What is the management approach for a patient with right-sided heart failure, potentially complicated by underlying conditions such as pulmonary hypertension, coronary artery disease, or cardiomyopathy, and a history of alcohol use disorder?

Management of Right-Sided Heart Failure

The cornerstone of right-sided heart failure management is identifying and treating the underlying cause—whether left heart disease, pulmonary hypertension, or primary RV pathology—while optimizing preload, reducing RV afterload, and maintaining RV coronary perfusion pressure. 1

Initial Assessment and Diagnosis

Determine the etiology systematically by categorizing RHF into three primary mechanisms 1:

• Decreased RV contractility: RV myocardial infarction, myocarditis, arrhythmogenic RV cardiomyopathy, or perioperative injury 1
• RV pressure overload: Pulmonary arterial hypertension, chronic thromboembolic pulmonary hypertension, left heart disease, pulmonary embolism, or pulmonary stenosis 1
• RV volume overload: Tricuspid regurgitation, pulmonary regurgitation, left-sided valvular disease, or pericardial disease 1

Assess RV function using echocardiography with specific parameters: TAPSE <16 mm, RV fractional area change <35%, or RV S' <9.5 cm/s indicate RV dysfunction 1. The TAPSE/PASP ratio provides a noninvasive surrogate for RV-arterial coupling 2.

Recognize that RV dysfunction carries significant prognostic weight: In HFrEF, RVD is present in approximately 48% of patients and confers a 2.4-fold increased risk of mortality, urgent transplantation, or LVAD placement at 90 days 1. In HFpEF, RVD occurs in 33% of patients and is associated with 2-year mortality of 45% versus 7% in those without RVD 1.

Hemodynamic Management

Optimize preload cautiously because the RV is preload-dependent but vulnerable to overdistension 2, 3:

• Avoid aggressive fluid resuscitation in most cases, as RV dilation worsens ventricular interdependence by shifting the interventricular septum leftward, compressing the LV and reducing cardiac output 1
• Use diuretics for volume overload with thiazides, loop diuretics, and aldosterone antagonists as appropriate 1
• Fluid restriction of 1.5-2 L/day is advised in advanced heart failure 1
• Sodium restriction is more important in advanced than mild heart failure 1

Maintain systemic blood pressure to preserve RV coronary perfusion 2, 4:

• Use norepinephrine as first-line vasopressor to maintain systemic arterial pressure close to RV systolic pressure, ensuring adequate RV perfusion 2, 4
• Target systolic blood pressure near RV systolic pressure because RV coronary flow occurs during both systole and diastole, unlike the LV 2

Afterload Reduction

Optimize oxygenation and ventilation aggressively 2, 3:

• Maintain SaO₂ >90% with supplemental oxygen to prevent hypoxic pulmonary vasoconstriction 2
• Avoid intubation if possible because positive pressure ventilation increases RV afterload and can precipitate acute decompensation 1, 3, 5
• Correct hypercapnia and acidosis as both worsen pulmonary vascular resistance 1

Consider pulmonary vasodilators for pulmonary arterial hypertension 6, 7, 5:

• Sildenafil (PDE-5 inhibitor) increases cGMP in pulmonary vascular smooth muscle, causing vasodilation 6
• Tadalafil provides similar pulmonary vasodilation with longer duration of action 7
• Contraindicated with nitrates or guanylate cyclase stimulators due to risk of severe hypotension 6, 7
• Inhaled pulmonary vasodilators may be required in severe cases and necessitate transfer to tertiary centers 5

Treatment of Underlying Conditions

Address left heart disease aggressively as it is the most common cause of RHF 1, 8:

• Control hypertension according to recommended guidelines (Class I, Level A) 1
• Treat coronary artery disease: Use nitrates and beta-blockers for angina; consider revascularization in patients with angina unresponsive to medical therapy 1
• Manage atrial fibrillation: Control ventricular response with beta-blockers (or amiodarone if contraindicated), and anticoagulate all patients with AF or prior thromboembolic events 1

Investigate for chronic thromboembolic pulmonary hypertension in patients with unexplained dyspnea or chronic RHF, as silent recurrent pulmonary embolism may be the cause 9.

Screen for connective tissue disease in patients with Raynaud phenomenon, arthralgias, or swollen hands presenting with dyspnea, as PAH associated with scleroderma carries poor prognosis 9.

Eliminate alcohol completely in alcoholic cardiomyopathy; otherwise, moderate intake (1-2 glasses of wine/day) is permitted 1.

Pharmacologic Therapy

Use beta-blockers unless contraindicated to reduce sudden death risk in patients with HF who have no or minimal fluid retention and have not recently required intravenous inotropes (Class I, Level A) 1.

Avoid NSAIDs and COX-2 inhibitors as they worsen heart failure 1.

Avoid Class I antiarrhythmic agents due to negative inotropic effects 1.

Consider inotropic support judiciously when medical management fails 10, 4:

• Dobutamine or milrinone may improve RV contractility enough to maintain cardiac output 4
• Use only after optimizing preload and afterload to avoid worsening outcomes 4

Advanced Therapies

Implantable cardioverter-defibrillator is indicated in patients with HF who have history of sudden death, ventricular fibrillation, or hemodynamically destabilizing ventricular tachycardia (Class I, Level A) 1.

Mechanical circulatory support should be considered early when medical management fails 10, 4, 5:

• Right ventricular assist devices or extracorporeal membrane oxygenation are increasingly used for acute RV failure refractory to medical therapy 4, 5
• Early consultation with pulmonary hypertension specialists and transfer to tertiary centers with mechanical support capabilities is advised 5

Cardiac transplantation remains the only established surgical approach for refractory heart failure, though availability is limited to approximately 2,500 patients yearly in the United States 1.

Critical Pitfalls to Avoid

Never treat the RV like the LV: The RV tolerates volume overload better than pressure overload, and aggressive fluid resuscitation can be catastrophic 2.

Recognize ventricular interdependence: RV dilation with pericardial constraint impairs LV filling more than reduced RV forward output, creating a vicious cycle 1.

Monitor for RV myocardial infarction in inferior MI, as functionally-relevant acute RVMI occurs in approximately 50% of patients with acute inferior MI 1.

In myocarditis with RVD, the presence of RV dysfunction by cardiac MRI confers a hazard ratio of 3.4 for death or heart transplantation and is the strongest predictor of death 1.