THE RISE AND FALL OF PULMONARY ARTERY WEDGE PRESSURE: TIME-DEPENDENT PRESSURE DECAY MAINTAINS LOW PULMONARY PRESSURES DURING SUBMAXIMAL EXERCISE

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It is now widely accepted that pulmonary arterial wedge pressure (PAWP) can rise significantly with exercise, even in health. The utility of exercise as a probe for hemodynamic abnormalities is an area of emerging interest, but has had limited success to date, in part due to low specificity of proposed ‘normal’ cut-off values. Recent works have identified ‘exaggerated’ patterns of PAWP responses to exercise as a marker of poor prognosis in heart failure cohorts. A detailed understanding of the ‘normal’ pattern of PAWP response to exercise may aid in the design of diagnostic protocols with appropriate normative data. The purpose of our study was to describe the PAWP response to submaximal exercise in healthy older adults. We hypothesized that PAWP would transiently increase during escalating work-rate, but subsequently decay as submaximal exercise is sustained. Twenty-eight healthy volunteers (17M/11F; mean age = 55±6 years) were studied at rest and during two consecutive stages of cycle-ergometry, with individualized work-rates designed to elicit heart rates (HR) of 100 bpm (Light Exercise) and 120 bpm (Moderate Exercise). Right heart catheterization was performed to directly measure pulmonary pressures. Pulmonary arterial and wedge pressures were measured early (2 minutes) and after sustained (7 minutes) exercise at each intensity. At control, HR was 63 ± 8 bpm, and mean right atrial pressure and PAWP were 6 ± 3 mmHg and 10 ± 3 mmHg, respectively. Pulmonary arterial systolic pressure was 25 ± 4 mmHg. Exercise data are presented in Table 1. With initiation of Light Exercise, target HR was achieved at approximately 2 minutes and then maintained. At 2 minutes of Light Exercise, PAWP increased from control by 100±34% and by 7 minutes of sustained exercise, PAWP then decayed by 57±26%. A further increase of exercise intensity (Moderate Exercise) failed to elicit a further increase in PAWP at 2 minutes, and by 7 minutes of Moderate Exercise, PAWP decayed further, matching resting Control measures despite significantly elevated HR and cardiac output. PAWP increases acutely and substantially with the initiation of exercise, but decays significantly within a period of minutes to that observed at rest. This time-dependent accommodation may be related to left-sided diastolic function, which may vary accordingly with age. Our data indicates that during sustained submaximal exercise, pressure across the pulmonary vasculature remains relatively low in health. Pulmonary hemodynamic response patterns to exercise may provide insight into hemodynamic abnormalities in clinical populations.