Exercise-induced pulmonary hypertension: physiological basis and methodological concerns

Abstract

Exercise stresses the pulmonary circulation through increases in cardiac output (.Q) and left atrial pressure. Invasive as well as noninvasive studies in healthy volunteers show that the slope of mean pulmonary artery pressure (mPAP)-flow relationships ranges from 0.5 to 3 mm Hg.min.L(-1). The upper limit of normal mPAP at exercise thus approximates 30 mm Hg at a .Q of less than 10 L.min(-1) or a total pulmonary vascular resistance at exercise of less than 3 Wood units. Left atrial pressure increases at exercise with an average upstream transmission to PAP in a close to one-for-one mm Hg fashion. Multipoint PAP-flow relationships are usually described by a linear approximation, but present with a slight curvilinearity, which is explained by resistive vessel distensibility. When mPAP is expressed as a function of oxygen uptake or workload, plateau patterns may be observed in patients with systolic heart failure who cannot further increase .Q at the highest levels of exercise. Exercise has to be dynamic to avoid the increase in systemic vascular resistance and abrupt changes in intrathoracic pressure that occur with resistive exercise and can lead to unpredictable effects on the pulmonary circulation. Postexercise measurements are unreliable because of the rapid return of pulmonary vascular pressures and flows to the baseline resting state. Recent studies suggest that exercise-induced increase in PAP to a mean higher than 30 mm Hg may be associated with dyspnea-fatigue symptomatology.

Figure 1.

Modeled mean pulmonary artery pressure–flow relationships at progressively increased pulmonary vascular distensibility expressed as % increase in diameter per mm Hg pressure (or α). α is normally less than 2%/mm Hg. A slight increase in vascular distensibility may result in marked decrease in pulmonary artery pressures at exercise.

Figure 2.

(A) Mean pulmonary artery pressure (mPAP)–$\stackrel{.}{\text{Q}}$ relationships at rest and at progressively increased workloads in normal subjects measured by echocardiography (n = 113). (B) mPAP–$\stackrel{.}{\text{Q}}$ relationships at rest and at progressively increased workloads in normal subjects measured by right heart catheterization (n = 24). The prediction bands are shown by the shaded areas. mPAP at $\stackrel{.}{\text{Q}}$ values of 10, 20, and 30 L/min are shown by the stippled lines. There was a good agreement on limits of normal between noninvasive and invasive measurements. Upper limits of normal are estimated as a slope of linearized mPAP–$\stackrel{.}{\text{Q}}$ of 3 mm Hg⋅min⋅L⁻¹ or mPAP less than 30 mm Hg at a $\stackrel{.}{\text{Q}}$ less than 10 L⋅min⁻¹. Adapted by permission from Reference .

Figure 3.

Changes in mean pulmonary artery pressure (mPAP) and $\stackrel{.}{\text{Q}}$ at maximum exercise and after 5, 10, and 20 minutes’ recovery in 25 healthy subjects. Both mPAP and $\stackrel{.}{\text{Q}}$ are almost back to baseline 5 minutes after maximum exercise. Reprinted by permission from Reference .

Figure 4.

Cardiac output versus workload (W) relationships at exercise. There is wide range of cardiac output values at any given workload. Reprinted by permission from Reference .

Figure 5.

Negative extrapolated pressure intercepts of mean pulmonary artery pressure (mPAP)–flow plots in patients with left heart failure. Group I and II: patients with left ventricular conditions and mPAP less than or greater than 19 mm Hg, respectively. Group III: pulmonary vascular disease. Extrapolated pressure intercepts of mPAP–$\stackrel{.}{\text{Q}}$ plots lower than left atrial pressure suggest pulmonary vasoconstriction at high pressures or flows. PAW = pulmonary artery wedge pressure. Reprinted by permission from Reference .