Cardiogenic Shock — Viva

Q1: Definition, classification and pathophysiology (2 min)

Examiner: Define cardiogenic shock and give the SHOCK-trial diagnostic criteria. Candidate: Cardiogenic shock is end-organ hypoperfusion due to cardiac pump failure. The SHOCK-trial criteria are: systolic blood pressure below 90 mmHg for at least 30 minutes (or vasopressors to maintain SBP at least 90); cardiac index at or below 2.2 L/min/m2; PCWP over 15 mmHg; and clinically evident hypoperfusion (oliguria under 30 mL/hour or cool extremities). Forrester subset IV uses wedge over 18 mmHg.^[1][9]

Examiner: What is the SCAI SHOCK classification and how is it used? Candidate: Five stages — A (at risk, no hypoperfusion; Jentzer hospital mortality 3.0 percent), B (beginning, hypoperfusion starting, 7.1 percent), C (classic shock, 12.4 percent), D (deteriorating despite escalating inotropes, 40.4 percent), E (extremis, 67.0 percent in Jentzer's CICU cohort — not an 80-percent figure). The B-to-C boundary is the appearance of hypoperfusion. Staging drives triage, escalation triggers and prognosis.^[8]

Examiner: Explain the pathophysiological spiral. Candidate: Acute myocardial injury reduces stroke volume and cardiac output; falling diastolic blood pressure reduces coronary perfusion pressure, particularly in the subendocardium (perfused only in diastole); the worsened ischaemia further reduces contractility, completing a self-perpetuating downward spiral. This is the biological reason early revascularisation works. Compensatory sympathetic, RAAS and vasopressin activation raise afterload and myocardial oxygen demand. In late shock, a SIRS/inflammatory phenotype (iNOS induction, excess nitric oxide and peroxynitrite) produces vasoplegia — the basis of the TRIUMPH trial testing the NOS inhibitor tilarginine, which did NOT reduce mortality.^[1]

Q2: Bedside assessment and investigations (3 min)

Examiner: The patient has acute MI with hypotension. Walk me through your immediate assessment and investigations. Candidate: ABCDE first — high-flow oxygen, NIV for pulmonary oedema, intubate if tiring. Arterial line, central access, urinary catheter, bedside echo within minutes. ECG drives emergency revascularisation of the infarct-related artery if STEMI. For the deteriorating patient a PA catheter gives wedge, cardiac index and cardiac power output (CPO equals MAP times cardiac output over 451 watts). Some AMI-CS protocols use CPO above 0.6 W as a resuscitation goal.^[7][9]

Examiner: The wedge is 24, CI is 1.6, lactate is 5 — which Forrester subset is this and what is its mortality? Candidate: Subset IV — cold and wet (PCWP over 18, CI below 2.2). This is classic cardiogenic shock, historical mortality 55.5 percent in Forrester's 1977 series.^[9]

Q3: Management (3 min)

Examiner: Outline your pharmacological and definitive management. Candidate: Pharmacological support: dobutamine or milrinone (CAPITAL DOREMI: primary composite 49 versus 54 percent, P equal to 0.47) plus first-line noradrenaline. Dopamine is not first-line — SOAP-II showed more arrhythmia (24.1 versus 12.4 percent) and, in the cardiogenic-shock subgroup, more 28-day deaths. Definitive management: emergency revascularisation of the infarct-related artery; CULPRIT-SHOCK showed culprit-lesion-only PCI reduced death or RRT at 30 days (45.9 versus 55.4 percent, RR 0.83). For refractory shock, escalate to MCS. Routine IABP did not reduce 30-day mortality in IABP-SHOCK II (39.7 versus 41.3 percent).^{[6][5][4][3][7]}

Examiner: How would you manage a RV infarct with shock? Candidate: The hallmark is clear-lung-fields shock — raised JVP with Kussmaul sign, hypotension, no pulmonary oedema. The RV is preload-dependent. I give a cautious fluid challenge to a raised JVP without pulmonary oedema, avoid nitrates, diuretics and beta-blockers, reperfuse the RCA by PCI, and add an inotrope if hypotension persists despite adequate preload. Maintain AV synchrony — atrial infarct and AV block are common, so atrioventricular sequential pacing may be needed.^[7]

Q4: Complications and prognosis (2 min)

Examiner: What are the complications and prognosis? Candidate: Cardiac complications include refractory VT/VF, pump failure and mechanical complications (papillary muscle rupture, VSR, free-wall rupture). Systemic complications include AKI, ischaemic hepatitis and stroke. Thirty-day mortality after AMI-CS is nearly 40 percent and 1-year about 50 percent; SCAI E hospital mortality was 67.0 percent in Jentzer's CICU validation. The SHOCK 1-year survival benefit was confined to patients younger than 75 years.^[7][8][2]

References9ShowHide

1. [1]Hochman JS, Sleeper LA, Webb JG, et al. Early revascularization in acute myocardial infarction complicated by cardiogenic shock. SHOCK Investigators N Engl J Med, 1999.PMID 10460813
2. [2]Hochman JS, Sleeper LA, White HD, et al. One-year survival following early revascularization for cardiogenic shock JAMA, 2001.PMID 11176812
3. [3]Thiele H, Zeymer U, Neumann FJ, et al. Intraaortic balloon support for myocardial infarction with cardiogenic shock N Engl J Med, 2012.PMID 22920912
4. [4]Thiele H, Akin I, Sandri M, et al. PCI Strategies in Patients with Acute Myocardial Infarction and Cardiogenic Shock N Engl J Med, 2017.PMID 29083953
5. [5]De Backer D, Biston P, Devriendt J, et al. Comparison of dopamine and norepinephrine in the treatment of shock N Engl J Med, 2010.PMID 20200382
6. [6]Mathew R, Di Santo P, Jung RG, et al. Milrinone as Compared with Dobutamine in the Treatment of Cardiogenic Shock N Engl J Med, 2021.PMID 34347952
7. [7]Samsky MD, Morrow DA, Proudfoot AG, et al. Cardiogenic Shock After Acute Myocardial Infarction: A Review JAMA, 2021.PMID 34751704
8. [8]Jentzer JC, van Diepen S, Barsness GW, et al. Cardiogenic Shock Classification to Predict Mortality in the Cardiac Intensive Care Unit J Am Coll Cardiol, 2019.PMID 31548097
9. [9]Forrester JS, Diamond GA, Swan HJ Correlative classification of clinical and hemodynamic function after acute myocardial infarction Am J Cardiol, 1977.PMID 835473