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At least 1,423 records · Page 79Linked to original sources
PubMed1986

Comparative effects of metabolic acidemia and hypoxemia on cardiac output and regional blood flows in unanesthetized newborn lambs.

We studied the comparative effects of HCl-induced metabolic acidemia (pH = 7.11 +/- 0.03, mean +/- SE) and hypoxemia (PO2 = 28 +/- 1 torr) on cardiac output and regional blood flows in newborn lambs 3 days after the surgical placement of catheters in the left atrium and aorta and pacing wires on the left atrium. Cardiac output decreased by 49 +/- 6% during metabolic acidemia in contrast to the 12 +/- 2% increase during hypoxemia. The adrenal glands and the diaphragm were the only organs that received increased blood flows during acidemia and hypoxemia. Cerebral and myocardial blood flows decreased during acidemia but increased during hypoxemia. Blood flows decreased to the carcass and gastrointestinal tract during acidemia but did not change significantly during hypoxemia. Renal and splenic blood flows decreased during both stresses, but the reductions were more severe during acidemia. The changes in regional blood flows were not a passive result of the respective changes in cardiac output. HCl-induced metabolic acidemia and hypoxemia each result in significant redistributions of available blood flows which are quantitatively and qualitatively different from each other.

Acidosis↗
PubMedDate not supplied

Effects of a calcium channel blocker on cardiac output distribution in conscious hypertensive dogs.

The effects of nitrendipine, 8 micrograms/kg/minute, were evaluated in six conscious dogs through measurements of arterial pressure and blood flow in the ascending aorta (cardiac output), mesenteric, renal, and iliac arteries before and after induction of chronic perinephritic hypertension. Before hypertension was induced, nitrendipine reduced mean arterial pressure 19 +/- 2.3% (from 95 +/- 3.2 mm Hg), decreased total peripheral resistance (60 +/- 2.6%), and increased cardiac output (108 +/- 10.5%). These values returned to baseline within 15 to 30 minutes. Nitrendipine caused the greatest increase in blood flow in the iliac bed (98 +/- 9.9%), an intermediate increase in the mesenteric bed (37 +/- 3.7%), and the least increase in the renal bed (7 +/- 2.2%). Two to six weeks after induction of hypertension, administration of nitrendipine elicited significant (p less than 0.01) decreases in mean arterial pressure (32 +/- 2.5% from 151 +/- 4.8 mm Hg) and total peripheral resistance (67 +/- 1.3%) compared with its administration in normotensive dogs, while the increase in cardiac output was not significantly changed (111 +/- 10.9%). These changes in arterial pressure and vascular resistances also were prolonged (i.e., hemodynamics returned to baseline after 75-90 minutes). The increase in iliac (99 +/- 16.8%) and renal (9 +/- 6.1%) blood flows after nitrendipine administration in hypertensive dogs was similar to that found in the normotensive dogs, but mesenteric blood flow doubled (84 +/- 8.4%). Thus, in conscious, hypertensive dogs, nitrendipine administration appears to markedly decrease arterial pressure and total peripheral and regional resistances, which also require more time to return to baseline, but appears to increase blood flow by a greater amount only in the mesenteric bed.

Animals↗
PubMed1986

Effects of supine and lateral positions on cardiac output and intracardiac pressures: an experimental study.

Hemodynamic measurements in human subjects and in experimental animals are generally made in the supine position; not much attention is paid to potential beneficial or harmful effects of right or left lateral positions on cardiac output or other hemodynamic variables. To evaluate the potential influence of such positional changes on cardiac performance, we measured cardiac output and left and right ventricular pressures (with micromanometer catheters) in anesthetized experimental animals (eight dogs and nine pigs) in the supine, right lateral, and left lateral positions. Cardiac output increased from supine to left lateral (mean +/- SD, 2.6 +/- 0.9 to 3.1 +/- 1.0 liters/min; p less than .001) and from supine to right lateral positions (2.6 +/- 0.9 to 3.1 +/- 1.1 liters/min; p less than .001). There was an associated decrease in arteriovenous oxygen saturation difference from supine to left lateral position (31 +/- 8% to 24 +/- 4%; p less than .001) and from supine to right lateral position (32 +/- 9% to 25 +/- 6%; p less than .001). Left ventricular systolic and end-diastolic pressures increased from supine to left lateral (128 +/- 17/9 +/- 2 to 147 +/- 19/16 +/- 4 mm Hg; both p less than .001) and from supine to right lateral positions (128 +/- 19/9 +/- 2 to 141 +/- 16/16 +/- 7 mm Hg; p less than .01 and p less than .001, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2000

Fludrocortisone and sleeping in the head-up position limit the postural decrease in cardiac output in autonomic failure.

Treatment with head-up tilt sleeping and low-dose fludrocortisone effectively minimizes orthostatic symptoms and increases orthostatic blood pressure in patients with neurogenic orthostatic hypotension. The aim of the present study was to examine whether the improvement in orthostatic blood pressure during combined treatment with low-dose fludrocortisone and nocturnal head-up tilt in patients with neurogenic orthostatic hypotension can be attributed to expansion of plasma volume or to increased total peripheral resistance. The effects of a 3-week treatment with fludrocortisone and nocturnal head-up tilting on the postural changes in arterial pressure, heart rate, and cardiac output (pulse contour) were evaluated in eight consecutive patients with orthostatic hypotension. The period during which the patients were able to remain in the standing position without orthostatic complaints increased minimally from 3 to 10 minutes. The decrease in arterial pressure after 1 minute of standing--(means with standard deviations in parentheses) systolic, 49 (20) mm Hg; diastolic, 18 (11) mm Hg--before treatment was produced by a greater than normal decrease in cardiac output: 37% (10%) in patients with neurogenic orthostatic hypotension versus -14% (8%) in control subjects. Treatment increased upright arterial pressure from 83 (19) mm Hg systolic and 55 (13) mm Hg diastolic to 114 (22) mm Hg systolic and 60 (16) mm Hg diastolic by limiting the decrease in cardiac output. Body weight increased but hematocrit did not change. Leg pressure-volume relationship decreased in the two patients studied. The responses of plasma renin activity and aldosterone to orthostatic stress prior to treatment were subnormal and became even lower after treatment. The improvement in upright blood pressure in orthostatic hypotension during treatment with fludrocortisone and nocturnal head-up sleeping is the result of a reduction in the orthostatic decrease in cardiac output. Preliminary data suggest that the expanded body fluid volume is allocated to the perivascular space rather than to the intravascular space.

Adult↗
PubMed1987

Cardiac output in exercise by impedance cardiography during breath holding and normal breathing.

Estimation of cardiac output by impedance cardiography (QZ) in exercise during normal breathing (NB) has been limited by motion artifact. Our objective was to obtain readable impedance cardiograms on five subjects during upright cycle exercise at 0, 50, 100, 150, and 200 W to permit comparisons of QZ during NB, expiratory breath hold (EXP) and inspiratory breath hold (INSP). Q was also determined using an equilibration CO2 rebreathing method [Q(RB)]. QZ during NB exceeded EXP QZ at 100, 150, and 200 W, and exceeded INSP QZ at 100 W (P less than 0.05). The low EXP QZ values were due to a significantly lower stroke volume at 100, 150, and 200 W (P less than 0.05). For the INSP QZ at 100 W, heart rate was lower than during EXP (P less than 0.05). Regression of QZ (NB) against Q(RB) resulted in a linear relationship (r = 0.93) over the range of Q = 7-26 1/min. The slope of the regression differed significantly from 1.0 (P less than 0.05). We conclude that QZ values obtained during EXP or INSP should not be assumed to represent QZ during NB, at least at work rates greater than 50 W. A consequence of the linear relationship between QZ(NB) and Q(RB) over the range of 0-200 W is that estimates of CO2 rebreathing cardiac output can be obtained by impedance cardiography if QZ is adjusted using an appropriate empirical factor.

Adult↗
PubMed2004

End-tidal CO2 for prediction of cardiac output following weaning from cardiopulmonary bypass.

This prospective study included 32 patients undergoing cardiopulmonary bypass (CPB) for elective coronary artery bypass grafting correlates the respiratory end-tidal CO2 (ETCO2) during partial separation from CPB with cardiac output (CO) following weaning from CPB. After induction of general anesthesia, a pulmonary artery catheter was inserted for measurement of cardiac output by thermodilution. Patients were monitored using a 5-lead ECG, pulse oximeter, invasive blood pressure monitoring, rectal temperature probe, and end-tidal capnography. At the end of surgery, patients were weaned from CPB in a stepwise fashion. Respiratory ETCO2 and in-line venous oximetry were continuously monitored during weaning. The ETCO2 was recorded at quarter pump flow and after complete weaning from CPB. Following weaning from CPB, CO was measured by thermodilution. The CO values were correlated with the ETCO2 during partial bypass and following weaning from bypass. Regression analysis of ETCO2 at quarter-flow and post-bypass CO showed significant correlation (r = 0.57, p < .001). Also, regression analysis of ETCO2 after complete weaning from bypass and post-bypass CO showed significant correlation (r = 0.6, p = .002). The correlation between ETCO2 and CO showed that an ETCO2 >30 mm Hg during partial CPB will always predict an adequate CO following weaning from CPB. An ETCO2 <30 mm Hg may denote either a low or a normal cardiac output and hence other predictive parameters such as SvO2 must be added.

Aged↗
PubMed1979

Distribution of cardiac output during induced isometric exercise in dogs.

Studies were designed to characterize the distribution of cardiac output during induced isometric exercise in anesthetized dogs. The response to isometric exercise involved significant increases in heart rate (+12 +/- 3%(SE)), mean arterial pressure (+13 +/- 2%), cardiac output (+26 +/- 8%), and respiratory minute volume (+75 +/- 26%); total peripheral resistance did not change significantly. Significant changes in blood flow were observed during isometric exercise in kidneys (-18 +/- 6%) and contracting limb muscles (+453 +/- 154%). Flow to liver (hepatic artery), spleen, brain, and myocardium remained near control values. Section of spinal dorsal roots L6-L7 abolished the responses to isometric exercise except for the increase in flow to exercising limb muscles. Alpha-adrenergic receptor blockade abolished the decrease in renal blood flow during isometric exercise; however, the increase in flow to exercising limb muscles was not affected by either alpha- or beta-adrenergic blockade.

Animals↗
PubMed1976

Cardiac output during human sleep.

Impedance cardiogram and sleep EEG were recorded from four male and four female subjects, aged 21 to 22 years, during one night in the laboratory following one adaptation night. Cardiac output fell approximately 26% during the night as a consequence of diminished stroke volume, the lowest values of both occurring during the latter portion of the night, dominated by SREM (rapid-eye-movement stage). Intracycle comparisons between SREM and SWS (slow wave sleep) or between eye movement burst and non-burst SREM showed no significant differences in stroke volume or cardiac output. Pre-ejection period and systolic ejection period were measured and discussed. The non-coincidence of the nadir of metabolic activity, expressed as cardiac output, and the apex of slow-wave sleep activity supported the concept of slow-wave sleep as a period of physiological restoration.

Adult↗
PubMed1988

Assessment of stroke volume and cardiac output by Doppler echocardiography.

The authors used the pulse and continuous-wave Doppler technique to perform 51 measurements of stroke volume and cardiac output in 37 persons. Results were compared with those obtained using Fick's principle of thermodilution (immediately subsequent or simultaneous). Regression analysis showed a close correlation between Doppler and haemodynamic values - r = 0.86 for stroke volume and 0.94 for cardiac output (p less than 0.001). Using the paired t-test, the methods did not differ significantly. Standard deviation of Doppler stroke volume values from reference haemodynamic values was 10%, and only two measurements differed by more than 25%. Doppler determination of cardiac output can be therefore recommended as an alternative method in patients with high-quality echo Doppler recordings.

Adult↗