Exercise stress echocardiography for the study of the pulmonary circulation

Abstract

Exercise stress tests have been used for the diagnosis of pulmonary hypertension, but with variable protocols and uncertain limits of normal.The pulmonary haemodynamic response to progressively increased workload and recovery was investigated by Doppler echocardiography in 25 healthy volunteers aged 19-62 yrs (mean 36 yrs). Mean pulmonary artery pressure (Ppa) was estimated from the maximum velocity of tricuspid regurgitation. Cardiac output (Q) was calculated from the aortic velocity-time integral. Slopes and extrapolated pressure intercepts of Ppa-Q plots were calculated after using the adjustment of Poon for individual variability. A pulmonary vascular distensibility a was calculated from each Ppa-Q plot to estimate compliance.Ppa increased from 14¡3 mmHg to 30¡7 mmHg, and decreased to 19¡4 mmHg after 5 min recovery. The slope of Ppa-Q was 1.37¡0.65 mmHg?min -1 ?L -1 with an extrapolated pressure intercept of 8.2¡3.6 mmHg and an a of 0.017¡0.018 mmHg -1 . These results agree with those of previous invasive studies. Multipoint Ppa-Q plots were well described by a linear approximation, from which resistance can be calulated. We conclude that exercise echocardiography of the pulmonary circulation is feasible and provides realistic resistance and compliance estimations. Measurements during recovery are unreliable because of rapid return to baseline. KEYWORDS: Echocardiography, exercise stress test, pulmonary arterial compliance, pulmonary hypertension, pulmonary vascular resistance P ulmonary arterial hypertension (PAH) is currently defined by a mean pulmonary artery pressure (P pa) of .25 mmHg, a left atrial pressure (Pla) f15 mmHg and a pulmonary vascular resistance (PVR) of .3 Wood units [1]. Previous definitions included P pa of .30 mmHg at exercise [2], but this has been abandoned because of uncertain limits of normal and unknown symptomatic relevance.Recently, however, TOLLE et al.[3] reported on exercise-induced PAH as a new clinical entity, characterised by a sharp increase in P pa of .30 mmHg as a cause of decreased exercise capacity. In that study, haemodynamic measurements were presented as log-log plots of P pa as a function of oxygen uptake (V9O 2 ), with plateau patterns typical of PAH and takeoff patterns representing a normal response. Since V9O 2 is related to cardiac output (Q), these patterns would appear at variance. Numerous studies have shown multipoint P pa-Q plots to be best described by linear or slightly curvilinear approximations [4,5]. REEVES et al.[6] modelled P pa as a function of Q invasively measured in exercising normal volunteers, and indeed found a slight curvilinearity which they explained by the natural distensibility of the resistive pulmonary arterioles.Even though the procedure has still not been validated, Doppler echocardiography is a recommended screening test for PAH [1,2] and has been used in combination with exercise for the diagnosis of overt or latent PAH [7]. A systolic pulmonary artery pressure (Ppa,sys) of 40 mmHg is usually taken as the upper limit of ...

Determinants of exercise-induced pulmonary arterial hypertension in systemic sclerosis

“…As previously described [20,21] and underlined by several recent reviews [4][5][6], the slope of the mPAP-LVCO relationship is probably the best way to demonstrate an abnormal increase in PAP during exercise and therefore for the diagnosis EIPH. However, duration of exercise in our population was really short and we rather focused on LV systolic and diastolic function.…”

“…The mPAP was estimated by the Chemla formula: mPAP = 0.61 × sPAP + 2. As previously described [20,21], left atrial pressure (LAP) was assessed by 1.9 + 1.24 LV E/e′ and pulmonary vascular resistance (PVR) was estimated as the ratio between (mPAP-LAP) and LVCO, both at rest and at peak exercise. The slope of mPAP/LVCO relationship was estimated as the ratio between changes (peak-rest value) in mPAP and changes in LVCO [19].…”

Clinical significance of dynamic pulmonary vascular resistance in two populations at risk of pulmonary arterial hypertension

“…However, multipoint sPAP-flow plots were well described by a linear or slightly curvilinear approximation in earlier studies. 16,31,42 In addition, there was a strong linear correlation between the slopes of the corrected ASD group, measured with 2 vs. 5 measurement points per patient (slope-2-points ¼ 1.26 × slope-5-points + 0.4; P , 0.001). Furthermore, echocardiographic measurements were not confirmed by right heart catheterization.…”

“…16 Furthermore, it is difficult to measure sPAP at peak exercise instead of immediately after because of the rapid decline during recovery. 31 Dynamic PVR will be less influenced by delayed measurement. In addition, in a recently published study of patients with SSc, sPAP at peak exercise was not predictive of PAH development.…”

The Role of Exercise Testing in the Modern Management of Pulmonary Arterial Hypertension

“…These have shown the ability to estimate systolic pulmonary artery pressure (sPAP) [43][44][45][46][47][48], PAOP by inference from E/e' ratio [49,50], CO from left ventricular outflow velocity-time integral [43,44], resistance [43,44], distensibility [43,44,51] and right ventricular function assessed by tricuspid annular plane systolic excursion (TAPSE) and tricuspid annular systolic velocity [52]. mPAP can be deduced from sPAP using one of the equations derived for this relationship [53,54].…”