What are the signs, symptoms, diagnosis, pathophysiology, and treatment of cardiogenic shock in patients?

Cardiogenic Shock: Clinical Overview

Definition and Diagnosis

Cardiogenic shock is defined as persistent hypotension (SBP <90 mmHg) despite adequate filling status with signs of end-organ hypoperfusion, carrying an in-hospital mortality rate of approximately 50%. 1

Diagnostic Criteria

Hemodynamic parameters:

• Systolic blood pressure <90 mmHg for ≥30 minutes OR requiring inotropes/vasopressors to maintain SBP >90 mmHg 1, 2
• Cardiac index <2.2 L/min/m² (normal: 2.2-4.0 L/min/m²) 1, 3
• Cardiac power output <0.6 W (most critical threshold for refractory shock) 1, 3
• Pulmonary capillary wedge pressure >15 mmHg 1, 3
• Central venous pressure >15 mmHg 3

Clinical signs of hypoperfusion:

• Altered mental status or confusion 1, 2
• Cool, clammy extremities with peripheral vasoconstriction 1, 4
• Urine output <0.5 mL/kg/hr 1, 2
• Elevated serum lactate >2 mmol/L 1
• Acute liver injury (elevated bilirubin ≥1.3 mg/dL predicts worse outcomes) 3
• Acute kidney injury 1, 2

Immediate Diagnostic Workup

All patients with suspected cardiogenic shock require immediate:

• 12-lead ECG to identify acute myocardial infarction 1
• Immediate transthoracic echocardiography to assess ventricular function, valvular function, loading conditions, and detect mechanical complications (ventricular septal rupture, acute mitral regurgitation, free wall rupture, tamponade) 1
• Invasive arterial line monitoring for accurate blood pressure measurement 1
• Laboratory evaluation including cardiac biomarkers, lactate, liver and kidney function tests 1

Pathophysiology

The pathophysiology involves a vicious spiral: myocardial dysfunction reduces cardiac output → systemic hypoperfusion → compensatory vasoconstriction (increased SVR) → increased afterload further impairs the failing heart → worsening ischemia and dysfunction 3, 5

Key hemodynamic derangements:

• Decreased cardiac output/cardiac index due to impaired myocardial contractility 3, 5
• Increased systemic vascular resistance as compensatory mechanism (opposite of distributive shock) 3, 5
• Elevated filling pressures (PCWP >15 mmHg, CVP >15 mmHg) from backward failure 3
• Myocardial stunning and hibernating myocardium enhance dysfunction 5
• Systemic inflammation and potential bacterial translocation from intestinal ischemia increase mortality 5

Treatment Algorithm

Step 1: Immediate Stabilization and Transfer

Transfer all patients with cardiogenic shock to a tertiary care center with 24/7 cardiac catheterization capability and mechanical circulatory support availability. 1, 6, 2

Step 2: Airway and Breathing

Respiratory support based on clinical status:

• Non-invasive positive pressure ventilation (CPAP, BiPAP) or high-flow nasal cannula for respiratory distress (respiratory rate >25 breaths/min, SaO₂ <90%) 1
• Endotracheal intubation and mechanical ventilation for inadequate oxygenation, excessive respiratory work, or hypercapnia from respiratory exhaustion 1
• Oxygen/mechanical respiratory support titrated according to blood gases 1

Step 3: Circulation - Revascularization (If ACS-Related)

In acute coronary syndrome-related cardiogenic shock:

• Immediate coronary angiography within 2 hours of hospital admission with intent to perform revascularization 1
• Immediate PCI is the treatment of choice if coronary anatomy is suitable 1
• Emergency CABG if coronary anatomy unsuitable for PCI or PCI has failed 1
• Consider complete revascularization during the index procedure 1
• If PCI-mediated reperfusion will be delayed >120 minutes, consider immediate fibrinolysis (after ruling out mechanical complications) and transfer to PCI center 1

Step 4: Hemodynamic Support - Pharmacologic

Initial fluid management:

• If no signs of overt fluid overload or congestion (collapsible IVC), attempt gentle volume loading (>200 mL over 15-30 minutes) after ruling out mechanical complications 1, 2
• Monitor central pressures; avoid volume overload in RV infarction as it worsens hemodynamics 1

Vasopressor therapy:

• Norepinephrine is the recommended first-line vasopressor when mean arterial pressure needs pharmacologic support 1, 6
• Titrate to maintain adequate mean arterial pressure and organ perfusion 1, 6

Inotropic therapy:

• Dobutamine (2-20 μg/kg/min) is the first-line inotropic agent to increase cardiac output when signs of low cardiac output persist 1, 6, 2
• Levosimendan may be used in combination with a vasopressor; improved hemodynamics in AMI-related shock when added to dobutamine and norepinephrine 1
• PDE3 inhibitors may be considered, especially in non-ischemic patients 1

Dopamine dosing (if used):

• Begin at 2-5 μg/kg/min for modest increments in heart force and renal perfusion 7
• In more seriously ill patients, begin at 5 μg/kg/min and increase gradually using 5-10 μg/kg/min increments up to 20-50 μg/kg/min as needed 7
• More than 50% of patients maintained on <20 μg/kg/min 7
• Monitor for diminished urine flow, increasing tachycardia, or new dysrhythmias as reasons to decrease dosage 7

Step 5: Mechanical Circulatory Support

Consider temporary mechanical circulatory support when end-organ function cannot be maintained by pharmacologic means or when there is inadequate response to inotropes. 1, 6

Intra-aortic balloon pump (IABP):

• Routine use of IABP is NOT recommended (IABP-SHOCK II trial showed no outcome improvement) 1
• Consider IABP only for hemodynamic instability due to mechanical complications (VSD, acute mitral regurgitation) before surgical correction 1
• May be considered during severe acute myocarditis or with acute myocardial ischemia before/during/after revascularization 1

Other mechanical circulatory support devices:

• Ventricular assist devices and other MCS may be used as "bridge to decision" or longer-term in selected patients 1
• Consider short-term MCS based on patient age, comorbidities, and neurological function 1
• Application should occur rapidly: IABP within 30 minutes, MCS within 1 hour from first weaning attempts 3

Step 6: Invasive Hemodynamic Monitoring

Pulmonary artery catheterization may be considered:

• For confirming diagnosis when clinical picture is unclear 1
• For guiding therapy in refractory shock 1
• To identify specific cardiogenic shock phenotype (LV-dominant, RV-dominant, or biventricular) 2, 3
• When escalating to mechanical circulatory support, invasive hemodynamic data should guide decisions 6, 3

Step 7: Management of Mechanical Complications

Mechanical complications require immediate surgical intervention after Heart Team discussion: 1

• Ventricular septal rupture 1
• Acute mitral regurgitation from papillary muscle rupture 1
• Free wall rupture with tamponade (requires immediate pericardial drainage) 1
• Natural history without surgery approaches 100% mortality 1

Step 8: Multidisciplinary Team Approach

Management by a multidisciplinary shock team experienced in cardiogenic shock is reasonable and associated with improved 30-day mortality. 1, 6, 2

Defining Refractory Cardiogenic Shock

Refractory shock is defined by persistent tissue hypoperfusion despite adequate doses of two vasoactive medications and treatment of underlying etiology: 3

• Cardiac power output <0.6 W (most critical threshold) 3
• Cardiac index <2.2 L/min/m² despite vasopressor and inotropic support 3
• SBP <80 mmHg despite maximal treatment or requiring high-dose vasopressors to maintain SBP >90 mmHg 3
• Progressive deterioration requiring increasing doses of inotropes and/or IABP 3

Common Pitfalls and Caveats

Critical mistakes to avoid:

• Do not use routine IABP—no mortality benefit demonstrated 1
• In RV infarction, avoid aggressive volume loading as it worsens hemodynamics 1
• Do not delay revascularization in ACS-related shock—no time limit should be set for invasive diagnosis and revascularization 1
• Avoid prolonged attempts at medical optimization in refractory shock—escalate to MCS within 1 hour 3
• Do not confuse late-stage septic shock with cardiogenic shock; septic shock maintains decreased SVR despite myocardial depression 3
• Diminishing urine flow, increasing tachycardia, or new dysrhythmias during inotrope therapy warrant dose reduction 7

Contraindications to mechanical circulatory support escalation:

• Anoxic brain injury 3
• Irreversible end-organ failure 3
• Prohibitive vascular access 3
• Do Not Resuscitate status 3

Monitoring for treatment response:

• Target cardiac index >2.0 L/min/m² with PCWP <20 mmHg 1, 6
• Reversal of mental confusion, loss of pallor, increased toe temperature, adequate nail bed capillary filling 7
• Urine output restoration (prognosis better when dopamine administered before urine flow decreases to 0.3 mL/min) 7
• Lactate clearance 1