Acute Right Ventricular Failure

Acute right ventricular failure is a rapid fall in right ventricular output from pressure overload, volume overload or loss of contractility. It causes systemic venous congestion and reduced left ventricular filling, leading to hypotension, hypoperfusion and shock. It has a high mortality unless the cause is reversed quickly.

Causes by frequency: acute pulmonary embolism, acute decompensation of pulmonary arterial hypertension or chronic lung disease, right ventricular infarction, acute respiratory distress syndrome with high airway pressures, after cardiac surgery or heart transplantation, left ventricular assist device implantation, acute myocarditis, tamponade and arrhythmia, sepsis, and drugs (negative inotropes, excess fluid).

Severity grading:

• Mild: raised jugular venous pressure and right sided congestion with normal blood pressure and perfusion.
• Moderate: hypotension (systolic blood pressure under 90 mmHg or a fall of 40 mmHg or more) that responds to treatment, or lactate 2 to 4 mmol/L.
• Severe: shock with lactate over 4 mmol/L, oliguria, and organ dysfunction despite initial therapy.
• Refractory: persisting shock on two or more vasoactive drugs, or cardiac arrest.

Pathophysiology.

The right ventricle is thin walled, compliant and adapts poorly to a sudden rise in afterload. Wall tension and oxygen demand increase while perfusion falls, because right coronary perfusion depends on aortic pressure.

Right ventricular dilatation shifts the septum toward the left ventricle (ventricular interdependence), reducing left ventricular filling and cardiac output. Falling aortic pressure lowers right coronary flow and drives a spiral of ischaemia and failure.

Hypoxia, hypercapnia and acidosis raise pulmonary vascular resistance and worsen the spiral.

Dyspnoea, syncope, chest pain, fatigue and abdominal discomfort. Signs: tachycardia, hypotension, raised jugular venous pressure with prominent v waves, a parasternal heave, loud pulmonary second sound, third heart sound, tricuspid regurgitation murmur, hepatomegaly, oliguria and cool peripheries with clear lungs. Cardiac arrest with pulseless electrical activity is a common end point.

Rapid investigations (completed within the first 15 to 30 minutes in parallel with resuscitation):

• ECG: sinus tachycardia, new right bundle branch block, right axis, S1Q3T3 pattern, T-wave inversion in V1 to V4, ST elevation in right sided leads (V4R) in right ventricular infarction.
• Bedside echocardiography: right ventricular dilatation (right to left ventricular basal diameter ratio over 1.0), septal flattening (D-shaped left ventricle), TAPSE under 17 mm, tricuspid annular S' under 9.5 cm/s, McConnell sign, plethoric inferior vena cava, tricuspid regurgitation, and thrombus in transit. An acutely loaded normal right ventricle rarely generates systolic pressures over 60 mmHg, so higher values point to chronic pulmonary hypertension.
• Troponin, NT-proBNP, lactate, arterial blood gas, creatinine, liver tests, D-dimer where appropriate, full blood count, coagulation screen and electrolytes.
• CT pulmonary angiography when stable enough, and bedside lung ultrasound.
• Invasive pressure monitoring: arterial line and, in shock, central venous pressure (over 15 mmHg suggests congestion) and consideration of pulmonary artery catheterisation.

Differential diagnosis.

• Left heart failure with secondary right heart failure.
• Cardiac tamponade and constrictive pericarditis.
• Septic or hypovolaemic shock, and severe tension pneumothorax.
• Acute severe asthma or exacerbation of chronic obstructive pulmonary disease, and aortic dissection.

First minutes (0 to 10).

• Move to a monitored resuscitation area. Oxygen to keep SpO2 over 92% (avoid hypoxia; high flow nasal oxygen preferred over intubation).
• Establish intravenous access and an arterial line.
• Identify and treat the cause immediately.
• Avoid intubation and positive pressure ventilation unless unavoidable: sedation and positive pressure can precipitate arrest. If intubation is necessary, use experienced operators, a haemodynamically stable induction agent (ketamine 1 to 2 mg/kg or etomidate 0.2 to 0.3 mg/kg), noradrenaline running, and low PEEP.

Treat the cause.

• Massive (high risk) pulmonary embolism: unfractionated heparin 80 units/kg intravenous bolus then 18 units/kg/h (aPTT 1.5 to 2.5 times control, checked at 6 hours); systemic thrombolysis with alteplase 100 mg intravenously over 2 hours (or 10 mg bolus then 90 mg over 2 hours; in cardiac arrest, 50 mg bolus, repeated once after 15 minutes if needed). Absolute contraindications: previous intracranial haemorrhage, ischaemic stroke within 6 months, intracranial neoplasm, active bleeding, recent major head trauma or surgery within 3 weeks. If contraindicated or failed: catheter directed therapy or surgical embolectomy.
• Right ventricular infarction: primary percutaneous coronary intervention as soon as possible. Avoid nitrates, diuretics and opioids that reduce preload. If hypotensive with clear lungs and low central venous pressure, give 250 to 500 mL of balanced crystalloid over 10 to 15 minutes and reassess. Pace for atrioventricular block (atrioventricular sequential pacing restores atrial kick).
• Acute decompensation of pulmonary arterial hypertension: identify trigger (infection, arrhythmia, non-adherence, anaemia, dehydration), continue or restart pulmonary vasodilators without interruption (for example intravenous epoprostenol starting at 2 ng/kg/min, increased in 1 to 2 ng/kg/min steps every 15 minutes or longer by response), and manage in a pulmonary hypertension centre.
• Arrhythmia: restore sinus rhythm quickly. Synchronised cardioversion 120 to 200 J (biphasic) for unstable atrial fibrillation or flutter or ventricular tachycardia. Amiodarone 300 mg intravenously over 20 to 60 minutes (or 150 mg over 10 minutes), then 900 mg over 24 hours via a central line.
• Tamponade: pericardiocentesis. Pneumothorax: decompress. Sepsis: antibiotics within 1 hour.

Haemodynamic support (0 to 60 minutes).

• Volume: if right atrial pressure or central venous pressure is under 8 mmHg and the inferior vena cava is small, give 250 to 500 mL of crystalloid. If central venous pressure is over 10 to 15 mmHg or the inferior vena cava is plethoric, do not give fluid.
• Decongestion: furosemide 40 to 80 mg intravenous bolus, then 5 to 20 mg/h infusion, titrated to urine output over 100 to 150 mL/h; add ultrafiltration if resistant; monitor potassium, magnesium and creatinine every 6 hours.
• Vasopressor: noradrenaline 0.05 to 0.5 microgram/kg/min, started early to restore mean arterial pressure over 65 mmHg and right coronary perfusion. Vasopressin 0.01 to 0.04 units/min may be added (it does not raise pulmonary vascular resistance).
• Inotrope when low output persists: dobutamine 2.5 to 10 microgram/kg/min (maximum 20); or milrinone 0.25 to 0.5 microgram/kg/min without a bolus (reduce dose in renal impairment, for example 0.2 to 0.33 microgram/kg/min at creatinine clearance under 30 mL/min), accepting the vasodilator effect and hypotension risk, ideally with a vasopressor.
• Pulmonary vasodilators when pulmonary vascular resistance is raised: inhaled nitric oxide 20 ppm (range 5 to 40 ppm) or inhaled epoprostenol 10 to 50 ng/kg/min via nebuliser, with methaemoglobin and rebound monitoring on withdrawal.
• Avoid systemic vasodilators, nitrates and non-dihydropyridine calcium channel blockers.

Ventilation and oxygenation. Treat hypoxia, hypercapnia and acidosis. Target SpO2 over 92%, pH over 7.35 and PaCO2 under 45 mmHg. If ventilated: tidal volume 6 mL/kg predicted body weight, plateau pressure under 27 cmH2O, lowest PEEP that gives oxygenation, and prone positioning for severe hypoxaemia with acute respiratory distress syndrome.

Mechanical support (refractory). Veno arterial extracorporeal membrane oxygenation, or a percutaneous or surgical right ventricular assist device, as a bridge to recovery, decision or transplantation. Early involvement of the multidisciplinary shock team.

Disposition. Admit all to intensive care or a cardiac care unit.

Monitoring. Continuous ECG, arterial pressure and oxygen saturation; lactate every 2 to 4 hours; hourly urine output; daily electrolytes, creatinine and liver tests; echocardiography every 24 hours or with change; central venous oxygen saturation and cardiac output where invasive monitoring is in place (target central venous oxygen saturation over 65%).

Referral and escalation. Escalate immediately to intensive care, cardiology and the shock or pulmonary embolism response team, and to a pulmonary hypertension centre for PAH. Consider early transfer to a centre with extracorporeal support and catheter based embolectomy if there is no response in 60 minutes.

Special groups.

• Pregnancy: left lateral tilt; alteplase and heparin are used in life threatening embolism; avoid warfarin and direct oral anticoagulants; involve obstetrics and plan delivery.
• Kidney impairment: avoid nephrotoxins, adjust milrinone, and use contrast sparingly.
• Older adults: lower fluid and drug doses, and discuss ceilings of care.