right heart failure

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 is commonly used if pharmacological rhythm control needed, though evidence specifically in PAH is limited.
• 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 oral absorption
• Elevated right-sided pressures → hepatic congestion → gut oedema → use IV loop diuretics until decongested; hepatic congestion also reduces hepatic drug metabolism — watch for drug accumulation
• Torsemide or bumetanide may be preferred over furosemide for more consistent oral bioavailability (80–100% vs. 10–100% for furosemide), though clinical superiority is not definitively established (TRANSFORM-HF (2023))
• Add thiazide (metolazone) for sequential nephron blockade when loop diuretic response is inadequate — see diuretic therapy for the full Mullens protocol and natriuresis-guided titration approach
• Acetazolamide 500 mg IV daily may be added upfront to prevent chloride depletion–driven diuretic resistance (see ADVOR protocol)
• MRAs (spironolactone, eplerenone) for further decongestion and potassium sparing — note these have slow onset and are primarily GDMT, not acute rescue agents
• Ultrafiltration if diuretic-refractory — last resort (see CARRESS-HF)
• Decongestion reduces tricuspid annular dilatation, TR severity, RV wall stress, and septal shift — but the RV is preload-dependent; aggressive volume removal can drop RV output and worsen LV filling
• Monitor weight daily; regular electrolytes and renal function; consider natriuresis-guided titration (spot urine Na⁺ at 2h) to optimise diuretic dosing

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

acute RV failure

avoid intubation

Positive pressure ventilation ↓ RV preload and ↑ RV afterload (Alviar, JACC. 2018). 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 with IV loop diuretics ± sequential nephron blockade. Clinical monitoring is essential — LV filling pressures may be normal or low despite RV overload. See diuretic therapy for dose-by-GFR tables, natriuresis-guided titration, and management of diuretic resistance.

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 (> 15 µg/min or > 0.2 µg/kg/min) may increase PVR; consider adding a second vasopressor at this threshold rather than uptitrating further
• Phenylephrine less preferred (pure alpha-agonist → ↑ PVR without inotropic benefit) — may be used as a second vasopressor in specific circumstances when noradrenaline exceeds 15 µg/min

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