Right heart failure

Contents

RV Physiology

The right ventricle is a thin-walled, crescent-shaped structure adapted to a low-pressure, high-compliance pulmonary circulation:

  • RV wall thickness: 3–5 mm (vs LV 8–12 mm)
  • Normal PAP: systolic 15–30 mmHg, mean 8–20 mmHg
  • Highly preload-dependent and exquisitely sensitive to acute increases in afterload
  • RV coronary perfusion is bi-phasic (systole and diastole, unlike the LV which perfuses mainly in diastole) — when RVSP rises acutely, RV perfusion pressure (= MAP − RVSP) falls → subendocardial ischaemia → contractile failure

RV–LV Interdependence

Both ventricles share the interventricular septum and pericardial space. Acute RV dilation under pressure shifts the septum leftward (D-sign on echo), compressing the LV, reducing LV preload and impairing LV filling. This creates a vicious cycle: RV failure → ↓ LV preload → ↓ CO → ↓ coronary perfusion → worsening RV failure.

Pathophysiology of RV Failure

Preload failure

Hypovolaemia, obstruction to venous return, cardiac tamponade.

Afterload failure (most common in ICU)

Acute ↑ PVR from:

  • Hypoxia → hypoxic pulmonary vasoconstriction
  • Hypercarbia, acidosis → pulmonary vasoconstriction
  • Positive pressure ventilation → ↑ intrathoracic pressure → compresses pulmonary capillaries → ↑ PVR; also ↓ venous return → ↓ RV preload
  • Massive PE, ARDS, acute or chronic pulmonary hypertension

Contractile failure

  • RV MI (proximal right coronary artery occlusion — accompanies ~30% of inferior STEMIs)
  • Post-cardiac surgery (cardioplegia, poor myocardial protection)
  • Septic cardiomyopathy, myocarditis

Causes in the ICU

Mechanism Examples
Acute ↑ PVR Massive PE, severe ARDS, hypoxia, hypercarbia, acidosis
RV MI Inferior STEMI — proximal RCA occlusion; volume-dependent management
Post-cardiac surgery After mitral valve surgery, congenital repair
Decompensated chronic PH Known PAH deteriorating from infection, surgery, hypoxia
Post-LVAD insertion LV unloading shifts demand to RV; unmasks latent RV failure
Septic cardiomyopathy Biventricular depression from inflammatory mediators

Clinical Recognition

Haemodynamic Signs

  • Hypotension with low CO (oliguria, cold peripheries, ↑ lactate)
  • Elevated JVP/CVP — high right-sided filling pressures
  • Clear lung fields — no pulmonary oedema (distinguishes from LV failure)
  • Hepatomegaly, ↑ LFTs from passive hepatic congestion

Echo Findings

  • RV:LV ratio >0.6 at end diastole — significant dilation
  • D-sign (septal bowing leftward) — RV pressure or volume overload
  • TAPSE <17 mm — impaired RV systolic function
  • IVC dilated with loss of respiratory variation (↑ RA pressure)

PA Catheter Profile (if in situ)

↑ CVP/RAP, ↑ PAP, ↓ PCWP (underfilled LV), ↓ CO/CI, ↑ PVR

Management

Four Pillars

1. Optimise preload (carefully)

  • RV is preload-dependent: hypovolaemia reduces output — cautious fluid challenge (250 mL with reassessment)
  • Excessive fluid worsens RV dilation, exacerbates septal shift, impairs LV filling — do not over-fill
  • Guided by echo and response to challenge

2. Reduce RV afterload

Inhaled nitric oxide (iNO):

  • Inhaled → selective pulmonary vasodilation → ↓ PVR without systemic hypotension
  • Dose 5–40 ppm; most response at lower doses; effective in ARDS, acute PH, post-surgery
  • Wean slowly — abrupt discontinuation causes rebound pulmonary hypertension

Inhaled prostacyclin (epoprostenol/iloprost): alternative to iNO; nebulised

Milrinone (IV PDE3 inhibitor): ↑ cAMP → inotropy + ↓ PVR; risk of systemic hypotension — use with vasopressor

Sildenafil (oral PDE5 inhibitor): for chronic PH or to facilitate iNO weaning

3. Maintain systemic pressure and RV coronary perfusion

  • Noradrenaline: first-line; maintains MAP → preserves RV perfusion pressure (MAP − RVSP)
  • Vasopressin 0.01–0.04 units/min: adjunct; relatively pulmonary-neutral
  • Angiotensin II: effective in catecholamine-refractory vasodilatory shock; see ATHOS-3
  • Dobutamine: β₁ inotropy + mild ↓ PVR via β₂; only use once systemic pressure protected (can cause profound hypotension)
  • Adrenaline: refractory shock; mixed α/β

4. Optimise mechanical ventilation

  • Use lowest effective PEEP — each cmH₂O increases RV afterload
  • Correct hypoxia and hypercarbia (both cause pulmonary vasoconstriction)
  • Consider prone positioning in ARDS-associated RV failure (redistributes flow, may ↓ PVR)

RV MI — Specific Management

  • Do NOT give nitrates or diuretics — reduce preload → precipitous haemodynamic collapse
  • Volume loading is the initial treatment: 250–500 mL challenges to maintain RV filling
  • Maintain sinus rhythm: AV block common (RCA supplies AV node in 90%); atropine, temporary pacing
  • Urgent primary PCI: reperfusion of the proximal RCA restores RV function rapidly

Mechanical Circulatory Support

  • RVAD: draws from RA, returns to pulmonary artery; short-term bridge
  • VA-ECMO: full support; note: retrograde aortic flow may ↑ LV afterload → may need LV venting

Viva Questions

1. Explain how mechanical ventilation worsens RV function and how you would mitigate this.

Positive pressure ventilation raises intrathoracic pressure, compressing pulmonary capillaries and increasing PVR — the primary determinant of RV afterload. Simultaneously, elevated intrathoracic pressure reduces venous return and RV preload. The RV, adapted to a low-pressure circuit, is unable to tolerate acute increases in afterload: it dilates, the septum bows leftward, LV filling is impaired, and cardiac output falls in a vicious cycle. High PEEP causing alveolar overdistension is particularly harmful — converting zone III to zone II conditions throughout the lung propagates vascular compression. Mitigation: use the minimum PEEP compatible with adequate oxygenation; target normocapnia (hypercarbia worsens pulmonary vasoconstriction); correct hypoxia; consider inhaled NO to reduce PVR directly; monitor RV function serially with echo; consider prone positioning in ARDS-associated RV failure, which may redistribute pulmonary blood flow and reduce PVR.

2. A patient with known pulmonary arterial hypertension deteriorates post-operatively with a dilated, hypokinetic RV on echo. What are your priorities?

This is decompensated PAH — a potentially fatal emergency with very high perioperative mortality. Priorities: (1) Identify and correct precipitants: hypoxia, hypercarbia, acidosis, sepsis, hypovolaemia — all worsen pulmonary vasoconstriction; (2) Restart PAH-specific therapy immediately if held peri-operatively (patients on IV epoprostenol cannot safely stop — rebound PH can be fatal); (3) Inhaled NO for acute pulmonary vasodilation; (4) Noradrenaline to maintain MAP and RV coronary perfusion pressure; (5) Vasopressin as adjunct; (6) Dobutamine or milrinone for RV inotropic support once systemic pressure protected; (7) Lowest possible PEEP and plateau pressures if ventilated; (8) Involve the specialist pulmonary hypertension team urgently; (9) VA-ECMO as rescue bridge if refractory. Avoid anything reducing preload or systemic vascular resistance without first protecting MAP.

3. How do you distinguish RV failure from cardiac tamponade, and why does the distinction matter?

Both present with hypotension, elevated JVP, and low cardiac output. Key differences: on echo, tamponade shows pericardial effusion with RA/RV diastolic collapse and a relatively normal-sized RV; RV failure shows a dilated RV, septal bowing (D-sign), TAPSE impaired, but no effusion (or a small one). Haemodynamically: tamponade produces equalisation of diastolic filling pressures (CVP = PCWP = PAD); RV failure produces high CVP, low PCWP (underfilled LV), and elevated PVR. Pulsus paradoxus >10 mmHg on spontaneous breathing suggests tamponade but is less reliable on PPV. The distinction matters because treatments are opposite: tamponade requires urgent drainage (pericardiocentesis or surgical); RV failure requires vasopressors, inotropes, and pulmonary vasodilators. Draining a non-existent effusion in RV failure achieves nothing; withholding vasodilators from tamponade is similarly unhelpful.