Right Ventricular Infarction

Right ventricular infarction is myocardial necrosis of the right ventricle, nearly always from proximal occlusion of the right coronary artery, before the acute marginal branches. It complicates 30 to 50% of inferior ST-elevation infarcts, and 10 to 15% cause significant haemodynamic compromise.

Isolated right ventricular infarction is rare. It is more common in right dominant systems and with proximal right coronary or, rarely, left circumflex occlusion.

The classic clinical triad is hypotension, clear lung fields and raised jugular venous pressure. In hospital mortality is about 25 to 30% when the right ventricle is involved, against about 6% without right ventricular involvement. Survivors usually recover right ventricular function after reperfusion.

Pathophysiology.

The thin right ventricle has low oxygen demand and a dual supply in systole and diastole, so infarction is less common than left sided, but an occlusion before the marginal branches reduces perfusion of the free wall.

An ischaemic, dilated right ventricle fails to deliver adequate blood to the left heart. Pericardial constraint and septal shift (ventricular interdependence) lower left ventricular filling and stroke volume, so the patient is preload dependent and hypotensive despite a normal left ventricular systolic function.

Atrioventricular block from nodal ischaemia, loss of atrial contraction, and a patent foramen ovale with right-to-left shunt (hypoxaemia) worsen the picture.

Chest pain, nausea and vomiting, dyspnoea, syncope and shock with inferior infarction. Signs: raised jugular venous pressure (with a Kussmaul sign), clear lungs, hypotension, a right sided third heart sound, tricuspid regurgitation murmur, bradycardia and heart block. Hypotension after nitrates, morphine or diuretics is characteristic.

• ECG: inferior ST elevation (ST elevation in III greater than in II suggests a right coronary culprit). ST elevation of 1 mm or more in lead V4R (right sided leads recorded in the first 10 hours). ST elevation in V1 with ST depression in V2, and atrioventricular block, also occur.
• Echocardiography: right ventricular dilatation and hypokinesia, TAPSE under 17 mm, septal flattening, plethoric inferior vena cava, tricuspid regurgitation, and a right-to-left shunt across a patent foramen ovale on agitated saline.
• Troponin; coronary angiography at once for reperfusion; invasive pressures where there is doubt (right atrial pressure 10 mmHg or more with right atrial to pulmonary capillary wedge pressure ratio over 0.8, and a dip-and-plateau trace).

Differential diagnosis.

• Pulmonary embolism, cardiac tamponade and constrictive pericarditis.
• Left ventricular failure with cardiogenic shock.
• Acute aortic dissection involving the right coronary ostium.
• Tension pneumothorax and sepsis with inferior ST changes.

Reperfusion. Primary percutaneous coronary intervention as soon as possible, with the target of first medical contact to wire passage within 120 minutes.

If this is not feasible, give fibrinolysis with tenecteplase within 10 minutes of diagnosis, then angiography at 2 to 24 hours.

• 30 mg under 60 kg.
• 35 mg for 60 to under 70 kg.
• 40 mg for 70 to under 80 kg.
• 45 mg for 80 to under 90 kg.
• 50 mg for 90 kg or over.
• Half dose from age 75.

Rescue angioplasty when ST resolution is under 50% at 60 to 90 minutes.

Antithrombotic therapy.

• Aspirin 150 to 300 mg orally loading dose, then 75 to 100 mg daily.
• Ticagrelor 180 mg orally loading dose, then 90 mg twice daily for 12 months.
• Alternatives to ticagrelor: prasugrel 60 mg loading dose then 10 mg daily (5 mg when weight is under 60 kg or age is 75 or over), or clopidogrel 600 mg loading dose, then 75 mg daily.
• Unfractionated heparin 70 to 100 units/kg intravenous bolus during primary percutaneous coronary intervention (60 units/kg with a glycoprotein IIb/IIIa inhibitor), or enoxaparin 0.5 mg/kg intravenously.
• With fibrinolysis in patients under 75: enoxaparin 30 mg intravenous bolus, then 1 mg/kg subcutaneously every 12 hours (maximum 100 mg for the first two doses; once daily when creatinine clearance is under 30 mL/min).
• From age 75, enoxaparin 0.75 mg/kg every 12 hours without bolus.

Haemodynamic support.

• Maintain right ventricular preload: if hypotensive with clear lungs and low jugular venous pressure, give crystalloid 250 to 500 mL over 10 to 15 minutes and reassess; up to 1 to 2 litres in total.
• Stop fluid when right atrial pressure exceeds 15 mmHg, when the jugular venous pressure rises further without a rise in blood pressure, or when septal shift increases, since overload dilates the right ventricle and reduces left ventricular filling.
• Avoid nitrates, diuretics, morphine, ACE inhibitors, angiotensin receptor blockers and beta blockers in hypotension, because they reduce preload.
• Inotropy when output is low after volume: dobutamine 2.5 to 10 microgram/kg/min (maximum 20). Noradrenaline 0.05 to 0.5 microgram/kg/min to maintain mean arterial pressure over 65 mmHg and right coronary perfusion.
• Pulmonary vasodilator for raised pulmonary vascular resistance: inhaled nitric oxide 20 ppm (range 5 to 40 ppm).
• Restore atrioventricular synchrony: atrial or atrioventricular sequential temporary pacing for high degree block (single chamber right ventricular pacing loses atrial contribution and may worsen output).
• Atropine 0.5 mg intravenously, repeated every 3 to 5 minutes to a maximum of 3 mg, for symptomatic bradycardia while pacing is arranged.
• Synchronised cardioversion 120 to 200 J (biphasic) for atrial fibrillation with instability, as loss of atrial kick is poorly tolerated.
• If cardioversion fails: amiodarone 300 mg intravenously over 20 to 60 minutes then 900 mg over 24 hours (central line).
• Refractory shock: mechanical support with a percutaneous right ventricular assist device, intra-aortic balloon counterpulsation, or veno arterial extracorporeal membrane oxygenation.
• Hypoxaemia not corrected by oxygen: suspect right-to-left shunt through a patent foramen ovale, with later closure.

Secondary prevention. Atorvastatin 40 to 80 mg once daily (LDL cholesterol under 1.4 mmol/L), ACE inhibitor (ramipril 2.5 mg daily, titrated to 10 mg) and beta blocker (metoprolol succinate 25 mg daily titrated to 200 mg) once haemodynamics recover and filling pressures are normal. Eplerenone 25 to 50 mg daily when ejection fraction is 40% or under with heart failure or diabetes (potassium under 5.0 mmol/L). Cardiac rehabilitation and risk factor control.

Monitoring. Continuous ECG for 48 to 72 hours, haemodynamics hourly, lactate every 2 to 4 hours in shock, creatinine and potassium daily, echocardiography at 24 to 48 hours, at discharge and at 3 months.

Referral and escalation. All patients need immediate cardiology and catheter laboratory activation. Refer to a shock team for hypotension persisting after volume, or for mechanical complications (tricuspid regurgitation, septal rupture, free wall rupture).

Special groups.

• Older adults: reduce fluid boluses and tenecteplase dose, and watch bleeding.
• Kidney impairment: adjust enoxaparin and minimise contrast.
• Pregnancy: rare (spontaneous coronary artery dissection is usual); treat in a specialist cardio obstetric centre.
• Region specific: where primary angioplasty is not available, fibrinolysis followed by early transfer is the usual approach.