01OverviewDefinition, clinical context and the essential points that orientate the chapter.
Cardiogenic shock is a dynamic syndrome that may begin before profound hypotension. Serial perfusion assessment and lactate trajectory are more informative than waiting for multi-organ failure.
Treatment has three simultaneous arms: restore oxygenation and perfusion, identify and reverse the cardiac cause, and decide early whether conventional support is succeeding or a shock/MCS centre is required.
The haemodynamic phenotype matters. LV congestion, RV preload dependence, mechanical rupture and mixed septic-cardiogenic shock require different fluid, vasopressor and device strategies.
Key points
- Shock is inadequate tissue perfusion, not a blood-pressure number alone: look for altered mentation, cool/mottled skin, oliguria, narrow pulse pressure, rising lactate and metabolic acidosis.
- Common causes are acute MI, decompensated HFrEF, fulminant myocarditis, severe tachy/bradyarrhythmia, acute valve or post-MI mechanical complication and acute RV failure.
- Bedside echo must rapidly distinguish LV failure, RV failure, tamponade, acute MR, VSD and major valve disease; a single estimated EF does not define the whole shock state.
- In ACS shock, urgent culprit-vessel revascularisation is central; routine immediate non-culprit multivessel PCI is not the default.
- Give fluid only when hypovolaemia or clear preload deficiency is present; repeated empirical boluses worsen pulmonary oedema and RV/LV congestion.
- Use noradrenaline for hypotension and add an inotrope such as dobutamine when low output persists; doses are continuously titrated in critical care, not prescribed as fixed ward doses.
- Vasoactive support is a bridge to cause control, recovery, temporary mechanical support or advanced therapy—not a definitive plan.
- NICE 2026 restricts catheter-based LV microaxial flow pumps to designated PPCI centres with on-site intensive-care expertise and evidence-generation/governance arrangements.
02AetiologyUnderlying causes, associations and risk factors, with why each one matters.
Acute myocardial infarction
Acute myocardial infarction can abruptly impair enough left-ventricular or right-ventricular myocardium to reduce output. Loss of contractility, ischaemic arrhythmia and mechanical complications may each cause or compound shock.
Mechanical or valvular failure
Papillary muscle rupture with acute mitral regurgitation, ventricular septal rupture, prosthetic-valve dysfunction or sudden native-valve failure can obstruct or divert forward flow and may deteriorate rapidly after infarction or intervention.
Diffuse myocardial dysfunction
Decompensated chronic cardiomyopathy, fulminant myocarditis or stress-related myocardial stunning can cause extensive biventricular dysfunction. Limited reserve makes infection, ischaemia or medication interruption important precipitants.
Electrical instability
Sustained ventricular tachycardia, very rapid atrial fibrillation, complete heart block or severe bradycardia can reduce filling time, heart rate or effective contraction, sometimes causing shock despite previously adequate ventricular function.
03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.
- 1Forward flow falls
Loss of contractility, coordinated rhythm or valve competence reduces stroke volume and cardiac output. Tissue hypoperfusion may begin while compensatory vasoconstriction still preserves the measured blood pressure.
- 2Compensation increases cardiac work
Sympathetic and renin–angiotensin activation cause tachycardia, vasoconstriction and fluid retention. These responses may initially support arterial pressure but increase myocardial oxygen demand and afterload, while ongoing retention can worsen congestion.
- 3Filling pressures rise
Left-sided failure can raise pulmonary venous pressure, causing oedema and hypoxaemia. A right-sided phenotype may instead cause systemic venous congestion and inadequate left-ventricular filling; fluid may help demonstrated underfilling but can worsen congestion if given empirically.
- 4A self-sustaining shock cycle develops
Inadequate perfusion and adrenergic stress can raise lactate, while evolving acidaemia, renal and hepatic dysfunction, and inflammation alter vascular tone. Coronary hypoperfusion and acidaemia can further impair contractility, accelerating multi-organ failure.
04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.
Confusion, agitation, cool mottled extremities, weak pulse, oliguria and rising lactate can precede severe hypotension.
Pulmonary oedema, low output and poor LV function after MI or decompensated cardiomyopathy; acute MR or VSD may be the hidden driver.
Raised JVP, hypotension and relatively clear lungs with RV dilation/dysfunction; consider RV infarction, PE or pulmonary-hypertension crisis.
New murmur, abrupt pulmonary oedema, biventricular failure, tamponade/PEA or sudden decline after MI demands surgical-level urgency.
Sustained VT, very rapid AF, complete heart block or severe bradycardia can cause or compound shock; use RCUK peri-arrest pathways.
Fever, vasodilation, infection or inflammatory injury may coexist with cardiac dysfunction; reassess vascular tone, filling and infection rather than assuming a pure phenotype.
05InvestigationsWhat to request, why it matters and how to interpret it.
Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.
- 01
Continuous ECG and immediate 12-lead ECGFirst step - Why
- Detect STEMI/NSTE-ACS, arrhythmia or conduction disease.
- Interpretation and limitations
- STEMI or ongoing ischaemia activates the cath-lab pathway without waiting for biomarkers.
- 02
Point-of-care and formal echocardiography - Why
- Define LV/RV function, valves, VSD, tamponade and gross filling.
- Interpretation and limitations
- Repeat when physiology changes; echo estimates guide but do not replace clinical perfusion or invasive data when shock persists.
- 03
Arterial blood gas, lactate and serial acid-base assessment - Why
- Measure global hypoperfusion and respiratory failure.
- Interpretation and limitations
- Failure of lactate to clear or worsening acidosis despite treatment suggests ongoing inadequate flow and need to escalate.
- 04
FBC, U&E/eGFR, glucose, magnesium, LFT, coagulation, troponin and group-and-save - Why
- Find cause, bleeding, metabolic triggers and end-organ injury and prepare for intervention.
- Interpretation and limitations
- Trend rather than rely on a single value; renal/hepatic injury and thrombocytopenia also affect MCS risk.
- 05
Coronary angiography - Why
- Identify and treat an acute coronary culprit.
- Interpretation and limitations
- In MI shock, revascularise the culprit urgently; stage other lesions unless a specific multidisciplinary reason changes the approach.
- 06
Invasive arterial and selected central/pulmonary haemodynamics - Why
- Titrate vasoactive support and clarify refractory or mixed shock.
- Interpretation and limitations
- Use by experienced critical-care/shock teams; device selection should follow the ventricle and haemodynamic problem, not habit.
06Differential diagnosisRealistic alternatives and the features that help distinguish them.
Septic or distributive shock
Infection, warm vasodilated peripheries and low vascular tone favour distributive shock, although myocardial depression and cardiogenic shock may coexist. The clinical context, cultures, echocardiography and repeated haemodynamic assessment help define a mixed phenotype.
Hypovolaemic or haemorrhagic shock
Fluid loss, bleeding, low venous pressure and small hyperdynamic ventricles favour hypovolaemia. Pulmonary or systemic congestion and impaired ventricular function favour cardiogenic shock, but mixed hypovolaemic and cardiogenic shock may follow infarction or intervention.
High-risk pulmonary embolism
Pulmonary embolism causes obstructive rather than primary pump shock, although secondary right-ventricular failure can be prominent. Sudden dyspnoea, thromboembolic risk and acute right-ventricular pressure overload with a relatively underfilled left ventricle support this diagnosis.
Cardiac tamponade
Tamponade can resemble right-sided cardiogenic shock with raised JVP and low output. A pericardial collection with compatible chamber collapse and respiratory filling variation supports external compression requiring urgent drainage assessment; no single echo sign excludes it.
07ManagementImmediate care, first-line treatment, alternatives and escalation.
01First-lineRecognise and mobiliseFirst stepFirst lineSuspected cardiogenic shock+
- 1Start ABCDE, high-acuity monitoring, arterial blood gas/lactate, ECG, IV access and targeted oxygen/ventilation; call cardiology and critical care immediately.
- 2Obtain urgent bedside echo and look for ACS, arrhythmia, tamponade, acute MR/VSD, RV failure, PE, bleeding or sepsis.
- 3Use cautious fluid only for demonstrated underfilling; avoid routine boluses in congestion.
- 4Insert arterial monitoring early when vasoactive therapy is needed and track urine output and lactate clearance.
02Second-lineRestore cause and perfusionSecond linePersistent hypoperfusion+
- 1For ACS, proceed to immediate angiography and culprit revascularisation; for structural rupture, activate cardiac surgery/intervention without delay.
- 2For unstable tachy/bradyarrhythmia, follow the RCUK electrical cardioversion/pacing route and correct ischaemia/electrolytes.
- 3Start noradrenaline for hypotension and add dobutamine when low output persists, titrating to perfusion rather than a supranormal BP.
- 4Use lung-protective ventilation while avoiding excessive intrathoracic pressure that worsens venous return/RV afterload.
03Third-lineShock-team escalationThird lineEscalationRising lactate, escalating vasoactive requirement or worsening organ injury+
- 1Reassess the diagnosis and correctable lesion with repeat echo, angiography and invasive haemodynamics when useful.
- 2Contact a regional shock/MCS centre before irreversible neurological, renal or hepatic injury develops.
- 3Select temporary support by phenotype and goal: bridge to recovery, intervention, decision, durable LVAD or transplant.
- 4EscalationFor a microaxial LV pump, follow NICE HTG775 centre, governance, consent and evidence-generation requirements; do not treat it as routine ward escalation.
04EscalationRefractory or non-recovering shockEscalationFailure to wean support or no reversible recovery+
- 1Run daily multidisciplinary neurological, cardiac and end-organ reassessment with an explicit recovery/bridge timeline.
- 2Consider durable LVAD or transplantation for eligible advanced-HF patients and VA-ECMO/temporary VAD for selected potentially reversible failure.
- 3Monitor and actively prevent MCS complications including bleeding, limb ischaemia, haemolysis, thrombosis, infection and LV distension.
- 4When recovery or advanced therapy is not achievable, align treatment with documented goals and provide specialist palliative care.
Key medicines and prescribing safety3 treatments · regimens, roles and cautions+
Noradrenaline
The cited ready-to-use SmPC, licensed for adults weighing over 50 kg, starts noradrenaline base at 0.05–0.15 micrograms/kg/min by central IV infusion pump, titrated in 0.05–0.1 micrograms/kg/min steps to perfusion/MAP; its maintenance range is 0.05–1.5 micrograms/kg/min.For this cited product use a central venous catheter and preferably arterial BP monitoring; do not transfer its concentration or limits to another preparation. Watch for arrhythmia, ischaemia and extravasation.
Dobutamine
Usually 2.5–10 micrograms/kg/min by continuous IV infusion, titrated to output and perfusion; higher doses are exceptional.Tachyarrhythmia, increased myocardial oxygen demand, ischaemia and hypotension; ICU/cardiology supervision only.
Furosemide IV
If pulmonary/systemic congestion coexists and perfusion permits, a loop-naive adult commonly starts 20–40 mg IV; prior loop exposure requires a higher response-led dose.Do not reflexively diurese an underfilled RV or profoundly hypovolaemic patient. Monitor BP, urine, renal function and electrolytes.
08ComplicationsImportant consequences, why they occur and why they matter clinically.
Multi-organ dysfunction
Sustained low flow causes acute kidney injury, hepatic injury, encephalopathy, gut ischaemia and lactic acidosis. Their progression narrows treatment options and signals failure to restore effective circulation.
Pulmonary oedema and respiratory failure
Raised left-sided filling pressure drives fluid into alveoli, worsening oxygenation and myocardial ischaemia. Ventilatory support may become necessary but can alter preload and haemodynamics in an unstable circulation.
Arrhythmia and cardiac arrest
Ischaemia, acidaemia, electrolyte disturbance and catecholamine exposure promote ventricular arrhythmia, while severe pump failure may end in pulseless electrical activity or asystole.
Peripheral and mesenteric ischaemia
Profound vasoconstriction and low output reduce limb and bowel perfusion; vasoactive support can intensify this trade-off, so abdominal pain, mottling and threatened extremities require active surveillance.
09Monitoring and follow-upTreatment response, safety checks and longer-term review.
- Continuous ECG, invasive arterial BP, oxygenation/ventilation and temperature.
- Hourly urine output, mental state, skin perfusion and serial lactate/pH to judge response.
- Creatinine/eGFR, potassium, magnesium, LFT, coagulation, haemoglobin and platelets at shock-appropriate frequency.
- Repeat echo for ventricular function, filling, valve/mechanical lesion and response to intervention/support.
- Vasoactive dose trajectory and cumulative fluid balance; escalating requirements are a trigger, not a routine endpoint.
- With MCS: distal limb perfusion, device flow/alarms, haemolysis, bleeding, thrombosis, infection and anticoagulation parameters.
10Special situationsVariants, exceptions and circumstances that change the usual approach.
Shock may be normotensive
Compensatory vasoconstriction can preserve cuff BP while tissue perfusion and lactate worsen.
Cause beats catecholamine
No vasopressor substitutes for opening the culprit artery, repairing a rupture, draining tamponade or correcting an unstable rhythm.
Lactate trajectory is dynamic
A single high lactate is non-specific; failure to fall after resuscitation supports persistent inadequate flow or a mixed cause.
Device choice follows phenotype
An isolated LV pump does not correct severe RV failure or provide oxygenation; VA-ECMO raises LV afterload and may require unloading.
NICE 2026 is not blanket approval
Microaxial-pump use remains bounded by centre expertise and special evidence/governance arrangements because benefit and complications vary by selection.
11Common pitfallsFrequent interpretation and management errors.
- 01
Waiting for severe hypotension before recognising shock despite worsening perfusion and lactate.
- 02
Giving repeated fluid boluses without defining LV/RV filling and congestion.
- 03
Escalating vasoactive doses while delaying reperfusion or surgical correction.
- 04
Performing routine immediate multivessel PCI in MI-related shock rather than prioritising the culprit lesion.
- 05
Choosing a mechanical device before defining the failing ventricle, oxygenation need, contraindications and bridge goal.