Right Ventricular Infarction

Historical Perspective

In 1930, Sanders reported the first clinical description of RVMI. During the following 4 decades, RVMI received attention mainly in autopsy series. At that time, any shock syndrome was considered the result of MI. This view was buttressed by evidence from open pericardium dog models in which destruction of the right ventricle was not associated with shock. The development of surgical procedures that bypassed the right ventricle, such as the Glenn and Fontan procedures, furthered the belief that the right ventricle is mainly a volume conduit contributing little to cardiac output.

In 1974, Cohn and coworkers first called attention to RVMI as a unique clinical and hemodynamic syndrome characterized, in its extreme form, by shock, distended neck veins, and clear lung fields. During the ensuing 2 decades of intense investigation into the syndrome, the crucial role of ventricular interdependence through the pericardium and the septum was recognized. Today, a rational approach to therapy of RVMI based on an understanding of its pathophysiology is possible.

Coronary Circulation and the Right Ventricle

In the 85% of patients with right dominant coronary circulation, the RV receives its blood supply almost exclusively from the right coronary artery (RCA), with the septum and part of the posterior wall supplied by the posterior descending artery and the anterior and lateral RV walls supplied by acute marginal branches of the RCA. The left anterior descending (LAD) artery supplies a small portion of the anterior wall of the right ventricle. In left dominant circulation, the left circumflex coronary artery supplies the posterior descending artery, and a nondominant RCA supplies the acute marginal branches. Isolated RV infarct without any LV involvement can occur with occlusion of a nondominant RCA.

The angiographic hallmark of RVMI is thrombotic occlusion of the RCA proximal to the origin of the acute marginal branches. Angiographic flow studies suggest that the status of RV branch perfusion is the critical determinant of RV ischemic dysfunction. Proximal RCA occlusions typically limit RV branch perfusion in contrast to distal RCA occlusions.

Not every case of proximal RCA occlusion results in RV infarction. This relative protection of the right ventricle from infarction is thought to be a consequence of its lower oxygen demand, its continued perfusion during systole, and the potential presence of collaterals from the LAD coronary artery, which, because of the lower systolic pressure on the right side, are more capable of supplying blood in the direction of the right ventricle than in the reverse direction. The LAD collaterals to the RV are mainly through the moderator band artery, a branch of the first septal perforator. Prior severe stenosis or occlusions of the LAD coronary artery can limit the development of collaterals to the right ventricle with an acute RCA occlusion increasing the degree of acute ischemic RV dysfunction.

Ventricular Interdependence

The concept of ventricular interdependence in RVMI is central to understanding the pathogenesis of the resultant low cardiac output state. Ventricular interdependence is mediated through the common pericardium and shared septum. The septum is an integral component—both physically and functionally—to the RV and even under physiologic conditions, septal contraction contributes to RV performance. In RVMI, acute RV dilation occurs. Because the RV shares a relatively fixed space with the LV, the pericardial pressure abruptly increases, leading to impaired LV filling. In animal models with the pericardium removed, it is difficult to induce hypotension with RVMI. When the pericardium is left intact, however, RVMI is associated with the full syndrome, as originally described by Cohn and coworkers. Incision of the pericardium leads to improvement in cardiac output, pressure equalization, and an increase in RV systolic pressure.

The increase in right-sided diastolic pressure that occurs in RVMI leads to a reversal of the normal left-to-right transseptal diastolic gradient. On echocardiography, the septum can be seen to flatten and encroach on the LV diastolic dimension. During systole, the septum can be seen to move paradoxically toward the RV, at times in a piston-like manner.

Except in rare cases of isolated RVMI, some degree of LVMI accompanies RVMI. The pericardial constraint and alterations in septal geometry lead to reduced LV filling; cardiac output is diminished further by the decrease in LV systolic function. Development of shock syndrome with isolated RV infarction proves, however, that LV systolic dysfunction is not necessary for the development of shock. Echocardiographic assessment in cases of hemodynamically severe RVMI has confirmed that shock may be present with preserved LV systolic function.

The hemodynamic hallmarks of RV infarction ( Box 14.1 ) are a decrease in cardiac output, elevation of right atrial pressure (>10 mm Hg), elevation of RV diastolic pressure, and decrease in RV systolic pressure. There is diastolic equalization of RV and LV pressures, as in cardiac tamponade and the ratio between right atrial and pulmonary capillary wedge pressure increases. This ratio, which normally is less than 0.65, is usually greater than 0.8 in RVMI. RV tracing reveals a delayed, depressed, and often bifid peak, indicating systolic RV failure. RV diastolic failure is also manifested by a dip and plateau pattern on the RV pressure tracing. In most studies, hemodynamic tracings showed a blunted x descent with a prominent y descent, suggesting decreased compliance of the RV, as seen in pericardial constriction ( Fig. 14.1 ). Although the hemodynamic criteria for RVMI are usually present on admission, volume loading may increase the identification of these abnormalities in some patients.

Clinical Presentation

Clinically significant RVMI usually occurs in patients with concomitant inferoposterior infarction of the LV, and many of the symptoms overlap. Necropsy studies suggest that RVMI occurs almost exclusively in patients with transmural posteroseptal MI. The size of the LV infarct does not correlate with RV infarct size. The size of the RV infarct influences the severity of RV dysfunction and presentation, however. What is unique to RVMI is the occurrence of a syndrome of RV diastolic and systolic failure that, in its extreme form, is characterized by a triad of signs: hypotension that can progress to cardiogenic shock, elevated neck veins, and clear lung fields.

When RVMI is hemodynamically significant, the physical examination is a sensitive method of detection. Dell'Italia and colleagues found elevated jugular venous pressure to be 88% sensitive, with a specificity of 69% for inferior wall MI with RV involvement. Kussmaul sign, an inspiratory increase in the jugular venous pressure, was found to be 100% sensitive and specific in the same series; Bellamy and coworkers found it to have a sensitivity of 59% and a specificity of 89%. Other associated findings include a high frequency of bradycardia, atrioventricular (AV) block, and atrial arrhythmias, including supraventricular tachycardias and atrial fibrillation or flutter. A right-sided fourth heart sound was described in 11 of 16 patients in one series, with 4 of 16 having a right-sided third heart sound. Tricuspid regurgitation may be audible. Pericardial friction rubs may be heard because infarction in the thin RV is usually transmural.

The differential diagnosis includes tension pneumothorax, cardiac tamponade, constrictive pericarditis, pulmonary embolism, and, rarely, atypical RV-variant takotsubo cardiomyopathy. When the full triad (hypotension, elevated neck veins, clear lungs) is present and ST segment elevations are observed in inferior leads, the diagnosis is straightforward. A potential pitfall is the occurrence of isolated RV branch infarction, which may manifest with the full clinical picture of RVMI but without evidence of MI on the standard 12-lead electrocardiogram (ECG) or with ECG evidence of a presumed anterior infarct. Harnett et al. recently presented a case series of two isolated RV branch MIs that were initially missed on angiography owing to an ECG pattern consistent with an anterior STEMI. Given the anatomic location, an isolated RVMI can mimic the clinical and ECG picture of an anterior LVMI. Consequently, anterior ST elevation in the precordial leads without reciprocal changes and lack of significant left coronary disease should prompt careful attention to the RV branch at time of angiography ( Box 14.2 ).

Pulmonary embolism (PE) occasionally mimics RVMI and may predispose to occult RVMI. Conversely, RVMI with secondary thrombus formation in the RV can lead to PE. Dyspnea is usually more severe in PE; RV systolic pressure, pulmonary artery pressure, and pulmonary vascular resistance are usually higher with PE than with RVMI. Cardiac tamponade may be acute and may manifest with a similar triad of elevated neck veins, hypotension, and clear lungs; it can be distinguished easily at the bedside with echocardiography, however. Pulsus paradoxus, a hallmark of tamponade, is unusual in RVMI, which tends to more closely resemble pericardial constriction.

Diagnosis

Electrocardiographic Diagnosis

ST Segment.

The ECG remains the most useful tool for the diagnosis of RVMI. The hallmark of acute RV ischemia is ST segment elevation in the right precordial leads, a finding first reported in 1976 by Erhardt and coworkers, who used lead CR located in the fifth intercostal space at the right midclavicular line. The importance of obtaining right-sided chest leads on presentation in patients with suspected acute MI, particularly with evidence of inferior wall involvement, cannot be overemphasized ( Fig. 14.2 ).

Several studies have documented that ST segment elevation of 0.05 mV or greater (0.5 mm when using standard settings of 10 mm/mV) in lead V _4R in the setting of inferior MI is sensitive and specific for RV involvement, as documented by postmortem examination or by radionuclide, echocardiographic, hemodynamic, or angiographic studies. Infrequently, ST segment elevation in V _5R or V _6R occurs in the absence of elevation in V _4R . Zehender and colleagues confirmed the utility of 0.1-mV ST segment elevation in any of the right precordial leads (V _4R-V6R ) in a series of 200 patients, showing a sensitivity of 89% and a specificity of 83%.

The ECG findings in RVMI of right precordial ST segment elevations are the result of a rightward and anteriorly directed vector. Andersen and coworkers showed that ST segment elevation in lead III exceeding that in lead II (i.e., ST segment vector directed rightward) is reasonably sensitive (68%) in diagnosing RVMI. This criterion had a specificity of only 11% and a positive predictive value of 58% in Zehender's series of 200 patients with inferior MI but had a sensitivity of 95%.

Certain special situations with variant ECG findings that may cause confusion warrant mention. Geft and colleagues described five patients with ST segment elevations in leads V ₁ to V ₅ who on catheterization were shown to have RCA occlusion and acute RVMI. All five patients had minimal or absent ST segment elevations in the inferior leads. The authors speculate that in the usual cases of RVMI, ST segment elevations in leads V ₁ to V ₅ are blocked by the dominant electrical forces of inferoposterior MI, resulting in isoelectric or even depressed ST segments in the left precordium. When these forces are absent, because of isolated RVMI or with minimal posterior involvement, as may be seen in a patient with a codominant circulation, ST segment elevation in the left precordial leads mimicking anterior wall MI may be seen. A distinguishing characteristic in RV infarction may be that the ST segment elevations are highest in leads V ₁ or V ₂ and decrease toward lead V ₅ , a pattern opposite that usually seen in anterior MI.

If septal involvement can mimic RVMI, a left lateral wall infarction or a large true posterior infarction can be expected to cancel right precordial ST segment elevations. Such cases of false-negative findings have been described.

Most studies of right precordial lead ST segment elevation have been limited to patients with evidence of inferior wall MI. In anterior MI, ST segment elevation in the right precordial leads has also been documented and has been found to be predictive of proximal LAD occlusion before the first septal branch, suggesting that the right precordial lead ST segment elevations are the result of a septal current of injury. A distinguishing characteristic in cases of LAD occlusion is that the ST segment elevation has a leftward axis in contrast to the rightward ST segment in RV infarction, as emphasized by Hurst. Other causes of right precordial ST segment elevation in the absence of RVMI include pericardial disease, left anterior hemiblock, and PE.

The time course of ST segment elevation in RVMI warrants emphasis. Braat and colleagues reported that ST segment elevations in lead V _4R resolve within 10 hours after the onset of chest pain in half of patients. Similar findings were reported by Klein and colleagues. Thus, it is important to obtain a right-sided ECG soon after the patient's presentation.

Q Waves in Right Ventricular Infarction.

Because patients may present after the ST segments have returned to baseline, criteria using Q waves in the right precordial leads have been sought. In normal subjects, an rS pattern is always present in V _3R and usually (>90%) in V _4R . In one series of patients with autopsy-documented RV infarction, the presence of a Q wave in these leads (as a QS or a QR pattern) was 100% specific and 78% sensitive. The high specificity (>90%) of Q waves was confirmed in Zehender's series of 200 patients with inferior wall MI. Early in the course of infarction, Q waves are still absent and the sensitivity is low, particularly for patients presenting early. In patients admitted late (>12 hours after the onset of symptoms), the sensitivity increases to 95%.

Bundle Branch Block.

RVMI, especially when extensive, has been shown to be associated with an incomplete and often transient right bundle branch block. The block is postulated to occur distally. Because there may also be precordial ST segment elevation in RV infarction, the right bundle branch block may be difficult to detect in lead V ₁ . Kataoka and coworkers pointed to a cove-shaped ST-T elevation in lead V ₁ as suggestive of an underlying right bundle branch block.

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