Cardiogenic shock

• Cardiogenic shock is a state of low cardiac output and tissue hypoperfusion caused by pump failure, not by volume loss (hypovolaemic) or widespread vasodilation (distributive).
• It is uncommon but devastating: it follows a heart attack in up to 10% of patients, and 30-day mortality is about 40% and 1-year mortality around 50-58% even with modern care. ^[2]
• The cornerstone of treatment is treating the cause, above all early revascularisation in myocardial infarction, plus early norepinephrine to support perfusing pressure and an inotrope to support contractility.
• Severity is graded with the SCAI shock stages A to E, which move as the patient improves or deteriorates and which predict mortality strongly.
• Temporary mechanical circulatory support (intra-aortic balloon pump, Impella, venoarterial ECMO) is used for patients who do not stabilise on drugs, selected by a multidisciplinary shock team.

By the end of this page you should be able to:

1. Define cardiogenic shock clinically and hemodynamically, and distinguish it from other shock types.
2. Stage a patient with the SCAI classification and name the serum and hemodynamic thresholds that separate the stages.
3. Choose and justify first-line and second-line vasopressors and inotropes, with doses and cautions.
4. Match a patient with LV, RV or biventricular failure to the appropriate temporary mechanical circulatory support device.
5. Outline the stages-of-management algorithm for the hypotensive and the normotensive patient.
6. Communicate prognosis honestly and recognise situations in which continued escalation is unlikely to help.

Cardiogenic shock is therefore "cold" and usually "wet": the patient is poorly perfused and commonly congested. Two less recognised variants exist and are easy to miss. Normotensive cardiogenic shock occurs when compensatory vasoconstriction keeps the blood pressure normal despite a low cardiac output and severe hypoperfusion; it carries a similarly high mortality. "Cold and dry" shock occurs in patients with an already fall in output but little congestion, for example early decompensation of chronic heart failure; these patients may respond to diuretics as well as perfusion support. A "warm and wet" picture with low systemic vascular resistance points to a mixed cardiogenic-distributive picture, often with a systemic inflammatory response. ^{[4][6] [5]}

Cardiogenic shock sits at the extreme end of the spectrum of acute heart failure, and many textbooks describe it as a short paragraph inside that chapter. It deserves far more. In the 2021 European Society of Cardiology (ESC) Heart Failure Guidelines, acute heart failure is divided into four clinical phenotypes: acute decompensated heart failure, acute pulmonary oedema, isolated right ventricular failure and cardiogenic shock. Cardiogenic shock is the phenotype in which tissue hypoperfusion, rather than congestion alone, dominates, and it is the only one of the four in which inotropes and short-term mechanical circulatory support are central recommendations. The guideline stresses its syndromic nature: tissue hypoperfusion leading to multi-organ failure and death; the two routes by which it develops, an acute cardiac insult versus progression of advanced chronic heart failure; and the normotensive variant produced by compensatory vasoconstriction. ^[7]

A practical bedside framework borrowed from heart failure care separates patients by cold versus warm (perfusion) and wet versus dry (congestion). Classic cardiogenic shock is cold and wet. About one third of patients fall outside that picture. ^[5]

Cardiogenic shock is uncommon, but it is the commonest cause of inpatient death after acute myocardial infarction and a major cause of death in acute heart failure.

• Incidence. Around 5 to 10% of patients presenting with ST-elevation myocardial infarction and about 2.5% of those with non-ST-elevation myocardial infarction develop cardiogenic shock, which is an estimated 40,000 to 50,000 patients per year in the United States. The overall incidence has fallen since the introduction of early revascularisation. Cardiogenic shock now accounts for roughly 30% of cardiogenic shock admissions related to ischaemia and roughly 50% related to acute decompensated heart failure. ^[2][5]
• In the intensive care unit. Cardiogenic shock accounts for about 7 to 10% of ICU admissions overall and for far more in cardiac ICUs. ^[4]
• Acute myocardial infarction setting. Up to 10% of patients develop shock early after myocardial infarction. Shock that develops more than 48 hours after the infarct carries a higher mortality than early shock. ^[2][5]
• France, across three national registries. The proportion of infarcts complicated by shock fell so that it has become an uncommon complication, reported at 2.8% of acute myocardial infarctions in the most recent period. ^[4]
• Hospital course. Overall hospitalisations for cardiogenic shock roughly tripled between 2004 and 2018. ^[5]
• Sex. Reported mortality is higher in women than in men in some age groups, both in infarct-related and non-infarct-related shock. ^[5]

Mortality estimates differ by source and geography, which is worth holding in your head rather than smoothing over. Infarct-related shock is associated with about 40% mortality at 30 days and about 50% at one year in the major North American review, while a broader international perspective gives one-year mortality of about 58% and an ICU or in-hospital mortality for modern series in the 31 to 39% range. French registry data put one-year mortality for patients who develop shock after infarction at about 58%. The simplest clinical rule is that about one patient in three does not leave hospital once cardiogenic shock is established. ^[2][4][5]

The causes are best grouped by the structure that fails, because the first treatment follows from the site.

• Myocardium. Acute myocardial infarction (still about 30% of cases), acute-on-chronic heart failure (about 50% of admissions), myocarditis, Takotsubo syndrome, peripartum cardiomyopathy, sepsis-induced cardiomyopathy, post-cardiotomy failure, medication toxicity (beta-blockers, calcium-channel blockers, angiotensin-converting-enzyme inhibitors, opiates), myocardial contusion. ^[4]
• Pericardium. Cardiac tamponade, constrictive pericarditis.
• Valves. Acute regurgitation from endocarditis or chordal rupture, aortic stenosis, mitral stenosis, valve thrombosis.
• Conduction and rhythm. Sustained ventricular tachyarrhythmias, unstable supraventricular tachyarrhythmias, high-grade atrioventricular block, bradycardia.
• Right ventricle. Massive pulmonary embolism, severe right ventricular infarction, pulmonary arterial hypertension.
• Mechanical complications of infarction. Ventricular septal rupture, free wall rupture, acute severe mitral regurgitation from papillary muscle rupture.

The two largest aetiologies behave differently. Infarct-related shock is an abrupt event, usually with mildly to moderately reduced ejection fraction and a disproportionately severe hemodynamic picture, and it triggers a systemic inflammatory response. Acute-on-chronic shock builds on pre-existing vasoconstrictor upregulation (angiotensin, endothelin-1, catecholamines), higher systemic vascular resistance, adrenergic desensitisation, and often beta-blocker use; its mortality is lower than in de novo shock. ^[4][5]

Risk factors for shock developing after myocardial infarction are older age, anterior infarction, diabetes mellitus, multivessel coronary artery disease, previous infarction or angina, pre-existing heart failure, ST-elevation myocardial infarction and bundle branch block. ^[5]

The common pathway is a fall in cardiac output that triggers compensatory responses that initially help and then hurt.

1. Low output lowers mean arterial pressure and renal perfusion.
2. Sympathetic activation raises heart rate and systemic vascular resistance.
3. Renal hypoperfusion activates the renin-angiotensin-aldosterone system, causing sodium and water retention and vasoconstriction.
4. Splanchnic venoconstriction returns about half of the total blood volume from the splanchnic bed to the central circulation. ^[5]
5. These responses raise ventricular filling pressures, afterload and myocardial oxygen demand, worsening ischemia and falling contractility further.
6. Congestion raises pulmonary capillary and central venous pressures; venous congestion of the kidneys and liver produces organ dysfunction.
7. Eventually microcirculatory dysfunction, inflammation, anaerobic metabolism and oxidative stress overwhelm compensation. Lactic acidosis develops, catecholamine sensitivity falls, cytokines, nitric oxide and reactive oxygen species accumulate, vascular tone collapses and the picture becomes "vasoplegic" and refractory.

In acute infarct-related shock the insult is sudden and the ejection fraction is often only mildly to moderately reduced. In acute-on-chronic failure the same cycle develops on top of already low reserve. Lactate rises early: a pathologic threshold is over 2 mmol/L, and complete lactate clearance by 8 hours is an independent predictor of survival. ^{[2][4][5] [3][6]}

Ask, as always, for symptoms in the patient's own words, remembering that dyspnoea and fatigue are far commoner than chest pain.

• Symptoms of hypoperfusion. Confusion or lethargy (the relatives usually notice first), dizziness or syncope, oliguria (the patient reports passing very little urine), shortness of breath at rest or on minimal exertion.
• Symptoms of congestion. Orthopnoea, paroxysmal nocturnal dyspnoea, ankle or abdominal swelling, weight gain in recent days.
• Chest pain or palpitations. May indicate acute myocardial infarction or arrhythmia as the trigger.
• Context. Recent infarction; infection or non-adherence to treatment in a patient with known heart failure; new medication such as beta-blocker or calcium-channel blocker overdose; pregnancy; or major trauma.
• Arrhythmia. Atrial fibrillation occurs in around 20% of patients; ventricular fibrillation in 9 to 19%; high-grade atrioventricular block in 4.5 to 21%. ^[4]

• General inspection. Agitated or drowsy; cold, clammy, often grey or mottled peripheries; prolonged capillary refill; cyanosis.
• Pulse. Rapid, weak and thready; may be irregular. A narrow pulse pressure is common.
• Blood pressure. Systolic pressure under 90 mmHg in classic shock, but remember the normotensive variant and the delayed-time course.
• Jugular venous pressure. Raised in left-sided failure with congestion; very high in right ventricular or biventricular failure.
• Heart. Tachycardia, third heart sound (ventricular gallop S3), and sometimes a fourth sound; a new pansystolic murmur suggests papillary muscle rupture or ventricular septal defect. The apex may be displaced in chronic failure.
• Lungs. Crackles from pulmonary oedema, or clear lungs in "cold and dry" shock.
• Abdomen and peripheries. Right upper quadrant tenderness and hepatomegaly from congestion; ascites in chronic right failure; pitting oedema.
• Urine output. Under 30 mL per hour is a red flag for hypoperfusion. ^{[4][6] [5]}
• Monitoring values. Arterial lactate over 2 mmol/L marks hypoperfusion; complete normalisation by about 8 hours predicts survival. Central venous oxygen saturation and the veno-arterial carbon dioxide gap (elevated over 6 mmHg) are useful surrogates of low cardiac output. ^[4]

Cardiogenic shock must be separated from the other three mechanistic shock types (hypovolaemic, distributive, obstructive), from mixed shock and from "pseudo-shock" (severe hypotension from a reversible non-cardiac cause). The table summarises the discriminatory features.

Mixed cardiogenic-septic shock is common and difficult: sepsis causes cardiomyopathy and vasodilation, while fluid loading can precipitate pulmonary oedema. The relative contribution of each has to be reassessed repeatedly. ^[6]

• ECG. Looks for ST-elevation infarction, ischaemia, new bundle branch block or high-grade block, ventricular or supraventricular tachycardia. Repeat it whenever the clinical picture changes.
• Chest radiograph. Pulmonary oedema "bat's wings", Kerley B lines, cardiomegaly; may be normal in dry shock.
• Transthoracic echocardiography (TTE). The single most useful test. It gives biventricular function, valvular pathology, right ventricular function, pericardial effusion, and filling pressures, and it can be repeated at the bedside. It lets you classify the patient as LV-dominant, RV-dominant or biventricular. ^[4]
• Arterial blood gas, lactate, full blood count, urea and electrolytes, liver function tests, high-sensitivity troponin, natriuretic peptide (BNP or NT-proBNP). Troponin identifies myocardial injury; natriuretic peptides support a cardiac cause of pulmonary oedema.
• Urine output and creatinine. Quantify renal hypoperfusion.
• Point-of-care lung ultrasound. Detects B-lines (pulmonary congestion) with higher sensitivity than the chest radiograph.

• Transoesophageal echocardiography if transthoracic windows are poor or to guide device placement.
• Invasive haemodynamic monitoring with a pulmonary artery (Swan-Ganz) catheter in patients receiving mechanical circulatory support or with complex phenotypes: cardiac output, cardiac index, cardiac power output (mean arterial pressure times cardiac output divided by 451), pulmonary capillary wedge pressure (elevated over 18 mmHg), right atrial pressure (elevated over 12 mmHg), pulmonary artery pulsatility index (under 1.5 suggests right ventricular failure). These readings guide device selection and weaning. ^{[4] [5][6]}
• Coronary angiography in any patient with a suspected acute coronary cause; emergent revascularisation is the only therapy with proven mortality benefit in infarct-related shock. ^[2][4]
• Cardiac MRI or CT when the diagnosis is uncertain, for example in myocarditis or mechanical complications.

The most widely used research definition is that of the SHOCK trial, and it is a good modern teaching definition: hypotension (systolic blood pressure under 90 mmHg for 30 minutes or longer, or the need for support to keep it at 90 mmHg or above), end-organ hypoperfusion (cool extremities, urine output under 30 mL per hour, heart rate at least 60 per minute), cardiac index under 2.2 L/min/m² and pulmonary capillary wedge pressure at least 15 mmHg, secondary to cardiac dysfunction. ^{[5] [3][4]}

The Society for Cardiovascular Angiography and Interventions (SCAI) classification, endorsed by the main US and European cardiology, critical care and thoracic surgery societies, gives a universal language for severity. It runs from A (at risk) to E (extremis), with an (A) modifier for cardiac arrest with concern for anoxic brain injury. It is dynamic; a patient's stage changes as they respond or deteriorate, and the stages correlate strongly with mortality in every subgroup tested. ^[3][5][6]

Two practical points from the consensus: lactate can be normal early, or dissociated from hemodynamics in chronic heart failure, so normal lactate never excludes shock. And stage C is the moment at which the first intervention beyond fluid resuscitation must be started; the therapy given is what separates stage C from stage D. ^[3][5]

Forrester and Diamond's classification, expanded by later authors, separates patients by peripheral perfusion (cold versus warm) and volume status (wet versus dry), using invasive haemodynamic data. Classic shock is cold and wet; euvolaemic ("cold and dry") shock is more common in acute-on-chronic failure; "warm and wet" (vasodilatory or mixed) shock is common after infarction with systemic inflammation. ^[4][5]

Cardiac power output and aortic pulsatility index are useful advanced predictors of outcome; the former is more reliable in acute infarct shock and the latter in acute decompensated failure. ^[5]

Management runs in parallel, not in sequence: treat the cause, stabilise perfusion, decongest, provide respiratory support, monitor, and escalate mechanically if needed.

1. Call the shock team and, when relevant, arrange transfer to an experienced high-volume centre within a hub-and-spoke network. Shock teams include an advanced heart failure cardiologist, interventional cardiologist, cardiothoracic surgeon and intensivist. ^[6]
2. Airway, oxygen, ventilation. Acute respiratory failure occurs in 50 to 88% of patients and over 80% need some respiratory support. Start with oxygen; escalate to non-invasive ventilation or intubation depending on mental status and gas exchange. Positive-pressure ventilation lowers preload and afterload and reduces the work of breathing. ^[4]
3. Vascular access. Large-bore peripheral or central; arterial line for continuous pressure.
4. Identify and treat the cause now. In infarct-related shock, emergent percutaneous coronary intervention of the culprit lesion is the only therapy shown to improve survival. Complete multivessel PCI of all lesions at the index procedure is not supported; the CULPRIT-SHOCK trial showed that a culprit-lesion-only strategy reduced the composite of 30-day mortality or severe renal failure requiring renal replacement therapy (45.9% versus 55.4%) and 30-day mortality (43.3% versus 51.6%). ^[2][4]
5. Ultrasound. Formal transthoracic echocardiography as soon as possible for phenotyping and for excluding tamponade, mechanical complications and severe valvular disease.
6. Fluids only when clearly needed. Fill only if hypovolaemic or with low filling pressures; most patients are "wet" or euvolaemic, and unneeded fluid worsens congestion.
7. Start vasoactive drugs early. Do not wait for full staging; begin norepinephrine in hypotensive shock and add an inotrope when cardiac index remains low.

The aim is to restore perfusion pressure and cardiac output at the lowest possible dose for the shortest possible time, because every one of these drugs increases myocardial oxygen demand and can provoke arrhythmias. ^[4][5]

Practical rule of thumb from current consensus documents: ^[5][6]

• Hypotensive shock (low MAP): inopressor first. Norepinephrine is recommended as first-line vasopressor in cardiogenic shock. It increases systemic vascular resistance and, in cardiogenic shock, blood pressure rises with an increase in cardiac index without an increase in heart rate. Its average half-life is 2 to 3 minutes, so it is titrated rapidly. ^[4][5]
• Concurrent or sequential inotrope: dobutamine or milrinone is added once perfusion pressure is supported, because vasopressors alone raise afterload. Dobutamine is the usual first-choice inotrope; milrinone is an alternative, particularly when renal function is adequate or beta-blocker use makes levosimendan attractive. Levosimendan is usually reserved for patients on chronic beta-blocker therapy. ^[4][5][6]
• Normotensive or stabilised hypotensive shock: inodilator alone (dobutamine or milrinone), once mean arterial pressure is adequate with or without low-dose vasopressor.
• Avoid dopamine as single agent; it is associated with higher mortality and more arrhythmias, particularly in the cardiogenic shock subgroup of the SOAP II trial. ^[4][5]
• Epinephrine should not be first choice. Compared with norepinephrine it produces more arrhythmias, tachycardia, lactic acidosis and refractory shock at the same haemodynamic efficacy; an individual-patient meta-analysis reported a three-fold increase in death. Low-dose epinephrine remains reasonable in selected situations (for example severe bradycardia or post-cardiotomy). ^[4][5]
• Vasopressin (V1a and V2 effects, fixed dose 0.01 to 0.03 units per minute, not titrated) is added to norepinephrine in mixed vasodilatory shock requiring high doses. ^[6][8]

Trial evidence worth knowing for examinations, kept short: norepinephrine beat dopamine in the cardiogenic shock subgroup of the SOAP II trial; epinephrine caused more refractory shock than norepinephrine in the OPTIMA-CC trial; milrinone and dobutamine were equivalent for the composite outcome in the DOREMI trial; levosimendan did not improve 180-day mortality over dobutamine in SURVIVE. ^[4][5]

Persistent congestion at 24 hours predicts worse outcomes. In venous congestion, loop diuretics plus thiazide (or thiazide-like) give sequential nephron blockade and more effective diuresis, with careful electrolyte replacement. Vascular congestion (volumes to keep below RA pressure 10-12 mmHg, pulmonary capillary wedge pressure 15-18 mmHg) ^[6] should be a daily target.

Vasodilators (nitroprusside, nitroglycerin) can be used as a bridge in normotensive or hypertensive cardiogenic shock with adequate contractile reserve; nitroglycerin is more venodilating and is often used when volume overload or acute coronary syndrome is present. Amiodarone is the first-line anti-arrhythmic in shock with structural heart disease. ^[4][6]

Use positive-pressure ventilation when there is respiratory distress: it improves oxygenation and decarboxylation, unloads respiratory muscles and improves cardiac output by reducing preload and afterload. Modality (oxygen mask, CPAP, BiPAP, invasive mechanical ventilation) is chosen by consciousness level, acidosis and haemodynamics. Non-invasive ventilation is first-line in cooperative patients with acute cardiogenic pulmonary oedema and without absolute contraindications; in cardiogenic shock it should generally be started after some haemodynamic stabilisation. ^[4]

The second half of management is etiology-specific and should not be deferred.

• Acute myocardial infarction. Emergent culprit-lesion PCI; consider urgent coronary artery bypass grafting for non-revascularisable lesions or mechanical complications. ^[2][4]
• Mechanical complications. Ventricular septal rupture, free wall rupture and acute severe mitral regurgitation need urgent surgical repair, often with temporary support.
• Valvular disease. Percutaneous balloon valvuloplasty, transcatheter aortic valve replacement or edge-to-edge mitral repair can bridge or cure; endocarditis-related deterioration generally needs surgery.
• Arrhythmia. Immediate cardioversion for unstable ventricular arrhythmias; amiodarone (300 mg over 20 minutes, then repeat 150 mg, then 1 mg/min infusion) for electrical storm; atropine or temporary transvenous pacing for high-grade block. ^[4]
• Takotsubo, myocarditis, peripartum cardiomyopathy. Supportive, often with immunosuppression or supportive care as the trigger dictates.
• Tamponade or massive pulmonary embolism. Pericardiocentesis or thrombolysis/thrombectomy as appropriate.

Mechanical support should be considered by the shock team when tissue perfusion remains inadequate despite vasoactives, or when the patient is in extremis. It supports perfusion and unloads the ventricle without increasing myocardial oxygen demand, as a bridge to recovery, intervention or advanced heart-failure therapies. Device selection weighs the site of failure (left, right or biventricular), required flow, need for oxygenation, feasibility and operator expertise. Evidence from randomised trials is limited, and practice is largely team and centre-dependent. ^[6]

• Intra-aortic balloon pump (IABP). Counterpulsation in the descending aorta; gives modest support (roughly 0.5 to 1 L/min) and the easiest bedside placement, with a good safety profile. It was not associated with reduced mortality in the IABP-SHOCK II trial of infarct-related shock, but observational data in heart-failure-related shock are encouraging, with "super-responders" who stabilise without further escalation. It remains a reasonable first device when end-organ function is relatively preserved and collapse is not imminent, and is contraindicated in severe aortic regurgitation. ^[6]
• Impella (percutaneous ventricular assist device). Axial flow from the left ventricle to the aorta gives direct unloading; the CP model provides up to 4 L/min, the axillary 5.5 up to 5.5 L/min. The IMPRESS trial showed no mortality benefit over IABP in infarct-related shock, and many centres now reserve the CP as short-term support or a bridge to transfer. ^[6]
• Venoarterial ECMO. Full cardiopulmonary support; bypasses the right ventricle and provides gas exchange, and can be placed percutaneously at the bedside. It increases left ventricular afterload, so LV venting is often needed. The ECLS-SHOCK trial showed no reduction in 30-day mortality with early ECMO in infarct-related shock and more bleeding and limb ischaemia; ECMO should be reserved for carefully selected refractory patients and is not first-line for all. ^{[6] [4]}
• TandemHeart. Transseptal centrifugal pump, 4 to 6 L/min, needs specific expertise. ^[6]
• Right-sided devices. Impella RP and ProtekDuo for right ventricular shock; ProtekDuo can be configured with an oxygenator.

Durations approved by the US regulator are short but off-label use for longer courses is common. Multidisciplinary shock teams are the practical answer to device selection and timing. ^[6]

Transfer to a shock centre within a hub-and-spoke network should be considered early; patients treated at high-volume centres have better outcomes. Invasive haemodynamic monitoring with a pulmonary artery catheter is particularly valuable when mechanical support is in place. After stabilisation, optimise guideline-directed medical therapy for the underlying heart failure. Palliative care involvement should not be delayed in patients with refractory shock or severe comorbidity; a third of patients do not survive the first hospitalisation, and recovery, when it happens, can still leave lasting morbidity. ^[4][6]

• Progressive multi-organ failure. Kidney and liver dysfunction, gut ischaemia, encephalopathy.
• Arrhythmias. Atrial fibrillation in about 20%, ventricular fibrillation in 9 to 19%, high-grade atrioventricular block in 4.5 to 21%. ^[4]
• Mechanical complications of infarction. Ventricular septal rupture, free wall rupture, acute severe mitral regurgitation.
• Device complications. Vascular injury, bleeding, haemolysis and renal failure (especially with Impella CP), limb ischaemia, "north-south" syndrome on ECMO, infection.
• Thrombosis and stroke. From reduced output, arrhythmia and indwelling devices.
• Respiratory failure. Common and may require mechanical ventilation.

Mortality remains high. About 40% die at 30 days after infarct-related shock and about 50% at one year, with broader international series reporting one-year mortality around 58% and 30-day survival nearer to 50%. Non-infarct-related shock has better survival than infarct-related shock in some series, and acute-on-chronic failure does better than de novo shock. About one third of patients do not survive the first hospitalisation. Survivors have high readmission rates and may develop chronic heart failure. ^[2][4][5]

Factors associated with worse outcome include older age, female sex in certain age groups, delayed shock (over 48 hours after infarction), high SCAI stage, elevated and poorly clearing lactate, high vasopressor doses, mechanical ventilation, renal dysfunction, large infarct size and prior comorbidity. ^[5]

• Pregnancy. Cardiogenic shock in pregnancy (peripartum cardiomyopathy, massive pulmonary embolism, amniotic fluid embolism) needs obstetric, cardiology and critical-care teams; delivery timing depends on maternal stability.
• Older adults. Higher mortality; mechanical support and transplantation may be less appropriate; goals of care should be discussed early.
• Children. Rare and usually a separate entity; outside this page's scope.

• A single transthoracic echocardiogram is the pivotal test: look for reduced ventricular function, a large effusion or a valve catastrophe whenever a hypotensive patient does not respond to fluids.
• Norepinephrine and dobutamine are cheap and widely available; a peripheral noradrenaline infusion through a large vein with close monitoring is acceptable when central access is delayed.
• Intra-aortic balloon pumps are cheaper than Impella or ECMO and may be the only mechanical support available; ECMO requires experienced perfusion and surgical teams.
• Early transfer to a centre with shock capability is usually better than persisting locally; arrhythmia control, inotropes and careful fluid balance are the universal first steps.
• Vasopressin and levosimendan are often not available; rely on norepinephrine and dobutamine.

• Cardiogenic shock is pump failure producing low cardiac output and hypoperfusion, usually with congestion; recognition does not require hypotension.
• Infarct-related shock affects up to 10% of infarct patients; acute decompensated heart failure is now a comparably common overall cause.
• Common causes group into myocardial, pericardial, valvular, rhythm/conduction and right-ventricular aetiologies; mechanical complications are surgical emergencies.
• Staging with SCAI A to E (plus the cardiac-arrest modifier) gives a shared, dynamic severity language.
• Early revascularisation of the culprit artery is the only therapy proven to improve survival in infarct-related shock; culprit-only PCI beat multivessel PCI in CULPRIT-SHOCK.
• Norepinephrine is first-line vasopressor; add dobutamine or milrinone for inotropy; avoid dopamine; avoid epinephrine as first choice; vasopressin and levosimendan are second line/selected use.
• Target a perfusing mean arterial pressure (around 65 mmHg is a common rule of thumb, although not firmly evidenced in cardiogenic shock) ^[4], a cardiac index over 2.2 L/min/m² and falling filling pressures. ^[6]
• Mechanical support (IABP, Impella, venoarterial ECMO, right-sided devices) is selected by a shock team; IABP-SHOCK II and ECLS-SHOCK showed no mortality benefit for routine early use in infarct-related shock.
• Positive-pressure ventilation, early decongestion, cause-specific treatment and early transfer to a high-volume centre complete the package.
• Mortality is 40% at 30 days and 50 to 58% at one year; trajectory over the first hours is the best predictor.

Acute myocardial infarction; acute decompensated heart failure; acute pulmonary oedema; shock of all types (hypovolaemic, distributive, obstructive); venoarterial extracorporeal membrane oxygenation; intra-aortic balloon pump; Impella and other percutaneous ventricular assist devices; heart transplantation and durable ventricular assist devices; arrhythmia management; acute kidney injury; critical care and intensive care monitoring.