right heart failure

RV failure in pulmonary hypertension is the primary driver of morbidity and mortality. Management centres on three physiological targets: preload reduction (diuresis), afterload reduction (PAH-targeted therapy), and contractility augmentation (inotropes). Acute decompensation carries very high mortality and requires ICU-level care with a focus on avoiding intubation and aggressive volume removal.

chronic RV failure

general supportive measures

Supplemental O₂ to maintain SpO₂ > 92%
Maintain sinus rhythm — atrial arrhythmias are poorly tolerated (loss of atrial kick further compromises RV filling). Cardiovert promptly when feasible; amiodarone preferred if pharmacological rhythm control needed.
Iron repletion if deficient (common in PAH; IV iron preferred for reliable absorption)
Monitor NT-proBNP and troponin longitudinally — rising biomarkers signal progressive RV dysfunction and inform escalation decisions

diuretics

Loop diuretics (furosemide, bumetanide, torsemide) are the mainstay — large doses often required due to neurohormonal activation and gut oedema reducing absorption
Torsemide may be preferred over furosemide for more consistent oral bioavailability, though clinical superiority is not definitively established
Add thiazide for sequential nephron blockade when loop diuretic response is inadequate
MRAs (spironolactone, eplerenone) may be added for further decongestion and potassium sparing
Ultrafiltration if diuretic-refractory
Decongestion reduces tricuspid annular dilatation, TR severity, RV wall stress, and septal shift — but avoid excessive volume depletion (may compromise LV filling and cardiac output)
Monitor weight daily; regular electrolytes and renal function

afterload reduction

Optimise PAH-targeted therapy — this is the primary strategy to reduce RV afterload. Up-front combination therapy (endothelin antagonist + PDE5i/sGC stimulator) is standard of care for intermediate- and high-risk PAH. In newly diagnosed PAH with low cardiac output, consider early initiation of IV/SC prostacyclin analogues.

inotropes

Digoxin may reduce symptoms in chronic RV failure, but evidence is mixed. Avoid in hypoxaemia and hypokalaemia (↑ toxicity risk).
Ambulatory milrinone/dobutamine infusions: reasonable as bridge to transplant or MCS (AHA/ACC/HFSA 2022 Class 2a). Not recommended for long-term use outside of palliation or bridge therapy (Class 3: Harm).

refractory RV failure

Durable RV assist device (RVAD) or total artificial heart — only if PVR is not severely elevated (severely elevated PVR → risk of pulmonary haemorrhage with RVAD)
Lung or heart-lung transplantation in selected patients

palliative care

Introduce palliative care early and in parallel with pharmacological therapy. Advance care planning should be discussed when curative options are limited, not deferred to end-stage disease.

acute RV failure

acute decompensation

Acute RV failure in PH carries very high mortality. Management requires ICU-level care with haemodynamic monitoring. Target MAP > 60 mmHg.

avoid intubation

Positive pressure ventilation ↓ RV preload and ↑ RV afterload. If intubation unavoidable:

Avoid hypotension at induction — use ketamine or etomidate; have vasopressin/noradrenaline running
Tidal volume ~6–8 mL/kg IBW; plateau pressure < 30 cmH₂O
Initial PEEP 3–5 cmH₂O; titrate cautiously (higher PEEP ↑ RV afterload)
Avoid hypercapnia (↑ PVR) — permissive hypocapnia is acceptable

volume management

Most decompensated PH patients are volume-overloaded, not volume-depleted. Excess preload worsens RV dilatation and septal shift → ↓ LV filling. Diurese aggressively (IV loop diuretics ± thiazide). Clinical monitoring is essential — LV filling pressures may be normal or low despite RV overload.

exception: acute RV infarction and massive PE

In acute PE or RV infarction without chronic RV remodelling, cautious fluid administration (≤ 500 mL crystalloid bolus) may improve cardiac output if CVP is low. This does not apply to chronically dilated RVs in PH, where additional volume worsens function.

vasopressors

Vasopressin (0.01–0.04 U/min) is preferred — ↑ SVR without ↑ PVR. Caution at higher doses (> 0.04 U/min may cause coronary vasoconstriction).
Noradrenaline as second-line at moderate doses — at higher doses (> 0.2 µg/kg/min) may increase PVR
Avoid phenylephrine (pure alpha-agonist → ↑ PVR without inotropic benefit)

inotropes (acute)

Dobutamine (2.5–10 µg/kg/min) — first-line inotrope for acute RV failure
Milrinone (0.125–0.5 µg/kg/min; consider omitting loading dose) — inodilator with pulmonary vasodilatory effect. Caution: systemic vasodilatation → hypotension → RV ischaemia; often paired with vasopressin.

inhaled pulmonary vasodilators

Inhaled nitric oxide (10–40 ppm) and/or inhaled epoprostenol — selectively ↓ PVR without systemic hypotension

systemic prostacyclins

IV epoprostenol as last resort (short half-life allows rapid titration; start 2 ng/kg/min, ↑ by 2 ng/kg/min q15min)
Monitor for systemic hypotension and worsening V/Q mismatch

monitoring in acute RV failure

Arterial line for continuous BP and ABG monitoring
CVP / ScvO₂: rising CVP with falling ScvO₂ signals worsening RV failure; target ScvO₂ > 65%
Serial echocardiography: RV size, septal motion, TAPSE, IVC collapsibility to guide therapy
NT-proBNP and troponin: trending values to assess trajectory
Urine output and lactate: end-organ perfusion markers

mechanical support

VA-ECMO: bridge to recovery, transplant, or PEA in refractory cases