Cardiology & Cardiac Surgery – Full Test
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Question 1 of 66
1. Question
Hint
PVR = MPAP-PCWP/CI (Woods). SI = Woods x 80, pHTN = mPAP >20mm Hg + PCWP >15mm Hg, LVSWI = SVI*MAP-PCWP*0.0136, right ventricular dysfunction, over-distended underperforming RV creating low cardiac output syndrome, inotropy/inodilators, iNO, diuresis/ultrafiltration, MCS
Resource: Hoeper et al. Eur Respir J 2019 (pulm HTN definition); Mebazaa et al. ICM 2018
Royal College Competency: 1.3.2.2, 1.3.12.2, 2.4.3.1, 2.4.14.3 -
Question 2 of 66
2. Question
Hint
Damped waveform
MAP accurate, measured systolic lower, measured diastolic higher
Catheter kinking, blood clot or air bubbles in the tubing, lack of pressurization of the transducer (the pressure bag not pressurized or empty) or leak in the system would all cause thisResource: Lakhal et al. ICM 2011 (arterial line accuracy); Tobin MV
Royal College Competency: 1.3.12.2, 3.4.1.1 -
Question 3 of 66
3. Question
Hint
Aortic valve endocarditis with abscess
Investigations: Echo, Blood cultures
Definitive Management: Cardiac surgery with AVR and excision aortic root abscess =/- root replacement.Resource: Baddour et al. Circulation 2015 (AHA IE Guidelines)
Royal College Competency: 2.4.3.1, 2.4.11.1 -
Question 4 of 66
4. Question
Hint
Rapid atrial fibrillation increases transvalvular pressure gradient across mitral valve increasing left atrial pressure and pulmonary capillary pressure resulting in pulmonary edema
MS most significant
Most important management rhythm control (cardioversion, amio/betablocker)
Benefits decreased transmural pressure gradient, recruitment.Resource: Vahanian et al. ESC Valvular Guidelines 2021; Nohria et al. JACC 2008
Royal College Competency: 1.3.2.2, 2.4.3.1 -
Question 5 of 66
5. Question
Hint
Automated cuff technique: oscillometry – variations in BP cuff due to arterial pulse sensed by monitor. MAP = pressure with maximal oscillations. SBP/DBP derived
Most accurate component: MAPResource: Pickering et al. Hypertension 2005 (BP measurement guidelines)
Royal College Competency: 1.3.12.2, 3.4.1.1 -
Question 6 of 66
6. Question
Hint
Assisted end-diastolic pressure not below unassisted.
Timing: Late deflation
Physiologic effect: Increased afterload increased myocardial O₂ consumption.Resource: Bolooki Clinical Application of IABP
Royal College Competency: 1.3.11.4, 1.3.12.2, 3.4.1.1 -
Question 7 of 66
7. Question
Hint
Curve A higher CO
Justification: cardiac output is inversely proportional to the area under the curveResource: Swan et al. NEJM 1970; Pulmonary artery catheter physiology
Royal College Competency: 1.3.12.2, 3.4.1.1 -
Question 8 of 66
8. Question
Hint
Abnormality: Pulsus paradoxus – exaggerated inspiratory decline (>10mm Hg) in blood pressure.
Physiology: Increased RV venous return with inspiration, leads to RV volume increase, leads to septal displacement, reducing LVOT and thus stroke volume. With external LV compression or exaggerated ventricular interdependence, pulsus paradoxus develops
Conditions: tamponade, severe asthma, COPD (profound intrathoracic pressure changes), pulmonary embolism, high PEEP, hypovolemiaResource: Shabetai Lancet 2004 (tamponade); Khasnis & Lokhandwala Postgrad Med 2002
Royal College Competency: 1.3.2.2, 1.3.12.2, 3.4.1.1 -
Question 9 of 66
9. Question
Hint
Plane: Parasternal Long Axis
Anatomical Structures: 1 proximal aorta 2 left atrium 3 interventricular septum 4 pericardium/left lung 5 lv cavityResource: Labovitz et al. JACC 2010; WINFOCUS POCUS Guidelines
Royal College Competency: 2.2.2, 3.4.2 -
Question 10 of 66
10. Question
Hint
Goals: High preload, high afterload, tachycardia (avoid bradycardia), normal contractility
Beck’s Triad: High JVP, hypotension, muffled heart soundsResource: Spodick Circulation 2003 (tamponade); Maisch et al. ESC Pericardial Guidelines 2015
Royal College Competency: 2.4.3.1, 3.4.2 -
Question 11 of 66
11. Question
Hint
Answer: Biventricular pacemaker with atrial pacing and internal defibrillator; cardiac resynchronization therapy. Indication: HFrEF, LBBB, QRS >150 ms, LVEF <35%.
Resource: Cleland et al. NEJM 2005 (CARE-HF); AHA/ACC CRT Guidelines 2012
Royal College Competency: 2.4.3.1, 3.4.1 -
Question 12 of 66
12. Question
Hint
Torsades de pointe
Prolonged Qtc
Magnesium infusion, overdrive pacing
Lidocaine infusion
AmiodaroneResource: Al-Khatib et al. JACC 2018 (AHA/ACC VT/VF Guidelines)
Royal College Competency: 1.3.9, 2.4.3.1 -
Question 13 of 66
13. Question
Hint
Failure to sense
Increase sensitivity (or decrease sensing threshold)Resource: Zipes et al. ACC/AHA Pacemaker Guidelines 2008; Epstein et al. Circulation 2008
Royal College Competency: 2.4.3.1, 3.4.1, 3.4.6.8 -
Question 14 of 66
14. Question
Hint
Etiology: Rheumatic
Anticipated tolerance: Poor tolerance, expect dyspnea, pulmonary edema
Justification: Fixed stenosis across valve results in decreased LV filling time with tachycardia, trans-mitral pressure gradient increaseResource: Vahanian et al. ESC Valvular Guidelines 2021
Royal College Competency: 1.3.2.2, 2.4.3.1 -
Question 15 of 66
15. Question
Hint
Mechanisms: Adenosine (other beta blocker, CCB, vagal)
Physiology: AV nodal blocker
Contraindication: contraindicated in severe asthma
Impact on rhythms: flutter will slow, show flutter waves and likely speed back up. sinus tachycardia will slow to reveal sinus rhythm and pick up back, more likely variably. SVT should abortResource: Al-Khatib et al. JACC 2018; Brugada et al. Circulation 1991
Royal College Competency: 1.3.9, 2.4.3.1 -
Question 16 of 66
16. Question
Hint
1st capnogram – gradual increased expired co2 on exhalation consistent with airflow obstruction
Physiologic explanation for ETCO2 change with cardiac arrest – Cardiac output decreases with CPR, thus pulmonary blood flow decreases, thus alveolar dead space increases, thus decreased expired (end-tidal) CO2
ROSC likely at 3 or 4 minutes
Bicarbonate expected to cause rapid transient increase in ETCO2
Theories for flow: thoracic pump (increased intrathoracic pressure with cardiac compression, forward flow, back flow prevented by cardiac and venous valves), cardiac compression theory )CPR compressing heart between sternum and spine, basically moving blood out of heart with each compressionResource: Neumar et al. Circulation 2010 (AHA CPR Guidelines); Meaney et al. Circulation 2013
Royal College Competency: 1.3.12.1, 3.4.1, 3.4.6.1 -
Question 17 of 66
17. Question
Hint
ACEi/ARB, beta-blocker, MRA, ARNI, ivabradine
Competencies: 1.3.9, 2.4.3.1
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Question 18 of 66
18. Question
Hint
PDE5 inhibitors increase cGMP intracellularly by inhibition of guanylyl cyclase. Nitrates increase cGMP via nitric oxide pathway.
The combination synergistically causes hypotension.Resource: McMurray et al. ESC Heart Failure Guidelines 2021; PARADIGM-HF NEJM 2014
Royal College Competency: 1.3.9, 2.4.3.1 -
Question 19 of 66
19. Question
Hint
Inferior STEMI, TPA: 15mg IV bolus + 50mg IV over 30 mins, then 35mg IV over 60 mins, Alteplase: 100mg IV over 2 hours, Tenecteplase/TNK: 0.53mg/kg, maintain preload, improve perfusion, minimize afterload, improve contractility, maintain sinus rhythm, complete or third-degree heart block. AV sequential pacing preferable to maintain synchrony.
Resource: O’Gara et al. JACC 2013 (ACC/AHA STEMI Guidelines); Zipes et al. Pacemaker Guidelines
Royal College Competency: 1.3.9, 2.4.3.1, 3.4.6 -
Question 20 of 66
20. Question
Hint
Septal rupture with VSD, step up oxygenation indicative of right to left shunt. Free wall rupture, papillary muscle rupture with acute MR, pseudoaneurysm
Resource: Steg et al. ESC STEMI Guidelines 2012; ACC/AHA STEMI Guidelines 2013
Royal College Competency: 1.3.2.2, 2.4.3.1 -
Question 21 of 66
21. Question
Hint
Neurological deficit, pulse/BP differential.
LR 33 means patients with finding are 33 times more likely to have AoD than patients without finding.
Investigation: CT-angiogram
Management: declare emergency/call for help, ABC IV O2 Monitor. Arterial line, central line, foley, SpO2, labetalol.
Agents: labetalol (bradycardia), nitroprusside (cyanide toxicity/VQ issue), nitroglycerine (rv dysfunction, headache). Emergency surgery consult.
Complications include: AI, tamponade, chf, ami, stroke, spinal ischemia, left plef, renal failure, intestinal ischemia, limb ischemia, rupture, pseudoaneurysm.Resource: Erbel et al. ESC Aortic Guidelines 2014; Hiratzka et al. ACC/AHA 2010
Royal College Competency: 1.3.9, 2.2.2, 2.4.3.1 -
Question 22 of 66
22. Question
Hint
140/60. 120/60. Bedside monitor does not interpret waveforms, it just calls the highest number systolic and lower number diastolic. Bedside monitor will interpret 140 as systolic when 140 is in fact this represents the augmented diastolic. IABP console recognizes difference. MAP is same on both monitors.
Resource: Bolooki IABP textbook
Royal College Competency: 1.3.11.4, 1.3.12.2, 3.4.1.1 -
Question 23 of 66
23. Question
Hint
RLL atelectasis/opacity, PAC good position middle 1/3 of left chest, ETT deep, RUQ drain
PA rupture
Female, atc, elderly, PAH, hypothermia, frequent PAC manipulation, mitral valve disease.
Pharmacologiy Strategy – phenyl/vaso and esmolol to increase BP by afterload rather than inotropy, decrease inotropy with elevated gradient, maybe fluidResource: Binanay et al. JAMA 2005 (ESCAPE); Swan-Ganz catheter complications literature
Royal College Competency: 1.3.12.2, 2.4.3.1, 3.4.1.1 -
Question 24 of 66
24. Question
Hint
Answers: Sinus bradycardia. Atropine blocks muscarinic parasympathetic receptors. Transplanted heart: denervated, higher resting HR (no vagal tone), exercise-induced HR increase via catecholamines not direct sympathetics. Atropine: no HR effect (no vagal innervation to block), anticholinergic systemic AEs. Alternatives: isoproterenol, pacing, epinephrine
Resource: Zipes et al. ACC Pacemaker Guidelines; Cardiac transplant pharmacology literature
Royal College Competency: 1.3.9, 2.4.14.3, 3.4.6 -
Question 25 of 66
25. Question
Hint
Ventricular escape rhythm. Wide QRS at slow rate with no obvious p waves. Regular pacing spikes seen in strip but no relationship to underlying rhythm. No sign of pacemaker sensing or capture. Interventions could include increasing pacemaker output until capture is obtained, switching leads or inserting new ground wire.
Resource: Epstein et al. ACC/AHA Pacemaker Guidelines 2008
Royal College Competency: 2.4.3.1, 3.4.6.7, 3.4.6.8 -
Question 26 of 66
26. Question
Hint
aortic blood pressure, ECG, ventricular pace, atrial pace, fixed rate (or asynchronous)
Resource: Bolooki IABP textbook; Royal College Competency: 1.3.11.4, 3.4.1.1
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Question 27 of 66
27. Question
Hint
Early inflation before the aortic valve has closed as indicated by the dicrotic notch. Will produce an increase in left ventricular afterload as the heart is trying to eject into the aorta with the balloon inflated. Increased LV afterload may decrease stroke volume and cardiac output in a failing ventricle; in addition increased LV afterload will increase myocardial oxygen consumption. Ruptured balloon, clamp, turn off machine/gas, remove, abcivo2monitor prep call for help, prep for hemodynamic collapse
Resource: Bolooki IABP textbook
Royal College Competency: 1.3.11.4, 3.4.1.1 -
Question 28 of 66
28. Question
Hint
Late deflation, increased afterload, increased myocardial oxygen consumption. Timing: pressure
Resource: Bolooki IABP textbook; Neumar et al. AHA CPR 2010
Royal College Competency: 1.3.11.4, 3.4.6.1 -
Question 29 of 66
29. Question
Hint
Dilutional thrombocytopenia from crystalloid, prolonged cpb time, aspirin anti-platelet effect, residual heparin effect. TEG shows residual heparin and platelet dysfunction or paucity. Protamine reaction, tamponade
Resource: Shore-Lesserson et al. Society of Cardiovascular Anesthesiologists TEG Guidelines;
Royal College Competency: 2.4.3.1, 2.4.7.1, 2.4.7.2, 3.4.1 -
Question 30 of 66
30. Question
Hint
Roles forETCO2 in arrest: Confirmation endotracheal tube placement, Good quality >20, ROSC sudden increase to near 40, <10 at 20m means futility
Phases: Baseline (0mm Hg)), expiratory upstroke (instrumental/anatomic deadspace), alveolar plateau (alveolar deadspace), inspiratory downstroke. Note PaCO2 – PetCO2 reflects dead space
Resource: Meaney et al. Circulation 2013; Bhavani-Shankar et al. Can J Anaesth 1992 (capnography phases)
Royal College Competency: 1.3.2.1, 1.3.12.1, 3.4.1, 3.4.6.1 -
Question 31 of 66
31. Question
Hint
mid-axillary line, 4th interspace, level of right atrium. If transducer is too high, measured pressure will be LOWER than true pressure by 14cm H2O which is 10mm Hg (14cm H2O/1.36mm Hg/cm H2O). CVP will now read 24mm Hg.
Resource: Monnet & Teboul ICM 2013 (CVP monitoring); Tobin MV
Royal College Competency: 1.3.12.2, 3.4.1.1 -
Question 32 of 66
32. Question
Hint
SVR = MAP-CVP/CO x 80, PVR = MPAP-PAWP/CO x 80, LVSWI =MAP-PAWP x SVI x 0.0136…svi = sv/bsa…sv = co/hr
Resource: Pulmonary artery catheter physiology references
Royal College Competency: 1.3.2.2, 1.3.12.2 -
Question 33 of 66
33. Question
Hint
Arterial oxygen = Hg x 1.3 x Sat + 0.003 x PaO2 =117, Alveolar pO2, PAO2 = (Patm – PH2O), FiO2 – PaCO2/RQ, 42-12.5= 30, Aa difference 30-25=5
Resource: Grocott et al. NEJM 2009 (Mount Everest expedition)
Royal College Competency: 1.3.2.1, 1.3.2.4 -
Question 34 of 66
34. Question
Hint
RV:LV ratio >0.6, loss of crescent shape (short axis) or triangle shape (4-chamber), paradoxical septal motion, decreased TAPSE <16 mm, RV wall thickness >1 cm (chronic).
Resource: Vieillard-Baron et al. ICM 2012; Rudski et al. JASE 2010 (RV assessment)
Royal College Competency: 1.3.12.2, 3.4.2 -
Question 35 of 66
35. Question
Hint
A, surgical mitral valve replacement, IABP to reduce LV afterload and lessen MR.
Resource: Thiele et al. NEJM 2012 (IABP-SHOCK II); Baran et al. JACC Heart Fail 2019 (SCAI cardiogenic shock classification); Ibanez et al. ESC STEMI Guidelines 2017; Lip et al. Chest 2011 (LV thrombus management)
Royal College Competency: 1.3.11.4, 2.4.3.1, 2.4.3.2 -
Question 36 of 66
36. Question
Hint
Etiology: Hypovolemic shock
Mgmt: IV fluid, pericardiocentesis
DDx pulsus: Hypovolemia, COPD, PE, high PEEP, asthmaResource: Connolly et al. Stroke 2012 (NCS SAH Guidelines); Maisch et al. ESC Pericardial Guidelines 2015; Spodick Circulation 2003 (tamponade physiology)
Royal College Competency: 2.4.1, 2.4.4.2, 3.4.2 -
Question 37 of 66
37. Question
Hint
Answers: PVR = 80x (PAm-PAOP/CO) = 44-38/5=96dyn/s/cm5. SVR 699 most supportive of distributive A – LOW afterload, B – HIGH contractility C – LOW preload. VO2 = 13.4xCOx(SaO2-SvO2)xHb = 13.4×5.8x(0.94-0.31)x11 = 538. DO2 = COxCaCO2 = CO x (1.34xHbxSaO2)+(PaO2x0.003) = 5.8 x (1.34x110x0.94)+(0.003×79) = 5..8×139.237 = 807mLO2/m. PPV increases CVP and PA pressures, may increase or decrease PVR depending on atelectasis, may decrease PAOP, increase CO
Resource: Nishimura et al. ACC/AHA Valvular Guidelines 2014 (MR management); Pinsky ICM 2003 (PAC and PPV interactions); Fick principle — West Respiratory Physiology;
Royal College Competency: 1.3.2.2, 1.3.12.2, 2.4.3.1, 3.4.1.1 -
Question 38 of 66
38. Question
Hint
Answers: A stroke volume (or cardiac output). B= preload (end-diastolic volume or filling pressure/LVEDP). C – Failing ventricle: flattened curve shifted downward and rightward — lower stroke volume achieved at any given preload, D – Normal ventricle: steep upsloping curve reaching high stroke volume plateau at moderate preload.
Resource: Katz Physiology of the Heart 5th ed.; Pinsky ICM 2016 (heart-lung interactions and Frank-Starling); West Cardiovascular Physiology 9th ed.
Royal College Competency: 1.3.2.2, 2.4.3.1 -
Question 39 of 66
39. Question
Hint
Class – Milrinone phosphodiesterase 3 inhibitor, Dobutamine synthetic catecholamine
MOA – Milrinone – inhibit cAMP metabolism, increase intracellular CA, Dobutamine – beta-agonist
Hemodynamics – Milrinone – Increase Dobutamine – Increase
Half-Life – Milrinone 4h, Dobutamine 2m
Metabolism – renally excreted unchanged, Dobutamine – metabolized to inactive by COMT, renally excretedResource: SCCM Cardiogenic Shock Guidelines; MacIver & Bhagra Cardiology textbook
Royal College Competency: 1.3.9, 2.4.3.1 -
Question 40 of 66
40. Question
Hint
A – unassisted systole B – unassisted aortic end-diastolic pressure C – assisted aortic end-diastolic pressure D – dicrotic notch E – diastolic augmentation F – assisted systole
Resource: Bolooki Clinical Application of IABP; Thiele et al. NEJM 2012 (IABP-SHOCK II)
Royal College Competency: 1.3.11.4, 1.3.12.2, 3.4.1.1 -
Question 41 of 66
41. Question
Hint
MOA: Vasopressin – V1 endothelial receptors cause vasoconstriction, V2 renal receptors impact renal salt retention. Norepinephrine alpha adrenergic induced vasoconstriction and beta adrenergic activation
Half Life: VP 20min NE 2min
Endogenous location: VP Hypothalamus, released by posterior pituitary NE adrenal gland, sympathetic nerve terminalsResource: VASST Trial (Russell et al. NEJM 2008); SCCM Sepsis Surviving Campaign 2021
Royal College Competency: 1.3.9, 2.4.1, 2.4.11.1 -
Question 42 of 66
42. Question
Hint
Answers: Pump thrombosis, re-operation (0.5 for heparin/tpa), no need for CPR if MAP good, hypovolemia low power low pi, ventricular recovery high power high pi. Cellular rejection – tacrolimus. AMR – steroids
Resource: Stulak et al. JACC 2014; LVAD management guidelines (ISHLT 2013)
Royal College Competency: : 1.3.9, 1.3.11.4, 2.4.3.2, 2.4.14.3, 3.4.1 -
Question 43 of 66
43. Question
Hint
Answers: Transition from negative to positive pressure ventilation with high mean airway pressure unmasked preload dependence (PPV 58%).
T1-2 contributor: Ventilator adjustment contributed more with 37% reduction, compared to 16% reduction in PPV from only 500mL
Pulsus paradoxus = exaggerated negative intrathoracic pressure swings during spontaneous inspiration causing biventricular interdependence, decreased stroke volume, PPV = positive pressure mechanical breaths increasing RV afterload and decreasing venous return suggesting preload responsiveness.
Clinical situations: spontaneous effort, non-sinus rhythm, low VT, open chest, RV failure, intra-abdominal hypertension, severe tachypnea
Resource: European Respiratory Journal: Pulsus Paradoxus, 2013; Intensive Care Medicine: PPV and fluid responsiveness
Royal College Competency: 1.3.2.1, 1.3.2.2, 1.3.12.2, 2.4.1 -
Question 44 of 66
44. Question
Hint
a) Diagnosis:
– Ventricular septal defect (VSD)
– Post-MI VSD / mechanical complication of MIb) PVR calculation and interpretation:
– PVR = (PA mean – PCWP) / CO × 80
– PVR = (40 – 38) / 1.8 × 80
– PVR = 2 / 1.8 × 80
– PVR = 89 dynes·sec·cm⁻⁵
– This is LOW (normal 150-250 dynes·sec·cm⁻⁵)c) Physiologic explanation (three points):
– Left ventricular dysfunction from ischemia/infarction causing decreased forward flow
– Left-to-right shunt through VSD increases PA saturations (step-up from RA 60% to PA 72%)
– Elevated PCWP (38 mmHg) from increased pulmonary venous return due to left-to-right shunt and LV dysfunction
– Low cardiac output (1.8 L/min) from cardiogenic shock and shunt “stealing” flow from systemic circulationd) Explanation for low RA saturation:
– Cardiogenic shock with low CO causing decreased systemic oxygen delivery
– Increased tissue oxygen extraction due to inadequate perfusion
– LV dysfunction contributing to poor forward flow
– Note: PA saturation artificially elevated by oxygenated blood from left-to-right shuntCompetency: 1.3.2.2, 1.3.12.2, 2.2.1, 2.4.3.1
Resource: — Crenshaw BS et al. Risk factors, angiographic patterns, and outcomes in patients with ventricular septal defect complicating acute myocardial infarction. Circulation 2000; 101:27-32 -
Question 45 of 66
45. Question
Hint
a) Parameters measured by PAC:
– Central venous pressure (CVP)
– Right atrial pressure (RAP)
– Right ventricular pressure (RVP)
– Pulmonary artery pressure (PAP)
– Pulmonary capillary wedge pressure (PCWP/PAOP)
– Cardiac output (CO)
– Mixed venous oxygen saturation (SvO2)b) Common clinical settings:
– Mixed/undifferentiated shock states
– Severe pulmonary hypertension
– Acute decompensated heart failure
– Cardiogenic shock
– SCAI stage D/E shock (consideration for mechanical circulatory support)
– High-grade cardiogenic shock requiring hemodynamic optimization
– Refractory shock of unclear etiologyc) Insertion distances:
– RA (right atrium): 15-20 cm from right internal jugular vein
– RV (right ventricle): 30-35 cm
– PA (pulmonary artery): 40-50 cm
– PA wedge: 45-55 cmd) MAP formula:
– MAP = DBP + 1/3(PP) where PP = pulse pressure = SBP – DBP
– OR MAP = DBP + 1/3(SBP – DBP)
– OR MAP = (SBP + 2×DBP) / 3e) SVR calculation:
– SVR = (MAP – CVP) / CO × 80
– SVR = (60 – 14) / 1.8 × 80
– SVR = 46 / 1.8 × 80
– SVR = 25.56 × 80
– SVR = 2044 dynes·sec·cm⁻⁵f) SVR interpretation:
– High (normal range 800-1200 dynes·sec·cm⁻⁵)g) Causes of low SVR:
– Sepsis / septic shock / distributive shock
– Anaphylaxis / anaphylactic shock
– Vasodilating antihypertensives (nitroprusside, hydralazine, calcium channel blockers)
– Neurogenic shock
– Severe liver disease / cirrhosis
– Thyrotoxicosish) Causes of high SVR:
– Hypovolemia / hypovolemic shock
– Cardiogenic shock
– Obstructive shock (massive PE, tamponade, tension pneumothorax)
– Vasopressor use (norepinephrine, vasopressin, phenylephrine)
– Hypothermia
– Pain or agitationCompetency: 1.3.12.2, 2.2.1, 3.4.1.1, 3.4.6.3
Resource: — Binanay C et al. Evaluation study of congestive heart failure and pulmonary artery catheterization effectiveness (ESCAPE). JAMA 2005; 294:1625-1633 -
Question 46 of 66
46. Question
Hint
a) Partial anomalous pulmonary venous return.
b) 1) Ultrasound confirmation of venous insertion site. 2) Pressure transduction confirming venous waveform. 3) Blood gas from CVL compared to simultaneous arterial sample showing paradoxically elevated PaO2. 4) Fluoroscopy to confirm catheter location in anomalous pulmonary vein.
c) Remove catheter and obtain alternative access; reposition catheter under fluoroscopic guidance.
Competency: 1.3.1; 1.3.12.2; 2.2.1; 2.2.2; 3.4.2.6; 3.4.6.3
Resource: Alzghoul B et al. Case Reports in Critical Care 2017; Article ID 3218063. doi:10.1155/2017/3218063 -
Question 47 of 66
47. Question
Hint
a) Initial CO2 from gastric gas (esophageal intubation); endotracheal tube migration out of the trachea after initial correct placement, cardiac arrest (reduced pulmonary perfusion)
Resource: Silvestri S et al. Ann Emerg Med 2005;45(5):497-503Competency: 3.4.4.2; 3.4.4.3; 2.2.1; 3.4.6.1
Resource: Silvestri S et al. Ann Emerg Med 2005;45(5):497-503 -
Question 48 of 66
48. Question
Hint
a) Poor quality CPR with inadequate cardiac output; massive pulmonary embolism causing dead space ventilation; dynamic hyperinflation reducing pulmonary blood flow. (1 mark each)
Competency: 3.4.6.1; 3.4.6.5; 2.2.1; 1.3.12.1
Resource: Kodali BS, Urman RD. J Emerg Trauma Shock 2014;7(1):37-40 -
Question 49 of 66
49. Question
Hint
a) Ventricular tachycardia.
b) Repeated ICD shocks are physically and psychologically traumatic, driving hyperadrenergic activation which is itself the substrate perpetuating VT — creating a self-exacerbating adrenergic cycle.
c) Medical: deep sedation (propofol or benzodiazepine); interventional: stellate ganglion block (alternate: radiotherapy)
d) Bridge to decision.
Competency: 2.4.3.1; 2.2.1; 2.4.3.2
Resource: Yartsev A. Management of super-refractory ventricular tachycardia. Chapter 352. Deranged Physiology 2025. -
Question 50 of 66
50. Question
Hint
a) No previous history of angina or MI; anterior location of infarct; age greater than 70 years. Additional accepted: female sex; ST elevation or Q waves on initial ECG; peak MB-CK greater than 150.
Competency: 2.4.3.1; 1.3.2.2
Resource: Hutchins KD et al. Am J Forensic Med Pathol 2002;23(1):78-82 -
Question 51 of 66
51. Question
Hint
a) Dynamic hyperinflation/autoPEEP: disconnect from ventilator to allow passive decompression. Tension pneumothorax: immediate needle decompression followed by chest tube insertion. Hypoxia from right mainstem intubation with lobar collapse: increase FiO2 and withdraw ETT to correct position. Additional accepted: severe hypercarbia and acidosis: increase minute ventilation.
Competency: 1.3.11.1; 2.4.2.1; 2.1.1
Resource: Leatherman J. Chest 2015;147(6):1671-1680 -
Question 52 of 66
52. Question
Hint
a) Unrecognized Tetralogy of Fallot.
b) Right-to-left intracardiac shunting through the non-restrictive VSD due to sepsis-induced reduction in systemic vascular resistance reversing the shunt direction.
c) Mechanisms: positive pressure ventilation increases RV afterload by raising pulmonary vascular resistance; reduced RV preload from decreased venous return. Non-invasive adjunct: inhaled nitric oxide. Alternate: high-flow nasal cannula oxygen.
d) MAP target 75 mmHg; a higher than standard MAP is required to increase systemic vascular resistance above pulmonary vascular resistance.
e) Dobutamine causes beta-2-mediated peripheral vasodilation, reducing SVR and worsening right-to-left shunting across the VSD.
Competency: 1.3.2.1; 1.3.2.2; 1.3.9.5; 1.3.11.1; 1.3.11.2; 2.4.1; 2.4.3.1; 2.4.11.1
Resource: Bernstein D. Cyanotic Congenital Heart Disease. Nelson Textbook of Pediatrics 2020; UpToDate: Pathophysiology of Tetralogy of Fallot. Updated 2024 -
Question 53 of 66
53. Question
Hint
a) 1 mark: methylene blue inhibits nitric oxide synthase and guanylate cyclase, reducing nitric oxide-mediated vasodilation;
1 mark: methylene blue monoamine oxidase inhibitor — risk of serotonin syndromeb) 1 mark: fentanyl inhibits serotonin reuptake.
1 mark for any two Hunter criteria already met: inducible clonus; lead-pipe rigidity with agitation or altered tone; spontaneous clonus; hyperreflexia with clonus.c) 1 mark for: analgesic alternatives: ketamine or acetaminophen IV.
d) 1 mark: target net negative fluid balance of 100 to 200 mL/hr initially. Titrate to avoid haemodynamic compromise;
Explanation: Repaired tricuspid valve and RV dysfunction mandate avoidance of aggressive fluid removal that reduces RV preload — RV is preload dependent post-repair and excessive ultrafiltration will reduce cardiac output;
Competency: 1.3.9.4; 1.3.9.5; 1.3.9.6; 1.3.2.2; 1.3.11.5; 2.4.1; 2.4.3.1; 2.4.5.1
Resource: Boyer EW, Shannon M. NEJM 2005;352(11):1112-1120 (serotonin syndrome); Mehaffey JH et al. Ann Thorac Surg 2017;103(2):510-515 (methylene blue vasoplegia); Ronco C et al. Lancet 2000;356(9223):26-30 (CRRT) -
Question 54 of 66
54. Question
Hint
a) Therapeutic hypothermia; propofol infusion syndrome. Additional accepted: raised intracranial pressure (Cushing reflex).
b) Discontinue propofol and initiate an alternative sedative agent; obtain urgent CT head and consult neurosurgery to exclude worsening intracranial pathology. Additional accepted: insert temporary transvenous pacemaker if hemodynamically compromised.
Competency: 1.3.12.3; 2.4.4.2; 1.3.9.1; 1.3.9.4
Resource: Kam PCA, Cardone D. Anaesthesia 2007;62(7):690-701 -
Question 55 of 66
55. Question
Hint
a) 2 marks: cardiac tamponade from clot accumulation causing chest tube occlusion (1 mark);
b) 2 marks — 1 mark each: post-surgical tamponade is commonly caused by loculated clot that is not amenable to needle drainage; risk of puncturing grafts, epicardial pacing wires, or cardiac structures in the post-surgical field.
c) 3 marks — 1 mark each for any 3: IV fluid bolus to augment preload and maintain stroke volume; avoid increasing PEEP or initiating positive pressure maneuvers that reduce venous return; consider reducing or stopping epinephrine temporarily if tachycardia-mediated; increase heart rate if bradycardic (tamponade physiology is rate-dependent for CO); urgent surgical re-exploration is definitiveCompetency: 1.3.2.2; 1.3.12.2; 2.4.1; 2.4.3.1; 3.4.5.2
Resource: Kuvin JT et al. Ann Thorac Surg 2002;74:1148–1153; Imazio M et al. Post-cardiac injury syndromes. Heart 2011;97:1463–1472 -
Question 56 of 66
56. Question
Hint
a) Augmented diastolic coronary perfusion pressure; reduction in LV afterload during systole.
b) Aortic dissection; limb or organ ischemia (renal, spinal cord, limb); balloon rupture; major hemorrhage; cerebral ischemia. Additional accepted: cholesterol emboli; worsened cardiac function from abnormal timing.
c) Significant aortic regurgitation (greater than mild); clinically significant abdominal aortic aneurysm or aortic dissection; uncontrolled sepsis. Additional accepted: uncontrolled bleeding disorder; severe peripheral artery disease not amenable to pretreating with stenting.
Competency: 1.3.11.4; 2.4.3.1; 2.4.3.2
Resource: Krishna M, Zacharowski K. Br J Anaesth 2009;102(2):151-158 -
Question 57 of 66
57. Question
Hint
a) 2 marks — 1 mark each: prolonged cardiopulmonary bypass causing consumption coagulopathy and platelet dysfunction; hypothermia (35.6°C) impairing enzymatic coagulation cascade and platelet function. Alternate acceptable: hypofibrinogenemia; thrombocytopenia from CPB-related platelet consumption and destruction.
b) 2 marks: cryoprecipitate or fibrinogen concentrate (1 mark);
c) 3 marks — 1 mark each for any 3: active rewarming to correct hypothermia (target ≥36.5°C); tranexamic acid if not already given peri-operatively; correct ionized hypocalcemia, surgical re-exploration to identify and control mechanical bleeding source; avoid further crystalloid dilutionCompetency: 1.3.2.2; 1.3.12.2; 2.4.1; 2.4.7.2; 3.1.1
Resource: Ranucci M et al. Patient blood management during cardiac surgery. J Cardiothorac Vasc Anesth 2018;32:2575–2591; ESA/EACTS Guidelines on patient blood management for adult cardiac surgery 2017 -
Question 58 of 66
58. Question
Hint
a) 3 marks: vasoplegia syndrome (1 mark); supported by: SVR critically low at 380 dynes·sec·cm⁻⁵ (1 mark); hypotension despite high ECMO flow and low filling pressures with warm vasodilated physiology (1 mark).
b) 2 marks — 1 mark per agent: vasopressin, norepinephrine. Alternate second agent: methylene blue, hydroxocobalamin
c) 1 mark: Peripheral VA-ECMO increases LV afterload risking LV distension and pulmonary edema in failing LVCompetency: 1.3.2.2; 1.3.9.5; 1.3.11.4; 1.3.12.2; 2.4.1; 2.4.3.2
Resource: Combes A et al. Extracorporeal membrane oxygenation for severe acute respiratory failure in adults. JAMA 2018;299:546–547; Jentzer JC et al. Cardiogenic shock classification. J Am Coll Cardiol 2019;74:2117–2128 -
Question 59 of 66
59. Question
Hint
Preload High Afterload High Heart Rate Low Contractilty Not increased (normal or low)
Resource: Bhonsale & Khandheria Circulation 2014 (HOCM management); Nallamshetty et al.
Royal College Competency: 1.3.2.2, 2.4.1, 3.4.2 -
Question 60 of 66
60. Question
Hint
a) 2 marks — 1 mark each: cardiac tamponade; acute RV failure (right ventricular dysfunction).
b) 2 marks — 1 mark each: urgent surgical re-exploration; volume resuscitation to maintain preload. Alternate for second mark: avoid positive pressure increases / minimize PEEP; urgent call to cardiac surgery.Competency: 1.3.2.2; 1.3.12.2; 2.4.1; 2.4.3.1
Resource: Kuvin JT, Harati NA, Pandian NG et al. Postoperative cardiac tamponade in the modern surgical era. Ann Thorac Surg 2002;74:1148–1153 -
Question 61 of 66
61. Question
Hint
a) 1 mark: abdominal compartment syndrome (1 mark);
b) 1 mark: external compression / transmitted intra-abdominal pressure.
c) 1 mark: NO – transmitted abdominal pressure, not lung compliance.
d) 2 marks — 1 mark each: direct renal venous compression; reduced renal perfusion pressure from elevated IAP.Competency: 1.3.2.2; 1.3.12.2; 2.4.1; 2.4.6.5; 2.2.1
Resource: Kirkpatrick AW et al. Intra-abdominal hypertension and abdominal compartment syndrome: updated consensus definitions. Intensive Care Med 2013;39:1190–1206; Cheatham ML. Abdominal compartment syndrome. Curr Opin Crit Care 2009;15:154–162 -
Question 62 of 66
62. Question
Hint
a) 1 mark: fluid responsive.
b) 1 mark: hyperdynamic / high-output septic shock.
c) 1 mark: fluid intolerance / pulmonary congestion. 1 mark: stop / minimize further fluid.
d) 2 marks — 1 mark each for two: pleural effusion; hepatic vein flow reversal, portal vein pulsatility, discontinuous renal vein pulsatile flow, tricuspid regurgitation.
e) 1 mark: positive pressure ventilation affects IVC. Alternate: atrial fibrillationCompetency: 1.3.2.2; 2.4.1; 2.4.11.1; 3.4.2.2; 3.4.2.7
Resource: Vieillard-Baron A et al. A decade of progress in critical care echocardiography. Intensive Care Med 2019;45:770–788; Spiegel R et al. The use of venous Doppler to predict fluid intolerance. Chest 2021;159:1394–1402 -
Question 63 of 66
63. Question
Hint
a) 1 mark each up to 2 total: Long QT Syndrome, Catecholaminergic polymorphone ventricular tachycardia, commotio cordis, hypoxic arrest/drowning. Alternate: idiopathic VF, Brugada (not classic with diving, water, cold)
b) 1 mark each up to 2 total: Hypertrophic cardiomyopathy, Arrhythmogenic right ventricular cardiomyopathy
c) 1 mark: Labetalol. Alternate. Non-dihydripyridine calcium channel blocker. 1 mark for 1 of: Nitroglycerine/prusside, clevidipine/nifedipine, enalaprit, hydralazineCompetency: ME 2.4.3
Resource: Sudden Cardiac Death in Young Athletes: JACC State-of-the-Art Review. JACC. 2024. Finocchiaro G, et al.Review -
Question 64 of 66
64. Question
Hint
Preload optimization with volume reduction, reduce afterload by minimizing mean airway pressure, pulmonary vasodilatation, increase HR, ensure coronary perfusion, prevent hypoxemia, hypercarbia, acidosis, increase RV contractility. Answer:
Specific = isoproterenol to increase HR, increase FiO2 for SpO2 >92%, increase freq to increase pH, furosemide for diuresis, inodilator (dobutamine/milrinone)Resource: Konstantinides et al. ESC PE Guidelines 2019; Jardin & Vieillard-Baron ICM 2003
Royal College Competency: 1.3.2.2, 2.4.3.1 -
Question 65 of 66
65. Question
Hint
Endocardial excursion, myocardial thickening (should be 30-40%), septal motion of anterior leaflet, LVOT VTI
Resource: Labovitz et al. JACC 2010 (POCUS in ICU); Rugolotto et al.
Royal College Competency: 1.3.12.2, 3.4.2 -
Question 66 of 66
66. Question
Hint
AV nodal reentry, A flutter, A fib, Vagal maneuvers, adenosine, b-blocker
Resource: Brugada et al. Circulation 1991 (WCT algorithm); Al-Khatib et al. JACC 2018
Royal College Competency: 2.4.3.1, 3.1.4