Cardiogenic and obstructive shock: Viva

Branch 1: Classification and recognition

The candidate should recognise that this boy is in cardiogenic shock. The cold, mottled peripheries, the capillary refill of 5 seconds, the gallop rhythm and the hepatomegaly are the signature of a cold, low-output state from pump failure, not the warm, vasodilated shock of early sepsis or the fluid-responsive hypovolaemia. A strong candidate states the problem representation clearly: a 10-year-old with a three-day viral prodrome and a cold low-output shock with a gallop and hepatomegaly, consistent with myocarditis until proven otherwise. [1]

If the examiner presses on the classification, the candidate should explain the four shock types (hypovolaemic, distributive, cardiogenic, obstructive) and the warm versus cold split. Cardiogenic and obstructive shock share the cold phenotype and are the two types where aggressive fluid resuscitation can harm. The candidate should distinguish cardiogenic shock (gallop, hepatomegaly, bilateral crackles) from obstructive shock (distended neck veins, muffled heart sounds or unilateral absent breath sounds) and explain that point-of-care ultrasound confirms the mechanism within minutes. [1][2]

Branch 2: Resuscitation and the fluid strategy

If asked about the immediate management, the candidate should give high-flow oxygen, assess the airway and breathing, and give a cautious fluid bolus of 5 mL per kg of isotonic crystalloid with reassessment, not the 20 mL per kg boluses of septic shock. The candidate must explain why: the failing myocardium cannot handle the volume, and pushing more fluid worsens the pulmonary oedema and the hepatic congestion. The candidate should start an adrenaline infusion at 0.05 to 0.5 micrograms per kg per minute after the first cautious bolus, because adrenaline increases contractility and peripheral vascular tone. [1][2]

A strong candidate anticipates the deterioration. The child with cardiogenic shock from myocarditis can decompensate rapidly into cardiopulmonary arrest, so the team should prepare for intubation and positive-pressure ventilation (which reduces left ventricular afterload but can drop venous return), secure central access, and arrange an urgent echocardiogram and a 12-lead ECG. The candidate should send a troponin and BNP, a blood gas for lactate and pH, and blood cultures to exclude a septic contribution. [4]

Branch 3: The investigation pathway and the role of mechanical support

If the examiner moves to the investigations, the candidate should state that the echocardiogram is the definitive test for cardiogenic shock: it assesses contractility (global or regional hypokinesis in myocarditis), structure (exclude congenital lesions, hypertrophic cardiomyopathy), valve function, and the presence of a pericardial effusion. The troponin and BNP are elevated in myocarditis. The 12-lead ECG may show ST changes, T wave inversion, or arrhythmia. Cardiac MRI may be needed for tissue characterisation once the child is stable. The American Heart Association 2021 scientific statement on myocarditis in children guides the diagnostic pathway. [4]

If asked about escalation to mechanical support, the candidate should describe the role of veno-arterial extracorporeal membrane oxygenation (VA-ECMO) for refractory cardiogenic shock that does not respond to inotropes. The SAVE score (Schmidt 2015) predicts survival after VA-ECMO using pre-cannulation variables including the underlying diagnosis, pre-ECMO cardiac arrest, age, weight and renal function. The candidate should state that ECMO is most effective when the cause is potentially reversible, such as fulminant myocarditis, and when it is cannulated before irreversible end-organ damage sets in. The candidate should involve the paediatric intensivist, the cardiologist and the ECMO service early. [5]