Chest

Chest

Volume 114, Issue 1, Supplement, July 1998, Pages 101S-106S
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The Pressure-Overloaded Right Ventricle in Pulmonary Hypertension

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DETERMINANTS OF OUTCOME IN PRIMARY PULMONARY HYPERTENSION

Figure 1 gives “point estimates” (ie, odds ratios + 95% confidence limits) for various factors that could influence outcome in PPH based on published data from the PPH registry.2 As can be seen in Figure 1, parameters that reflect RV function, such as right atrial mean pressure and cardiac output, are significantly associated with prognosis. The only other factor associated with prognosis is pulmonary vascular resistance, which, as will be discussed, is a major determinant in RV function. The

HOW THE RV DIFFERS FROM THE LV

Under normal loading conditions and when function is not compromised, the RV ejects blood against approximately 25% of the afterload of the LV. As a result RV wall thickness is much less than in the LV, the LV wall thickness being greater in order to minimize wall stress via the LaPlace relationship (Fig 2). Because wall thickness is less in the RV, it is more compliant and can accommodate more rapidly to volume overload.8 Because of the thin chamber wall and the higher compliance, the RV does

THE RV IN PPH

In PPH or congenital heart disease associated with increased RV afterload, the RV becomes LV-like in character, assuming a wall thickness of 0.6 to 1.5 cm by MRI measurements (unpublished data). However, the RV is still geometrically different from the LV, as illustrated in Figure 3. In PPH, the RV is characterized by increased end-diastolic volume, change of the normal ventricular conformation tetrahedron to a crescentic trapezoid, and varying degrees of RV hypertrophy.9 The RV in severe PPH

ALTERED GENE EXPRESSION IN PPH RVS

What are the changes in gene expression that occur in the pressure-overloaded RV and how do they produce intrinsic contractile dysfunction (ie, load-independent decreases in systolic function)? Shown in Table 1 are changes in gene expression that we have described in failing, hypertrophied RVs examined in PPH subjects. The decrease in the gene and protein expression of β1-adrenergic receptors and adenylyl cyclase contributes to β1-receptor pathway desensitization, which is produced in response

TREATMENT OF RV FAILURE FROM SEVERE PRESSURE OVERLOAD

The prominent British cardiologist Celia Oakley has written that “When faced with an irremovable increase in afterload, … right ventricular failure is untreatable and easily made worse.”22 While this was generally true in the 1980s when the statement was made, there is now considerable hope in the treatment of RV failure from PPH. In reality, the definitive treatment of heart failure from severe pressure overload is the same in the RV as in the LV—that is, to relieve the obstruction and lower

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    Copyright © 1998 The American College of Chest Physicians. Published by Elsevier Inc. All rights reserved.