33 research outputs found
Cardiac output by model flow method from intra-arterial and finger tip pulse pressure profiles
No full textModelflow®, when applied to non-invasive fingertip pulse pressure recordings, is a poor predictor of cardiac output (Q’ litre· 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’ withModelflow®, 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 (Q’porta) was significantly (P < 0.05) higher than that computed from the intra-arterial recordings (Q’pia). The line relating beat-by-beat Q’porta and Q’pia was y = 1.55x - 3.02 (r2 = 0.640). The bias was 1.44 litre · min-1 and the precision was 2.84 litre · min-1.The slope of this line was significantly higher than 1, implying a systematic overestimate of Q’ by Q’porta with respect to Q’pia. 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
Simultaneous determination of the kinetics of cardiac output, systemic O2 delivery and lung O2 uptake at exercise onset in men.
No full textWe tested whether the kinetics of systemic O2 delivery (Q'aO2) at exercise start was faster than that of lung O2 uptake (V' O2), being dictated by that of cardiac output (Q'), and whether changes in Q' would explain the postulated rapid phase of the V'O2 increase. Simultaneous determinations of beat-by-beat (BBB) Q' and Q' aO2, and breath-by-breath V'O2 at the onset of constant load exercises at 50 and 100 W were obtained on six men (age 24.2 +/-3.2 years, maximal aerobic power 333 +/- 61 W). V'O2 was determined using Grønlund’s algorithm. Q' was computed from BBB stroke volume (Qst, from arterial pulse pressure profiles) and heart rate (fH, electrocardiograpy) and calibrated against a steadystate method. This, along with the time course of hemoglobin concentration and arterial O2 saturation (infrared oximetry) allowed computation of BBB Q'aO2. The Q', Q'aO2 and V'O2 kinetics were analyzed with single and double exponential models. fH, Qst, Q', and V'O2 increased upon exercise onset to reach a new steady state. The
kinetics of Q'aO2 had the same time constants as that of Q'. The latter was twofold faster than that of V'O2. The V'O2 kinetics were faster than previously reported for muscle phosphocreatine decrease. Within a two-phase model, because of the Fick equation, the amplitude of phase I Q' changes fully explained the phase I of V'O2 increase. We suggest that in unsteady states, lung V' O2 is dissociated from muscle
O2 consumption. The two components of Q' and Q'aO2 kinetics may reflect vagal withdrawal and sympathetic activation
Simultaneous determination of kinetics of cardiac output, systemic O2 delivery, and lung O2 uptake at exercise onset in men.
No full textWe tested whether the kinetics of systemic O(2) delivery (QaO(2)) at exercise start was faster than that of lung O(2) uptake (Vo(2)), being dictated by that of cardiac output (Q), and whether changes in Q would explain the postulated rapid phase of the Vo(2) increase. Simultaneous determinations of beat-by-beat (BBB) Q and QaO(2), and breath-by-breath Vo(2) at the onset of constant load exercises at 50 and 100 W were obtained on six men (age 24.2 +/- 3.2 years, maximal aerobic power 333 +/- 61 W). Vo(2) was determined using Grønlund's algorithm. Q was computed from BBB stroke volume (Q(st), from arterial pulse pressure profiles) and heart rate (f(h), electrocardiograpy) and calibrated against a steady-state method. This, along with the time course of hemoglobin concentration and arterial O(2) saturation (infrared oximetry) allowed computation of BBB QaO(2). The Q, QaO(2) and Vo(2) kinetics were analyzed with single and double exponential models. f(h), Q(st), Q, and Vo(2) increased upon exercise onset to reach a new steady state. The kinetics of QaO(2) had the same time constants as that of Q. The latter was twofold faster than that of Vo(2). The Vo(2) kinetics were faster than previously reported for muscle phosphocreatine decrease. Within a two-phase model, because of the Fick equation, the amplitude of phase I Q changes fully explained the phase I of Vo(2) increase. We suggest that in unsteady states, lung Vo(2) is dissociated from muscle O(2) consumption. The two components of Q and QaO(2) kinetics may reflect vagal withdrawal and sympathetic activation
Factors determining the kinetics of VO2max decay during bed-rest: implications for VO2max limitation
No full textThe aim of this study was to characterize the time course of maximal oxygen consumption (V'O2 max) changes during bedrests longer than 30 days, on the hypothesis that the decrease in V'O2 max tends to asymptote. On a total of 26 subjects who participated in one of three bedrest campaigns without countermeasures, lasting 14, 42 and 90 days, respectively, V'O2 max, maximal cardiac output (Qmax) and maximal systemic O2 delivery (QaO2max) were measured. After
all periods of HDT, V'O2 max; Qmax and QaO2max were significantly lower than before. The V'O2 max decreased less than Qmax after the two shortest bedrests, but its percent decay was about 10% larger than that of Qmax after 90-day bedrest. The V'O2 max decrease after 90-day bedrest was larger than after 42- and 14-day bedrests, where it was similar. The Qmax and QaO2max decline after 90-day bedrest was equal to those after 14- and 42-day bedrest. The average daily rates of the V'O2 max; Qmax and QaO2max decay during bedrest were less if the bedrest duration was longer, with the exception of that of V'O2 max in the longest bedrest. The asymptotic V'O2 max decay demonstrates the possibility that humans could keep working effectively even after an extremely long time in microgravity. Two components in the V'O2 max decrease were identified, which we postulate were related to cardiovascular deconditioning and to impairment of peripheral gas exchanges due to a possible muscle function deterioration
Factors determining the time course of V'O2 max decay during bedrest: implications for V'O2 max limitation.
No full textThe aim of this study was to characterizethe time course of maximal oxygen consumption (V'O2 max) changes during bedrests longer than 30 days,on the hypothesis that the decrease in V'O2 max tends toasymptote. On a total of 26 subjects who participatedin one of three bedrest campaigns without countermeasures,lasting 14, 42 and 90 days, respectively,_VO2 max maximal cardiac output (Qmax) and maximalsystemic O2 delivery (QaO2max) were measured. Afte rall periods of HDT, V'O2 max; Q'max and Q'aO2max weresignificantly lower than before. The 'V O2 max decreasedless than 'Qmax after the two shortest bedrests, but itsper cent decay was about 10% larger than that of _Qmaxafter 90-day bedrest. The 'V O2 max decrease after90-day bedrest was larger than after 42- and 14-daybedrests, where it was similar. The 'Qmax and 'QaO2maxdeclines after 90-day bedrest was equal to those after14- and 42-day bedrest. The average daily rates of the_VO2 max; Q'max and Q'aO2max decay during bedrest wereless if the bedrest duration were longer, with theexception of that of V'O2 max in the longest bedrest. Theasymptotic V'O2 max decay demonstrates the possibilitythat humans could keep working effectively even afteran extremely long time in microgravity. Two componentsin the 'VO2 max decrease were identified, which wepostulate were related to cardiovascular deconditioningand to impairment of peripheral gas exchanges dueto a possible muscle function deterioration
Cardiac output, O2 delivery and V’O2 kinetics during step exercise in acute normobaric hypoxia.
No full textPhase I dynamics of cardiac output, systemic O2 delivery, and lung O2 uptake at exercise onset in men in acute normobaric hypoxia
No full textWe 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 (Q˙aO2), and breath-by-breath lung oxygen uptake (V˙O2) 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 Q˙aO2 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 V˙ O2 were unchanged.Q˙aO2 was unchanged at rest and lower at exercise. During transients, amplitude of phase I (A1) for V˙O2 was unchanged. For fH, Q˙and Q˙aO2, A1 was lower. Phase I time constant (tau1) forQ˙aO2 and V˙O2 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 Q˙aO2, neural (vagal) and mechanical (venous return increase by muscle pump action), would rather be confirmed
The time course of the decrease in maximal oxygen consumption during long-term bed rest in humans
No full textThe time course of the decrease in maximal oxygen consumption during long-term bed rest in human
Kinetics of cardiac output, systemic O2 delivery and lung O2 uptake in normoxia and normobaric hypoxia in men
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