Cardiogenic shock

Contents

Definition and Haemodynamics

Cardiogenic shock (CS) is a state of primary cardiac pump failure resulting in tissue hypoperfusion that is not corrected by volume alone.

Classic haemodynamic profile:

Parameter Value
Cardiac index (CI) <2.2 L/min/m²
PCWP >18 mmHg
SVR ↑
SBP <90 mmHg (or MAP <60 mmHg for ≥30 min despite adequate filling)

Tissue hypoperfusion markers: elevated lactate, oliguria, cool peripheries, altered mentation.

SCAI Classification

The Society for Cardiovascular Angiography and Interventions (SCAI) staging classifies CS from A to E, reflecting escalating severity and mortality:

Stage Description Approximate mortality
A At risk — no current haemodynamic compromise <5%
B Beginning — mild hypotension or tachycardia ~10%
C Classic CS — hypoperfusion requiring intervention 20–35%
D Deteriorating despite initial intervention 40–60%
E Extremis — cardiac arrest or refractory shock >50%

Aetiology

Acute myocardial infarction: most common cause (40–50%); large anterior MI most likely; right ventricular MI can cause CS with clear lungs.

Other causes:

Category Examples
Acute decompensated HF DCMP, acute-on-chronic
Acute valvular pathology Acute MR (papillary muscle rupture post-MI), acute AR (dissection, endocarditis), critical AS
Myocarditis Viral, giant cell, immune checkpoint inhibitor
Mechanical complications of MI Free wall rupture, VSD, papillary muscle rupture
Post-cardiotomy Low cardiac output syndrome after CPB
Arrhythmia Sustained VT, complete heart block
Takotsubo cardiomyopathy Catecholamine surge, apical ballooning

Pathophysiology

CS creates a vicious cycle of deterioration:

↓ Cardiac output
       ↓
↓ Coronary perfusion pressure
       ↓
↓ Myocardial oxygen supply + ↑ demand (tachycardia, wall stress)
       ↓
↓ Myocardial function → worsening shock

Systemic effects:

  • Compensatory ↑ SVR (catecholamine-mediated) → ↑ afterload → further ↓ CO
  • Neurohormonal activation: RAAS, ADH → salt and water retention
  • Inflammatory cascade in severe CS: cytokine release (TNF-α, IL-1, IL-6) → iNOS-mediated vasodilation → vasodilatory component superimposed on cardiogenic (mixed shock)
  • Lactic acidosis from tissue hypoperfusion → myocardial depression

Right ventricular MI: occlusion of dominant right coronary artery → RV infarction → ↓ RV output → ↓ LV preload → ↓ CO despite preserved LV function; ventricular interdependence (septal shift); characteristic: hypotension + ↑ JVP + clear lungs; treated with aggressive fluid loading and avoiding nitrates/diuretics.

Assessment and Monitoring

Clinical:

  • Cool, clammy peripheries; prolonged CRT; oliguria; altered mentation
  • Signs of pulmonary oedema (LV failure); clear lungs (RV MI, hypovolaemic component)

Bedside echocardiography:

  • LVEF, regional wall motion, valvular pathology, RV function, pericardial effusion, septal defect
  • Haemodynamic estimation: LVOT VTI, mitral inflow, IVC collapsibility

Invasive haemodynamics (pulmonary artery catheter or Impella-derived):

  • Confirm diagnosis, differentiate from distributive shock
  • Guide inotrope and fluid titration

Investigations: ECG (STEMI, LBBB, complete heart block), troponin, BNP/NT-proBNP, ABG (lactate, pH), echo, CXR.

Management

1. Treat the underlying cause

  • AMI-CS: primary PCI is the priority; door-to-balloon time applies; revascularise culprit artery (see CULPRIT-SHOCK below)
  • Arrhythmia: cardioversion or pacing
  • Valvular emergency: urgent surgical or TAVI/MitraClip consultation

2. Fluid management

  • Judicious fluid challenge only if evidence of hypovolaemia or RV MI
  • Avoid fluid loading in LV failure with elevated PCWP — worsens pulmonary oedema
  • RV MI is an exception: cautious fluid to optimise LV preload

3. Vasopressors

  • Noradrenaline is first-line: raises MAP via α₁-mediated vasoconstriction; preferred over dopamine (↓ arrhythmia, less tachycardia)
  • Target MAP ≥65 mmHg; avoid excessive SVR elevation which worsens LV afterload

4. Inotropic support

Agent Mechanism Notes
Dobutamine β₁ > β₂ agonism ↑ CO, mild ↓ SVR; tachycardia and arrhythmia at higher doses
Milrinone PDE3 inhibitor → ↑ cAMP Inodilator: ↑ contractility + vasodilation; lusitropic (↑ relaxation); longer half-life; caution in hypotension
Adrenaline Mixed α/β agonism Reserved for refractory shock; raises CO and SVR; causes lactic acidosis (β₂-mediated); arrhythmogenic
Levosimendan Calcium sensitiser + K-ATP channel opener Inodilator; no increase in myocardial O₂ demand; limited acute haemodynamic evidence vs dobutamine

5. Mechanical circulatory support (MCS)

  • IABP (intra-aortic balloon pump): counterpulsation; ↓ afterload in systole, ↑ diastolic aortic pressure; simple to insert; modest haemodynamic benefit (see IABP-SHOCK II)
  • Impella (microaxial flow pump): continuous axial flow from LV to aorta; provides up to 5.5 L/min unloading; more invasive; haemodynamic benefit greater than IABP
  • VA-ECMO: full cardiopulmonary bypass circuit; provides >4 L/min; note: ↑ LV afterload (retrograde aortic flow); may need LV venting (Impella + ECMO = "ECPella")
  • Tandem Heart: LA-to-aorta; rarely used in UK

6. Organ support

  • Renal: often requires RRT (AKI common)
  • Respiratory: NIV or mechanical ventilation for pulmonary oedema/ARDS component
  • Sedation: minimise myocardial depression

Key Trials

Trial Question Finding
IABP-SHOCK II (Thiele, Lancet 2012) IABP vs no IABP in AMI-CS undergoing early revascularisation No difference in 30-day mortality (39.7% vs 41.3%); changed guidelines — IABP no longer routinely recommended
CULPRIT-SHOCK (Thiele, NEJM 2017) Culprit-only PCI vs multivessel PCI in AMI-CS with multivessel disease Culprit-only PCI reduced 30-day death/RRT (45.9% vs 55.4%); multivessel PCI increased risk — now standard to revascularise culprit only acutely
OPTICS / various MCS trials Impella vs IABP Impella provides superior haemodynamic support but survival benefit in unselected CS not definitively established in adequately powered RCTs

Viva Questions

1. What is the haemodynamic profile of cardiogenic shock and how does it differ from distributive shock?

Cardiogenic shock is characterised by low cardiac index (<2.2 L/min/m²), elevated filling pressures (PCWP >18 mmHg), and high SVR — the body compensates for low output by vasoconstriction. Distributive shock (e.g. sepsis) has low SVR and often a normal or elevated cardiac output. Mixed shock occurs when both components co-exist, as in severe sepsis with pre-existing cardiomyopathy. Clinical differentiation uses echocardiography and invasive monitoring; cool extremities with pulmonary oedema suggests cardiogenic; warm vasodilated peripheries with hypotension suggests distributive. The distinction matters because treatment differs fundamentally — fluids help in distributive shock but worsen pulmonary congestion in cardiogenic shock.

2. Why has IABP fallen out of favour in AMI-related cardiogenic shock?

The IABP-SHOCK II trial (Thiele 2012) randomised 600 patients with AMI-CS undergoing early revascularisation to IABP versus no IABP and found no difference in 30-day mortality (39.7% vs 41.3%). The trial was well-powered and the finding was replicated at long-term follow-up. Physiologically, the IABP augments diastolic pressure and offloads the LV, but the haemodynamic benefit is modest (<0.5 L/min CO improvement). More powerful unloading devices (Impella) provide larger haemodynamic effects but have not yet demonstrated consistent mortality benefit in adequately powered trials in unselected CS populations. IABP may still have a role in specific mechanical complications (acute MR, VSD) or as a bridge to surgery.

3. How would you approach escalating haemodynamic support in a patient with cardiogenic shock not responding to initial inotropes?

I would follow a systematic escalation. First, confirm the diagnosis — bedside echo to exclude tamponade, new valvular pathology, RV failure, or mechanical complication of MI, all of which require specific treatment. Ensure optimum filling (guided by echo or invasive monitoring) and treat any arrhythmia. If LV failure predominates: escalate inotropes (dobutamine → adrenaline), add vasopressin if vasoplegic component, consider pulmonary artery catheter for precise haemodynamic guidance. Mechanical support: Impella provides more robust unloading than IABP. VA-ECMO is the most powerful rescue option but increases LV afterload (retrograde aortic flow), which may worsen myocardial recovery — LV venting with an Impella device ("ECPella") can counteract this. Simultaneously: refer to a heart failure/transplant centre early if refractory, to consider bridging strategies (LVAD, transplantation). Set clear decision-making windows and goals of care discussions with the patient/family.

4. What are the specific management principles for right ventricular MI?

RV MI most commonly results from right coronary artery occlusion in inferior STEMI. The RV infarcts and fails, reducing LV preload and thereby CO. The classic triad is hypotension, raised JVP, and clear lung fields (normal PCWP). Management differs crucially from LV-CS: (1) Fluid resuscitation — the failing RV is preload-dependent; cautious fluid boluses to optimise LV filling; target CVP 15–18 mmHg; (2) Avoid nitrates and diuretics — both reduce preload and cause catastrophic hypotension; (3) Maintain AV synchrony — atrial kick contributes significantly to RV filling; temporary pacing for complete heart block; (4) Revascularise — PCI of the culprit RCA restores RV perfusion; RV is often ischaemic rather than infarcted and recovers with reperfusion; (5) Inotropes: dobutamine for RV contractile support; (6) Vasopressors if refractory hypotension. Most RV MI with supportive care and reperfusion recover meaningful RV function within days.