Marcel Azabji Kenfack

Correction of cardiac output obtained by Modelflow from finger pulse pressure profiles with a respiratory method in humans

The beat-by-beat non-invasive assessment of cardiac output (Q litre x min(-1)) based on the arterial pulse pressure analysis called Modelflow can be a very useful tool for quantifying the cardiovascular adjustments occurring in exercising humans. Q was measured in nine young subjects at rest and during steady-state cycling exercise performed at 50, 100, 150 and 200 W by using Modelflow applied to the Portapres non-invasive pulse wave (Q(Modelflow)) and by means of the open-circuit acetylene uptake (Q(C2H2)). Q values were correlated linearly ( r = 0.784), but Bland-Altman analysis revealed that mean Q(Modelflow) - Q(C2H2) difference (bias) was equal to 1.83 litre x min(-1) with an S.D. (precision) of 4.11 litre x min(-1), and 95% limits of agreement were relatively large, i.e. from -6.23 to +9.89 litre x min(-1). Q(Modelflow) values were then multiplied by individual calibrating factors obtained by dividing Q(C2H2) by Q(Modelflow) for each subject measured at 150 W to obtain corrected Q(Modelflow) (Qcorrected) values. Qcorrected values were compared with the corresponding Q(C2H2) values, with values at 150 W ignored. Data were correlated linearly ( r = 0.931) and were not significantly different. The bias and precision were found to be 0.24 litre x min(-1) and 3.48 litre x min(-1) respectively, and 95% limits of agreement ranged from -6.58 to +7.05 litre x min(-1). In conclusion, after correction by an independent method, Modelflow was found to be a reliable and accurate procedure for measuring Q in humans at rest and exercise, and it can be proposed for routine purposes.

Cardiac output by Modelflow® method from intra-arterial and fingertip pulse pressure profiles

Modelflow, when applied to non-invasive fingertip pulse pressure recordings, is a poor predictor of cardiac output (Q, litre x min(-1)). The use of constants established from the aortic elastic characteristics, which differ from those of finger arteries, may introduce signal distortions, leading to errors in computing Q. We therefore hypothesized that peripheral recording of pulse pressure profiles undermines the measurement of Q with Modelflow, so we compared Modelflow beat-by-beat Q values obtained simultaneously non-invasively from the finger and invasively from the radial artery at rest and during exercise. Seven subjects (age, 24.0 +/- 2.9 years; weight, 81.2 +/- 12.6 kg) rested, then exercised at 50 and 100 W, carrying a catheter with a pressure head in the left radial artery and the photoplethysmographic cuff of a finger pressure device on the third and fourth fingers of the contralateral hand. Pulse pressure from both devices was recorded simultaneously and stored on a PC for subsequent Q computation. The mean values of systolic, diastolic and mean arterial pressure at rest and exercise steady state were significantly ( P < 0.05) lower from the finger than the intra-arterial catheter. The corresponding mean steady-state Q obtained from the finger (Qporta) was significantly ( P < 0.05) higher than that computed from the intra-arterial recordings (Qpia). The line relating beat-by-beat Qporta and Qpia was y =1.55 x -3.02 ( r2 = 0.640). The bias was 1.44 litre x min(-1) and the precision was 2.84 litre x min(-1). The slope of this line was significantly higher than 1, implying a systematic overestimate of Q by Qporta with respect to Qpia. Consistent with the tested hypothesis, these results demonstrate that pulse pressure profiles from the finger provide inaccurate absolute Q values with respect to the radial artery, and therefore cannot be used without correction with a calibration factor calculated previously by measuring Q with an independent method.

PHASE I DYNAMICS OF CARDIAC OUTPUT, SYSTEMIC O2 DELIVERY AND LUNG O2 UPTAKE AT EXERCISE ONSET IN MEN IN ACUTE NORMOBARIC HYPOXIA

We tested the hypothesis that vagal withdrawal plays a role in the rapid (phase I) cardiopulmonary response to exercise. To this aim, in five men (24.6+/-3.4 yr, 82.1+/-13.7 kg, maximal aerobic power 330+/-67 W), we determined beat-by-beat cardiac output (Q), oxygen delivery (QaO2), and breath-by-breath lung oxygen uptake (VO2) at light exercise (50 and 100 W) in normoxia and acute hypoxia (fraction of inspired O2=0.11), because the latter reduces resting vagal activity. We computed Q from stroke volume (Qst, by model flow) and heart rate (fH, electrocardiography), and QaO2 from Q and arterial O2 concentration. Double exponentials were fitted to the data. In hypoxia compared with normoxia, steady-state fH and Q were higher, and Qst and VO2 were unchanged. QaO2 was unchanged at rest and lower at exercise. During transients, amplitude of phase I (A1) for VO2 was unchanged. For fH, Q and QaO2, A1 was lower. Phase I time constant (tau1) for QaO2 and VO2 was unchanged. The same was the case for Q at 100 W and for fH at 50 W. Qst kinetics were unaffected. In conclusion, the results do not fully support the hypothesis that vagal withdrawal determines phase I, because it was not completely suppressed. Although we can attribute the decrease in A1 of fH to a diminished degree of vagal withdrawal in hypoxia, this is not so for Qst. Thus the dual origin of the phase I of Q and QaO2, neural (vagal) and mechanical (venous return increase by muscle pump action), would rather be confirmed.

Prolonged head down bed rest-induced inactivity impairs tonic autonomic regulation while sparing oscillatory cardiovascular rhythms in healthy humans.

Background Physical inactivity represents a major risk for cardiovascular disorders, such as hypertension, myocardial infarction or sudden death; however, underlying mechanisms are not clearly elucidated. Clinical and epidemiological investigations suggest, beyond molecular changes, the possibility of an induced impairment in autonomic cardiovascular regulation. However, this hypothesis has not been tested directly. Methods Accordingly, we planned a study with noninvasive, minimally intrusive, techniques on healthy volunteers. Participants were maintained for 90 days strictly in bed, 24 h a day, in head-down (−6°) position (HDBR). Physical activity was thus virtually abolished for the entire period of HDBR. We examined efferent muscle sympathetic nerve activity, as a measure of vascular sympathetic control, baroreceptor reflex sensitivity, heart rate variability (assessing cardiovagal regulation), RR and systolic arterial pressure and low-frequency and high-frequency normalized components (as a window on central oscillatory regulation). Measures were obtained at rest and during simple maneuvers (moderate handgrip, lower body negative pressure and active standing) to assess potential changes in autonomic cardiovascular responsiveness to standard stimuli and the related oscillatory profiles. Results HDBR transiently reduced muscle sympathetic nerve activity, RR, heart rate variability and baroreceptor reflex sensitivity late during HDBR or early during the recovery phase. Conversely, oscillatory profiles of RR and systolic arterial pressure variability were maintained throughout. Responsiveness to test stimuli was also largely maintained. Conclusion Prolonged inactivity as induced by HDBR in healthy volunteers reduces both cardiovagal and vascular sympathetic regulation, while largely maintaining peripheral responsiveness to standardized stimuli and sparing the functional structure of central oscillatory cardiovascular regulation.

Cardiac output, O2 delivery and V˙O2 kinetics during step exercise in acute normobaric hypoxia

We hypothesised that phase II time constant (τ2) of alveolar O2 uptake ( [Formula: see text] ) is longer in hypoxia than in normoxia as a consequence of a parallel deceleration of the kinetics of O2 delivery ( [Formula: see text] ). To test this hypothesis, breath-by-breath [Formula: see text] and beat-by-beat [Formula: see text] were measured in eight male subjects (25.4±3.4yy, 1.81±0.05m, 78.8±5.7kg) at the onset of cycling exercise (100W) in normoxia and acute hypoxia ( [Formula: see text] ). Blood lactate ([La]b) accumulation during the exercise transient was also measured. The τ2 for [Formula: see text] was shorter than that for [Formula: see text] in normoxia (8.3±6.8s versus 17.8±3.1s), but not in hypoxia (31.5±21.7s versus 28.4 5.4±5.4s). [La]b was increased in the exercise transient in hypoxia (3.0±0.5mM at exercise versus 1.7±0.2mM at rest), but not in normoxia. We conclude that the slowing down of the [Formula: see text] kinetics generated the longer τ2 for [Formula: see text] in hypoxia, with consequent contribution of anaerobic lactic metabolism to the energy balance in exercise transient, witnessed by the increase in [La]b.