Marie M. Budev, DO, MPH, Alejandro C. Arroliga, MD, Herbert P. Wiedemann, MD, and Richard A. Matthay, MD

Disclosures

Semin Respir Crit Care Med. 2003;24(3) 

In This Article

Interaction Between the Pulmonary Vasculature and the Right Heart

The right ventricle is a crescent-shaped chamber composed of a concave free wall and a convex interventricular septum[18,19] (Fig. 1). Right ventricular contraction is produced by three main mechanisms: an initial shortening of the trabeculae and papillary muscles forcing the tricuspid valve toward the ventricular apex; a subsequent decrease in the longitudinal axis, causing minimal ejection of blood; and finally, movement of the free wall toward the interventricular septum leading to a contraction followed by a secondary contraction of the circular fibers and resulting in an increased curvature of the interventricular septum. The concave free wall, along with the increased curvature of the interventricular septum, leads to a bellows-like action with subsequent expulsion of blood from the right ventricle. Right ventricular contractions are aided by a passive gradient between the two regions within the chamber, the inflow and outflow areas. Right ventricular contractions are more passive than left ventricular contractions. Because of the thin walls and crescent shape of the right ventricle, it is compliant and can accommodate and eject relatively large amounts of blood with limited myocardial shortening.[20] Therefore, it can accommodate large increases in blood volume rather than pressure, in contrast to the muscular left ventricular pressure pump. If right ventricular afterload is increased because of pulmonary artery constriction, stroke volume rapidly decreases. In contrast, if right ventricular preload is increased or atrial preload is increased by volume expansion, the stroke volume or work remains constant[21,22] (Fig. 2). Under normal circumstances, the compliant thin-walled right ventricle empties into the pulmonary vasculature, which provides low resistance to outflow.

Figure 1.

The anatomic relationship of the right ventricle (RV) to the left ventricle (LV) illustrating the crescent shape of the right ventricle and the globular shape of the heart. Left atrium (LA) and right atrium (RA). (From Guyton[24] with permission.)

Figure 2.

Effect of increasing afterload (A) and preload (B) on the right and left ventricle. (From McFadden and Braunwald[22] with permission.)

In normal persons, the pulmonary vasculature can react to wide fluctuations in flow without much change in pressure so that the right ventricle is not pressure-overloaded. This accommodation is effected by recruitment of previously nonperfused vessels in the superior portions of the lung and distention of the vessels in dependent areas. During periods of intense exercise, pulmonary blood flow may increase up to fivefold, whereas pulmonary vascular resistance may increase only minimally through recruitment of small arterioles and capillaries thereby enabling the pulmonary vascular bed to accommodate an increase in cardiac output while systolic pulmonary artery pressure rarely exceeds 20 mmHg.[23] In fact, two thirds of the lung must be destroyed before pulmonary artery pressure increases at rest. Even after pneumonectomy, pulmonary artery pressure remains near normal as long as no further pulmonary vascular change occurs.[6]

The response of the right ventricle to acute increases in pulmonary vascular resistance has been studied in animal models.[24] Figure 3 depicts the changes in mean systemic arterial pressure, mean pulmonary artery pressure, mean right ventricular pressure, and mean right atrial pressure that occur as the main pulmonary artery is progressively constricted over 4 to 5 minutes. During this process, the right ventricle was able to generate increasing pulmonary artery pressure and maintain cardiac output until the mean pulmonary artery pressure was about 40 mmHg, at which point sudden circulatory collapse ensued.

Figure 3.

Measurement of mean pulmonary pressures in a dog over a 4- to 5-minute period. The right ventricle is unable to generate a mean pulmonary artery pressure > 40 mmHg, leading to sudden circulatory collapse. (From Wiedemann and Matthay[24] with permission.)

Wiedemann and Matthay described the pathophysiology of such acute circulatory collapse as the "vicious cycle" of acute right failure (Fig. 4).[24] Increasing right ventricular volume (preload) is an important mechanism for maintaining systolic function in the presence of pulmonary artery hypertension. However, as right ventricular volume increases, ventricular wall stress and oxygen demand increase, tricuspid valve insufficiency occurs, and left ventricular diastolic compliance decreases. These events, which impair the performance of the ventricles, eventually cause systemic hypotension. As aortic pressure drops, right coronary artery perfusion is adversely affected, with further decline in right ventricular function and further right ventricular dilation. Without intervention, these events rapidly spiral into irreversible shock.

Figure 4.

Pathophysiology of acute right heart failure: the vicious cycle. (From Wiedemann and Matthay[24] with permission.)

In patients with chronic cor pulmonale, acute decompensation may occur during exacerbations of pulmonary disease when compensatory measures (such as dilation and hypertrophy) fail. Other factors leading to right ventricular failure may include reduced right ventricular preload due to hyperinflation in patients with obstructive lung disease with decreased venous return. Reduced right ventricular filling in these patients may result from increased intrathoracic pressure or decreased intravascular volume owing to diuretic therapy. In patients with restrictive lung disease, loss of distensibility and relative stiffness of the intrathoracic structures may limit cardiac filling leading to right ventricular collapse.[25] Also, poor right ventricular response or overt failure due to pressure overload may be caused by impairment of right ventricular blood supply. In systemic hypertension, the left ventricle has increased myocardial oxygen demand. In turn, coronary artery perfusion pressure increases with an increase in diastolic pressure to meet this myocardial oxygen demand. In patients with pulmonary artery hypertension, right ventricular myocardial oxygen demand is also increased. Right ventricular myocardial perfusion occurs during both diastole and systole but systolic flow to the right coronary artery is diminished because of elevations in right ventricular pressure.[11] In addition, perfusion pressures may decrease with a reduction in cardiac output. Even with normal coronary arteries, the blood flow to the right coronary artery can be limited at high pulmonary artery pressures, possibly leading to right ventricular failure due to myocardial ischemia.[6]

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