Cardiogenic shock

Article written and reviewed by Dr Luca Moretti

Cardiogenic shock is a state of acute circulatory failure in which primary cardiac dysfunction produces cardiac output inadequate to meet tissue requirements, with hypoperfusion, despite sufficient or correctable intravascular volume. Hypotension is frequent but not essential: vasoconstriction may temporarily maintain blood pressure while lactate, oliguria, cold skin or neurological impairment documents perfusion failure. It is not a uniform entity. Left ventricular, right ventricular or biventricular phenotypes, congestion or relative underfilling, vasoconstriction or vasoplegia, and ischemic, inflammatory, valvular or arrhythmic causes produce different requirements; effective therapy requires serial phenotyping, not automatic application of the same device to every patient. Mortality remains high and increases with delayed reperfusion, arrest, neurological injury, organ failure and progression of SCAI stage. Diagnosis, transfer, revascularization and decisions about support must therefore take place in parallel.

Acute coronary syndrome is a major cause, but a growing proportion arises from acute decompensation of chronic heart failure. Fulminant myocarditis, Takotsubo syndrome, pulmonary embolism, right ventricular infarction, tamponade, endocarditis, prosthetic dysfunction and mechanical complications are time-sensitive alternatives. The SCAI classification from A to E describes risk, from the at-risk phase to extreme shock, and must be updated after every intervention. Cardiac arrest and neurological injury are modifiers; the stage trajectory in the first few hours has greater prognostic value than the initial category; treatment addresses the cause, blood pressure, oxygenation, vasoactive drugs and selected temporary support. Contemporary evidence has ruled out a benefit from indiscriminate routine use of IABP and ECLS, while DanGer-Shock demonstrated benefit and more complications with a microaxial pump in a highly selected STEMI population.

Etiology, pathogenesis and pathophysiology

In extensive myocardial infarction, myocardial loss and residual ischemia reduce stroke volume and blood pressure; coronary perfusion falls, increasing ischemia and dysfunction; tachycardia and catecholamines increase demand and create an ischemic spiral. Papillary muscle rupture, a ventricular septal defect and free-wall rupture produce regurgitation, a shunt or tamponade. They may cause shock disproportionate to ejection fraction and require echocardiography and urgent surgical or percutaneous correction; right ventricular infarction limits pulmonary blood flow and left ventricular preload. The physiology requires rhythm management, revascularization and cautious volume administration, avoiding nitrates and excessive filling.

In chronic heart failure, shock may result from progression, arrhythmia, infection, ischemia, treatment withdrawal or vasoplegia; a dilated ventricle may tolerate very high pressures but lose cardiac output after a small change in rhythm or afterload. Fulminant myocarditis and Takotsubo syndrome may recover, making support a bridge to recovery; giant cell or eosinophilic myocarditis requires diagnosis and specific immunotherapy; biopsy is selected when it changes management. Peripartum cardiomyopathy, toxicity and endocrine crises are partially reversible causes. The history and context must be obtained during resuscitation.

Acute mitral or aortic regurgitation, critical stenosis and prosthetic thrombosis alter pressure and flow without necessarily producing major dilation; valve correction is the definitive therapy, while drugs and support provide stabilization as a bridge. Tamponade and acute constriction are forms of obstructive shock of cardiac origin but require drainage or surgery, rather than inotropes as the primary treatment. High-risk pulmonary embolism requires reperfusion and right ventricular support. Fast or slow arrhythmias may be the sole cause or an amplifier. Cardioversion, pacing and electrolyte correction must precede unnecessary escalation.

Low cardiac output reduces oxygen delivery; tissues increase extraction until reserve is exhausted, after which lactate rises. Lactate is also influenced by catecholamines, the liver and seizures, so trends and clearance are more useful than a single value. Vasoconstriction maintains blood pressure but increases afterload and reduces cutaneous, renal and splanchnic blood flow. In advanced stages, inflammation, acidosis and drugs may produce mixed vasoplegia, with warm extremities and low vascular resistance despite a cardiac origin; elevated venous pressure reduces organ perfusion and contributes to renal, hepatic and intestinal dysfunction. Shock is therefore not simply equivalent to insufficient arterial pressure.

The right ventricle fails because of afterload, ischemia or volume. Dilation and septal displacement reduce left ventricular filling; isolated left ventricular support may not receive flow; the pulmonary artery pulsatility index and RAP/wedge ratio help recognize right ventricular predominance. Mechanical ventilation modifies both ventricles. PEEP reduces venous return and may increase right ventricular afterload, but unloads the left ventricle and improves hypoxia; the choice is adapted to the dominant chamber. VA-ECMO increases perfusion but also left ventricular afterload and may cause distension and pulmonary edema; unloading is considered according to ejection, pressures and stasis, without definitive evidence for a universal strategy.

Microcirculatory dysfunction may persist after cardiac output is restored. The endothelium, glycocalyx, inflammation and distributive shunting make the relationship between macrohemodynamics and tissues incomplete; venous oxygen saturation and lactate must be interpreted alongside urine output, skin and consciousness. Multiorgan injury becomes progressively self-sustaining: AKI, hypoxic hepatitis, intestinal ischemia, coagulopathy and encephalopathy reduce the probability of recovery; the window for support does not coincide with terminal hypotension. Arrest adds global ischemia and neurological prognostic considerations. Temperature, sedation and shock confound examination; multimodal assessment is deferred until the appropriate time.

Clinical manifestations

Classic findings are hypotension, tachycardia, cold extremities, sweating, oliguria and altered mental status. However, systolic blood pressure above 90 mmHg does not rule out shock if vasopressors are required or signs of hypoperfusion are present; a narrow pulse pressure suggests low stroke volume; a wide pulse pressure with vasoplegia may mask the cardiac component. Mean arterial pressure must be interpreted in relation to the usual value and perfusion. Jugular veins, crackles, edema and ascites define congestion. Clear lung fields with elevated jugular venous pressure point toward right ventricular infarction, embolism or tamponade, but no triad is sufficiently sensitive.

Chest pain, dyspnea, nausea and syncope accompany myocardial infarction; a new murmur suggests a mechanical complication; the absence of a murmur does not rule out acute regurgitation when ventricular and atrial pressures equalize. Fever, a viral prodrome, pregnancy, chemotherapy or medications point toward other causes; a collateral history from family members and records is essential in a confused or intubated patient. Palpitations or device shocks may identify an arrhythmia. A bradyarrhythmia in an inferior infarction or infiltrative setting may be the correctable precipitant.

SCAI stage B includes instability without overt hypoperfusion; C is classic shock requiring intervention, D is deterioration despite treatment and E is extreme collapse. Criteria include clinical, biochemical and hemodynamic findings and are applied serially. Progression toward SCAI D or E, rising lactate and a need for multiple vasopressors signal failure and require reassessment of the cause, device and eligibility. Arrest is not equated with shock but modifies its risk. The initial rhythm, no-flow time and neurological response weigh on proportionate decisions.

Mottled skin, capillary refill time and peripheral temperature are simple measures but are influenced by age, drugs and the environment; hourly urine output is a sensitive indicator, although CKD, diuretics and obstruction modify it. Confusion, agitation and drowsiness reflect perfusion, hypoxia, hypercapnia or drugs; new neurological asymmetry requires investigation for stroke or a procedural complication. Abdominal pain, persistently elevated lactate and ileus may indicate mesenteric ischemia. The absence of early signs does not rule it out in a sedated patient.

The therapeutic response includes increased blood pressure and cardiac output, reduced lactate and vasopressor requirements, recovery of urine output and improved consciousness; normalization of a single number does not equate to recovery if the drug dose is increasing. The hemodynamic balance is reassessed after revascularization, a cautious fluid challenge, an inotrope or support; failure to respond suggests an uncorrected cause, involvement of another chamber or irreversible injury. Congestion may worsen while blood pressure improves, especially with ECMO or volume administration. Ultrasound and pressures guide the new balance.

Investigations and diagnosis

A 12-lead ECG and right-sided leads, bedside echocardiography and laboratory tests are performed immediately. Troponin, complete blood count, electrolytes, renal function, liver function, coagulation, blood gases and lactate define the etiology and organ involvement; cultures and inflammatory tests are added if infection is suspected; echocardiography identifies function, chambers, valves, the septum, pericardium, aorta and volume. The urgent anatomical diagnosis of papillary muscle rupture, VSD, tamponade or embolism changes treatment more than a precise ejection fraction. Transesophageal echocardiography is used when transthoracic imaging is insufficient or during procedures; transport for advanced imaging is avoided in unstable patients unless essential.

Arterial monitoring provides beat-to-beat blood pressure and blood gas sampling; central venous access allows vasoactive drug administration and oxygen saturation measurement, but a normal ScvO2 does not rule out shunting or reduced extraction. The arteriovenous CO2 difference may complement assessment of flow; the pulmonary artery catheter measures right atrial, pulmonary artery and wedge pressures and cardiac output and calculates cardiac power, vascular resistance and right ventricular indices. In complex shock, invasive phenotyping helps select and wean support. Errors in zeroing, wedge pressure, thermodilution and Fick measurements may lead to incorrect decisions. Trends and consistency with echocardiography and clinical findings are mandatory.

Cardiac power output combines mean arterial pressure and cardiac output and identifies risk; a cardiac index below approximately 2.2 L/min/m² is common but does not define shock on its own. Small body size, sepsis and support devices make thresholds variable; pulmonary artery pulsatility index, TAPSE and strain assess the right ventricle, but are load-dependent. The RAP/PCWP ratio helps recognize disproportionate right ventricular involvement and risk with left ventricular support. The response to a passive maneuver or a small bolus may assess preload responsiveness, but filling an already congested ventricle worsens interdependence.

In STEMI, coronary angiography and PCI of the culprit vessel are urgent. In multivessel disease with shock, CULPRIT-SHOCK supports initial revascularization of the culprit lesion, deferring the others except for anatomical exceptions. CT angiography is used for embolism or dissection if the patient can be transported; magnetic resonance imaging has no place in the unstable phase; myocardial biopsy is selected in fulminant myocarditis when the result changes immunotherapy or prognosis. Toxicology, endocrine and infectious tests follow clinical suspicion; an extensive workup must not delay reperfusion or mechanical correction.

The differential diagnosis includes distributive, hypovolemic and obstructive shock, often overlapping. Ultrasound, hemodynamics and response distinguish septic vasoplegia with myocardial depression, hemorrhage, tamponade and embolism. Defining mixed shock is important: increasing only the inotrope in vasoplegia worsens oxygen consumption, while using only a vasopressor in severe low cardiac output increases afterload. Serial documentation includes SCAI stage, cause, phenotype, arrest, organ involvement and doses; this language allows comparisons and team decisions.

Treatment and prognosis

The first treatment is correction of the cause. In myocardial infarction, timely revascularization is the only intervention with robust historical evidence of benefit; mechanical complications require urgent surgery or procedures; tamponade requires drainage, embolism reperfusion, and arrhythmia cardioversion or pacing. A shock team coordinates interventional cardiology, intensive care, surgery, heart failure care and perfusion. Early transfer to a center with support capabilities is preferable to late escalation without options. Oxygenation, ventilation, temperature, glucose, electrolytes and antibiotics when indicated are part of resuscitation. Nutrition and prevention of complications begin after stabilization.

Norepinephrine is the first-choice vasopressor in most hypotensive profiles because it increases blood pressure with fewer arrhythmias than dopamine. The blood pressure goal is individualized according to perfusion, age and comorbidities, avoiding doses that excessively increase afterload. Dobutamine or milrinone is used as an inotrope for low cardiac output with supported blood pressure; milrinone is renally cleared and vasodilatory, while dobutamine is a beta-agonist. DOREMI did not show clear superiority; the lowest effective dose reduces arrhythmias and oxygen consumption. Epinephrine is associated with more lactate elevation and tachycardia and is reserved for selected settings or arrest. Vasopressin may be added in vasoplegia.

Fluids are not automatic therapy; a small bolus is appropriate with documented underfilling, right ventricular infarction or fluid loss, while high pressures, edema and dilation indicate diuresis or unloading. Hemorrhage requires blood components and control of the source. Diuretics treat concomitant congestion when perfusion is supported; renal replacement therapy is used for standard indications or refractory volume overload, with the modality adapted to instability. Invasive ventilation reduces work, but induction may cause collapse. A vasopressor ready for use, preoxygenation and drug selection are essential.

IABP does not reduce mortality when used routinely in myocardial infarction with shock without a mechanical complication, but may be considered in acute regurgitation, VSD or as a selected bridge. A microaxial pump unloads the left ventricle and increases flow, but causes bleeding, ischemia and AKI. DanGer-Shock showed lower 180-day mortality with a microaxial pump in selected STEMI patients, excluding post-arrest coma, severe right ventricular involvement and mechanical complications. Patient selection is part of the result and does not allow indiscriminate extension. VA-ECMO provides biventricular and respiratory support, but ECLS-SHOCK did not show benefit from unselected early routine use in myocardial infarction and increased complications.

Device selection begins with the chamber, required flow, oxygenation, access, aorta, valves and goal. Right ventricular support, a left ventricular pump, ECMO or a combination produces different effects; none compensates for an uncorrected mechanical cause; monitoring for hemolysis, limb complications, bleeding and distension is daily. Anticoagulation and access are adapted to the device and risk; weaning requires resolution of the cause, reduced vasoactive support, recovering organs and adequate hemodynamics at decreasing flow. A failed trial leads to optimization, a change in strategy or assessment for durable support.

If recovery does not occur, LVAD or transplantation is considered before irreversible injury. Age, neurological status, renal function, liver function, infection, malignancy, frailty and support determine eligibility; a temporary device is a bridge to decision, not a promise of definitive therapy. Prognosis depends on the cause, SCAI stage, arrest, lactate, cardiac power and number of organs involved; progression in the first 24 hours identifies greater risk than an initial measurement. When recovery or replacement is not possible, palliative care and communication guide proportionate withdrawal of support and symptom treatment, together with the family and team.

Complications

AKI results from hypoperfusion, congestion, contrast, hemolysis and inflammation and may require dialysis; creatinine lags behind the insult; urine output, potassium, acidosis and volume guide decisions. Hypoxic hepatitis causes very high aminotransferases, coagulopathy and altered drug metabolism. Pre-existing congestion increases susceptibility. Mesenteric ischemia and bacterial translocation may produce pain, ileus, lactate elevation and sepsis; delayed recognition is often fatal.

Ventricular arrhythmias, fibrillation and conduction blocks worsen cardiac output. Catecholamines, ischemia and electrolyte disturbances increase risk; cardioversion, pacing and ablation are used according to the mechanism; electrical storm requires sedation, correction of triggers, drugs and ablation, with support if instability prevents the procedure. Arrest adds anoxic injury and aspiration; neurological prognostication follows standardized timing and methods.

Temporary devices cause bleeding, thrombosis, hemolysis, limb ischemia, stroke, infection and vascular injury; a microaxial pump may cause aortic or mitral injury and suction events; ECMO may cause left ventricular distension and differential oxygenation. Harlequin syndrome occurs in peripheral VA-ECMO when the heart ejects poorly oxygenated blood toward the brain while retrograde flow oxygenates the lower body. Right radial oxygen saturation and the cannulation strategy are crucial. Thrombocytopenia and coagulopathy require distinguishing consumption, drugs and HIT. Indiscriminate transfusions add volume and risk.

Catheter infections, pneumonia and sepsis convert shock into a mixed form. Fever may be absent, and increasing vasoplegia must prompt a search for a source; antibiotics are guided by probability and cultures. Delirium, acquired weakness and pressure injuries increase with sedation and immobility; early rehabilitation begins when support allows. Malnutrition and intestinal ischemia make nutrition complex; cautious enteral feeding is preferred after stability is achieved, avoiding overfeeding during active shock.

Survival may be followed by heart failure, renal dysfunction, neurological deficits, anxiety and post-traumatic stress disorder. Cardiology and rehabilitation follow-up addresses the cause, ejection fraction, rhythm and prevention. Recurrent shock or inotrope dependence signals advanced heart failure; late assessment reduces the options for LVAD or transplantation. The burden on family members and decisions during incapacity require frequent communication. Goals, probabilities and criteria for the success of support must be explicit from implantation onward.