Why does this statement matter?
A patient with oedema, rising creatinine and a dilated right ventricle may need decongestion. A hypotensive patient with right ventricular infarction and relative volume depletion may need a different approach. Both can have right heart failure, but the same treatment can have very different consequences.
The Heart Failure Society of America (HFSA) statement positions right heart failure as a distinct, prognostically important syndrome. It synthesises published evidence and expert guidance; it is not a new randomised trial or a universally validated treatment protocol. Its organising principle is to identify the physiology driving deterioration and reassess the response to treatment.
What should the initial assessment establish?
The right ventricle (RV) must move blood through the pulmonary circulation, accommodate systemic venous return and provide adequate left ventricular filling. Failure can produce congestion, reduced cardiac output and organ dysfunction in different combinations.
Assessment therefore needs to establish the cause, volume status and adequacy of perfusion. The statement describes renal and hepatic dysfunction as important systemic consequences. Pulmonary hypertension, left-heart disease, pulmonary embolism, myocardial injury and valvular disease require different therapeutic pathways.
Transthoracic echocardiography is first-line. Combine RV size and function, tricuspid regurgitation, ventricular interaction and estimated pressures. Tricuspid annular plane systolic excursion (TAPSE) and tissue Doppler measurements are load- and angle-dependent; previous cardiac surgery may further limit their interpretation. Cardiac magnetic resonance can help when echocardiography is inadequate or discordant with the clinical picture.
Right heart catheterisation can clarify haemodynamics and pulmonary hypertension phenotype. Consider invasive assessment particularly when volume status remains uncertain, renal function worsens or instability complicates treatment. A high right atrial pressure with a normal or low pulmonary artery wedge pressure can represent substantial isolated right-sided congestion; a normal wedge pressure does not by itself argue against diuresis. [1]
How should preload be managed?
Preload optimisation is not synonymous with fluid loading. Excess volume can worsen RV dilatation, wall tension, tricuspid regurgitation and ventricular interaction. Conversely, excessive fluid removal can reduce output and cause hypotension, especially in low-output failure.
Loop diuretics remain central when congestion is present. An inadequate response may warrant combination treatment with a thiazide diuretic. Follow renal function and electrolytes alongside haemodynamics and clinical response. Persistent congestion with worsening renal dysfunction may prompt consideration of ultrafiltration rather than automatic escalation of fluid administration.
Intravenous fluids have a selective role in relative volume depletion, including some patients with RV infarction. The decision requires a volume assessment and repeated evaluation of benefit or deterioration.
When are inotropes and vasopressors useful?
In acute RV failure with inadequate output, dobutamine and milrinone can improve haemodynamics. Their pharmacology helps guide selection, but direct comparative evidence is limited.
| Agent | Practical distinction in the statement | Important limitation |
|---|---|---|
| Dobutamine | Rapid onset and a short half-life favour titration during acute instability; it may cause less vasodilation than milrinone. | Hypotension, arrhythmias and myocardial ischaemia remain concerns. |
| Milrinone | Greater pulmonary and systemic vasodilation; its action is downstream of the beta receptor, which may be useful after beta-blocker exposure. | Longer action and renal accumulation complicate use in kidney impairment. |
| Norepinephrine or vasopressin | Preferred vasopressor options described for profound hypotension and threatened perfusion. | Selection and titration require ongoing assessment of output and organ perfusion. |
The statement discusses a suggested mean arterial pressure of 70–75 mmHg to preserve aortic pressure and right coronary perfusion, while explicitly noting that alternative targets have not been directly compared in RHF. This is a physiological suggestion, not a trial-established universal target. [1]
Why must afterload treatment follow the cause?
Pulmonary arterial hypertension (PAH) is a setting in which targeted treatment can reduce pulmonary vascular load. The statement directs clinicians to contemporary PAH guidance; advanced disease may require parenteral prostacyclin treatment and specialist consideration of transplantation.
In selected acute settings, inhaled nitric oxide or inhaled epoprostenol may lower pulmonary vascular resistance. Inhaled treatment offers greater pulmonary selectivity, while systemic therapies can cause hypotension and other adverse effects. Nitric oxide requires careful weaning because abrupt withdrawal can produce rebound pulmonary hypertension.
| Underlying condition | Cause-specific direction |
|---|---|
| Pulmonary hypertension from left-heart disease | Treat the underlying heart failure. Routine pulmonary vasodilators are not recommended because benefit is unproven and harm, including fluid retention, may occur. |
| Chronic thromboembolic pulmonary hypertension | Specialist multidisciplinary assessment for pulmonary endarterectomy, balloon pulmonary angioplasty and appropriate medical treatment. |
| Symptomatic severe tricuspid regurgitation | Consider intervention after optimal medical treatment, taking account of RV function, anatomy, symptoms and procedural risk. |
For transcatheter tricuspid interventions, the statement highlights improvements in symptoms and quality of life. It does not establish a long-term mortality benefit. [1]
How do rhythm and respiratory support affect the RV?
Atrial contraction and atrioventricular synchrony contribute to RV filling. Supraventricular tachyarrhythmias can compromise output. Cardioversion may be considered, although success varies in critical illness. Beta-blockers and nondihydropyridine calcium-channel blockers require caution because negative inotropy and hypotension may worsen decompensation.
Hypoxia, hypercapnia and acidosis can worsen pulmonary vasoconstriction. High airway pressures and lung overdistension can increase RV afterload, while positive-pressure ventilation can reduce cardiac filling.
The statement advocates judicious use of mechanical ventilation and non-invasive support when feasible. Where invasive ventilation is necessary, low tidal volumes and avoidance of excessive positive end-expiratory pressure are important physiological considerations. Induction and intubation require careful planning because sedation-related hypotension and changes in loading conditions can precipitate collapse.
When should care escalate?
Acute RHF refractory to medical treatment may require temporary mechanical circulatory support. Options include RV assist devices and venoarterial extracorporeal membrane oxygenation (VA-ECMO). The choice depends on isolated versus biventricular failure, oxygenation needs, anatomy, reversibility, organ function and institutional expertise.
Support may provide a bridge to recovery, a decision or transplantation. Serial reassessment must guide escalation and weaning; device availability alone does not determine suitability.
Where does uncertainty remain?
The authors identify inconsistent definitions, limited RHF-specific endpoints, inadequate phenotyping in registries and a lack of broadly applicable risk models. PAH and post-LVAD risk scores serve particular populations and should not be assumed to perform equally across all causes of RHF.
The statement reports no funding and discloses several authors’ relationships with drug and device companies. Its practical framework is useful, but the strength of evidence differs across treatments and settings.
Clinical takeaway
Assess the congested circulation and the underperfused patient together. Optimise preload, address the cause of increased RV afterload and support output when required, while protecting rhythm and respiratory physiology. The HFSA statement provides a structured approach; continuing reassessment and recognition of its evidence limits remain essential.
Full reference
1. Kanwar MK, Carnicelli AP, Belkin MN, Esposito ML, Coons JC, Molina EJ, Airhart S, Cascino TM, Blumer V, Tedford RJ. Heart Failure Society of America Scientific Statement on Right Heart Failure. Journal of Cardiac Failure. 2026. Article in press in the supplied PDF; final volume, issue and pagination not verified. doi:10.1016/j.cardfail.2026.04.026.