Diagnostic Algorithm for Right Ventricular Failure
Begin with bedside transthoracic echocardiography (TTE) as the first-line diagnostic tool to assess RV size, function, and identify the underlying etiology—this is the cornerstone of RV failure diagnosis and should be performed immediately in any patient with suspected RV failure. 1, 2, 3
Initial Clinical Assessment
Look for specific signs of RV failure:
- Elevated jugular venous pressure with prominent V waves 4
- Peripheral edema and hepatomegaly 4
- Hypotension with narrow pulse pressure 5, 4
- Signs of low cardiac output (cool extremities, altered mental status) 5
- Tachycardia and tachypnea 5
Obtain immediate laboratory studies:
- Cardiac biomarkers (troponin, BNP/NT-proBNP) to assess myocardial injury and wall stress 1, 5
- Arterial blood gas to evaluate hypoxemia and acid-base status 5
- Complete blood count and metabolic panel 6
Echocardiographic Evaluation (Primary Diagnostic Tool)
Assess RV size and function using standardized views:
- Apical four-chamber view: Measure RV/LV end-diastolic surface area ratio (>0.6 indicates RV enlargement) 1
- Parasternal long-axis view: Measure RV/LV end-diastolic diameter ratio 1
- Subcostal view: Evaluate RV free wall thickness (>5mm suggests acute RV failure when associated with RV dilatation) 1
Identify specific echocardiographic features of RV failure:
- Paradoxical septal motion (D-shaped left ventricle) 1
- Septal flattening during systole and/or diastole 1
- Dilated inferior vena cava (IVC) with minimal or absent respiratory variation (<50% collapse) 1
- Reduced tricuspid annular plane systolic excursion (TAPSE <16mm) 1
- Reduced RV free wall strain on speckle tracking if available 1
Evaluate for specific etiologies:
- Pulmonary embolism: Look for McConnell's sign (RV free wall hypokinesis with apical sparing), though this is not specific 1
- RV infarction: Regional wall motion abnormalities in subcostal short-axis view, inter-atrial septal bowing into left atrium 1
- Valvular disease: Assess tricuspid and pulmonary valve morphology and function 1
- Pericardial disease: Rule out pericardial effusion with tamponade physiology 1
Risk Stratification Based on Etiology
If pulmonary embolism is suspected:
- Classify as high-risk if cardiogenic shock or persistent hypotension is present 5, 7
- Classify as intermediate-risk if hemodynamically stable but with RV dysfunction on imaging or elevated biomarkers 5, 7
- Proceed immediately to bedside echocardiography before CT if patient is unstable 1, 7
If RV infarction is suspected:
- Obtain 12-lead ECG looking for ST elevation in right-sided leads (V3R-V4R) 1
- Perform urgent coronary angiography if acute coronary syndrome is confirmed 1
If chronic pulmonary hypertension is suspected:
- Estimate RV systolic pressure from tricuspid regurgitation velocity 1
- Assess for signs of chronic RV remodeling (RV hypertrophy, RV dilation) 1
Advanced Imaging When Initial Assessment is Inconclusive
Cardiac MRI is the gold standard for anatomical and functional RV assessment when:
- Echocardiographic windows are inadequate 2, 3
- Precise quantification of RV volumes and ejection fraction is needed 2
- Tissue characterization is required (fibrosis, infiltration) 2
- Arrhythmogenic cardiomyopathy is suspected 1
CT pulmonary angiography when:
- Pulmonary embolism remains in differential but patient is hemodynamically stable 7
- Detailed assessment of pulmonary vasculature is needed 1
Cardiac catheterization when:
- Hemodynamic confirmation is required (measure RV pressures, pulmonary artery pressures, cardiac output) 1, 2
- Coronary anatomy needs evaluation in suspected RV infarction 1
- Pulmonary hypertension severity and reversibility testing is needed 1
Common Pitfalls to Avoid
Do not delay echocardiography for other imaging modalities in unstable patients—bedside TTE provides immediate diagnostic and prognostic information that guides urgent management decisions 1. The sensitivity and specificity of point-of-care TTE for identifying RV dysfunction is sufficient to initiate treatment 1.
Do not rely solely on Doppler gradients to assess RV pressure—always correlate with tricuspid regurgitation velocity and integrate clinical findings, as Doppler measurements can overestimate or underestimate true pressures in certain conditions 1.
Do not miss biventricular involvement—assess left ventricular function simultaneously, as many conditions causing RV failure also affect the LV, and ventricular interdependence means RV failure impairs LV filling 1, 6.
Do not overlook IVC assessment—a non-dilated IVC effectively rules out significant RV failure and cardiac tamponade, while a dilated IVC with minimal respiratory variation strongly supports the diagnosis 1.