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PubMed2006

Redistribution of cardiac output during hemorrhagic shock in sheep.

OBJECTIVE: Our goal was to evaluate the robustness of one of the assumptions used by esophageal Doppler monitors to compute systemic stroke volume and cardiac output; i.e., a constant flow proportion between supra-aortic vessels and descending aorta. For this purpose, we measured ascending and descending aortic blood flows during acute hemorrhage in anesthetized ewes. DESIGN: Prospective, experimental study. SETTING: Animal research facility. SUBJECTS: Adult ewes. INTERVENTIONS: Anesthetized animals were implemented with an aortic pressure transducer and two ultrasound transit time flowmeters placed around ascending and descending aorta, respectively. After baseline measurements, three incremental blood withdrawals were followed by progressive blood restitution in three similar steps. MEASUREMENTS AND MAIN RESULTS: Ascending and descending aortic blood flows were reduced in a proportional manner after hemorrhage (-48% and -46%, respectively; p < .05 vs. baseline). Following blood restitution, flows were not fully restored, but ascending aortic flow was reduced by 27% with respect to initial control values while descending aortic flow was only 15% below. The agreement between ascending aortic flow and cardiac output calculated as descending aortic flow divided by 0.7 was characterized by a bias of 0.07 L/min and limits of agreement of +1.24 L/min and -1.10 L/min. CONCLUSIONS: Minor blood flow redistribution between supra-aortic and descending aortic territories was seen only following blood restitution but not during hemorrhage in these anesthetized ewes. This observation supports the robustness of the assumption of constant flow proportion used by the esophageal Doppler monitor to calculate systemic stroke volume from descending aortic flow measurements.

Animals↗
PubMed1995

Relation between pulmonary venous flow and pulmonary wedge pressure: influence of cardiac output.

Multiple factors affect the systolic and diastolic components of pulmonary venous flow. It has been suggested that left ventricular function might influence the effects of filling pressures on indexes of pulmonary venous flow. The present study was designed to evaluate the effect of the pulmonary wedge pressures, left ventricular function, and cardiac output on the pulmonary vein flow pattern. Forty-five patients undergoing cardiac surgery were included in this study. Pulmonary venous flow and mitral flow variables were obtained by transesophageal echocardiography with hemodynamic variables obtained simultaneously. In the total group, there was no consistent relation between the pulmonary venous flow or the mitral flow parameters and the capillary wedge pressures. When patients were grouped according to normal (> 2.2 L/min/m2) or low (< 2.2 L/min/m2) cardiac index, a significant and positive relation was found between the systolic component of the pulmonary venous flow and the pulmonary wedge pressure in patients with normal cardiac index (r = 0.69; p = 0.003). Conversely, in patients with low cardiac index there was also a significant although negative correlation between the systolic velocity integral and the pulmonary wedge pressure (r = -0.58; p < 0.001). In conclusion, the systolic component of the pulmonary venous flow correlates closely and significantly with the capillary wedge pressures. The direction of this relation depends to a large extent on the total cardiac output and to a lesser extent on the left ventricular systolic function as assessed by the ejection fraction.

Adult↗
PubMed1979

Effect of alpha-methyldopa on cardiac output in hypertension.

Hemodynamic and blood volume changes, systolic time intervals, and baroreflex mechanisms were studied in 20 patients with hypertension after methyldopa (12 +/- 0.9 mg/kg/day). The drug was administered orally during 7 days' hospitalization on a normal sodium diet (110 mEq/day). There was a fall in blood pressure and in total peripheral resistance, without significant change in cardiac index, heart rate, and stroke index. There were increases in plasma and blood volume (p less than 0.05) but no change in cardiopulmonary blood volume or systolic time intervals. The unchanged heart rate was associated with an increased sensitivity ( less than 0.05) of the baroreflex mechanisms. The study supports the view that the unchanged cardiac output after methyldopa is related to important changes in control of cardiac output, including redistribution of blood volume and modifications in baroreflex mechanisms.

Adult↗
PubMed1997

Noninvasive cardiac output estimation: a preliminary study.

The availability of a simple-to-use, automatic measurement system for noninvasive flow estimation is imperative, given the clinical demand for an acceptable noninvasive procedure rather than the standard invasive procedure of thermodilution. A method for calculating cardiac output from noninvasively derived pressure pulses has been developed, and the results of a preliminary evaluation study on post-cardiac surgery patients for whom invasive flow measures were readily available for comparison are provided in this report. The proposed method relies on fast Fourier transform (FFT) analysis of pulses measured externally at the carotid and femoral pressure points. A transfer function of the aorta is computed from digitally filtered pulse measurements, and a tapered model of the aorta is parametrically adapted using a simplex optimization algorithm so that its transfer function matches that derived experimentally. An aortic input impedance term is obtained from the optimized model and utilized along with the carotid pulse (analogous to input voltage) to compute aortic flow. In addition to its automation, attractive features of this method include the requirement for relatively few pulses for analysis as well as considerable resistance to noise artifact. For 59 data records collected from 54 post-cardiac surgery patients, the average flow measurements computed over several pulses compare well with the standard, invasive method of thermodilution. Preliminary results also indicate a strong potential for tracking changes in cardiac output over time, and invite further use of the method in monitoring hemodynamically unstable patients.

Cardiac Output↗
PubMed1976

A computer module for the continuous monitoring of cardiac output in the operating theatre and the ICU.

A new pulse contour method to determine stroke volume and cardiac output continuously in patients on a beat-to-beat basis from the aortic pressure wave has been implemented in the form of a simple, inexpensive, fully automatic computing module for a commercially available patients monitoring system (Philips Medical Systems). Its reliability has been tested and shown in a computer analog, in experimental studies in 10 dogs (not reported here), in 22 hemodynamic studies on 20 young healthy volunteers and during 41 days in 20 postsurgical patients in the ICU, the most important result being that erros figures (15 and 19% respectively in the two human studies) are of the same order as when two standard methods, Fick and dye dilution are compared. The clinical studies have further indicated the easy applicability of the module 1 degree in the monitoring of critically ill patients in ICU's, 2 degrees as a monitor of the systemic circulation during anesthesia, and 3 degrees as a tool for studying the hemodynamic effects of pharmacological agents. The instrument consitutes no burden to the patients and has, several times during the course of the evaluation, provided an early warning of a deteriorating hemodynamic status of the patient to the physician.

Age Factors↗
PubMed1996

Cardiac output is not affected during intraoperative testing of the automatic implantable cardioverter defibrillator.

INTRODUCTION: Perioperative mortality of patients undergoing implantation of automatic implantable cardioverter defibrillators (ICDs) has been reduced dramatically following the availability of transvenous-subcutaneous defibrillation leads. However, patients with severely reduced left ventricular function show a substantial rate of nonsudden cardiac mortality within the first year. Whether repeated intraoperative inductions of ventricular tachycardia/fibrillation (VT/VF) during implantation lead to hemodynamic deterioration and thus might contribute to development of end-stage heart failure in these patients is unknown. The purpose of the present study was to determine cardiac output and hemodynamic performance during transvenous-subcutaneous ICD implantation in patients with severe left ventricular dysfunction. METHODS AND RESULTS: In 11 patients with a left ventricular ejection fraction (EF) < or = 0.35, cardiac output was measured automatically with a combined continuous cardiac output/mixed venous oxygen saturation pulmonary artery catheter system. ICD implantation was performed during standardized general anesthesia. In the 11 patients (EF = 27 +/- 2% [mean +/- SEM]) a total of 95 episodes of VT/VF followed by defibrillation were induced (episodes per patient = 9 +/- 1; range 6 to 11). Cardiac index was 2.2 +/- 0.2 L.min-1.m-2 after induction of anesthesia (before start of surgery), and 1.9 +/- 0.1 L.min-1.m-2 immediately before first induction of VT/VF. After the last episode of VT/VF, cardiac index was 2.1 +/- 0.2 L.min-1.m-2. Cardiac index measured 1, 2, and 3 minutes after induction of VT/VF was not significantly different when compared to the preinduction value during any episode of VT/VF induction. Similarly, stroke volume index was 39 +/- 5 mL.m-2 immediately before first induction of VT/VF and 36 +/- 3 mL.m-2 after the last episode of VT/VF (NS). At the end of surgery, hemodynamic parameters did not exhibit any significant difference when compared to the data obtained before start of ICD implantation and testing. CONCLUSION: Extensive defibrillation tests during transvenous-subcutaneous ICD implantation in patients with severe left ventricular dysfunction are not associated with acute deterioration of cardiac performance.

Cardiac Output↗
PubMed1990

Positive correlation between 'the arterial oxygen extraction tension' and mixed venous pO2 but lack of correlation between 'the oxygen compensation factor' and cardiac output in 38 patients.

pH and blood gases were measured in simultaneous samples of arterial blood from the radial artery and mixed venous blood from the pulmonary artery using an ABL300 and OSM3 (Radiometer A/S, Denmark). Cardiac output was measured by thermodilution. The patients were suffering from chronic obstructive pulmonary disease or adult respiratory distress syndrome. The data indicate that patients respond to a decreased arterial oxygen availability by allowing the mixed venous pO2 to fall rather than by increasing the cardiac output to maintain a normal mixed venous pO2. In other words, the arterial oxygen extraction tension and the oxygen compensation factor were both highly correlated to the mixed venous pO2 but unrelated to the cardiac index. For this reason the arterial oxygen extraction tension appears to be a more relevant parameter of the overall arterial oxygen availability than the oxygen compensation factor. Comparison of the arterial and mixed venous data confirms the accuracy of the Oxygen Status Algorithm for calculating the various oxygen parameters, including the p50, the estimated 2,3-diphosphoglycerate concentration, and the estimated physiological shunt, on the basis of a single arterial blood sample.

2,3-Diphosphoglycerate↗
PubMedDate not supplied

Effect of exercise on cardiac output and other cardiovascular parameters of heavy turkeys and relevance to the sudden death syndrome.

The cardiovascular response to treadmill exercise was studied in 14-to-18-week-old male and female heavy turkeys. Arterial blood pressure, cardiac output, body temperature, and heart rate were measured before and during each period of exercise. Total peripheral resistance, stroke volume, and stroke index were calculated from those parameters. Systolic, diastolic, and mean blood pressures significantly decreased during exercise. Cardiac output increased during exercise in males and females by 64% and 23%, respectively, while total peripheral resistance fell by approximately 40% in both sexes. Exercise had no significant effect on stroke volume and stroke index. The cardiac functional capacity of the heavy turkey in response to mild exercise appears very limited. This failure of the cardiovascular system to adequately respond to increased metabolic needs suggests that hemodynamic failure is a major component in the pathogenesis of sudden death syndrome of turkeys.

Animals↗
PubMed1995

Comparison of cardiac output measurements by thermodilution and thoracic electrical bioimpedance in critically ill versus non-critically ill patients.

Thoracic electrical bioimpedance (TEB) has been proposed as an alternative to thermodilution (TD) for the measurement of cardiac output in settings such as the Emergency Department where invasive monitoring is not available. Validation studies comparing TEB with TD suggest a wide range of variability in the agreement between the two methods. This prospective study tests the hypothesis that this variability may be related to the severity of patient illness. Fifteen non-critically ill patients undergoing cardiac catheterization and 13 critically ill patients who underwent Swan-Ganz catheterization in the medical intensive care unit (MICU) were enrolled. Fifty-one pairs of data from the catheterization laboratory and 49 pairs of data from the MICU were obtained. The patients were graded retrospectively according to the APACHE II scoring system. The mean difference (bias) between TEB and TD results was calculated for each patient using the method suggested by Bland and Altman. A pooled t-test was performed to determine whether there was any significant difference between the APACHE II scores or cardiac output measurements obtained by TEB and TD in the two groups. APACHE II scores were 4.7 +/- 1.2 for the catheterization laboratory and 14.2 +/- 5.0 for the intensive care unit patients (P < .001). The catheterization laboratory (cath lab) group bias was 0.23 +/- 2.19, whereas the MICU bias was .002 +/- 2.33. There was no significant difference in the bias between the two groups despite significant differences in the APACHE II scores. Standard deviations of the bias were less than 15% different from each other.(ABSTRACT TRUNCATED AT 250 WORDS)

APACHE↗
PubMed1984

Accuracy of absolute left ventricular volumes and cardiac output determined by radionuclide cardiography.

We determined left ventricular (LV) volumes and derived variables by gated equilibrium radionuclide imaging at rest and during exercise in 12 patients without valve disease or intracardiac shunts. LV volume was determined as the product of the background-corrected LV count rate and an individual attenuation correction factor divided by the count rate in peripheral blood. Attenuation correction was based on measurement of LV depth within the chest from an initial first pass study in the left lateral view and a linear attenuation coefficient of 0.156 cm-1 determined in phantom studies. The average LV depth was 8.0 cm (range 6.9-9.1) in agreement with an average depth measured by echocardiography of 8.2 cm (6.3-9.4), P much greater than 0.05. The correlation between radionuclide (RC) and simultaneous thermodilution (TD) measurements was for cardiac output (CO): r = 0.95; CO (RC) = 1.00 X CO (TD) + 0.10 1/min with a standard error of the estimate (SEE) of 0.79 1/min; for stroke volume (SV): r = 0.90; SV(RC) = 0.93 X SV (TD) + 5 ml; SEE = 8 ml; for end-diastolic volume (EDV): r = 0.96; EDV(RC) = 1.06 X EDV(TD) -14 ml; SEE = 27 ml; and for end-systolic volume (ESV): r = 0.98; ESV(RC) = 1.05 X ESV (TD) -6 ml; SEE = 20 ml. The interobserver variation, expressed as the coefficient of variation, was for cardiac output 6%, for stroke volume 6%, for end-diastolic volume 4%, and for end-systolic volume 5%. This method permits non-invasive determination of LV volume and total LV output per beat based exclusively on data obtained during radionuclide imaging.

Adult↗
PubMed1979

Determination of cardiac output in the mouse.

A technique is described for determination of cardiac output in the mouse. The method is basically a tracer dilution technique using 86-rubidium as soluble indicator, where a microsampler is used for blood collection and in which the gamma function fitting is applied for area determination.

Animals↗
PubMed1978

Mechanism of cardiac output response to hypertonic sodium chloride infusion in dogs.

Hypertonic sodium chloride and tris(hydroxymethyl)amino-methane (Tris) hydrochloride (0.3 mmol/kg.min) were infused intravenously into chloralose-anesthetized dogs over a 20-min period. Cardiac output, maximum left ventricular dP/dt, and (dP/dt)/P increased by 55, 33, and 23%, respectively, during NaCl infusion, but Tris HCl infusion had no effects. NaCl infusion did not change heart rate or left ventricular end-diastolic pressure. Mean systemic and pulmonry arterial blood pressures increased, whereas total peripheral and pulmonary vascular resistances decreased. Responsiveness of cardiac beta-adrenergic receptors, as determined by serial intravenous injections of epinephrine, was not affected by NaCl infusion. Plasma catecholamine concentration, however, increased during NaCl infusion. In addition, the increases in cardiac output, maximum left ventricular dP/dt and (dP/dt)/P were abolished by prior treatment with practolol, a cardioselective beta-adrenergic receptor blocking agent. These results suggest that the hemodynamic effects of NaCl infusion were caused, at least in part, by the inotropic action of catecholamines.

Animals↗
PubMed1992

Amrinone and dobutamine as primary treatment of low cardiac output syndrome following coronary artery surgery: a comparison of their effects on hemodynamics and outcome.

This study was undertaken in order to compare the effectiveness of amrinone and dobutamine as primary treatment of a low cardiac output (CO) after coronary artery bypass graft (CABG) surgery. Thirty patients with preoperative left ventricular dysfunction participated in this open-label randomized study. Patients were included if they failed to separate from cardiopulmonary bypass (CPB) without inotropic support or if they had a cardiac index (CI) less than 2.4 L/min/m2 after CPB regardless of the blood pressure, in the presence of adequate filling pressures. The treatment objectives were to separate from CPB and achieve a CI > or = 2.4 L/min/m2 and a mean arterial pressure > or = 70 mmHg. Patients treated with amrinone received 0.75 mg/kg followed by 10 micrograms/kg/min; when the objectives were not achieved within five minutes, another 0.75 mg/kg was given. Patients treated with dobutamine received an initial infusion of 5 micrograms/kg/min increased stepwise to 15 micrograms/kg/min if necessary. Eleven of 15 amrinone versus 6 of 15 dobutamine patients achieved the predefined treatment objectives with the test drug alone (P = NS). Comparisons of hemodynamics in patients treated solely with amrinone (n = 7) or dobutamine (n = 6) after CPB showed no significant differences between the treatment groups. The incidence of myocardial ischemia as detected by Holter monitor was 36% with amrinone and 33% with dobutamine. Two patients suffered ventricular fibrillation and two had significant supraventricular tachyarrhythmias (heart rate > 130/min) during treatment with dobutamine alone, whereas no significant arrhythmias occurred in the amrinone group (P = NS). Six dobutamine patients (40%) had postoperative myocardial infarction (MI) as opposed to none among the amrinone patients (P = 0.017). These results indicate that amrinone compares favorably with dobutamine as a primary treatment of low CO after CABG. Further study in a larger number of patients will be required in order to determine if the lower incidence of MI in the amrinone group was due to the treatment drug.

Amrinone↗
PubMed1958

Cardiac output during excitation of chemoreflexes in the cat.

In cats under chloralose anaesthesia the reflex fall of blood pressure and heart rate caused by injection of veratrine, amidines, diphenhydramine, or ethyl acetoacetate was accompanied by a fall in cardiac output. After veratrine and amidines there was a fall in mean pulmonary arterial pressure and after veratrine no significant change in pulmonary vascular resistance. After diphenhydramine and ethyl acetoacetate there was a rise in mean pulmonary arterial pressure and after diphenhydramine an increase in pulmonary vascular resistance. The effects of veratrine and amidines, but not those of diphenhydramine and ethyl acetoacetate, were abolished by section of the vagi. The main change leading to the fall of cardiac output after amidines was bradycardia.

Animals↗
PubMed1980

[Interrelationship of cardiac output and myocardial contractility].

On examination of 56 persons, 4 were found to have no abnormalities of the cardiovascular system, in all of the others the diagnosis of ischemic heart disease was confirmed. The cardiac output was determined by means of a thermodiluter. The stroke work index, the total peripheral resistance, and the segmental contraction of the left-ventricular wall were calculated. Changes in the stroke volume in response to a stress test, left ventriculography, were studied. It was found that changes in the stroke volume do not correlate with the clinical and coronarographic manifestations of the disease and the condition of the contractility of segments of the left-ventricular wall in the absence of clinical symptoms of circulatory insufficiency. The trend of stroke volume changes recorded during the stress test showed a dependence on the volume and degree of left-ventricular asynergy. Changes in the stroke volume were determined by the initial value of the cardiac output. High sensitivity of the left-ventricular function curve in detecting dysfunction of the left ventricle as well stroke volume-total peripheral resistance feedback were revealed.

Cardiac Catheterization↗
PubMed1992

Behavior of cardiac output during progressive exercise tests: a preliminary report.

The behavior of cardiac output (Q) during progressive incremental exercise tests was studied in young healthy men. Q approached a plateau and leveled off at almost the same work rate at which oxygen uptake (VO2) attained its maxima, while heart rate (HR) still continued to rise. This suggests that the limiting factor for maximal aerobic capacity in healthy subjects is Q. The rate of increase in Q and HR accelerated from a work rate which is close to the ventilatory anaerobic threshold (AT). The prime cause of the progressive augmentation in cardiac activity is probably an accelerated release of plasma catecholamine and/or potassium. There is a possibility that these substances might also affect the AT.

Adolescent↗
PubMed1990

Estimation of cardiac output by bioimpedance cardiography.

Changes in thoracic electrical bioimpedance during the cardiac cycle have been related to the ejection of the stroke volume of blood during cardiac systole. Refinements in the recording and analysis of these changes permit estimation of cardiac output. Encouraging reports comparing results obtained by this method and those obtained simultaneously using the current standard invasive method have been published. While there are limitations, the advantages of this technique are sufficient to make bioimpedance cardiography attractive to the military physician. It is for these reasons that the principles of this technology are reviewed in this paper.

Cardiac Output↗