Cardiogenic shock

12 min read Last updated April 8, 2026

Surgical approach (where relevant)

  • Cardiogenic shock is a syndrome, not an operation; surgical/cath-lab interventions are often definitive treatment.
  • If acute MI-related shock
    • Urgent coronary angiography ± PCI (culprit lesion revascularisation; consider complete revascularisation later).
    • If mechanical complication suspected: urgent echo then surgery (VSD repair, papillary muscle rupture/acute MR repair/replacement, free wall rupture).
  • If acute valvular catastrophe (e.g. acute severe MR/AR, prosthetic valve thrombosis)
    • Emergency valve surgery or thrombolysis/catheter intervention depending on pathology and stability.
  • If obstructive/structural causes
    • Tamponade: pericardiocentesis or surgical drainage.
    • Massive PE with shock: thrombolysis, catheter-directed therapy, or surgical embolectomy; consider ECMO as bridge.
  • Mechanical circulatory support (MCS) procedures
    • IABP insertion (usually femoral; less common as routine in MI shock).
    • Percutaneous LV assist (Impella) insertion in cath lab.
    • VA-ECMO cannulation (peripheral femoral-femoral ± distal limb perfusion; or central in theatre).

Anaesthetic management (typical scenarios: cath lab, emergency theatre, ICU procedures)

  • Type of anaesthesia
    • Often requires GA for airway control, ventilation, and procedures (PCI in unstable patient, MCS insertion, emergency cardiac surgery).
    • Selected stable patients: local anaesthesia + minimal sedation for cath lab procedures; avoid oversedation.
    • Regional anaesthesia rarely appropriate in active shock (sympathectomy → collapse).
  • Airway
    • ETT usually preferred (aspiration risk, need for controlled ventilation, high FiO2/PEEP, procedures).
    • SGA generally avoided in severe shock/active pulmonary oedema.
  • Duration
    • Variable: PCI 1–2 h; MCS insertion 0.5–2 h; emergency cardiac surgery 4–8+ h; ongoing ICU resuscitation days.
  • Pain
    • Underlying ischaemia/MI is painful; procedures range from minimally painful (lines) to very painful (sternotomy).
  • Induction principles (if GA)
    • Resuscitate first: vasopressor running, arterial line ideally pre-induction, pre-oxygenate, senior help, defib pads on.
    • Choose haemodynamically stable technique: etomidate or ketamine (cautious in tachyarrhythmia/ischaemia), opioid-based, low-dose induction, avoid large propofol doses.
    • Paralysis: rocuronium (RSI if aspiration risk); avoid long apnoea; be ready for peri-intubation arrest.
    • Ventilation: avoid excessive PEEP if RV failure/low preload; treat pulmonary oedema with careful PEEP/FiO2 and afterload reduction only if BP allows.
  • Monitoring and access
    • A-line, central access (preferably multi-lumen), large-bore IV, urinary catheter, temperature, capnography, frequent ABGs/lactate.
    • Echo (TTE/TOE) early to define phenotype (LV vs RV vs mechanical/obstructive) and guide therapy.
    • Consider advanced monitoring: ScvO2, pulse contour, PAC in selected cases (esp. RV failure/complex shock).
  • Intra-procedural haemodynamic goals
    • MAP ≥ 65 mmHg (individualise: chronic HTN, cerebral perfusion).
    • Optimise oxygen delivery: Hb, SaO2, CO; reduce oxygen demand (analgesia, sedation, treat fever/shivering).
    • Avoid tachycardia and hypotension (worsen ischaemia).

Definition and diagnostic criteria

  • Cardiogenic shock = critical end-organ hypoperfusion due to primary cardiac pump failure (LV, RV, or both), often with elevated filling pressures and pulmonary congestion.
  • Pragmatic bedside definition: hypotension (SBP < 90 mmHg or MAP < 65 mmHg) or need for vasopressors + signs of hypoperfusion (cold clammy peripheries, oliguria, altered mentation, lactate > 2 mmol/L).
  • Haemodynamic (classic) criteria (where measured): CI < 2.2 L/min/m² with PCWP > 15 mmHg (LV failure phenotype).
  • SCAI shock stages (A–E): At risk → Beginning → Classic → Deteriorating → Extremis; useful for communication and escalation to MCS.

Aetiology (think: pump failure, mechanical, electrical, obstructive)

  • Pump failure
    • Acute MI (most common), myocarditis, Takotsubo, decompensated cardiomyopathy, post-cardiotomy stunning.
    • RV infarction, severe pulmonary hypertension with RV failure.
  • Mechanical complications (esp. post-MI)
    • Acute severe MR (papillary muscle rupture), VSD, free wall rupture → tamponade, acute AR, prosthetic valve dysfunction.
  • Electrical
    • Bradyarrhythmias/heart block, VT/VF, rapid AF/flutter causing loss of filling time and CO.
  • Obstructive mimics to exclude early (management differs)
    • Massive PE, cardiac tamponade, tension pneumothorax, dynamic LVOT obstruction (e.g. HOCM/Takotsubo).

Pathophysiology (exam-friendly)

  • Reduced contractility/forward flow → ↓CO → hypotension → coronary hypoperfusion → worsening ischaemia (vicious cycle).
  • Compensatory sympathetic vasoconstriction increases SVR (maintains BP but increases afterload and myocardial oxygen demand).
  • Elevated filling pressures → pulmonary oedema → hypoxaemia → further myocardial dysfunction.
  • Microcirculatory dysfunction and systemic inflammation may develop; mixed cardiogenic–distributive shock is common in late stages.
  • RV failure: ↓LV preload + systemic venous congestion; very preload- and afterload-sensitive (PEEP, hypoxia, acidosis worsen).

Clinical features

  • Hypoperfusion: cool mottled peripheries, delayed cap refill, oliguria, confusion, rising lactate/metabolic acidosis.
  • Congestion: raised JVP, pulmonary crackles, hypoxaemia, S3, peripheral oedema (may be absent early).
  • Clues to phenotype
    • RV infarct/PE: raised JVP, clear lungs, hypotension; ECG inferior MI; echo RV dilation/poor RV function.
    • Mechanical MR/VSD: new loud murmur, acute pulmonary oedema, rapid deterioration; confirm with echo.
    • Tamponade: hypotension + raised JVP + muffled heart sounds (often incomplete), pulsus paradoxus; echo diagnostic.

Investigations (prioritise bedside and actionable)

  • ECG: STEMI/NSTEMI, arrhythmia, heart block, RV infarct (right-sided leads).
  • Bloods: ABG/VBG (lactate, acid-base), FBC, U&E/creatinine, LFTs, coagulation, troponin, glucose, CRP; group & save/crossmatch.
  • CXR: pulmonary oedema, cardiomegaly, alternative diagnoses (pneumothorax).
  • Echocardiography (key test): LV/RV function, regional wall motion, valve lesions, VSD, tamponade, LVOT obstruction; estimate filling pressures.
  • Invasive haemodynamics (selected): CVP/ScvO2; PAC if unclear phenotype, RV failure, or to guide MCS; interpret trends not single numbers.
  • Coronary angiography urgently if MI suspected and patient suitable for reperfusion.

Immediate management (structured approach)

  • Call for help early: ICU/cardiology/cardiothoracic/cath lab; consider early MCS referral (SCAI C–E, escalating inotropes/vasopressors, rising lactate).
  • A–E with simultaneous actions
    • Airway/Breathing: high-flow O2; NIV/CPAP for pulmonary oedema if cooperative; intubate if failing oxygenation/ventilation, exhaustion, or for procedures.
    • Circulation: attach defib pads; treat arrhythmias; establish arterial line; 2 large-bore IV/central access; start vasopressor early.
    • Disability/Exposure: glucose, temperature, look for bleeding/sepsis triggers, signs of mechanical complication.
  • Fluids: cautious and guided (echo, dynamic response); avoid large boluses in LV failure/pulmonary oedema; RV infarct may need small boluses to optimise preload.
  • Vasopressors/inotropes (typical first-line)
    • Noradrenaline to target MAP (preferred vasopressor in cardiogenic shock).
    • Add inotrope if low output persists despite adequate MAP: dobutamine or milrinone (milrinone useful in RV failure/pulmonary HTN but causes vasodilation; needs vasopressor).
    • Adrenaline: potent inotrope/vasopressor but higher risk of tachyarrhythmia and lactate rise; consider refractory shock.
    • Vasopressin can be added to reduce catecholamine dose in mixed shock/vasoplegia.
  • Treat the cause (time-critical)
    • MI: urgent reperfusion (PCI); antiplatelet/anticoagulation per cardiology; manage complications.
    • Arrhythmia: DC cardioversion for unstable tachyarrhythmia; pacing for high-grade block; correct electrolytes.
    • Mechanical: urgent echo and surgical/cath intervention.
  • Ventilation strategy: avoid hypoxia/hypercapnia/acidosis (increase PVR and worsen RV); use lung-protective ventilation; titrate PEEP to oxygenation while monitoring haemodynamics.
  • Renal and metabolic: aim urine output > 0.5 mL/kg/h; avoid nephrotoxins; correct K+/Mg2+/Ca2+; treat severe acidosis (usually by improving perfusion; bicarbonate rarely).

Mechanical circulatory support (MCS): indications and key points

  • Indications: persistent hypoperfusion despite optimisation (adequate preload, MAP with vasopressor, inotrope), rising lactate, recurrent arrhythmia, or as bridge to definitive therapy (PCI/surgery/transplant).
  • IABP
    • Diastolic augmentation + afterload reduction; modest CO increase.
    • Best for: mechanical complications (e.g. acute MR/VSD) as bridge; refractory angina; not routine in MI-related shock.
    • Contraindications: severe AR, aortic dissection, severe PAD, uncontrolled sepsis/bleeding relative.
  • Impella (percutaneous LVAD)
    • Direct LV unloading and forward flow; requires adequate RV function/preload.
    • Risks: haemolysis, limb ischaemia, bleeding, aortic/valve injury; anticoagulation needed.
  • VA-ECMO
    • Provides circulatory + oxygenation support; useful in biventricular failure or refractory arrest (ECPR).
    • Key issue: increases LV afterload → LV distension/pulmonary oedema; may need LV venting (IABP/Impella/atrial septostomy/surgical vent).
    • Complications: bleeding, thrombosis, limb ischaemia, stroke, infection; requires anticoagulation and meticulous monitoring.

Drug summaries (high-yield)

  • Noradrenaline: α1>β1; ↑SVR and MAP with modest inotropy; first-line vasopressor.
  • Dobutamine: β1>β2; ↑inotropy and HR, ↓SVR; good for low output with adequate BP; may worsen hypotension/arrhythmias.
  • Milrinone: PDE3 inhibitor; inotrope + lusitrope + vasodilator; helpful in RV failure/pulmonary HTN; long half-life, renal clearance; often needs noradrenaline.
  • Adrenaline: β and α dose-dependent; strong inotropy/vasopressor; tachyarrhythmia, hyperlactataemia; consider refractory shock.
  • Vasopressin: V1 vasoconstriction; adjunct in vasoplegia/mixed shock; minimal pulmonary vasoconstriction compared with catecholamines.
  • GTN: venodilator/arterial dilator; useful in pulmonary oedema/ischaemia if BP tolerates; avoid in RV infarct and severe AS; stop if hypotensive.
  • Diuretics: for congestion once perfusion pressure adequate; avoid reflexively in profound shock.

Differential diagnosis of shock with low BP (FRCA framing)

  • Distributive (sepsis/anaphylaxis): warm peripheries early, low SVR; may coexist with cardiogenic shock.
  • Hypovolaemic: history of bleeding/fluid loss, flat JVP, small collapsible IVC on echo.
  • Obstructive: PE/tamponade/tension pneumothorax; echo and clinical exam key.
  • Neurogenic: bradycardia with hypotension, warm peripheries; spinal injury context.
You are called to ED: 68-year-old with chest pain, SBP 75, SpO2 88% on O2, cold peripheries, lactate 5. Outline your immediate management of suspected cardiogenic shock.

Structure by A–E, early echo, early vasopressor, treat cause.

  • Call for help: ICU + cardiology/cath lab; activate pathway for urgent reperfusion if MI suspected.
  • A/B: high-flow O2; consider CPAP/NIV for pulmonary oedema if conscious; intubate if failing oxygenation/ventilation or for cath lab/instability.
  • C: defib pads; 2 IV lines; arterial line; bloods including ABG/lactate; start noradrenaline early to MAP ≥ 65; cautious small fluid bolus only if echo suggests underfilled/RV infarct.
  • Early bedside echo: LV/RV function, tamponade, acute MR/VSD, LVOT obstruction; guides inotrope vs fluids vs urgent procedure.
  • Add inotrope if low output persists: dobutamine (or milrinone if RV failure/pulmonary HTN with vasopressor support).
  • Treat arrhythmias: DC cardioversion if unstable tachyarrhythmia; pacing for high-grade block; correct K+/Mg2+.
  • Definitive: urgent PCI for MI; consider MCS if escalating drugs/rising lactate or peri-arrest.
Define cardiogenic shock and describe how you would differentiate it from other causes of shock at the bedside.

Give a pragmatic definition + bedside phenotype clues + echo.

  • Definition: hypotension requiring vasopressors and/or SBP < 90/MAP < 65 with signs of hypoperfusion due to primary cardiac pump failure (often with congestion).
  • Bedside: cold clammy peripheries, narrow pulse pressure, raised JVP, pulmonary oedema, oliguria, altered mentation, raised lactate.
  • Differentiate: sepsis/anaphylaxis often warm early with low SVR; hypovolaemia has flat JVP and no congestion; obstructive causes have specific signs (tamponade/PE/tension pneumothorax).
  • Echo is decisive: LV/RV function, tamponade, PE signs, valve/mechanical lesions, LVOT obstruction; integrate with ECG and CXR.
Discuss your choice of vasoactive drugs in cardiogenic shock (including rationale and pitfalls).

Aim: perfusion pressure first, then augment contractility; avoid tachycardia/ischaemia.

  • Noradrenaline first-line to restore MAP and coronary perfusion with less tachycardia than adrenaline.
  • If low output persists: add dobutamine (watch hypotension/arrhythmia) or milrinone (good for RV failure/pulmonary HTN; vasodilates; renal clearance).
  • Adrenaline reserved for refractory shock/peri-arrest; risk tachyarrhythmia, increased myocardial O2 demand, lactate rise (interpret lactate carefully).
  • Vasopressin as adjunct in vasoplegia/mixed shock to reduce catecholamine dose.
  • Avoid pure vasoconstriction without inotropy if severe LV failure (may worsen CO); use echo/clinical response to titrate.
A patient with inferior STEMI is hypotensive with raised JVP and clear lungs. How does this change your management?

This suggests RV infarction: preload-dependent, avoid preload reduction and excessive PEEP.

  • Suspect RV infarct: obtain right-sided ECG leads; urgent echo for RV function and exclude tamponade/PE.
  • Fluids: cautious small boluses to optimise RV preload (guided by echo and response).
  • Avoid GTN/diuretics and avoid high PEEP if possible (reduce preload).
  • Vasoactives: noradrenaline for MAP; consider dobutamine or milrinone if RV contractility poor (milrinone needs vasopressor).
  • Definitive: urgent reperfusion (PCI) is key; treat bradyarrhythmias/AV block with pacing if needed.
Describe the role of echocardiography in cardiogenic shock and what key findings you would look for.

Echo defines the shock phenotype and identifies time-critical reversible causes.

  • LV: global vs regional dysfunction; estimate filling pressures; look for LV thrombus; assess for LVOT obstruction.
  • RV: size/function, septal flattening, TR, estimated pulmonary pressures; RV failure phenotype.
  • Valves/mechanical: acute MR, VSD, acute AR, prosthetic dysfunction.
  • Pericardium: tamponade signs (effusion, chamber collapse, IVC plethora).
  • Volume status: IVC size/variability (interpret cautiously in ventilated patients).
You need to intubate a patient in cardiogenic shock with pulmonary oedema. How will you do it safely?

Peri-intubation hypotension/arrest is a major risk; resuscitate and plan.

  • Preparation: senior help; full monitoring; defib pads; suction; difficult airway plan; pre-oxygenate (CPAP/NIV if tolerated).
  • Haemodynamics: start noradrenaline infusion before induction; consider push-dose vasopressor; aim MAP ≥ 65; arterial line if feasible pre-induction.
  • Induction: low-dose etomidate or ketamine + opioid; avoid large propofol doses; rapid sequence if aspiration risk.
  • Ventilation: gentle ventilation, avoid excessive PEEP initially; titrate PEEP to oxygenation while watching BP; avoid hypercapnia/acidosis.
  • Post-intubation: reassess with echo, ABG, lactate; adjust vasoactives; consider early MCS if escalating support.
What are the indications, contraindications, and complications of an intra-aortic balloon pump?

Know mechanism + key contraindications (severe AR, dissection).

  • Mechanism: inflates in diastole (↑coronary perfusion), deflates in systole (↓afterload).
  • Indications: bridge in mechanical complications (acute MR/VSD), refractory ischaemia, perioperative support; not routine for MI shock.
  • Contraindications: severe aortic regurgitation, aortic dissection, severe PAD/aneurysm, uncontrolled bleeding/sepsis (relative).
  • Complications: limb ischaemia, bleeding/haematoma, infection, balloon rupture, thrombocytopenia, embolism, aortic injury.
Outline the principles of VA-ECMO in cardiogenic shock and the key anaesthetic/ICU considerations.

VA-ECMO supports circulation and oxygenation; beware LV distension and complications.

  • Indications: refractory cardiogenic shock, biventricular failure, ECPR, bridge to recovery/decision/transplant.
  • Physiology: increases systemic perfusion but may increase LV afterload → LV distension/pulmonary oedema; consider unloading strategies.
  • Cannulation issues: limb ischaemia risk (distal perfusion catheter), bleeding, vascular injury; anticoagulation and monitoring required.
  • Monitoring: flows, pressures, oxygenator function, ABGs (differential hypoxia in peripheral VA-ECMO), haemolysis markers, lactate trends.
A shocked post-MI patient has a new pansystolic murmur and flash pulmonary oedema. What is your differential and immediate plan?

Think acute MR vs VSD; both need urgent echo and surgical/cath input.

  • Differential: papillary muscle rupture → acute severe MR; post-infarct VSD; less likely TR/functional MR.
  • Immediate: urgent echocardiography; stabilise with noradrenaline ± inotrope; consider IABP as bridge; intubate/ventilate if needed.
  • Definitive: urgent cardiothoracic surgery (or percutaneous closure in selected VSD) alongside coronary management.
How would you set haemodynamic targets in cardiogenic shock and how do you assess response to treatment?

Targets are perfusion-based; use clinical + biochemical + echo trends.

  • Targets: MAP ≥ 65 (individualise), improving mentation, warm peripheries, UO > 0.5 mL/kg/h, falling lactate, improving acid-base.
  • Assess: serial lactate, capillary refill/skin mottling, urine output, ABGs, echo reassessment (stroke volume, filling, RV/LV function), ScvO2 trends if available.
  • Avoid fixation on single numbers (e.g. CVP alone); interpret in context (ventilation, RV failure, tamponade).
Explain why cardiogenic shock can become 'mixed' shock and how that changes management.

Late cardiogenic shock often has vasoplegia/inflammation; vasopressors become more important.

  • Mechanisms: systemic inflammatory response, ischaemia–reperfusion, endotoxin translocation, vasodilatory mediators → reduced SVR.
  • Implication: may need higher vasopressor doses (noradrenaline ± vasopressin) alongside inotropy; avoid excessive fluids; consider sepsis workup and antibiotics if indicated.
  • MCS may be required earlier because escalating catecholamines increase myocardial oxygen demand and arrhythmia risk.

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