Unexplained exertional dyspnea caused by low ventricular filling pressures: results from clinical invasive cardiopulmonary exercise testing

Pulmonary Circulation, March 2016, Vol. 6 Issue: Number 1
p55-62, 8p;

Abstract: To determine whether low ventricular filling
pressures are a clinically relevant etiology of unexplained dyspnea on
exertion, a database of 619 consecutive, clinically indicated invasive
cardiopulmonary exercise tests (iCPETs) was reviewed to identify
patients with low maximum aerobic capacity (V̇o2max) due to inadequate
peak cardiac output (Qtmax) with normal biventricular ejection
fractions and without pulmonary hypertension (impaired: n= 49, V̇o2max
= 53% predicted [interquartile range (IQR): 47%–64%], Qtmax = 72%
predicted [62%–76%]). These were compared to patients with a normal
exercise response (normal: n= 28, V̇o2max = 86% predicted [84%–97%],
Qtmax = 108% predicted [97%–115%]). Before exercise, all patients
received up to 2 L of intravenous normal saline to target an upright
pulmonary capillary wedge pressure (PCWP) of ≥5 mmHg. Despite this
treatment, biventricular filling pressures at peak exercise were lower
in the impaired group than in the normal group (right atrial pressure
[RAP]: 6 [IQR: 5–8] vs. 9 [7–10] mmHg, P= 0.004; PCWP: 12 [10–16] vs.
17 [14–19] mmHg, P< 0.001), associated with decreased stroke volume
(SV) augmentation with exercise (+13 ± 10 [standard deviation (SD)] vs.
+18 ± 10 mL/m2, P= 0.014). A review of hemodynamic data from 23
patients with low RAP on an initial iCPET who underwent a second iCPET
after saline infusion (2.0 ± 0.5 L) demonstrated that 16 of 23 patients
responded with increases in Qtmax ([+24% predicted [IQR: 14%–34%]),
V̇o2max (+10% predicted [7%–12%]), and maximum SV (+26% ± 17% [SD]).
These data suggest that inadequate ventricular filling related to low
venous pressure is a clinically relevant cause of exercise
intolerance.