Medicine chapters
Cardiogenic shock and multi-organ failure
Shock caused by pump failure, most often after a large myocardial infarction: how to recognise it, how it differs from other shock, emergency treatment with revascularisation and inotropes, and how multi-organ failure follows.
- Cardiogenic shock is tissue hypoperfusion from pump failure: low blood pressure (systolic below 90 mmHg), cold clammy peripheries, low urine output, raised JVP and pulmonary oedema; commonest cause is a large MI.
- Haemodynamics: low cardiac output, high filling pressures (CVP and wedge), high systemic vascular resistance.
- Treat the cause (urgent revascularisation in MI), give oxygen, careful fluids only if filling is low, then inotropes (dobutamine) and vasopressors (noradrenaline), with mechanical support if needed.
On this page
Overview
Shock is a state of inadequate tissue perfusion and oxygen delivery. In cardiogenic shock the problem is the pump: the heart cannot push out enough blood even though the circulating volume is adequate.
It is the most severe form of acute heart failure (Killip class IV after MI). Mortality is high, and the only treatment shown to change the outcome after infarction is to open the blocked artery quickly. Untreated, poor perfusion leads to multi-organ failure.
Types of shock: where cardiogenic fits
| Type | Problem | Examples |
|---|---|---|
| Hypovolaemic | Low circulating volume | Haemorrhage, burns, vomiting and diarrhoea |
| Cardiogenic | Pump failure | Myocardial infarction, myocarditis, arrhythmia, acute valve failure |
| Obstructive | Blocked filling or outflow | Cardiac tamponade, tension pneumothorax, massive pulmonary embolism |
| Distributive | Vessel dilation and leak | Sepsis, anaphylaxis, neurogenic shock |
Causes (aetiology)
Myocardial
- Acute myocardial infarction with a large area of left ventricle lost: the commonest cause.
- Right ventricular infarction (with inferior MI).
- Acute myocarditis, end-stage cardiomyopathy, myocardial contusion, drug overdose (beta-blockers, calcium channel blockers).
Mechanical complications of MI
- Acute mitral regurgitation from papillary muscle rupture: sudden pulmonary oedema and shock.
- Ventricular septal rupture: new pansystolic murmur and shock; untreated mortality is very high.
- Rupture of the ventricular wall: tamponade and electromechanical dissociation; usually fatal.
Others
- Arrhythmias: sustained VT, very fast AF, complete heart block.
- Acute valve failure: endocarditis, prosthetic valve thrombosis, aortic dissection with acute aortic regurgitation.
Tamponade, tension pneumothorax and massive PE cause shock with a high JVP, but they are obstructive, not cardiogenic. The heart muscle is fine; filling or outflow is blocked. Treat the obstruction.
Pathophysiology (the vicious circle)
- The left ventricle fails, so stroke volume and cardiac output fall.
- Blood pressure falls, so coronary perfusion falls, causing more ischaemia and more pump failure.
- Sympathetic and renin-angiotensin activation cause vasoconstriction and tachycardia. This raises afterload and myocardial oxygen demand, which makes things worse.
- Back-pressure raises left atrial and pulmonary capillary pressure, causing pulmonary oedema and hypoxia.
- Tissues switch to anaerobic metabolism, causing lactic acidosis, then organ failure.
Clinical features
Signs of shock (shared with all shock)
- Hypotension: systolic BP below 90 mmHg (or a large fall from baseline).
- Tachycardia, weak or thready pulse.
- Cold, clammy, pale peripheries, slow capillary refill, sweating.
- Oliguria: urine output below 0.5 mL/kg per hour.
- Confusion, restlessness, drowsiness.
- Fast breathing from metabolic (lactic) acidosis.
Signs of the failing heart (point to cardiogenic)
- Raised JVP.
- Basal crackles, pulmonary oedema, breathlessness.
- Gallop rhythm (S3), pulsus alternans.
- New murmur: mitral regurgitation or VSD after MI.
- Chest pain or ECG changes of infarction.
Cold peripheries + high JVP + crackles + hypotension = cardiogenic shock. Warm peripheries + bounding pulse + hypotension = septic (distributive) shock.
Killip classification after MI
| Class | Findings |
|---|---|
| I | No crackles, no S3 |
| II | Crackles in under half the lung fields, or an S3 |
| III | Crackles in over half the lung fields (pulmonary oedema) |
| IV | Cardiogenic shock |
After MI, the one treatment that clearly improves survival in cardiogenic shock is early revascularisation, usually primary PCI.
Haemodynamic patterns
| Shock | CVP / wedge pressure | Cardiac output | Systemic vascular resistance |
|---|---|---|---|
| Cardiogenic | High | Low | High |
| Hypovolaemic | Low | Low | High |
| Septic (early) | Low or normal | High | Low |
| Tamponade | High (pressures equalise) | Low | High |
BP 80/50 mmHg
MAP = diastolic + (systolic − diastolic) / 3
MAP = 50 + (80 − 50) / 3 = 50 + 10 = 60 mmHg → below the usual target of about 65 mmHg
Investigations
- ECG at once: STEMI, new LBBB, arrhythmia, heart block.
- Echocardiography (urgent, bedside): poor LV function, RV infarction, acute MR, septal rupture, tamponade. This is the key test to find the cause.
- Bloods: troponin, arterial blood gas and lactate (severity marker), urea and creatinine, electrolytes, liver function, full blood count, clotting, glucose. BNP or NT-proBNP supports heart failure.
- Chest X-ray: pulmonary oedema, heart size.
- Coronary angiography if ischaemic cause.
- Monitoring: arterial line, central venous line, urinary catheter. A pulmonary artery (Swan-Ganz) catheter can measure wedge pressure and cardiac output when the fluid state is unclear.
Emergency management
General
- Admit to CCU or ICU; continuous ECG, BP, oxygen saturation and urine output.
- Oxygen; non-invasive ventilation (CPAP) or intubation if hypoxic and tiring.
- Correct arrhythmias (cardioversion for unstable tachycardia, pacing for heart block), electrolytes, acidosis (treat the cause; bicarbonate only for extreme acidosis).
- Fluids: a small careful challenge only if filling pressures are low (for example right ventricular infarction). Most patients already have high filling pressures and pulmonary oedema.
Treat the cause
- Acute MI: urgent revascularisation by primary PCI (or CABG). This is the most important step.
- Mechanical complications (papillary muscle rupture, VSD): stabilise and send for early surgery.
- Tamponade: pericardiocentesis. Massive PE: thrombolysis.
Drugs
| Drug | Main receptor / action | Use |
|---|---|---|
| Dobutamine | β1 agonist (some β2): raises contractility and output, mild vasodilation | First-line inotrope for low output |
| Noradrenaline | α agonist: vasoconstriction, raises BP | Persistent hypotension |
| Dopamine | Low dose dopamine receptors, medium β, high dose α | Used less now |
| Adrenaline | α and β | Refractory hypotension, arrest |
| Milrinone | Phosphodiesterase III inhibitor: inotrope plus vasodilator | Patients on beta-blockers or with receptor down-regulation |
| Levosimendan | Calcium sensitiser | Resistant cases |
| Diuretics, nitrates | Reduce preload | Pulmonary oedema once BP is adequate |
Dobutamine raises output; noradrenaline raises pressure. A common pairing is dobutamine for the pump plus noradrenaline if the BP stays low.
All inotropes increase myocardial oxygen demand and can extend an infarct or trigger arrhythmias. Use the lowest effective dose. Nitrates and morphine must be used with care, because they drop BP further.
Mechanical circulatory support
- Intra-aortic balloon pump (IABP): a balloon in the descending aorta inflates in diastole (raising coronary and cerebral perfusion) and deflates in systole (reducing afterload). Used as a bridge to surgery, for example in acute MR or post-infarct VSD. Contraindicated in significant aortic regurgitation and aortic dissection.
- Ventricular assist devices or ECMO as a bridge to recovery or transplant in selected centres.
The balloon pump "pushes in diastole, pulls in systole": inflation feeds the coronaries, deflation unloads the left ventricle.
Complications
- Multi-organ failure (below).
- Arrhythmias, cardiac arrest.
- Acute kidney injury, shock liver, mesenteric ischaemia.
- Hypoxic brain injury.
- Disseminated intravascular coagulation.
- Complications of treatment: line sepsis, bleeding, limb ischaemia from IABP.
Multi-organ failure (multiple organ dysfunction syndrome)
Definition: progressive failure of two or more organ systems in an acutely ill patient, so that homeostasis cannot be kept without support. Triggers include any prolonged shock, sepsis, major trauma, pancreatitis and burns. Mortality rises with the number of organs that fail.
| Organ | How it fails |
|---|---|
| Lungs | ARDS: often the first organ involved; hypoxia, bilateral infiltrates |
| Kidneys | Acute kidney injury (acute tubular necrosis), oliguria, rising creatinine |
| Liver | Ischaemic hepatitis ("shock liver"), jaundice, high transaminases |
| Heart and circulation | Hypotension needing vasopressors |
| Blood | DIC, low platelets |
| Gut | Ileus, stress ulcer bleeding, ischaemic colitis, acalculous cholecystitis |
| Brain | Confusion, reduced consciousness, coma |
| Metabolic | Lactic acidosis, high glucose early, low glucose late |
The SOFA score is used in intensive care to measure organ dysfunction.
Management
Treat the cause, restore perfusion, and support each failing organ: ventilation for ARDS, renal replacement for AKI, blood products for DIC, nutrition (enteral where possible), ulcer and thrombosis prophylaxis, and glucose control.
Expect: the commonest cause of cardiogenic shock (large MI); signs that separate it from septic and hypovolaemic shock (cold peripheries, raised JVP, crackles); the haemodynamic table (low output, high wedge pressure, high SVR); Killip class IV; dobutamine as the inotrope and noradrenaline as the vasopressor; urgent PCI as definitive treatment; how an IABP works and its contraindications; mechanical complications of MI; and the organs involved in multi-organ failure, with ARDS often first.
Quick revision
- Cardiogenic shock = pump failure with hypoperfusion; systolic BP below 90 mmHg, oliguria, cold clammy skin.
- Raised JVP, crackles and S3 point to the heart as the cause.
- Low output, high wedge pressure, high SVR.
- Commonest cause: large anterior MI; Killip IV.
- Primary PCI is the key treatment after MI.
- Dobutamine for output, noradrenaline for pressure, milrinone if on beta-blockers.
- IABP inflates in diastole, deflates in systole; avoid in aortic regurgitation.
- Multi-organ failure: lungs (ARDS), kidneys, liver, blood (DIC), gut, brain.
Written by The House Job from standard references (Kumar and Clark's Clinical Medicine).
FAQ
How do you tell cardiogenic shock from septic shock at the bedside?
Cardiogenic shock gives cold, clammy peripheries with a raised JVP and lung crackles. Early septic shock usually gives warm peripheries, a bounding pulse and a low or normal JVP.
Why should fluids be given cautiously in cardiogenic shock?
Filling pressures are usually already high, so extra fluid worsens pulmonary oedema. A small challenge is reasonable only if filling is low, as in right ventricular infarction.
Which inotrope is used first in cardiogenic shock?
Dobutamine, a β1 agonist that increases contractility and cardiac output. Noradrenaline is added if blood pressure remains low.
What is multi-organ failure?
Failure of two or more organ systems after a severe insult such as shock or sepsis; the lungs, kidneys, liver, clotting system and brain are commonly involved.