How to diagnose cardiogenic shock in a patient using 2D (two-dimensional) echocardiography?

Diagnosing Cardiogenic Shock with 2D Echocardiography

Immediate transthoracic echocardiography (TTE) should be performed when cardiogenic shock is suspected, as it is the most valuable initial diagnostic tool for confirming both the presence and underlying cause of shock while providing critical hemodynamic information. 1, 2, 3

Primary Echocardiographic Assessment

Left Ventricular Evaluation

• Assess LV systolic function and ejection fraction - cardiogenic shock most commonly results from severe LV dysfunction with LVEF typically reduced, though shock can occur with preserved EF 1, 2
• Evaluate regional wall motion abnormalities - these indicate acute myocardial infarction as the underlying cause, with shock typically requiring loss of at least 40% of LV myocardium 1
• Measure stroke volume and cardiac output - reduced stroke volume and cardiac index <2.2 L/min/m² confirm inadequate cardiac output 1, 2
• Assess LV filling pressures - elevated filling pressures distinguish cardiogenic from other shock types 1, 2

Right Ventricular Assessment (Critical and Often Overlooked)

• Evaluate RV size and function - RV infarction is a classic cause of shock with normal LVEF and presents with RV dilatation, dyssynergy, and paradoxical septal motion 1, 4
• Measure TAPSE (tricuspid annular plane systolic excursion) - values <17 mm indicate RV dysfunction 1, 4
• Look for McConnell sign - RV free wall akinesis with preserved apical function suggests RV infarction 4
• Assess for tricuspid regurgitation - presence with low pulmonary pressures suggests RV infarction rather than pulmonary hypertension 4

Valvular Assessment

• Evaluate for acute severe mitral regurgitation - both severity and presence are major predictors of mortality in cardiogenic shock 1, 5
• Look for mechanical complications - papillary muscle rupture causing severe MR, ventricular septal rupture (visible defect with color Doppler), or LV free wall rupture 1, 4
• Assess for acute severe aortic or mitral valve dysfunction - can cause shock with preserved systolic function 4

Additional Critical Findings

• Examine pericardial space - even small effusions can cause tamponade and shock if accumulation is rapid (e.g., RV perforation during pacing) 1
• Evaluate for dynamic LVOT obstruction - hyperdynamic small LV cavity with systolic anterior motion of mitral valve indicates obstruction rather than pump failure, requiring beta-blockers and fluids instead of inotropes 1
• Assess IVC diameter and collapsibility - dilated IVC without respiratory variation suggests elevated right-sided pressures 1

Key Diagnostic Patterns

Shock with Reduced LVEF

• Depressed global LV function with regional wall motion abnormalities 1
• Decreased stroke volume and cardiac output 1
• Elevated LV filling pressures 1, 2
• Secondary mitral regurgitation common 1, 5

Shock with Preserved LVEF (Critical to Recognize)

• RV infarction pattern: RV dilatation, dyssynergy, TAPSE <17 mm, paradoxical septal motion, tricuspid regurgitation with low PA pressures 4
• Mechanical complications: acute severe MR, ventricular septal rupture, free wall rupture with tamponade 4
• Dynamic LVOT obstruction: small hyperdynamic LV, systolic anterior motion, secondary MR 1, 4
• Acute valvular disease: severe aortic stenosis, acute aortic or mitral regurgitation 4

Critical Pitfalls to Avoid

• Don't overlook RV function - RV failure is frequently missed but is a critical cause of shock with preserved LVEF 4
• Beware of hyperdynamic small LV - this may indicate severe hypovolemia, RV failure with LV underfilling, or dynamic LVOT obstruction rather than good cardiac function 1, 4
• Don't assume large effusions are needed for tamponade - rapid accumulation of even small amounts can cause shock 1
• Recognize that normal LV and RV function with normal valves virtually rules out cardiogenic shock - look for other causes of shock 3

When TTE is Inadequate

• Proceed to transesophageal echocardiography (TEE) when transthoracic windows are suboptimal 1
• Consider invasive hemodynamic monitoring with pulmonary artery catheterization when echo findings are equivocal or don't match clinical picture 4, 2

Hemodynamic Information from Echo

• Stroke volume calculation via LVOT velocity-time integral (VTI) 4, 2
• Cardiac output estimation 1, 6
• Assessment of filling pressures through mitral inflow patterns and tissue Doppler 1, 2
• Evaluation of pulmonary pressures via tricuspid regurgitation velocity 6