Stroke volume response during exercise measured by acetylene uptake and MRI

Abstract

The intra-breath technique to measure acetylene absorption offers the possibility to determine augmentation of the pulmonary blood flow per heart beat (Q(C)) as an estimate of the stroke volume response during exercise. However, this method has not been compared with a validated test until now. Therefore, the aim of this study was to compare Q(C) with stroke volume (SV(MRI)) determined by magnetic resonance imaging (MRI) at rest and during exercise in healthy subjects and patients. For this purpose, ten healthy subjects and ten patients with idiopathic pulmonary arterial hypertension (iPAH) with expected impaired stoke volume response during exercise were measured by both methods. Exercise-induced changes in Q(C) and SV(MRI) were correlated in healthy controls (r = 0.75, p < 0.05). Compared to healthy controls, Q(C) increased less during exercise in iPAH patients (11 +/- 17 ml versus 33 +/- 12 ml, p < 0.05). A similar difference in stroke volume response to exercise between the two groups was measured by MRI (-0.6 +/- 8 ml versus 23 +/- 12 ml, p < 0.05, respectively). Hence, intra-breath and MRI measurements showed similar differences in exercise-induced changes in stroke volume between controls and patients. From these results it can be concluded that the intra-breath measurement of acetylene absorption might be of value as a non-invasive tool to estimate stroke volume augmentation during exercise and can detect differences in stroke volume responses between iPAH patients and healthy subjects.

Prognostic value of exercise pulmonary haemodynamics in pulmonary arterial hypertension

“…6MWD in moderate-tosevere PAH patients is determined by maximal cardiac output [20,21]. As in PAH, cardiac output cannot adapt due to an inability to increase heart rate and stroke volume [19,22], it is not surprising to find a significant association between 6MWD and exercise cardiac index in our relatively small population of patients.…”

“…A role in this finding for the lower workload in the NYHA IV group is unlikely, as exercise heart rate was similarly increased in all NYHA groups and the low exercise cardiac index in the NYHA IV group was chiefly ascribable to the absence of increase in stroke volume from rest to exercise, a well-known mechanism of inadequate adaptation to exercise in severe PAH [19]. 6MWD in moderate-tosevere PAH patients is determined by maximal cardiac output [20,21].…”

Belastungstests bei pulmonal-arterieller Hypertonie

“…Tatsächlich ist der rechte Ventrikel vom Aufbau her nicht gut geeignet, auf eine erhöhte Nachlast zu reagieren. Infolgedessen zeigen PAH-Patienten ein niedriges Schlagvolumen, das unter Belastung nicht zunimmt [9], sodass der Anstieg der Auswurfleistung primär durch Erhöhung der Herzfrequenz erreicht wird [10]. Jedoch ist PAH auch dadurch gekennzeichnet, dass die Herzfrequenz nicht auf den zu erwartenden Höchstwert gesteigert werden kann, sodass die maximale Auswurfleistung unter Belastung zugleich durch das niedrige Schlagvolumen und die veränderte chronotrope Reaktion begrenzt wird [8,9,10].…”

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

“…However, unlike TTE it cannot provide information on pressure and a significant minority of subjects fail to tolerate the test because of claustrophobia [66]. Additionally exercise measurements so far in PAH have been taken in the immediate post-exercise phase because of the difficulty in cycling whilst inside the bore of the scanner [67]. The validity of this is questionable as values of pressure and flow post-exercise fall rapidly [44,68].…”

“…Nevertheless, the feasibility of the technique to estimate SV during exercise in PAH and detect the effects of disease targeted therapy on exercise SV, have both been demonstrated [67,71]. Lee et al [71] also showed that, if SV is the variable of interest, then changes in supine resting SV provided as much information as erect exercise values, indicating the importance of preload as a stressor for assessing the pulmonary circulation.…”