Overview

Cardiogenic shock is a life-threatening clinical syndrome in which cardiac dysfunction causes inadequate cardiac output and tissue hypoperfusion. Hypotension is common but is not essential; patients may initially maintain blood pressure through marked vasoconstriction while organ perfusion deteriorates.¹

Acute myocardial infarction is a major cause, but cardiogenic shock may also complicate acute or advanced heart failure, myocarditis, severe valvular disease, mechanical complications of myocardial infarction, arrhythmias and right ventricular failure. Early recognition, rapid identification of the cause and repeated assessment of the patient’s shock trajectory are essential.¹

Anatomy & Physiology

Cardiac output is determined by heart rate and stroke volume. Stroke volume depends on preload, myocardial contractility and afterload. Adequate tissue perfusion also requires sufficient arterial pressure and appropriate distribution of blood flow.

The left ventricle provides systemic blood flow. The right ventricle delivers blood through the pulmonary circulation and maintains left ventricular preload. Failure of either ventricle may therefore cause shock, although the haemodynamic pattern and treatment priorities differ.

Aetiology & Risk Factors

Aetiology

• Acute myocardial infarction with extensive left ventricular injury
• Mechanical complications of myocardial infarction, including ventricular septal rupture, papillary muscle rupture causing acute severe mitral regurgitation, and free-wall rupture with cardiac tamponade
• Acute decompensated heart failure
• Fulminant myocarditis
• Stress cardiomyopathy
• Acute severe mitral or aortic regurgitation
• Critical aortic stenosis
• Prosthetic valve dysfunction
• Right ventricular infarction or other severe right ventricular failure
• Massive pulmonary embolism
• Sustained tachyarrhythmia or severe bradyarrhythmia
• Pericardial tamponade, which is more precisely classified as obstructive shock but may present with overlapping cardiovascular features
• Post-cardiotomy myocardial dysfunction

Risk Factors

The risk of cardiogenic shock is increased by:

• Large or anterior myocardial infarction
• Delayed presentation or delayed coronary reperfusion
• Previous myocardial infarction or heart failure
• Multivessel or left main coronary artery disease
• Older age and frailty
• Diabetes mellitus
• Chronic kidney disease
• Peripheral vascular disease
• Pre-existing left or right ventricular dysfunction

Pathophysiology

Severe myocardial dysfunction reduces stroke volume and cardiac output. The resulting fall in arterial pressure activates the sympathetic nervous system and renin–angiotensin–aldosterone system, causing tachycardia, vasoconstriction and fluid retention.

These compensatory responses may temporarily preserve blood pressure but increase myocardial oxygen demand and ventricular afterload. Coronary perfusion may fall, worsening myocardial ischaemia and contractility. Elevated ventricular filling pressures produce pulmonary or systemic congestion.

Persistent hypoperfusion causes anaerobic metabolism, lactate accumulation, endothelial dysfunction, inflammation and progressive renal, hepatic, neurological and gastrointestinal injury. Vasodilatation may develop in advanced shock, creating a mixed cardiogenic–vasodilatory phenotype.^1,3

Clinical Manifestations

Presentation depends on the cause, ventricle involved and stage of shock.

• Chest pain or other symptoms of myocardial ischaemia
• Dyspnoea, orthopnoea or acute pulmonary oedema
• Fatigue, weakness or exercise intolerance
• Palpitations
• Presyncope or syncope
• Confusion or reduced consciousness
• Reduced urine output
• Cold or mottled extremities

Signs of hypoperfusion

• Cool, pale, clammy or mottled skin
• Delayed capillary refill
• Narrow pulse pressure
• Weak peripheral pulses
• Altered mental state
• Oliguria
• Hypotension
• Tachycardia, although bradycardia may occur
• Elevated lactate or metabolic acidosis

Signs suggesting the underlying phenotype

• Pulmonary crepitations, hypoxaemia or pulmonary oedema suggest left-sided congestion
• Elevated jugular venous pressure, peripheral oedema or hepatomegaly suggest systemic venous congestion
• Elevated jugular venous pressure with relatively clear lungs may suggest predominant right ventricular failure
• A new systolic murmur after myocardial infarction may indicate acute mitral regurgitation or ventricular septal rupture
• Marked pulse-pressure variation or muffled heart sounds may suggest cardiac tamponade
• Fever and warm peripheries may indicate a mixed cardiogenic–vasodilatory state

Diagnosis

Cardiogenic shock is a clinical and haemodynamic syndrome rather than a diagnosis established by one test. It should be suspected when cardiac dysfunction is accompanied by evidence of tissue hypoperfusion. Persistent hypotension, commonly a systolic blood pressure below 90 mmHg or the need for circulatory support, strengthens the diagnosis but is not mandatory.^1,2

Assessment should occur concurrently with initial resuscitation.

Immediate assessment

• Airway, breathing and circulation
• Continuous cardiac rhythm, blood pressure and oxygen-saturation monitoring
• Focused history, including chest pain, heart failure symptoms, medications and the timing of deterioration
• Examination for hypoperfusion, congestion, murmurs and signs of the underlying cause
• Serial reassessment of mental state, urine output, peripheral perfusion, lactate and haemodynamic support requirements

Investigations

• 12-lead ECG: identifies acute ischaemia, infarction or arrhythmia.
• Bedside echocardiography: assesses left and right ventricular function, regional wall-motion abnormalities, filling, valvular disease, pericardial effusion and mechanical complications.
• Arterial or venous blood gas: evaluates lactate, pH, oxygenation and ventilation.
• Blood tests: full blood count, electrolytes, renal and liver function, glucose, troponin, coagulation studies and other tests directed by the suspected cause.
• Chest radiograph: may demonstrate pulmonary oedema or an alternative respiratory diagnosis.
• Coronary angiography: urgently indicated when acute coronary occlusion is suspected and revascularisation is appropriate.^4,5
• Pulmonary artery catheterisation: may help define left-, right- or biventricular shock, clarify mixed phenotypes and guide escalation or temporary mechanical circulatory support in selected patients.¹

Important alternatives and contributors include hypovolaemic, distributive and obstructive shock. Mixed shock states are common, particularly after cardiac arrest, prolonged shock, infection or systemic inflammation.

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Classification

The Society for Cardiovascular Angiography and Interventions (SCAI) SHOCK classification describes shock severity and should be reassessed over time.²

An A modifier denotes cardiac arrest. Prognosis also depends on the cause, shock phenotype and non-modifiable factors such as age, neurological injury and frailty.²

Treatment

Management requires simultaneous stabilisation, treatment of the cause and prevention of further organ injury. Early involvement of a multidisciplinary shock team and transfer to an advanced shock centre should be considered when shock is severe or progressing.¹

Immediate management

• Provide oxygen for hypoxaemia and ventilatory support when required.
• Establish arterial and reliable venous access.
• Monitor cardiac rhythm, blood pressure, urine output, lactate and end-organ function.
• Correct severe electrolyte, glucose, acid–base and temperature abnormalities.
• Give cautious fluid challenges only when low preload is suspected; indiscriminate fluid administration may worsen pulmonary oedema.
• Avoid unnecessary delays in definitive treatment while pursuing haemodynamic measurements.

Haemodynamic support

• Vasopressors: norepinephrine is commonly preferred when vasopressor support is required to maintain perfusion pressure.¹
• Inotropes: dobutamine or a phosphodiesterase-3 inhibitor may be considered when low cardiac output persists despite adequate perfusion pressure, although both may provoke hypotension or arrhythmias.
• Use the lowest effective dose and reassess frequently because vasoactive drugs increase myocardial workload and have not been shown to correct the underlying cause.

Cause-specific treatment

• Acute myocardial infarction: urgent coronary angiography and revascularisation. In multivessel disease with shock, the initial percutaneous intervention generally targets the culprit vessel rather than routine immediate multivessel intervention.^4,5
• Mechanical complication: urgent cardiothoracic and interventional assessment for repair or surgery.
• Arrhythmia: electrical or pharmacological treatment according to haemodynamic stability and the rhythm.
• Acute severe valvular disease: stabilisation followed by urgent surgical or transcatheter intervention where appropriate.
• Myocarditis or acute heart failure: treat the cause and assess for advanced heart-failure support when recovery is uncertain.

Temporary mechanical circulatory support

Temporary mechanical circulatory support may be considered for selected patients with persistent or deteriorating shock despite initial treatment. Device selection should match the ventricular phenotype, oxygenation requirements, treatment goal, contraindications and local expertise.¹

Options include an intra-aortic balloon pump, percutaneous ventricular assist devices and venoarterial extracorporeal membrane oxygenation. Routine unselected use is not supported: early extracorporeal life support did not reduce 30-day mortality in infarct-related cardiogenic shock and increased complications in the ECLS-SHOCK trial.⁶

Complications & Prognosis

Complications

• Multiorgan failure
• Acute kidney injury
• Ischaemic hepatitis
• Encephalopathy or hypoxic–ischaemic brain injury
• Mesenteric or peripheral limb ischaemia
• Acute respiratory failure
• Ventricular and supraventricular arrhythmias
• Cardiac arrest
• Thromboembolism
• Bleeding, infection, haemolysis or vascular injury related to invasive procedures and circulatory-support devices
• Death

Prognosis

Cardiogenic shock has a high short-term mortality despite modern reperfusion, critical care and circulatory-support strategies. Prognosis depends on the reversibility of the cause, severity and duration of hypoperfusion, response to initial treatment and development of neurological or multiorgan injury.^1,3

Poor prognostic features include:

• Higher or worsening SCAI stage
• Cardiac arrest with neurological injury
• Persistent or rising lactate
• Progressive acidosis
• Oliguria or worsening renal and hepatic function
• Biventricular failure
• Increasing vasopressor or mechanical-support requirements
• Advanced age, frailty and major comorbidity
• Failure to correct the underlying cause

Survivors require reassessment of ventricular function, guideline-directed cardiovascular therapy where tolerated, cardiac rehabilitation and follow-up for heart failure, arrhythmias and device-related complications.

References

1. Sinha SS, Morrow DA, Kapur NK, Kataria R, Roswell RO. 2025 concise clinical guidance: an ACC expert consensus statement on the evaluation and management of cardiogenic shock. J Am Coll Cardiol. 2025;85(16):1618–1641. doi:10.1016/j.jacc.2025.02.018
2. Naidu SS, Baran DA, Jentzer JC, et al. SCAI SHOCK stage classification expert consensus update: a review and incorporation of validation studies. J Soc Cardiovasc Angiogr Interv. 2022;1(1):100008. doi:10.1016/j.jscai.2021.100008
3. van Diepen S, Katz JN, Albert NM, et al. Contemporary management of cardiogenic shock: a scientific statement from the American Heart Association. Circulation. 2017;136(16):e232–e268. doi:10.1161/CIR.0000000000000525
4. McDonagh TA, Metra M, Adamo M, et al. 2021 ESC guidelines for the diagnosis and treatment of acute and chronic heart failure. Eur Heart J. 2021;42(36):3599–3726. doi:10.1093/eurheartj/ehab368
5. Rao SV, O’Donoghue ML, Ruel M, et al. 2025 ACC/AHA/ACEP/NAEMSP/SCAI guideline for the management of patients with acute coronary syndromes. Circulation. 2025;151(13):e771–e862. doi:10.1161/CIR.0000000000001309
6. Thiele H, Zeymer U, Akin I, et al. Extracorporeal life support in infarct-related cardiogenic shock. N Engl J Med. 2023;389(14):1286–1297. doi:10.1056/NEJMoa2307227