Management of Cardiogenic Shock
Immediately transfer the patient to a tertiary center with 24/7 cardiac catheterization capability, initiate invasive arterial monitoring, perform urgent echocardiography and ECG, start norepinephrine as the first-line vasopressor if mean arterial pressure requires support, add dobutamine if low cardiac output persists after fluid challenge, and proceed to emergency coronary angiography within 2 hours if acute coronary syndrome is suspected. 1, 2
Immediate Diagnostic Assessment
Obtain ECG and echocardiography immediately in all patients with suspected cardiogenic shock to identify the underlying cardiac cause, assess ventricular and valvular function, detect mechanical complications (ventricular septal rupture, acute mitral regurgitation, free wall rupture), and evaluate loading conditions. 1
Hemodynamic Definition
Cardiogenic shock is defined by:
- Persistent systolic blood pressure <90 mmHg despite adequate filling status 1, 2
- Signs of hypoperfusion: oliguria (<0.5 mL/kg/h), cold extremities, altered mental status, lactate >2 mmol/L, or metabolic acidosis 1, 2
- Hemodynamic criteria: cardiac index <2.2 L/min/m², cardiac power output <0.6 W, pulmonary capillary wedge pressure >15 mmHg 2, 3
Invasive Monitoring
- Place an arterial line immediately for accurate continuous blood pressure measurement 1
- Consider pulmonary artery catheterization when diagnosis is unclear or the patient fails to respond to initial therapy, as recent observational evidence suggests improved outcomes with complete hemodynamic profiling 1, 4
Initial Hemodynamic Support Strategy
Step 1: Fluid Challenge (When Appropriate)
Administer a cautious fluid challenge of approximately 200 mL over 15-30 minutes in hypotensive patients with normal perfusion and no signs of congestion, only after ruling out mechanical complications by echocardiography. 1, 2
Critical caveat: In right ventricular infarction, avoid volume overload as it may worsen hemodynamics through ventricular interdependence. 1, 2
Step 2: Vasopressor Selection
Norepinephrine is the recommended first-line vasopressor when mean arterial pressure needs pharmacologic support, targeting MAP ≥65 mmHg. 1, 2, 5, 4
- Norepinephrine is preferred over dopamine because it is associated with lower mortality and fewer arrhythmias (12% vs 24% arrhythmia rate) 5, 6
- Do not use dopamine as it increases arrhythmia risk and mortality compared to norepinephrine 5
- Do not use epinephrine in cardiogenic shock; it should be restricted to cardiac arrest only 5
Step 3: Inotropic Support
Dobutamine is the first-line inotropic agent to increase cardiac output when signs of low cardiac output persist after adequate fluid resuscitation. 1, 2, 5, 4
- Initial dose: 2-3 μg/kg/min, titrate up to 20 μg/kg/min based on hemodynamic response 5, 7
- Dobutamine increases cardiac output and stroke volume without excessive chronotropic effects 5
If inadequate response to dobutamine plus norepinephrine:
- Consider levosimendan as it may be used in combination with a vasopressor in cardiogenic shock following acute myocardial infarction, improving cardiovascular hemodynamics without causing hypotension, particularly in patients on chronic beta-blocker therapy 1, 5, 7
- Alternatively, consider PDE3 inhibitors (e.g., milrinone), especially in non-ischemic patients 1
Critical principle: Rather than combining multiple inotropes, escalate to mechanical circulatory support if there is inadequate response to pharmacologic therapy. 1, 5
Treatment of Underlying Cardiac Cause
Acute Coronary Syndrome-Related Cardiogenic Shock
Perform immediate coronary angiography within 2 hours of hospital admission with intent to revascularize the culprit lesion. 1, 2
- Emergency PCI is the only therapy proven to reduce mortality in cardiogenic shock complicating acute myocardial infarction 2
- If coronary anatomy is not suitable for PCI or PCI fails, proceed directly to emergency CABG 1, 2
- Consider complete revascularization during the index procedure in selected patients with cardiogenic shock 1, 2
- Do not perform routine multivessel PCI at the time of primary PCI; treat only the culprit lesion as multivessel intervention increases mortality and renal failure risk 2
Special scenario: In STEMI patients with cardiogenic shock where PCI-mediated reperfusion would be delayed >120 minutes, give immediate fibrinolysis and transfer to a PCI center, then perform emergent angiography on arrival regardless of ST-segment resolution or time elapsed. 1, 2
Mechanical Complications
Identify and treat mechanical complications early after multidisciplinary Heart Team discussion, including ventricular septal rupture, acute mitral regurgitation, and free wall rupture. 1, 2
Respiratory Support
Provide oxygen or mechanical ventilation to maintain oxygen saturation >90% according to blood gas analysis. 1
- Endotracheal intubation with positive end-expiratory pressure is usually required for patients with respiratory failure and pulmonary edema 2
Mechanical Circulatory Support Initiation
When to Consider MCS
Consider short-term mechanical circulatory support in refractory cardiogenic shock defined by persistent tissue hypoperfusion despite adequate doses of two vasoactive medications and treatment of the underlying etiology. 1, 2
Specific hemodynamic thresholds for refractory shock:
- Cardiac power output <0.6 W (most critical threshold) 2, 3
- Cardiac index <2.2 L/min/m² despite vasopressor and inotropic support 2, 3
- Systolic blood pressure <80 mmHg despite maximal treatment 2
- Progressive deterioration requiring increasing doses of inotropes 2
Device Selection by Phenotype
For left ventricular-dominant refractory shock (cardiac power output <0.6 W, PCWP >15 mmHg, RA <15 mmHg):
For right ventricular-dominant shock (cardiac power output <0.6 W, RA >15 mmHg, PCWP <15 mmHg):
- Consider right ventricular support devices 2
For biventricular shock (cardiac power output <0.6 W, both RA >15 mmHg and PCWP >15 mmHg):
IABP Recommendations
Do not use routine intra-aortic balloon pump as randomized trials (IABP-SHOCK II) showed no mortality benefit. 1, 2
Exception: IABP may be considered for hemodynamic instability/cardiogenic shock due to mechanical complications such as ventricular septal rupture or acute mitral regurgitation. 1, 2
Routine veno-arterial ECMO is not recommended as it has not shown a survival benefit in routine use. 2
Monitoring Parameters and Treatment Targets
Continuously monitor:
- Cardiac output/cardiac index (target >2.0 L/min/m²) 1, 2, 5
- Mean arterial pressure (target ≥65 mmHg) 2, 5
- Systolic blood pressure (target >90 mmHg) 1, 2
- Urine output (target >0.5 mL/kg/h) 2
- Lactate clearance as a marker of treatment response 2
- Mental status and peripheral perfusion 2, 5
- Pulmonary capillary wedge pressure (target <20 mmHg) 1, 2
Frequent laboratory monitoring during intravenous therapy:
Systems-Based Approach
All patients with cardiogenic shock should be rapidly transferred to a tertiary care center with:
- 24/7 cardiac catheterization service 1, 2
- Dedicated ICU/CCU with availability of short-term mechanical circulatory support 1, 2
- Multidisciplinary shock team (cardiology, cardiac surgery, critical care, nursing) 2, 4
Implement standardized protocols with multidisciplinary shock teams as this approach has been associated with improved 30-day all-cause mortality. 2, 4
Critical Pitfalls to Avoid
- Do not delay revascularization: In-hospital mortality remains 40-50% despite modern therapies; emergency coronary revascularization is the only therapy proven to reduce mortality 1, 2, 9
- Do not use routine IABP as it provides no mortality benefit 1, 2
- Do not perform multivessel PCI at primary intervention as it increases mortality and renal failure 2
- Do not combine multiple inotropes without considering mechanical support: If dobutamine plus norepinephrine fails, escalate to MCS rather than adding more drugs 1, 5
- Do not use dopamine or epinephrine as first-line agents due to increased arrhythmias and mortality 5
- Do not delay pericardiocentesis if pericardial effusion with tamponade physiology is present, as it can cause acute anuric renal failure reversible after drainage 5
- Avoid volume overload in right ventricular infarction as it worsens hemodynamics 1, 2
- Revascularization may be futile in patients with severe multiorgan failure and should be reconsidered 2