Contents

1. Why is the Right Ventricle Important?
2. The least you need to know
3. What causes Right Ventricular Infarction?
4. Pathogenesis and Pathophysiology of RVI.
5. Diagnosis of RVI.
6. Complications associated with RVI.
7. Treatment of RVI.
8. Prognosis.
9. Key Points

• The right ventricle has the same cardiac output as the left
• RV is anatomically and physiologically designed to serve the low pressure pulmonary circulation
• Muscle mass RV is only 15% of LV
• RV stroke work is 25% of LV
• Pulmonary is 10% of Systemic vascular resistance
• Coronary blood flow occurs in both systole and diastole in the right ventricle in the absence of right ventricular hypertrophy.
• The main blood vessel is the right coronary artery (serves the lateral wall, the posterior wall and posterior interventricular septum by the post descending a).
• The anterior wall is supplied by the conus artery and the LAD.
• The RV is like a pocket, wrapped around the LV, sharing the interventricular septum and pericardium.

• The lower afterload and myocardial oxygen demand of the right ventricle [as compared with the left] explain its lower oxygen extraction at rest and its relative resistance to irreversible ischemic damage during right coronary occlusion.

• The increased incidence of right ventricular infarction in patients without a history of preinfarction angina may result from a lack of adequately formed collateral vessels.

• Right ventricular infarction complicates 30-50% of inferior wall MIs, and 10% of anterior wall infarcts.
• The most reliable ECG finding is ST segment elevation in the right precordial leads, particularly RV4, with associated ST segment elevation in II, III & aVF.
• Clinical signs are: high central venous pressure, clear lung fields and systemic hypotension.
• With a large infarction, the RV may, essentially, become a conduit from the systemic veins to the pulmonary circulation.
• Management is centered on volume loading to CVP 16 –20 and the early use of inotropes (dobutamine) to maintain blood flow to the LV [Preload] and to maximize cardiac output.

WHAT CAUSES RIGHT VENTRICULAR INFARCTION?

• Right ventricular infarction occurs when there is an occlusion of the right coronary artery proximal to the acute marginal branches, but it may also occur with an occlusion of the left circumflex artery in patients who have left-dominant coronary circulation
• RVI less commonly may occur as a result of occlusion of the LAD.
• RVI is strongly associated with Inferior wall myocardial infarcts – 30%
• Haemodynamic insufficiency in the presence of inferior wall myocardial infarction suggests additional right ventricular infarction.
• Isolated RVI is extremely rare – 2% of autopsies.

Pathogenesis and Pathophysiology of Right Ventricular Infarction.

• Haemodynamic sequelae include: ­ Right atrial pressure, ­ Right atrial end diastolic pressure, normal LVEDP.

• "Backward Failure" – raised JVP
• Ischaemia induced RV systolic failure and enlargement of the RV, the restraining effect of the pericardium leads to ¯ in left ventricular size and consequent reduced LV performance.

• Remember that normally the tension developed with the contraction of the left ventricle is transmitted to the RV and this assists in the propulsion of blood into the pulmonary arteries.
• In RV infarction, this is less effective:

Due to LV dysfunction

Due to flaccidity of the RV free wall and a reduction in it’s contribution to contractility.

• As a result, it is vital to maintain LV preload and RV afterload to minimise LV dysfunction.

Because of the pathophysiology of right ventricular infarction, its management differs substantially from the routine management of left ventricular infarction. Early, accurate diagnosis is imperative. Since hemodynamically important right ventricular infarction typically occurs in patients with an acute inferior myocardial infarction, suspicion is warranted in any patient presenting with such an infarction.

• The clinical triad of hypotension, clear lung fields, and elevated jugular venous pressure in a patient with an inferior infarction is virtually pathognomonic for right ventricular infarction. However, this triad has a sensitivity of less than 25 percent.
• Caution must be exercised in relying on such findings, since they are readily masked by volume depletion and because the physical and hemodynamic signs of right ventricular infarction often emerge only after volume loading.
• Kussmaul's sign (­ JVP on inspiration) has been shown to be highly sensitive and specific for right ventricular infarction .
• Other physical findings may include right ventricular gallops, tricuspid regurgitation, and atrioventricular dissociation.
• ­ CVP > PCWP

• A right precordial lead (V_4R) is the investigation of choice. ST-segment elevation in lead V_4R remains the most predictive electrocardiographic finding for right ventricular infarction. A 1-mm ST-segment elevation in this lead was 70 percent sensitive and 100 percent specific for right ventricular infarction. In one series, 48 percent of the patients had resolution of electrocardiographic changes within 10 hours of the onset of symptoms. Thus, it is imperative to record the electrocardiogram through the accessory right precordial leads as early as possible.
• It is important to recognize the transient nature of ST-segment elevation
• Right bundle-branch block and complete heart block are the most frequent conduction abnormalities associated with right ventricular infarction .

• Two-dimensional echocardiography: abnormal findings include right ventricular dilatation, right ventricular wall asynergy, and abnormal interventricular septal motion caused by a reversal of the transseptal pressure gradient due to the increased right ventricular end-diastolic pressure.
• The short-axis view has been shown to have the highest sensitivity (82 percent), with a specificity ranging from 62 percent to 93 percent for hemodynamically important right ventricular infarction
• Interatrial septal bowing toward the left atrium, indicative of an increased right atrial-left atrial pressure gradient, is an important prognostic marker in right ventricular infarction. Patients with this finding have more hypotension, more heart block, and higher mortality than patients without it
• Doppler echocardiography is particularly helpful in detecting such complications of right ventricular infarction as tricuspid regurgitation, ventricular septal defect and premature opening of the pulmonary valve [which indicates a noncompliant right ventricle].

• Shock.
• 2^nd or 3^rd degree heart block [indicates a poor prognosis & occurs in as many as 48 percent of right ventricular infarctions].
• Atrial fibrillation [1/3 of RVIs}.
• Ventricular arrhythmias.
• Ventricular septal rupture [in patients with right ventricular infarction and transmural posterior septal infarction].
• Right ventricular thrombus formation and subsequent pulmonary embolism,
• Tricuspid regurgitation
• Pericarditis [due to the frequent transmural injury of the relatively thin-walled right ventricle].
• Right-to-left shunt through a patent foramen ovale [should be suspected in patients who have hypoxemia that is not responsive to the administration of oxygen].

Volume load – eg. iv Hartmann’s / Saline / Gelo

Although volume loading increases RAP and PCWP, it does not increase cardiac output

Avoid nitrates, diuretics, morphine boluses [these ¯ preload]

Maintain atrioventricular synchrony:

AV sequential pacing for complete heart block

Prompt cardioversion for atrial fibrillation

Dobutamine is the agent of choice, then adrenaline or noradrenaline, dopamine.

Dobutamine increases cardiac output, stroke volume index and RVEF, consequently unloading the right ventricle.

Intraaortic balloon counterpulsation

Vasodilators [sodium nitroprusside]

Caution: these may also ¯ LV preload and thus cardiac output.

Thrombolytic Agents

Direct angioplasty

 

Effect of Reperfusion on Biventricular Function and Survival after Right Ventricular Infarction

Terry R. Bowers, William W. O'Neill, Cindy Grines, Mark C. Pica, Robert D. Safian, James A. Goldstein

N Engl J Med April 1998;338:933-40

Background. Although the salutary effects of reperfusion in patients with left ventricular infarction are well documented, the benefits in patients with acute right ventricular infarction are less clear.

Methods. To determine whether primary angioplasty improves right ventricular function and the clinical outcome in patients with right ventricular infarction, we performed echocardiographic studies before and after angioplasty in 53 patients with acute right ventricular infarction.

Results. Complete reperfusion, defined as normal flow in the right main coronary artery and its major right ventricular branches, was achieved in 77 percent of patients, leading to prompt and striking recovery of right ventricular function. 23 percent had unsuccessful reperfusion. Unsuccessful reperfusion was associated with lack of recovery of right ventricular function, as well as persistent hypotension and low cardiac output and a high mortality rate (58 percent, vs. 2 percent for those with successful reperfusion; P = 0.001).

Conclusions. In patients with right ventricular infarction, complete reperfusion of the right coronary artery by angioplasty results in the dramatic recovery of right ventricular performance and an excellent clinical outcome. In contrast, unsuccessful reperfusion is associated with impaired recovery of right ventricular function, persistent hemodynamic compromise, and a high mortality rate.

• When inferior myocardial infarction is complicated by right ventricular infarction, however, the in-hospital mortality may be as high as 31 percent, as compared with 6 percent for patients with inferior myocardial infarction and no right ventricular involvement.

• Several studies have found that right ventricular dysfunction after a myocardial infarction is an independent risk factor for higher long-term mortality.

• Other studies suggest that long-term outcome depends on the degree of concomitant left ventricular dysfunction.

Dell'Italia LJ. Right ventricular infarction. J Intensive Care Med 1986;1:246-56.

 

• In the vast majority of survivors of right ventricular infarction, manifestations of right ventricular dysfunction return to normal. Clinical and haemodynamic recovery eventually occurs even in patients whose right ventricular function remains depressed for weeks or months. This return to normal may be due to the amelioration of concomitant left ventricular dysfunction, resulting in a reduction in right ventricular afterload, or to a gradual stretching of the pericardium with amelioration of its restraining effect

NEJM Right Ventricular Infarction, Review, April 28, 1994 -- Volume 330, Number 1

Key Points

1. The Right Ventricle is anatomically and physiologically designed to serve the low pressure pulmonary circulation.

2. Right ventricular infarction occurs when there is an occlusion of the right coronary artery proximal to the acute marginal branches.

3. Right ventricular infarction complicates 30-50% of inferior wall MIs, and 10% of anterior wall infarcts.

4. Haemodynamic insufficiency in the presence of inferior wall myocardial infarction suggests additional right ventricular infarction.

5. The clinical triad of hypotension, clear lung fields, and elevated jugular venous pressure in a patient with an inferior infarction is virtually pathognomonic for right ventricular infarction.

6. It is vital to maintain LV preload and RV afterload to minimise LV dysfunction.

7. The most reliable ECG finding is ST segment elevation in the right precordial leads, particularly RV4, with associated ST segment elevation in II, III & aVF.

8. Right bundle-branch block and complete heart block are the most frequent conduction abnormalities associated with right ventricular infarction.

9. Complications associated include - shock, heart block, arrhythmias, septal rupture, thrombus, embolism tricuspid regurgitation & pericarditis.

10. Treatment Strategy: 1. Maintain Right Ventricular Preload,2. Inotropic support, 3. Reduce Right ventricular afterload, 4. Reperfusion

11. In-hospital mortality may be as high as 31 percent.

12. Long-term outcome depends on the degree of concomitant left ventricular dysfunction.