Right Ventricular Infarction

Introduction
Background

Right ventricular infarction was first recognized in a subgroup of patients with inferior wall myocardial infarctions who demonstrated right ventricular failure and elevated right ventricular filling pressures despite relatively normal left ventricular filling pressures. Increasing recognition of right ventricular infarction, either in association with left ventricular infarction or as an isolated event, emphasizes the clinical significance of the right ventricle to total cardiac function.

Interest in recognizing right ventricular infarction noninvasively has grown because of the therapeutic implications of distinguishing patients with right ventricular dysfunction from those with the more usual clinical presentation of left ventricular dysfunction. Patients with right ventricular infarctions associated with inferior infarctions have much higher rates of significant hypotension, bradycardia requiring pacing support, and in-hospital mortality than isolated inferior infarctions.1

Pathophysiology

The right ventricle is a thin-walled chamber that functions at low oxygen demands and pressure. It is perfused throughout the cardiac cycle in both systole and diastole, and its ability to extract oxygen is increased during hemodynamic stress. All of these factors make the right ventricle less susceptible to infarction than the left ventricle.

The posterior descending branch of the right coronary artery usually supplies the inferior and posterior walls of the right ventricle. The marginal branches of the right coronary artery supply the lateral wall of the right ventricle. The anterior wall of the right ventricle has a dual blood supply: the conus branch of the right coronary artery and the moderator branch artery, which courses from the left anterior descending artery.2

Interestingly, right ventricular infarction noted at necropsy usually involves the posterior septum and posterior wall rather than the right free wall. The relative sparing of the right ventricular anterior wall apparently arises from a high degree of collateralization. This collateral blood flow is thought to be derived from the thebesian veins and diffusion of oxygen directly from the ventricular cavity. A direct correlation exists between the anatomic site of right coronary artery occlusion and the extent of right ventricular infarction. Studies have demonstrated that more proximal right coronary artery occlusions result in larger right ventricular infarctions.3 On occasion, the right ventricle can be subjected to infarction from occlusion of the left circumflex coronary artery.4

Because the right ventricle is considered a low-pressure volume pump, its contractility is highly dependent on diastolic pressure. Hence, when contractility and associated diastolic dysfunction are impaired attendant to right ventricular infarction, the right ventricular diastolic pressure increases substantially and systolic pressure decreases. In such a scenario, concomitant left ventricular dysfunction, with increase in right ventricular afterload, is possible. In such a setting, right ventricular output can decrease dramatically, and the only driving force remaining is elevated right atrial pressure. In such a circumstance, the right ventricle serves as a poorly functioning conduit between the right atrium and the pulmonary artery.

Elevation of right atrial pressure secondary to right ventricular infarction has been noted to serve as a stimulus for secretion of atrial natriuretic factor. Increased levels of this polypeptide can be detrimental to normal left ventricular filling pressures. This occurs by virtue of the potent vasodilating, natriuretic, diuretic, and aldosterone-inhibiting properties of atrial natriuretic factor. Inappropriately elevated levels of atrial natriuretic factor may worsen the clinical syndrome of right ventricular infarction.5 The potential hemodynamic derangements associated with right ventricular infarction render the afflicted patient unusually sensitive to diminished preload (ie, volume) and loss of atrioventricular synchrony. These 2 circumstances can result in a severe decrease in right and, secondarily, left, ventricular output.6,7,8

Early thrombolysis or mechanical reperfusion of an occluded coronary artery resulting in right ventricular infarction is associated with prompt reduction in right atrial pressure. This is extremely important because persistently elevated right atrial pressure has been associated with increased in-hospital mortality rate when associated with myocardial infarction. The extent of right ventricular infarction varies greatly and is dependent on the site of occlusion of the right ventricular arterial supply. If occlusion occurs before the right ventricular marginal branches, and collateral blood flow from the left anterior descending coronary artery is absent, then the size of infarction generally is greater. Extent of infarction depends somewhat on flow through the thebesian veins.9 In general, any major reduction in blood supply to the right ventricular free wall portends an adverse prognosis in association with this disorder.

Frequency
United States

Isolated infarction of the right ventricle is extremely rare; right ventricular infarction usually is noted in association with inferior wall myocardial infarction. The incidence of right ventricular infarction in such cases ranges from 10-50%, depending on the series.10

The frequency of right ventricular infarction, which can be detected by right-sided precordial leads, in association with non–ST-segment elevation or non–Q-wave myocardial infarction is not known and currently is being investigated. Although right ventricular infarction is clinically evident in a sizable number of cases, the incidence is considerably less than that found at autopsy.11,12,13,14 A major reason for the discrepancy is the difficulty in establishing the presence of right ventricular infarction in living subjects. Additionally, right ventricular dysfunction and stunning frequently is of a transient nature, such that estimation of its true incidence is even more difficult.

Criteria have been set forth to diagnose right ventricular infarction; even when strictly employed, however, the criteria lead to underestimation of the true incidence of right ventricular infarction.15,16,17
Clinical
History
Although right ventricular infarction occurs in more than 30% of patients with inferior posterior left ventricular myocardial infarction, hemodynamically significant right ventricular infarction occurs in less than 10% of these patients.18,19
A right ventricular infarct should be considered in all patients who present with an acute inferior wall myocardial infarction, especially in the setting of a low cardiac output.
Patients may describe symptoms consistent with hypotension.
A subtle clue to the presence of hemodynamically significant right ventricular infarction is a marked sensitivity to preload-reducing agents such as nitrates, morphine, or diuretics.20
Other presentations include high-grade atrioventricular block, tricuspid regurgitation, cardiogenic shock, right ventricular free wall rupture, and cardiac tamponade.
Should a patient with right ventricular infarction experience unexplained hypoxia despite administration of 100% oxygen, right-to-left shunting at the atrial level in the presence of right ventricular failure and increased right atrial pressure must be considered.21,22 Despite its rarity, this complication of right ventricular infarction must always be considered when a patient with myocardial infarction is thought to have hypoxia secondary to clinically silent pulmonary emboli. The mechanism for right-to-left shunting in the absence of increased pulmonary arterial pressure resides in patency of the foramen ovale in association with poor right ventricular compliance and increased right atrial filling pressures.
Patients with extensive right ventricular necrosis are at risk for right ventricular catheter–related perforation, and passage of a floating balloon catheter or pacemaker must always be performed with great care in such a setting.
Physical
The classic clinical triad of right ventricular infarction includes distended neck veins, clear lung fields, and hypotension.23
Infrequent clinical manifestations include right ventricular third and fourth heart sounds, which are typically audible at the left lower sternal border and increase with inspiration.
On hemodynamic monitoring, disproportionate elevation of right-sided filling pressures compared with left-sided hemodynamics represents the hallmark of right ventricular infarction.

http://emedicine.medscape.com/article/157961-overview