Noninvasive cardiac output measurement by arterial pulse analysis compared with inert gas rebreathing

1993 ◽  
Vol 74 (6) ◽  
pp. 2687-2693 ◽  
Author(s):  
W. J. Stok ◽  
F. Baisch ◽  
A. Hillebrecht ◽  
H. Schulz ◽  
M. Meyer ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Pulse Contour ◽  
Inert Gas ◽  
Lower Body ◽  
Arterial Pulse ◽  
Saline Loading ◽  
Intravenous Saline ◽  
Pulse Analysis

Noninvasive cardiac output (CO) measured by arterial pulse analysis was compared with that measured by inert gas rebreathing in six healthy male volunteers. Pulse contour analysis was applied to the pressure wave output of a Finapres, which noninvasively measures continuous arterial pressure in a finger. Data were collected before, during, and after a 10-day 6 degrees head-down tilt experiment. Intravenous saline loading and lower body negative pressure stimuli varied CO over 2.8–9.6 l/min, as measured by the rebreathing technique. Because pulse contour provides only relative changes in CO, to obtain absolute values it must be calibrated against another measurement. Pulse contour data were calibrated every measurement day against the mean of two to four control rebreathing CO measurements before the lower body negative pressure or intravenous saline loading stimuli. Using one averaged calibration factor per subject for a total of 27 days, we compared the results of both methods. The linear regression between pulse contour (Pc CO) and rebreathing CO (Rebr CO) was Pc CO = 0.15 + 0.98(Rebr CO) (r = 0.96). The standard deviation of the difference of the two methods was 0.5 l/min (n = 205), excluding data used for calibration. By monitoring pulse contour CO before and during rebreathing, the rebreathing maneuver itself was shown to produce a substantial increase in CO that was mainly related to an increase in heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Arterial pulse pressure and vasopressin release in humans during lower body negative pressure

1993 ◽  
Vol 264 (5) ◽  
pp. R1024-R1030 ◽  
Author(s):  
P. Norsk ◽  
P. Ellegaard ◽  
R. Videbaek ◽  
C. Stadeager ◽  
F. Jessen ◽  
...  
Keyword(s):  
Pulse Pressure ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Venous Pressure ◽  
Plasma Norepinephrine ◽  
Lower Body ◽  
Arterial Pulse ◽  
Vasopressin Release ◽  
Arterial Pulse Pressure ◽  
Arterial Plasma

The hypothesis was tested that narrowing of arterial pulse pressure (PP) is a determinant of arginine vasopressin (AVP) release in humans. Six normal males completed a two-step lower body negative pressure (LBNP) protocol of -20 and -50 mmHg, respectively, for 10 min each. None of these subjects experienced presyncopal symptoms. Arterial plasma AVP and plasma renin activity (PRA) (at 2-min intervals) only increased subsequent to a decrease in PP (invasive brachial arterial measurements) and stroke volume (ultrasound Doppler technique, n = 4). Simultaneously, mean arterial pressure did not change. A selective decrease in central venous pressure and left atrial diameter (echocardiography, n = 4) at LBNP of -20 mmHg did not affect AVP or PRA, whereas arterial plasma norepinephrine increased (n = 4). During LBNP, significant (P < 0.05) intraindividual linear correlations were observed between log(AVP) and PP in four of the subjects with r values from -0.75 to -0.99 and between log(PRA) and PP in all six subjects with r values from -0.89 to -0.98. In conclusion, these results are in compliance with the hypothesis that narrowing of PP in humans during central hypovolemia is a determinant of AVP and renin release.

Venous and arterial reflex responses to positive-pressure breathing and lower body negative pressure

1997 ◽  
Vol 82 (6) ◽  
pp. 1889-1896 ◽  
Author(s):  
Jochen K. Peters ◽  
George Lister ◽  
Ethan R. Nadel ◽  
Gary W. Mack
Keyword(s):  
Cardiac Output ◽  
Vascular Resistance ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Venous Pressure ◽  
Transmural Pressure ◽  
Right Atrial ◽  
Positive Pressure ◽  
Lower Body ◽  
Reflex Responses

Peters, Jochen K., George Lister, Ethan R. Nadel, and Gary W. Mack. Venous and arterial reflex responses to positive-pressure breathing and lower body negative pressure. J. Appl. Physiol. 82(6): 1889–1896, 1997.—We examined the relative importance of arteriolar and venous reflex responses during reductions in cardiac output provoked by conditions that increase [positive end-expiratory pressure (PEEP)] or decrease [lower body negative pressure (LBNP)] peripheral venous filling. Five healthy subjects were exposed to PEEP (10, 15, 20, and 25 cmH2O) and LBNP (−10, −15, −20, and −25 mmHg) to induce progressive but comparable reductions in right atrial transmural pressure (control to minimum): from 5.9 ± 0.4 to 1.8 ± 0.7 and from 6.5 ± 0.6 to 2.0 ± 0.2 mmHg with PEEP and LBNP, respectively. Cardiac output (impedance cardiography) fell less during PEEP than during LBNP (from 3.64 ± 0.21 to 2.81 ± 0.21 and from 3.39 ± 0.21 to 2.14 ± 0.24 l ⋅ min−1 ⋅ m−2with PEEP and LBNP, respectively), and mean arterial pressure increased. We observed sustained increases in forearm vascular resistance (i.e., forearm blood flow by venous occlusion plethysmography) and systemic vascular resistance that were greater during LBNP: from 19.7 ± 2.91 to 27.97 ± 5.46 and from 20.56 ± 2.48 to 50.25 ± 5.86 mmHg ⋅ ml−1 ⋅ 100 ml tissue−1 ⋅ min ( P < 0.05) during PEEP and LBNP, respectively. Venomotor responses (venous pressure in the hemodynamically isolated limb) were always transient, significant only with the greatest reduction in right atrial transmural pressure, and were similar for LBNP and PEEP. Thus arteriolar rather than venous responses are predominant in blood volume mobilization from skin and muscle, and venoconstriction is not intensified with venous engorgement during PEEP.

Norepinephrine kinetics and cardiac output during nonhypotensive lower body negative pressure

1991 ◽  
Vol 260 (5) ◽  
pp. H1708-H1712 ◽  
Author(s):  
R. G. Baily ◽  
U. Leuenberger ◽  
G. Leaman ◽  
D. Silber ◽  
L. I. Sinoway
Keyword(s):  
Cardiac Output ◽  
Continuous Infusion ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Normal Subjects ◽  
Systemic Clearance ◽  
Lower Body ◽  
Radiotracer Technique ◽  
Low Cardiac Output ◽  
Arterial Plasma

Recently we have shown that arterial norepinephrine (NE) concentration increases significantly during lower body negative pressure (LBNP) of -15 mmHg. Interestingly, the increase was found to be related predominantly to a decrease in arterial NE clearance. We postulated that this reduction in clearance would be related to a reduction in cardiac output. Accordingly, we measured both cardiac output (2-dimensional echocardiographic/Doppler technique) and arterial NE kinetics ([3H]NE continuous infusion radiotracer technique) during LBNP of -15 mmHg. These measures of cardiac output and arterial NE spillover and clearance were obtained in 12 normal subjects at baseline, 5 and 10 min (Early) and 25 and 30 min (Late) of LBNP. We found that arterial NE concentration increased significantly, by 25% Early and 22% Late (P = 0.001). Spillover, however, did not change (P = 0.258), whereas clearance decreased by 12% Early and 19% Late (P = 0.014), and cardiac output decreased by 15% Early and 19% Late (P = 0.001). These reductions in clearance and cardiac output correlated significantly (r = 0.61, P = 0.001). No correlation was noted between spillover and cardiac output (r = 0.027, P = 0.874). We conclude that the increases in arterial NE concentration during nonhypotensive LBNP are predominantly due to decreased cardiac output with resultant decreases in systemic clearance of NE. These findings suggest that the ability to clear NE from the circulation is linked to the level of cardiac output and that low cardiac output states by themselves may lead to an elevation in arterial plasma NE concentrations.

Neurohormonal responses to oscillatory lower body negative pressure in healthy subjects

2021 ◽  
Author(s):  
Akanksha Singh ◽  
Shival Srivastav ◽  
Kavita Yadav ◽  
Dinu S. Chandran ◽  
Ashok Kumar Jaryal ◽  
...  
Keyword(s):  
Negative Pressure ◽  
Healthy Subjects ◽  
Lower Body Negative Pressure ◽  
Lower Body

Bradykinin has no acute effect on the response of forearm blood flow to sympathetic stimulation in man

1990 ◽  
Vol 78 (4) ◽  
pp. 399-401 ◽  
Author(s):  
M. J. Cullen ◽  
J. R. Cockcroft ◽  
D. J. Webb
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Negative Pressure ◽  
Enzyme Inhibitor ◽  
Lower Body Negative Pressure ◽  
Acute Effect ◽  
Acute Administration ◽  
Lower Body ◽  
Resistance Vessels ◽  
Sympathetic Responses

1. Six healthy male subjects received 0.9% (w/v) NaCl (saline) followed by incremental doses of bradykinin (1, 3 and 10 pmol/min), via the left brachial artery. Blood flow and the response of blood flow to lower-body negative pressure were measured in both forearms during infusion of saline and each dose of bradykinin. 2. Bradykinin produced a moderate and dose-dependent increase in blood flow in the infused, but not the non-infused, forearm. Lower-body negative pressure produced an approximately 15–20% reduction in blood flow in both forearms, and this response was unaffected by local infusion of bradykinin. 3. Bradykinin, in contrast to angiotensin II, had no acute effect on peripheral sympathetic responses to lower-body negative pressure. We conclude that, in forearm resistance vessels in man, withdrawal of angiotensin II, rather than accumulation of bradykinin, is likely to account for the attenuation of peripheral sympathetic responses after acute administration of a converting-enzyme inhibitor.

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