An improved procedure for determination of cardiac output by a conductivity method

1960 ◽  
Vol 15 (6) ◽  
pp. 1062-1064 ◽  
Author(s):  
Edward J. Hershgold ◽  
Sheldon H. Steiner ◽  
Leo A. Sapirstein

The applicability of the hematocrit dilution technique employing arterial blood conductivity changes to the determination of the cardiac output has been extended by a) electronic damping of the detecting circuits, which permits greater amplification of the signal without increasing the variability of the base line that occurs during each cardiac cycle, and by b) development of a solution isoosmolar and isoconductive with plasma that substitutes for autogenous plasma in the procedure. The preparation of the synthetic solution is described. It is shown that this solution gives results indistinguishable from those obtained with plasma. Values are given for the conductivity and osmolarity of dog plasma. Submitted on December 3, 1959

1989 ◽  
Vol 256 (3) ◽  
pp. R778-R785 ◽  
Author(s):  
M. I. Talan ◽  
B. T. Engel

Heart rate, stroke volume, and intra-arterial blood pressure were monitored continuously in each of four monkeys, 18 consecutive h/day for several weeks. The mean heart rate, stroke volume, cardiac output, systolic and diastolic blood pressure, and total peripheral resistance were calculated for each minute and reduced to hourly means. After base-line data were collected for approximately 20 days, observation was continued for equal periods of time under conditions of alpha-sympathetic blockade, beta-sympathetic blockade, and double sympathetic blockade. This was achieved by intra-arterial infusion of prazosin, atenolol, or a combination of both in concentration sufficient for at least 75% reduction of response to injection of agonists. The results confirmed previous findings of a diurnal pattern characterized by a fall in cardiac output and a rise in total peripheral resistance throughout the night. This pattern was not eliminated by selective blockade, of alpha- or beta-sympathetic receptors or by double sympathetic blockade; in fact, it was exacerbated by sympathetic blockade, indicating that the sympathetic nervous system attenuates these events. Because these findings indicate that blood volume redistribution is probably not the mechanism mediating the observed effects, we have hypothesized that a diurnal loss in plasma volume may mediate the fall in cardiac output and that the rise in total peripheral resistance reflects a homeostatic regulation of arterial pressure.


2005 ◽  
Vol 288 (4) ◽  
pp. G677-G684 ◽  
Author(s):  
Jens H. Henriksen ◽  
Søren Møller ◽  
Stefan Fuglsang ◽  
Flemming Bendtsen

Patients with cirrhosis have hyperdynamic circulation with abnormally distributed blood volume and widespread arteriovenous communications. We aimed to detect possible very early (i.e., before 4 s) and early (i.e., after 4 s) central circulatory transits and their potential influence on determination of central and arterial blood volume (CBV). Thirty-six cirrhotic patients and nineteen controls without liver disease undergoing hemodynamic catheterization were given central bolus injections of albumin with different labels. Exponential and gamma variate fits were applied to the indicator dilution curves, and the relations between flow, circulation times, and volumes were established according to kinetic principles. No significant very early central circulatory transits were identified. In contrast, early (i.e., 4 s to maximal) transits corresponding to a mean of 5.1% (vs. 0.8% in controls; P < 0.005) of cardiac output (equivalent to 0.36 vs. 0.05 l/min; P < 0.01) were found in cirrhotic patients. These early transits averaged 7.7 vs. 12.7 and 17.2 s of ordinary central transits of cirrhotic patients and controls, respectively ( P < 0.001). Early transits were directly correlated to the alveolar-arterial oxygen difference in the cirrhotic patients ( r = 0.46, P < 0.01) but not in controls ( r = 0.04; not significant). There was good agreement between the CBV determined by the conventional indicator dilution method and that determined by separation of early and ordinary transits by the gamma variate fit method (1.51 vs. 1.53 liter; not significant). In conclusion, no very early central circulatory transits were identified in cirrhotic patients. A significant part of the cardiac output undergoes an early transit, probably through pulmonary shunts or areas with low ventilation-perfusion ratios in cirrhotic patients. Composite determination of CBV by the gamma variate fit method is in close agreement with established kinetic methods. The study provides further evidence of abnormal central circulation in cirrhosis.


1986 ◽  
Vol 60 (6) ◽  
pp. 2063-2070 ◽  
Author(s):  
S. M. Albelda ◽  
J. H. Hansen-Flaschen ◽  
P. N. Lanken ◽  
A. P. Fishman

To determine the effect of an increase in spontaneous minute ventilation on lung fluid balance, we added external dead space to the breathing circuit of six tracheostomized, unanesthetized, spontaneously breathing sheep in which lung lymph fistulas had been created surgically. The addition of 120–180 ml of dead space caused minute ventilation to increase by 50–100% (secondary to increases in both tidal volume and frequency), without changing pulmonary arterial pressure, pulmonary capillary wedge pressure, cardiac output, or arterial blood gas tensions. The increase in spontaneous ventilation was associated with an average increase of 27% in lung lymph flow (P less than 0.05) and an average reduction of 11% in the lymph-to-plasma concentration ratio (L/P) for total protein (P less than 0.05). Lymph flow and L/P for total protein approached stable values after 2–3 h of hyperpnea, and the increase in lymph flow persisted for at least 18 h of dead-space breathing. Removal of dead space was associated with a rapid return (within 45 min) of lymph flow to base-line levels. These results suggest that hyperpnea increases the pulmonary transvascular filtration rate. Since no changes in vascular pressures or cardiac output were observed, this increase in transvascular filtration is most likely due to a fall in interstitial fluid pressure.


1985 ◽  
Vol 58 (4) ◽  
pp. 1225-1230 ◽  
Author(s):  
S. Gelman ◽  
K. C. Fowler ◽  
S. P. Bishop ◽  
L. R. Smith

Cardiac output distribution and regional blood flow were studied during hypocarbia independent of changes in ventilatory parameters. Fifteen cynomolgus monkeys were anesthetized with methohexital sodium (8 mg/kg im) and hyperventilated through an endotracheal tube. Hypocarbia at two levels, 28 +/- 1.8 and 17 +/- 0.6 Torr, was achieved by a stepwise decreasing CO2 flow into the semiclosed system. Regional blood flow was determined with labeled microspheres. At each stage of experiments two sets of microspheres (9 and 15 microns diam) were used simultaneously. The use of two microsphere sizes allowed evaluation of the relationship between total (nutritive and nonnutritive) tissue blood flow, determined with 15-microns spheres, and nutritive blood flow, determined with 9-microns spheres. There was no change in cardiac output or arterial pressure during both degrees of studied hypocarbia. Hypocarbia was accompanied by a decrease in myocardial blood flow determined with 15-microns spheres and preservation of the flow determined with 9-microns spheres. Splenic blood flow was decreased, whereas hepatic arterial blood flow was increased during both levels of hypocarbia. Blood flow through the brain, renal cortex, and gut showed a biphasic response to hypocarbia: during hypocarbia at 28 +/- 1.8 Torr, blood flow determined with 15-microns spheres was unchanged (in the gut) or decreased (in the brain and kidneys), whereas blood flow determined with 9-microns spheres was decreased. During hypocarbia at 17 +/- 0.6 Torr, blood flow determined with 9-microns spheres had a tendency to restore to base-line values.


1966 ◽  
Vol 7 (3) ◽  
pp. 235-243 ◽  
Author(s):  
Tan WATANABE ◽  
Kazuzo KATO ◽  
Hiroshi WATANABE ◽  
Shintaro KOYAMA

1977 ◽  
Vol 232 (5) ◽  
pp. H534-H536
Author(s):  
D. G. Wantzelius ◽  
K. L. Goetz

We describe an inexpensive circuit designed to correct base-line drift of electromagnetic flowmeters automatically when cardiac output is being measured. The circuit measures the flowmeter output voltage during a portion of each diastole when blood flow in the aorta is assumed to be zero. Any deviation of the flowmeter output voltage from zero during this time represents either base-line offset or drift. The output voltage obtained during zero flow conditions is stored throughout the next cardiac cycle and subtracted continuously from the flowmeter output during each beat, thus giving a beat-by-beat correction of any base-line drift.


1989 ◽  
Vol 256 (2) ◽  
pp. H527-H532 ◽  
Author(s):  
F. Heusser ◽  
J. T. Fahey ◽  
G. Lister

We previously found limited tolerance to acute reduction in cardiac output in lambs at the nadir of their physiological anemia [Am. J. Physiol. 253 (Heart Cir. Physiol. 12): H100-H106, 1987]. To determine the effect of hemoglobin concentration [Hb] on critical cardiac output, critical systemic O2 transport, and peripheral O2 extraction, we performed 31 experiments in 12 one-mo-old lambs at four [Hb] (means +/- SD in g/dl): 7.4 +/- 0.6, 10.5 +/- 0.5, 14.5 +/- 0.5, and 16.5 +/- 0.6. Desired [Hb] was obtained by exchange transfusion with packed red cells or plasma. Cardiac output was reduced by inflation of a balloon-tipped catheter in the right atrium, and critical levels were defined at the point where O2 consumption decreased and/or arterial blood lactate concentration increased in response. With lower [Hb], cardiac output was unchanged, systemic O2 transport was reduced, and fractional O2 extraction was increased, keeping O2 consumption constant at base line. As [Hb] was reduced, critical cardiac output was significantly higher, whereas critical systemic O2 transport was independent of [Hb], as were fractional O2 extraction and mixed venous PO2 at the critical point. Thus peripheral O2 extraction was not affected by changes in [Hb] during progressive decreases in cardiac output. We conclude that 4-wk-old lambs have decreased tolerance to reductions in cardiac output and systemic O2 transport because their relative anemia provides them with a base-line cardiac output and systemic O2 transport close to the critical level.


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