: a systematic review and meta-analysis." Intensive care medicine 40.5 (2014): 629-639.

Low, D., D. Healy, and N. Rasburn. "The use of the BERCI DCI® Video Laryngoscope for teaching novices direct laryngoscopy and tracheal intubation." Anaesthesia 63.2 (2008): 195-201.

Aziz, Michael F., et al. "Routine Clinical Practice Effectiveness of the Glidescope in Difficult Airway ManagementAn Analysis of 2,004 Glidescope Intubations, Complications, and Failures from Two Institutions." Anesthesiology: The Journal of the American Society of Anesthesiologists 114.1 (2011): 34-41.

College answer

Potential causes

Microcirculatory disturbance secondary to DIC/Vasopressor requirement/worsening septic state.

Suggested by:
Clinical deterioration of patient: escalating vasopressor requirements, worsening acidosis etc. Likely a gradual change not clearly temporally associated with line insertion
Likely to see similar changes in the other limbs
Radial pulse present, arterial waveform present/normal.
Doppler USS, arteriography: - no abnormalities
 

Traumatic Injury to artery secondary to line insertion
Suggested by:
May be history of difficult insertion, multiple attempts. Other limbs not affected
Likely to manifest relatively quickly after line insertion. Pulse may not be present, arterial waveform abnormal
Imaging may reveal arterial dissection flap, lack of flow distal to line.

Embolic/thrombotic phenomena (including inadvertent drug administration via line)
Rapid onset
History of drug administration through arterial line
ay be other embolic phenomena
May have patchy ischaemic changes over digits
Waveform may be absent or present/normal depending on site of embolus
Imaging may demonstrate thrombus.

Examiners Comments:

Candidates listed the causes, but commonly did not outline how they would distinguish between them. The answer template focussed on history and clinical examination, whereas the candidates’ answers focussed mainly on extensive investigations which would not have been appropriate. This meant that the answers often lacked depth, and therefore did not score well.

Discussion

One can only add very little to what the college had already

The possibilities are:

• Complication of line insertion
  • Possible complications which threaten limb perfusion include:
    • Mis-sized catheter (resulting in vessel occlusion)
    • Haematoma causing compression
    • Laceration causing vasospasm
    • Intimal dissection
    • Vessel  thrombosis
  • Distinguishing features:
    • Rapid onset
    • Evidence of multiple attempts
    • Pain and swelling at the insertion site
    • Dissection or thrombosis detected on angiography or ultrasonography of the affected limb
• Complication of critical illness
  • Severe shock may give rise to poor limb perfusion
  • Distinguishing features:
    • Gradual onset
    • All limbs will be poorly perfused
    • Vasopressor requirements will be high
    • Angiography or ultrasonography of the affected limb will demonstrate normal patent vessels
• Embolic phenomena
  • ​​​​​​​Due to 
    • Air embolism from the counterpressure set
    • Accidental administration of medications
    • Thrombi (from the line insertion site or from upstream, eg. in the context of AF)
    • Cholesterol emboli (also could be from line insertion)
    • Forgotten guidewire
  • Distinguishing features:
    • Rapid onset
    • History of drug administration or guidewire mismanagement
    • Vessel obstruction detected on angiography or ultrasonography of the affected limb

References

Scheer,Perel and Pfeiffer.Complications and risk factors of peripheral arterial catheters used for haemodynamic monitoring in anaesthesia and intensive care medicine. Crit Care. 2002; 6(3): 199–204.

College answer

Not available.

Discussion

References

College answer

Not available.

Discussion

This is a well worded and highly relevant question that should form a part of the revision process for future candidates, because - though it may never be repeated again - the clinical importance of the subject matter transcends its exam importance. In other words, you need to know this stuff to be a good intensivist, and not just to pass the exam.

The detailed discussion of site selection in arterial line placement for some reason ended up in the First part Exam revision notes, even though there are no First Part Exam revision questions on this topic. Reasons for why it remains there are largely related to the indolence of the author. 

The best layout for this thing would probably be a table with this sort of structure:

References

College answer

Not available.

Discussion

This is indeed a square wave test, demonstrating an underdamped arterial waveform.  We know this, even though "(Image removed from exam report.)", because this question is identical to Question 11.2 from the first paper of 2010.  The underdamping is revealed by the multiple oscillations and the systolic overshoot.

The dynamic response testing of arterial lines is discussed in greater detail elsewhere.

In brief: the under-damped trace will overestimate the systolic, and there will be many post-flush oscillations.

References

College answer

Not available.

Discussion

They only wanted six things. However...

• Information from arterial line amplitude
  • Heart rate
  • Systolic pressure
  • Diastolic pressure (coronary filling)
  • Mean arterial pressure (systemic perfusion)
  • Pulse pressure (high in AR, low in cardiac tamponade or cardiogenic shock)
  • Changes in amplitude associated with respiration (pulse pressure variation)
• Information from arterial line frequency
  • Heart rate
  • Rhythm
  • Effect of rhythm on MAP
• Information from arterial waveform shape
  • Slope of anacrotic limb represents aortic valve and LVOT flow
  • Slurred wave in AS
  • Collapsing wave in AS
  • Rapid systolic decline in LVOTO
  • Bisferiens wave in HOCM
  • Low dicrotic notch in states with poor peripheral resistance

References

College answer

Not available.

Discussion

Determinants of central venous pressure, where you can pick any four of the following:

• Reference level of the transducer
• Intravascular volume
  • and the distribution of this volume between the venous and arterial compartment
• Central venous compliance
• Right ventricular compliance
  • myocardial or pericardial disease; tamponade
• Right ventricular systolic function
• Cardiac rhythm (i.e. AF vs. sinus rhythm)
• Tricuspid valve disease
• Pulmonary vascular resistance
• Intrathoracic pressure

Characteristic CVP waveforms are seen in the following settings (pick four, any four):

• AF: absent a waves
• Junctional rhythm, VT, complete heart block: cannon fused ac waves
• Tricuspid regurgitation: fused cv waves
• Triciuspid stenosis: prominent a wave
• Pericardial constriction or poor RV compliance: bifid CVP wave
• Cardiac tamponade: prolonged y descent

Passive leg raise autotransfusion:

• Process:

  1) Drop the patient's torso to supine position

  2) Raise both legs to 45° using the mechanical bed

  3) Keep them up for 60-90 seconds
  4) Measure the change in stroke volume 

• Interpretation:
  A 10% increase in the measured stroke volume is interpreted as a positive result.
  Other acceptable surrogates would be an increase in cardiac output, an decrease in pulse pressure variation, or (less reliably) an increase in blood pressure
• Physiological basis:
  The autotransfusion of ~ 500ml of venous blood from the legs acts as a reversible fluid bolus. Ergo, if the patient's cardiac output increases as the result of this manoeuvre, it will also increase following a fluid bolus.
• Reliability:
  Sensitivity of 97% and a specificity of 94%, in predicting fluid responsiveness 
  Reliable irrespective of the mode of ventilation
  Stroke volume and cardiac output measurements are the most reliable, whereas pulse pressure variation is less reliable (Cherpanath et al, 2016)
• Limitations:
  You need a patient with both legs intact
  You rely on an intact pelvis, so this excludes a lot of messy trauma patients (in whom it would be very useful)
  It can't be done if you have a balloon pump in situ, or post angiography (because you need to lie flat) - and thus a lot of low-cardiac-output cardiogenic shock patients are excluded, which is a pity
  It can't be done if you are even slightly concerned about your intracranial pressure.

References