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PubMed1976

Estimation of cardiac output by an N2O rebreathing method in adults and children.

A nitrous oxide rebreathing method was used to measure recirculation time and cardiac output (as pulmonary blood flow) in adults and children during exercise. The method was compared with the indirect (CO2) Fick rebreathing method in almost simultaneous measurements of cardiac output. Recirculation time varied from about 15 s at rest to 8.5 s at high levels of exercise, and was slightly longer in children than adults. Cardiac output estimated by both methods was within the normal range for children and adults, being lower for a given oxygen consumption in children. For the adults the mean intrasubject variability of the N2O rebreathing method, measured as the coefficient of variation of cardiac output, was in the range of 6-8% at all levels of work. This was lower than reported for other N2O rebreathing methods, and similar to values based on the indirect (CO2) Fick, direct (O2) Fick, and dye-dilution methods of estimating cardiac output. The method is therefore proposed as a noninvasive technique suitable for rapid, accurate, and reproducible measurements of cardiac output.

Adult↗
PubMed1989

Circulatory and renal control by prostaglandins and renin in low cardiac output in dogs.

Changes of neurohumoral factors including vasodilatory prostaglandins (PGs) were investigated in an experimental model of moderate low-cardiac-output status induced by rapid right ventricular pacing (240 beats/min). After 7 days of pacing, we studied the response of renal, hormonal, and hemodynamic parameters to cyclooxygenase inhibition by indomethacin and the effects of the renin system by converting-enzyme blockade in addition to the inhibition of PG synthesis. Lowering cardiac output increased plasma levels of norepinephrine and atrial natriuretic peptide. Plasma renin concentration was suppressed, despite a fall in cardiac output and blood pressure and a stimulation of sympathetic nerve activity. Urinary excretion of PGE2 was increased (P less than 0.04); plasma levels of PGE2 and 6-keto-PGF1 alpha were unchanged as measured in blood from the renal vein, pulmonary artery, and aorta. During low cardiac output, we found a significant decrease of glomerular filtration rate, whereas renal blood flow and renal and peripheral vascular resistances were unchanged. Administration of indomethacin decreased plasma and urinary PGs significantly, markedly reduced renal blood flow, and increased renal vascular resistance without affecting peripheral vascular resistance. The additional blockade of the renin-angiotensin system by captopril showed mainly a vasodilator effect on peripheral arterial resistance vessels, resulting in an increase of cardiac output. Our results suggest that, in moderate low-cardiac-output status, renal blood flow is maintained by renal vasodilator PGs, which counterbalance vasoconstrictor mechanisms like the activated sympathetic nerve activity. We indirectly showed the importance of angiotensin II in preserving glomerular filtration rate, which declines when renin secretion is suppressed, as it may be the case in moderate heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1992

Hemodynamics during liver transplantation: the interactions between cardiac output and portal venous and hepatic arterial flows.

Liver blood flow and systemic hemodynamics were measured intraoperatively in 34 patients after liver transplantation. Ultrasound transit-time flow probes measured hepatic arterial and portal venous flow over 10 to 75 min 1 to 3 hr after reperfusion. Cardiac output was measured by thermodilution. Mean cardiac output was 9.5 +/- 2.8 L/min; the mean total liver blood flow of 2,091 +/- 932 ml/min was 23% +/- 11% of cardiac output. Mean portal flow of 1,808 +/- 929 ml/min was disproportionately high at 85% +/- 10% of total liver blood flow. Correlation analysis showed a significant (p less than 0.01; r = 0.42) correlation between cardiac output and portal venous flow and a trend toward negative correlation (p = 0.087) between cardiac output and hepatic arterial flow. These data show that increased flow in the newly transplanted liver is predominantly portal venous flow and is associated with high cardiac output and reduced hepatic arterial flow. In the last 13 patients studied, portal flow was reduced by 50% and the hepatic artery response was measured. We saw a significant (p less than 0.05) increase in hepatic artery flow from 322 +/- 228 to 419 +/- 271 ml/min, indicating an intact hepatic arterial buffer response. The hepatic artery response also showed that it is a reversible rather than a fixed resistance that contributes to the low hepatic artery flow in these patients.

Blood Pressure↗
PubMed1986

Ventilation and cardiac output during the onset of exercise, and during voluntary hyperventilation, in humans.

Three normal subjects performed rest--exercise transitions on a cycle ergometer, from rest to unloaded pedalling (0 W), 50, 100 and 150 W. Each experiment was performed in triplicate, with randomized work load order, in two sessions. Ventilation was obtained breath-to-breath by integration of a pneumotachygraph signal, and cardiac output beat-to-beat by a new development of the Doppler technique. Results were bin-averaged in 4 s bins over the first 20 s, and compared to resting values. Both ventilation and cardiac output increased significantly in the first 2 s. This initial rise in ventilation was due entirely to an increase in rate, the subsequent rise mainly to increase in tidal volume. Cardiac output increased predominantly through change in rate with smaller increases in stroke volume. A striking feature was a tendency for ventilation and cardiac output responses to be biphasic with an initial rise followed by a slight fall at the 14 s mark, and a subsequent rise, at all work loads. Overall correlation between ventilation and cardiac output was therefore high (r = 0.92). Six normal subjects hyperventilated for 45 s voluntarily, (a) at rate 24/min and normal tidal volume; (b) at normal rate and tidal volume of 1.5 l; (c) at rate 24/min and tidal volume of 1.5 l. Cardiac output, averaged over 10-45 s, rose by 0.4, 0.5, and 1.0 l min-1 respectively, with falls in end-tidal PCO2 of 4, 6, and 8 mmHg. Six normal subjects hyperventilated for 60 s with rate 24/min and tidal volume of 1.4 l, and end-tidal PCO2 maintained at 38 +/-2 mm Hg. Cardiac output, averaged from 10-60 s, rose by 1.0 l min-1. With increased rate and tidal volume, whether isocapnic or hypocapnic, cardiac output responses showed an overshoot with a peak value at about 30 s. The hypothesis of 'cardiodynamic hyperpnoea' considers a possible effect of increasing cardiac output on ventilation. The effects of ventilation on cardiac output must also be considered. We propose an extended hypothesis involving stable positive feed-back.

Adult↗
PubMed1975

Cardiac output response to altered acid-base status during diethyl ether anaesthesia.

The effects of acid-base changes on cardiac output during diethyl ether anaesthesia were studied in 25 mongrel dogs prepared by surgically implanting a plastic encased non-ferrous core electromagnetic probe on the ascending aorta. The findings are: (1) Metabolic acidaemia produced only slight decrease in cardiac output but a more marked fall became evident with decreasing pH(2) Respiratory acidaemia led to a slight rise in cardiac output. (3) Respiratory alkalaemia decreased cardiac output. (4) Metabolic alkalaemia also produced a decline in cardiac output.

Acid-Base Equilibrium↗
PubMed1990

Cardiac output determined by ultrasound-Doppler: clinical applications.

A non-invasive method for cardiac output determination (COD) based on ultrasound-Doppler technique was evaluated in patients with cardiac disease at rest and during exercise, including patients with heart transplants. The aortic blood flow velocity was measured with pulsed Doppler technique from the jugulum, placing the sample volume just above the aortic valve, and the area from a parasternal 2-D echocardiographic measurement of the aortic annulus diameter assuming a circular area. Cardiac output was calculated as the product of the systolic velocity integral, the aortic annulus area and the heart rate. A high correlation was found between this method and a simultaneously performed invasive cardiac output (COF) and stroke volume (SVF) determination by the direct Fick method (COD = 0.3 + 0.9 x COF, r = 0.96, SDres = 0.5 l min-1 and SVD = 3.9 + 0.92 x SVF, r = 0.94, SDres = 6.9 ml). However, looking just at the systolic velocity integral compared to stroke index determined with the Fick method we found a low correlation, especially in patients with heart transplants. We conclude that cardiac output can reliably be measured non-invasively with this method--also in patients with heart transplants. The systolic velocity integral alone can be used for assessing changes in stroke volume but for absolute values of stroke volume and stroke index flow area should also be determined.

Adult↗
PubMed2000

An alternative thermodilution method to measure cardiac output in a rat model of stagnant hypoxia.

Rats are often used to study hemodynamics in animal research. We have established an alternative method to measure cardiac output in a conscious rat using a thermodilution technique via a left ventricular injection. The validity of this method was evaluated in conscious rats and compared with the results obtained using the radiolabeled microspheres (reference sample method). Using 20 male Sprague-Dawley rats, a baseline cardiac index was measured by thermodilution to determine the baseline cardiac index and to evaluate between animal variability. The baseline cardiac index was compared to the reference sample method with 6 rats. Following baseline measurements, an intra-atrial balloon was inflated in a stepwise manner to create 2 to 3 different cardiac outputs, and the cardiac index was computed. For each measurement, the cardiac index was first measured by thermodilution and immediately followed by the reference sample method. A total of 21 measurements were obtained, and the results were analyzed by a Bland-Altman plot and the correlation coefficient was calculated. Although the agreement between the two methods was poor, both methods had a good correlation (r2 = 0.59). With the thermodilution technique, we demonstrated a small coefficient of variation in each measurement, with a low intra-animal and inter-animal variability. As there is no gold standard method to measure cardiac output in rats, we believe that left ventricular thermodilution is a reliable method, and overcomes several technical difficulties such as heat loss, one of the significant limitations of the conventional thermodilution method (via right atrial injection). This new thermodilution technique (via the left ventricle) is therefore an attractive alternative method to measure cardiac output in rats.

Animals↗
PubMed1988

Interpretation of nitrate plasma concentrations. Effect of cardiac output on nitroglycerin pharmacokinetics in experimental animals.

We tested the hypothesis that the pharmacokinetics of nitroglycerin might be governed by haemodynamics, viz: cardiac output. The steady state pharmacokinetics of nitroglycerin, both in arterial and in venous plasma, were investigated in 11 rats after sequential infusions either of nitroglycerin alone (10 micrograms kg-1 min-1) or of nitroglycerin plus vasopressin (the latter at 5.5 mU kg-1 min-1). Cardiac output was estimated twice in each animal using 85Sr and 141Ce microspheres. Nitroglycerin systemic clearance in arterial plasma was found to be correlated strongly with cardiac output (r = 0.784, N = 22, P less than 0.001). Using the distribution ratio of nitroglycerin between red blood cells and plasma, we determined the systemic clearance of nitroglycerin in arterial blood to be about 3/4 of cardiac output. Vasopressin co-infusion decreased both the cardiac output and the arterial nitroglycerin clearance, but it also increased the arteriovenous extraction of nitroglycerin. Thus, vasopressin had no net effect on the venous plasma clearance of nitroglycerin. In animals infused with nitroglycerin alone, cardiac output also significantly correlated with nitroglycerin venous plasma clearance (P less than 0.01) and arteriovenous extraction (P less than 0.05). These data indicate that haemodynamic alterations may have profound effects on the observed plasma concentrations of nitroglycerin. These parameters need to be standardized and controlled if meaningful plasma concentrations of organic nitrates are to be obtained and interpreted.

Animals↗
PubMed1984

Effects of sodium nitroprusside on thermal trauma depressed cardiac output in the anaesthetized dog.

Thermal trauma to the anaesthetized dog results in an immediate significant decrease in cardiac output, an increase in peripheral resistance and no significant change in mean arterial blood pressure. The infusion of sodium nitroprusside, 5 or 8 micrograms/kg X min, produced a significant increase in cardiac output and a decrease in peripheral resistance. Mean arterial blood pressure fell during the infusion and returned to pre-injection values immediately upon cessation of infusion. Cardiac output and peripheral resistance also returned to pre-infusion values upon cessation of infusion. A comparison between the responses to infusion of sodium nitroprusside and the administration of verapamil showed that infusion of sodium nitroprusside produced a slower onset of increase in cardiac output and a lower maximum increase in cardiac output than observed after verapamil.

Animals↗
PubMedDate not supplied

Analysis of maternal circulation and renal function in physiologic pregnancies; parallel examinations of the changes in the cardiac output and the glomerular filtration rate.

OBJECTIVE: The aim of the study was to examine the temporal relations between the parameters of the maternal hemodynamics and homeostasis in different phases of pregnancy and the postpartum period. METHODS: Eleven healthy pregnant women were involved in the study. The value of the peripheric vasodilatation was measured by the ratio I/A of the maternal sphygmogram (I: incisure point, A: amplitude of the carotid pressure curve). The change of the cardiac output was determined by the ejection angle composed from maternal carotid sphygmogram and its first electrical derivate (dP/dT). The glomerular filtration rate (GFR) was measured with the in vitro radiofluorescent method. RESULTS: The primary peripheral vasodilatation and GFR increase occur early in the first trimester of a normal pregnancy, start to decrease at the end of the third trimester, and return to the normal value in the postpartum period. The increase of GFR precedes the increase of cardiac output. The cardiac output increases progressively from the first trimester and starts to decrease in the third trimester of a normal pregnancy. The extracellular volume increases at the beginning of first trimester progressively until the end of pregnancy and returns to the normal value in the postpartum period. DISCUSSION: The increase of GFR and the cardiac output during pregnancy are contributed to volume-establishment and to the cessation of the special "underfilled" condition of the maternal circulation in the normal pregnancy. We suppose that the maximal increase of GFR precedes the maximal increase of the cardiac output because the GFR increase is caused by maximal renal vasodilatation. The increase of cardiac output is caused in the first trimester by the shunt effect of the enhanced renal blood flow of maternal kidneys, and in the second and third trimester by the shunt effect of the feto-placental unit and the shunt effect of the maternal kidneys.

Adolescent↗
PubMed1990

Effect of neuropeptide Y on cardiac output, its distribution, regional blood flow and organ vascular resistances in the pithed rat.

1. The effects of neuropeptide Y on cardiac output, its distribution and organ vascular resistances were determined with tracer microspheres in pithed rats. 2. Neuropeptide Y increased blood pressure by increasing both cardiac output and total peripheral resistance. The increase in cardiac output was due to an increase in stroke volume as heart rate was not changed. Increased vascular resistance in the splenic, renal, testicular, epididymal, skeletal muscle, large intestinal and mesenteric vascular beds contributed to the increase in total peripheral resistance. Vasoconstriction was most pronounced in the mesenteric bed. 3. This study indicates that neuropeptide Y increases blood pressure by increasing cardiac output and total peripheral resistance. The increased cardiac output is possibly due to an increase in venous return, whilst the increased total peripheral resistance was due to regional vasoconstriction, particularly in the mesenteric bed.

Animals↗
PubMed1996

Effect of an irregular ventricular rhythm on cardiac output.

Impairment of cardiac function in atrial fibrillation has been attributed to loss of atrial contraction and to a rapid ventricular rate. The results of this study suggest that irregularity of the ventricular rhythm, independent of the ventricular rate, may also contribute to impairment of cardiac function during atrial fibrillation.

Atrial Fibrillation↗
PubMed1979

Normal cardiac output in relation to age and body size.

The resting cardiac output was measured in 151 healthy persons (109 males and 42 females) of 4 to 78 years of age by the earpiece dye-dilution method by using an automatic calibration device of dye concentration. Cardiac index had a significantly inverse correlation to age in 105 cases with the age higher than 20 years: r=-0.491 and y=-4.874-0.023x, where y is cardiac index (liters/min/m2) and x is age (years). Stroke index also decreased linearly by aging throughout all ages: r=-0.426 and y=71.0-0.26 x, where x is stroke index (ml/m2) and x is age. There is no significant difference between males and females. A significant difference was found between the young group below 14 years of age and the other group older than 15 years when cardiac output was correlated to body sizes such as height, weight and surface area. The former which is corresponding to the growth age showed significantly higher cardiac output than the latter. From these results, age-matched normal predicted values were presented. It is suggested that the measured cardiac index and stroke index should be taken as abnormal if those values deviate from the normal value by 30% or more.

Adolescent↗
PubMedDate not supplied

The effect of body mass and temperature on the heart rate, stroke volume, and cardiac output of larvae of the rainbow trout, Oncorhynchus mykiss.

The goal of this experiment was to determine whether the type of tight supply-and-demand relationship between cardiac output and metabolic demand for O2 seen in juvenile and adult fish applies during larval development. To this end, we looked at how the heart rate, stroke volume, and cardiac output of rainbow trout (Oncorhynchus mykiss) larvae varied in response to changes in tissue mass and incubation temperature. Previous studies have shown that both factors have a profound influence on metabolic rate. Heart rate and stroke volume were estimated using videomicroscopic methods and used to calculate cardiac output at five or six approximately evenly spaced intervals between hatch (approximately 15 mg wet tissue mass) and 150 accumulated thermal units (degrees C d) posthatch (approximately 50 mg tissue mass) at 5 degrees, 10 degrees, 12 degrees, and 15 degrees C. Cardiac output (range 0.2-20 microL min(-1)) increased significantly in response to increases in both tissue mass and incubation temperature. The increase in cardiac output with tissue mass reflected significant increases in stroke volume as well as heart rate. Temperature only had a significant effect on heart rate (i.e., stroke volume was unaffected). The rate of increase in cardiac output as a result of tissue growth was significantly faster than the rate at which O2 demand increased (the allometric mass exponent [+/-SE] for cardiac output was 1.78 +/- 0.08; literature values for O2 uptake average approximately 1.0), which suggests that the cardiovascular system was less important as a means of delivering O2 to the tissues in small larvae than it was in larger larvae and in juvenile and adult fish. Direct diffusion appeared to be the primary means of O2 delivery in small larvae and embryos.

Animals↗
PubMed1977

Postnatal development of cardiac output distribution measured by radioactive microspheres in rats.

Distribution of cardiac output was measured in rats, 9, 18, 25, 42 and 64 days old, by means of 85Sr-labelled microspheres 15 micrometer in diameter. The fractions of the cardiac output supplying the heart, lungs, cerebrum, hindbrain, kidney, liver, spleen, stomach, small intestine, large intestine, bones and muscles of the hindlegs and skin were estimated. The values obtained were further related to the relative weights of the respective organs. The distribution of cardiac output changed with age, the changes being most pronounced in the brain, kidney and small intestine.

Age Factors↗
PubMed1996

Circuit factors in the high cardiac output of sepsis.

PURPOSE: The increase of cardiac output (CO) in sepsis must be matched by an increase in venous return. Our goal was to determine which of the determinants of venous return are responsible in volume-loaded and nonvolume-loaded pigs with endotoxemia. The determinants include stressed volume, venous compliance (Cv), venous resistance (RVR) and right atrial pressure (Pra). We also tested the effect of the nitric oxide (NO) synthase inhibitor, N omega-nitro-L-arginine-methyl ester (L-NAME) after the hemodynamics with endotoxin stabilized. METHODS: Pigs were anesthetized and mechanically ventilated. We measured CO by thermodilution, mean circulatory filling pressure (MCFP) by inflating a balloon in the right atrium, blood volume by dye dilution, and Cv by rapid blood infusions. RVR was calculated from MCFP-Pra/CO). After baseline measurements, we infused 10 micrograms/(kg x h-1) of Escherichia coli endotoxin. Eight animals also received 30 mL x kg-1 of dextran over the 2 hours (volume treated), and seven did not (no volume). After 2 hours we injected 25 mg x kg-1 of the NO synthase inhibitor, L-NAME, and repeated the measurements. RESULTS: In volume-treated animals, CO increased from 3.9 +/- 0.7 to 5.4 +/- 0.8 L x min-1 (P < .05), and blood pressure (BP) fell from 118 +/- 9 to 76 +/- 12 mmHg. MCFP rose, and there was no change in RVR or Cv, whereas capacitance increased (ie, right shift of pressure-volume curve). Cardiac function (ie, Starling curve) did not change. In no-volume animals, CO fell from 4.47 +/- 0.64 to 2.50 +/- 0.86 L x min-1, BP from 114 +/- 10 to 9 +/- 13 mmHg and MCFP fell. Systemic vascular resistance did not change. Cardiac function was markedly depressed, and the heart rate increased from 143 +/- 13 to 203 +/- 30 beats x min-1. L-NAME restored BP in both groups but also increased RVR and depressed cardiac function. CONCLUSION: Changes in vascular tone during endotoxemia are dependent on volume status. The increased cardiac output in volume-treated septic animals occurred because of an increase in stressed volume due to the volume given in combination with a dilated vasculature. L-NAME restored arterial tone but decreased CO because of a rise in RVR and decrease in cardiac function.

Analysis of Variance↗
PubMed1993

Hemodynamic changes associated with thermodilution cardiac output determination in canine acute blood loss or endotoxemia.

Since the technique of thermodilution (TD) cardiac output measurement, per se, causes hemodynamic alterations, the author examined whether the alterations elicited by iced injectate are augmented in the presence of acute blood loss or endotoxemia, compromised conditions frequently associated with critically ill patients. Acute blood loss (N = 8) and endotoxemia (N = 8) were induced by withdrawing arterial blood approximately 20-30 ml.kg-1 over 30 min and by a slow intravenous infusion of E. coli endotoxin 2.5-3.0 mg.kg-1 over 10 min, respectively, in anesthetized dogs. The magnitudes of decreases in mean arterial and pulmonary artery pressures during slowing of heart rate (HR) following injection of iced injectate 3 ml were slightly less in acute blood loss than in normovolemia, whereas in endotoxemia the degree of mean arterial pressure decrease during slowing of HR following iced injectate 3 ml was slightly less as compared with that before endotoxemia. However, the alterations in other hemodynamic variables following injection of iced injectate 3 ml were similar between dogs with and without acute blood loss or endotoxemia. No profound hemodynamic changes were observed during any TD cardiac output measurements under both conditions. Cardiac output estimated by TD correlated closely with pulmonary blood flow measured by electromagnetic flowmeter in endotoxemia (r > 0.9) but not during acute blood loss. These results indicate that TD cardiac output determination does not cause serious hemodynamic alterations in endotoxemia or acute blood loss, and can estimate right ventricular output accurately in endotoxemia but not in acute blood loss.

Acidosis↗
PubMed1979

Effect of cardiac output on pulmonary shunt.

The effect of cardiac output on pulmonary shunt was studied in living lungs of human patients and dogs which had alveoli and blood vessels, and also in artificial lung (bubble-type oxygenator) which had no such structural factors. In spite of such a structural difference, quite similar results were observed in both living and artificial lungs, and this suggests that some common factors other than the change in blood vessels result in the change in pulmonary shunt. It was observed that pulmonary shunt increased as the saturation of mixed venous blood became higher. It was clarified that the oxygen-receiving capacity of blood decreased as the oxygen saturation of mixed venous blood became higher. It was clarified that the oxygen-receiving capacity of blood decreased as the oxygen saturation became higher, i.e., the amount of reduced hemoglobin became less. The reduction in oxygen-receiving capacity of blood results in the reduction in oxygen-transfer efficiency from alveoli to blood and hence pulmonary shunt increases, and this can be regarded as a kind of shunt-like effect. It can be concluded that the change in pulmonary shunt by cardiac output is not due to the change in the lung function but is caused by the change in the oxygen-receiving capacity of the mixed venous blood.

Animals↗