Cardiogenic Shock

Our mechanical circulatory support and ECMO guides assume the reader knows what cardiogenic shock is. This page fills that gap. Recognising early deterioration is a genuine physiotherapy contribution — we are often at the bedside, moving the patient, when the first signs appear.¹

Definition

Cardiogenic shock is a state of inadequate tissue perfusion due to primary cardiac dysfunction, despite adequate intravascular volume. Conventional haemodynamic criteria include a sustained systolic blood pressure below 90 mmHg (or the need for vasopressors to maintain it), together with evidence of end-organ hypoperfusion: cool peripheries, oliguria, altered mental state, and a rising lactate.^1,2

The SCAI shock classification stages severity from A ("at risk") through B ("beginning"), C ("classic"), D ("deteriorating") to E ("extremis"), and has become the common language across cardiology and critical care. It is worth knowing because the stage frames how much physiological reserve exists for any intervention, including ours.³

Pathophysiology

Reduced stroke volume lowers cardiac output and systemic perfusion. Compensatory vasoconstriction and tachycardia raise afterload and myocardial oxygen demand while coronary perfusion pressure falls — a self-reinforcing spiral. A systemic inflammatory response with inappropriate vasodilatation frequently develops, which is why some patients are simultaneously in cardiogenic and distributive shock. Congestion and hypoperfusion together produce cardiorenal and cardiohepatic injury.

Co-morbidities

Cardiogenic shock arises in hearts that were usually already compromised, and the surrounding disease shapes both the course and what rehabilitation is possible afterwards. Coronary artery disease and prior infarction are the commonest background; pre-existing heart failure, valvular disease and arrhythmia are frequent. Chronic kidney disease is both risk factor and casualty — cardiorenal injury develops rapidly and dialysis is often needed. Diabetes, chronic lung disease, peripheral vascular disease (which restricts device access sites) and frailty all worsen outcome. ⚠ Pre-morbid functional status is the single most useful predictor of what recovery will look like, and is worth establishing from family early rather than reconstructing later.

Prevalence

Cardiogenic shock complicates roughly 5–10% of acute myocardial infarctions, and although infarct-related shock has fallen as reperfusion has improved, the overall incidence has not declined — the non-ischaemic share, from acute decompensated heart failure, myocarditis and valvular disease, has risen to around half of cases in contemporary registries. It accounts for a small proportion of intensive care admissions but a disproportionate share of deaths, and remains the leading cause of in-hospital mortality after myocardial infarction.²

Causes

Acute myocardial infarction with left ventricular failure remains the most common cause, though the proportion arising from non-ischaemic causes is rising. Others include acute decompensated heart failure, fulminant myocarditis, mechanical complications of infarction (papillary muscle rupture, ventricular septal defect, free wall rupture), acute valvular failure, arrhythmia, right ventricular infarction, massive pulmonary embolism, cardiac tamponade, and stress cardiomyopathy (see Takotsubo).

Symptoms

Patients describe severe breathlessness, often at rest and worse lying flat, with profound fatigue and weakness disproportionate to anything they have done. Chest discomfort is present when the cause is ischaemic. Many are agitated, confused or drowsy — cerebral hypoperfusion, not anxiety, though it is easily read as the latter. Nausea, sweating and a sense of impending doom are common. Some appear deceptively settled until moved, which is precisely why our observations during activity carry information the resting chart does not.

Recognition — the part relevant at the bedside

Cardiogenic shock rarely announces itself. Signs that should prompt escalation, particularly if they are new or worsening during activity:

• Cool, mottled peripheries with delayed capillary refill and a narrow pulse pressure.
• New confusion, agitation or drowsiness.
• Falling urine output.
• Disproportionate breathlessness at rest or on minimal exertion, orthopnoea, or new crackles.
• Tachycardia with a blood pressure that falls rather than rises with activity.
• A rising lactate on the most recent gas — the single most useful number available to us.

⚠ A patient who becomes less alert or more mottled when sat out is not deconditioned; they are decompensating. Return them to a supported position and escalate.

Management

Treatment addresses the cause — primary percutaneous coronary intervention for infarction (see PCI), surgery for mechanical complications, and rhythm control where relevant — alongside haemodynamic support. Inotropes and vasopressors are used with caution given their oxygen cost. Mechanical circulatory support ranges from intra-aortic balloon counterpulsation through microaxial pumps to veno-arterial ECMO, used as a bridge to recovery, to decision, or to durable support or transplantation. Mortality remains high, around 40–50% at 30 days in registry data, though it has improved with organised shock-team pathways.^2,4,5

Medications

Inotropes (dobutamine, milrinone, levosimendan) raise contractility at the cost of myocardial oxygen demand and arrhythmia. Vasopressors (noradrenaline first-line) maintain perfusion pressure but raise afterload. Both are titrated continuously, and ⚠ the direction of travel over the last 24 hours tells us more than the absolute dose — rising support means deferring active work. Diuretics address congestion; anticoagulation is required for mechanical support circuits. ⏹ Chronic heart failure therapy is often withheld or reduced acutely and reintroduced during recovery, so a patient's medication list changes rapidly — check it rather than working from yesterday's chart.

Multi-system manifestations

Shock is a whole-body event. Acute kidney injury is near-universal in severe cases; hepatic dysfunction ("shock liver") and gut ischaemia follow hypoperfusion. Respiratory failure requires ventilatory support, and pulmonary oedema complicates weaning. Coagulopathy and thrombocytopenia are common, particularly on mechanical support, and limb ischaemia is a specific hazard of femoral arterial cannulation — ⚠ check distal perfusion before and after any movement of a cannulated limb. Delirium is the rule rather than the exception, and critical illness neuromyopathy develops within days. Stroke and systemic embolism occur.

Living with recovery from cardiogenic shock

Survivors are frequently unprepared for how long recovery takes. Profound weakness, fatigue, breathlessness and poor concentration persist for months, and many cannot climb a flight of stairs on discharge from a hospital that saved their life — which is bewildering without explanation. Post-intensive-care syndrome is common: anxiety, depression, post-traumatic stress and cognitive impairment. Some have no memory of the admission; others have vivid distressing recall. Family members carry their own trauma. Practical concerns are substantial — return to work and driving, device management for those on durable support, transplant assessment for some, and an implanted defibrillator for many. Explaining the trajectory realistically at the outset does more good than optimism.

Prognosis

Mortality remains high: roughly 40–50% at 30 days in registry data, and higher in SCAI stages D and E.^2,3 Organised shock-team pathways with early recognition and structured escalation have improved outcomes, though the trial evidence for individual devices is disappointing — neither routine intra-aortic balloon counterpulsation nor routine ECLS in infarct-related shock improved survival in randomised trials.^4,5 For those who survive to discharge, functional recovery is often substantial but slow, and continues over six to twelve months. Left ventricular function may recover partly or fully depending on cause — fulminant myocarditis and stress cardiomyopathy have notably better recovery than extensive infarction.

Role of the physiotherapist

During critical illness

Respiratory management of the ventilated or non-invasively supported patient; positioning for ventilation–perfusion matching, mindful that position changes alter preload and may not be tolerated; secretion clearance where indicated; and protection against the harms of immobility — passive movement, splinting and early activity within the limits the circulation allows. Interventions are negotiated with the bedside team against current support, and are frequently deferred rather than abandoned.

Early mobilisation

Mobilisation is feasible in selected patients on mechanical support, including those on femoral devices, but requires an explicit team plan, device-aware handling and clear stopping criteria.^6,7 The judgement is not whether the patient can be moved but whether the oxygen cost of movement is affordable today.

Recovery and rehabilitation

Survivors frequently have intensive care–acquired weakness, profound deconditioning, and the cognitive and psychological sequelae of critical illness. Rehabilitation is long and should be structured — see cardiorespiratory rehabilitation and ICU-acquired weakness where relevant. Underlying heart failure management continues alongside.

Warning signs

Part 1 · References

1. 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.
2. Thiele H, Ohman EM, de Waha-Thiele S, et al. Management of cardiogenic shock complicating myocardial infarction: an update 2019. Eur Heart J 2019;40(32):2671–2683.
3. Naidu SS, Baran DA, Jentzer JC, et al. SCAI SHOCK stage classification expert consensus update. J Am Coll Cardiol 2022;79(9):933–946.
4. Thiele H, Zeymer U, Neumann FJ, et al. Intraaortic balloon support for myocardial infarction with cardiogenic shock. N Engl J Med 2012;367(14):1287–1296.
5. Thiele H, Zeymer U, Akin I, et al. Extracorporeal life support in infarct-related cardiogenic shock (ECLS-SHOCK). N Engl J Med 2023;389(14):1286–1297.
6. Wells CL, Forrester J, Vogel J, et al. Safety and feasibility of early physical therapy for patients on extracorporeal membrane oxygenator. Crit Care Med 2018;46(1):53–59.
7. Hodgson CL, Stiller K, Needham DM, et al. Expert consensus and recommendations on safety criteria for active mobilization of mechanically ventilated critically ill adults. Crit Care 2014;18(6):658.

References are numbered in citation order (Vancouver/BMJ style) and were current at the time of writing. Guidelines are living documents — verify against the latest version before clinical use.