Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Cardiac Output”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 937 records · Page 52Linked to original sources

[Noninvasive determination of cardiac output in ventilated patients . Clinical evaluation of a simplified quick method].

OBJECTIVE: This study was performed to evaluate a new simplified rebreathing method to determine cardiac output (CO) in mechanically ventilated patients. METHODS: Using a rebreathing system (AMIS 2001, Innovision, Dänemark), effective pulmonary blood flow (PBF) and oxygen consumption (V(radical)O2) were determined non-invasively in 40 patients. After estimation of arterial (CaO2) and capillary oxygen (CcO2) content from the results of an arterial blood gas analysis, intrapulmonary shunt was calculated as Q(s)/Q(t) = [CcO2CaO2] * PBF/V(radical)O(2). Cardiac output was determined by the rebreathing method as CO(rb) = PBF/(1- Q(s)/Q(t)). The cardiac output measured by thermodilution (CO(thd)) was used to determine reference values, which were calculated as mean value of CO(thd) and CO(rb). Intrapulmonary shunt calculated from arterial and mixed-venous blood gas analyses served as reference for the non-invasive determination. In addition, reproducibility of the new method was determined in 15 patients. RESULTS: CO(thd) varied from 3.7-9.5 l/min (6.1 +/- 1.6 l/min; mean +/-SD). Bias and precision of CO(rb) determination accounted for 0.18 l/min (2.9%) and +/- 0.61 l/min (10%), respectively. Precision of intrapulmonary shunt measurement accounted for +/-2.1%. Reproducibility of the CO measurements accounted for 0.24 l/min or 3.9%. CONCLUSION: The rebreathing system evaluated in the present study allows the noninvasive determination of cardiac output with rather high accuracy and good reproducibility. However, technical improvement and further investigation in patients with extremely high cardiac output and shunt values will be needed before its routine clinical use.

Aged↗

Effects of alpha-adrenoceptor agonists on cardiac output and blood pressure in spinally anesthetized ganglion-blocked dogs.

The alpha-adrenoceptor agonist ST-1059 (2-amino-1-(2,5-dimethoxyphenyl) ethanol), the alpha 1-adrenoceptor agonist methoxamine, the alpha 2-adrenoceptor agonist clonidine and a nonselective alpha-adrenoceptor agonist norepinephrine, all increase cardiac output and dose-dependently increase arterial blood pressure in spinally anesthetized ganglion-blocked dogs. The increase in cardiac output may be the result of an increased venous return via the contraction of capacitance vessels, and the vasopressor responses are attributed to an increase in total peripheral resistance. The increases in cardiac output and pressor responses induced by ST-1059 and methoxamine were antagonized by the alpha 1-adrenoceptor antagonist prazosin (0.3 mg/kg i.v.), but those induced by clonidine were not inhibited. In contrast, the alpha 2-adrenoceptor antagonist yohimbine (0.3 mg/kg i.v.) had little or no effects on the increase in cardiac output or the pressor responses induced by ST-1059 and methoxamine, but strongly attenuated those of clonidine. Prazosin and yohimbine inhibited the norepinephrine-induced increase in cardiac output and pressor responses. These results suggest that the increases in cardiac output and blood pressure induced by ST-1059 were mediated by postjunctional alpha 1-adrenoceptor stimulation, such as by methoxamine, but that those induced by clonidine were mediated by postjunctional alpha 2-adrenoceptor stimulation in dogs. Not only the postjunctional alpha 1-adrenoceptors but also the postjunctional alpha 2-adrenoceptors may play an important role in the constriction of venous beds, as well as of the arterioles in spinally anesthetized ganglion-blocked dogs.

Adrenergic alpha-Agonists↗

Effect of cardiac output on extravascular lung water measurements made with the thermoconductivity method.

The authors tested the effects of injectate temperature and of changing cardiac output on the measurement of lung water by the thermoconductivity technique (ETVL). Cardiac output in dogs was increased and decreased with isoproterenol and halothane, respectively. Post mortem extravascular lung water (pulmonary extravascular tissue weight [PETW] was determined using a weighing technique. Cardiac output varied between 0.7 and 8.8 l/min and did not influence the ETVL measurement. The authors conclude ETVL measured by the thermoconductivity technique is not influenced by large changes in cardiac output.

Animals↗

Transient changes in ventilation and cardiac output at the start and end of exercise.

In order to clarify the nature of the regulatory mechanism of the hyperventilation observed at the transition from rest to exercise, cardiac output and ventilation changes in response to submaximal bicycle exercise given as a step function were studied in five healthy men. Cardiac output was determined non-inversively by using a type of impedance plethysmography. It was found that (1) both the cardiac output and ventilation started to increase during the first 10 sec after the start of exercise; (2) the rate of increase in the initial response was abrupt in ventilation but rather gradual in cardiac output: (3) the fast response was followed by a slow response with an exponential time course, the half response time of which ranged between 10 and 45 sec in cardiac output and between 5 and 80 sec in ventilation. The half time increased in proportion to an increase in the work rate and (4) end-tidal pressure of carbon dioxide monitored simultaneously showed a slight decrease at 10 to 15 sec after the start of exercise. It was therefore concluded from the above observation that the initial phase of the exercise-induced hyperpnea is probably of a neurogenic origin.

Adult↗

Cardiac output response to prostaglandin E2-induced abortion in the second trimester.

Maternal cardiac output changes were evaluated in 10 patients undergoing second-trimester abortion induced by prostaglandin E2 suppositories. The peak cardiac output increased by an average of 64.5% above preinduction values. This is similar to the percent increase described during oxytocin-induced labor at term. Inasmuch as resting cardiac output tends to be higher in midpregnancy than at term, absolute values during prostaglandin E2 induction were higher than those observed in laboring term patients.

Abortifacient Agents↗

Exercise cardiac output following Skylab missions: the second manned Skylab mission.

Cardiac output was measured during preflight and postflight exercise-stress tests on the Skylab astronauts. In the postflight tests immediately following the 28-, 59-, and 84-d earth orbital missions, the astronauts exhibited an approximate 30% decrease in cardiac output coupled with an approximate 50% decrease in cardiac stroke volume during exercise. These changes were accompanied by elevated heart rates and significant (p less than 0.01) increases in total systemic peripheral vascular resistance. Mean arterial pressure was unchanged. The hemodynamic alterations were transient in that all parameters returned to normal preflight values within 30 d of the end of the orbital period. Duration of the zero-G exposure did not appear to influence either the magnitude of the hemodynamic changes or the time-course of their return to normal. These results are discussed in relation to other cardiovascular findings and possible mechanisms responsible for the observations are outlined.

Adult↗

Effect of continuous positive pressure ventilation on cardiac output.

Ten mongrel dogs were placed on 5 and 10 cm. H20 of CPPV. Cardiac output, pulmonary vascular resistance and pleural pressures were measured. At 5 cm. H20/CPPV there was no significant change in cardiac output or pulmonary vascular resistance. At 10 cm. H20 CPPV cardiac output significantly decreased and pulmonary vascular resistance increased. The physiologic basis for these changes is discussed and related to the clinical situation.

Animals↗

Impedance cardiography for estimating cardiac output during submaximal and maximal work.

Impedance cardiography was used to estimate cardiac output in 10 men during rest and within 5 s after exercise on a bicycle ergometer, including work up to and including maximal aerobic capacity. An indwelling venous catheter permitted simultaneous sampling of venous blood for observing changes in hematocrit associated with each exercise level. Cardiac output, calculated from a standard equation which assumes a constant value of 150 omega.cm for the electrical resistivity of blood, was compared with corresponding calculations in which blood resistivity was individually determined as a function of hematocrit. It is concluded that many of the discrepancies in the literature related to values for cardiac output obtained during exercise by the impedance method may be inherent in calculations that do not consider the changing electrical resistivity of the blood with a changing hematocrit.

Adult↗

Approximate normal standards of maximal cardiac output during upright exercise in women.

The observed normal ranges of age- and weight-adjusted maximal oxygen uptake and age-adjusted maximal heart rate during upright exercise using the Bruce protocol are shown for 104 asymptomatic women. Cardiac output was measured during upright exercise in 11 normal women with the use of the direct Fick method. On the basis of the relation between oxygen uptake and cardiac output in these 11 women, the cardiac output and stroke volume were estimated by regression in the 104 women to provide normal ranges of age-adjusted values for cardiac output and stroke volume. The potential usefulness of these age-adjusted normal ranges is illustrated by analysis of 21 observations of maximal cardiac output in 16 women with heart disease.

Adult↗

Influence of cardiac output on oxygen exchange in acute pulmonary embolism.

We investigated interactions between cardiac output, VA/Q distribution pattern, pulmonary gas exchange, O2 transport, and tissue oxygenation in 16 patients during the acute phase of pulmonary embolism (PE). The effects of breathing room air, O2 therapy (FIO2 = 0.40) (11 patients), and dobutamine (four patients) were studied after right catheterization using the multiple inert gas elimination technique. The pattern of VA/Q ratio distributions was found to depend essentially on cardiac output level. The individual blood flow perfusing ventilated areas was found to be inversely related to the mean VA/Q ratio of blood flow distribution. PVO2 was directly related to cardiac index (p less than 0.02), and negatively related to the mean VA/Q of blood flow distribution. In view of the influence of low VA/Q ratios and PVO2 on arterial hypoxemia, our results showed that the heart's response to PE conditioned the strategy of pulmonary gas exchange and O2 transport. Oxygen breathing led to a slight but consistent fall in cardiac output (-0.6 +/- 0.5 L/min, p less than 0.01). However, although PaO2 remained normal and PVO2 was slightly improved, we found no evidence for a role of hypoxic pulmonary vasoconstriction in the pulmonary hypertension observed during the acute phase of PE. Administration of dobutamine improved O2 transport and tissue oxygenation, although PaO2 remained constant or even fell in some cases because of increased VA/Q mismatch.

Acute Disease↗

Effect of controlled halothane anaesthesia on splanchnic blood flow and cardiac output in the dog.

Effects of halothane anaesthesia on aplanchnic blood flow and cardiac output were studied in six dogs. Blood flows in the hepatic artery, the superior mesenteric artery and the portal vein were measured electromagnetically. Cardiac output was measured by thermodilution. Depth of anaesthesia, ventilation, acid-base state and body temperature were controlled. Cardiac output and blood flows in the hepatic artery, the superior mesenteric artery and the portal vein decreased significantly to 73%, 54%, 59% and 60% of control values, respectively. Total peripheral vascular resistance decreased significantly, while mesenteric and portal resistance remained essentially unchanged and hepatic arterial resistance showed a significant increase. It is suggested that the difference between the various vascular responses may be caused by a differentiated release from baroreceptor inhibition in various parts of the bulbar vasomotor center.

Anesthesia, General↗

Stress and cocaine elicit similar cardiac output responses in individual rats.

Cocaine use and behavioral stress elicit variable cardiovascular responses in individuals. In the present study, we examined the effects of cocaine or stress on arterial pressure, heart rate, and cardiac output in conscious rats. Rats were instrumented for determination of ascending aortic blood flow as an index of cardiac output using pulsed Doppler flow-metry. Cocaine administration elicited consistent decreases in cardiac output in some rats, whereas others had increases. In contrast, the pressor and heart rate responses were similar in these two groups of animals. Air jet stress also elicited a decrease in cardiac output only in a subset of conscious rats, yet produced equivalent pressor responses in all rats. Cardiac output responses to cocaine and air jet stress were closely correlated in individual rats, indicating that these stimuli evoke similar hemodynamic responses in individual rats. These observations suggest that the rat may provide a model for understanding differential cardiovascular sensitivity to cocaine and/or stress in humans.

Animals↗

Lack of agreement between bioimpedance and continuous thermodilution measurement of cardiac output in intensive care unit patients.

BACKGROUND: Bolus thermodilution is the standard bedside method of cardiac output measurement in the intensive care unit (ICU). The Baxter Vigilance monitor uses a modified thermodilution pulmonary artery catheter with a thermal filament to give a continuous read-out of cardiac output. This has been shown to correlate very well with both the 'gold standard' dye dilution method and the bolus thermodilution method. Bioimpedance cardiography using the Bomed NCCOM 3 offers a noninvasive means of continuous cardiac output measurement and has been shown to correlate with the bolus thermodilution method. We investigated the agreement between the continuous bioimpedance and continuous thermodilution methods, enabling acquisition of a large number of simultaneous measurements. RESULTS: A total of 2390 paired data points from seven patients were collected. There was no correlation (r2 = 0.01) between the methods. The precision (1.16 l/min/m2) of agreement between the Vigilance and the Bomed, assessed by the Bland-Altam method, was very poor although the bias (-0.16 l/min/m2) appeared fair. CONCLUSIONS: The Bomed NCCOM 3 bioimpedance monitor shows poor agreement with the Baxter Vigilance continuous thermodilution monitor in a group of general ICU patients and cannot be recommended for cardiac output monitoring in this situation.

Journal Article↗

[Relationship between cardiac output and PETco2 as well as Paco2 during high-dose fentanyl anesthesia].

We investigated the relationship between cardiac output and PETCO2 as well as blood PCO2 in 10 patients undergoing cardiac surgery of long duration under high-dose fentanyl anesthesia. After anesthetic induction, the minute ventilation was kept constant at 10 ml.kg-1 x 10 cycles.min-1 and a pulmonary artery catheter was inserted. PETCO2, PaCO2 and cardiac index (CI) were measured simultaneously. PaCO2 was corrected for body temperature, and alveolar dead space-to-tidal volume ratio was calculated as VD/VTalv = (PaCO2-PETCO2)/PaCO2. After body, temperature became stabilized, the measurements were started and repeated every 10 to 20 minutes during the prebypass period. One hundred and eight sets of data were taken from 10 patients. PETCO2 correlated positively with CI. Similarly, PaCO2 correlated positively with CI, but VD/VTalv, did not correlate with CI. PETCO2 correlated closely and positively with PaCO2, but it correlated negatively and only marginally with VD/VTalv. When examined in individual patients, PaCO2 correlated positively with PETCO2 in all patients, while VD/VTalv correlated negatively with PETCO2 only in 3 patients. By multiple regression analysis, VD/VTalv change accounted for only 22.3 +/- 15.0% of PETCO2 change, while PACO2 or PaCO2 change accounted for 77.6 +/- 15.0% of PETCO2 change. Decreased CI was associated with decreased CO2 delivery from the tissue to the lung (DCO2) and PaCO2 decreased with decreasing DCO2. Decreased CI was also associated with decreased oxygen uptake (VO2), and PaCO2 decreased with decreasing VO2. A decrease in CI resulted in an increase in VA/Q, and PaCO2 decreased when VA/Q increased. PETCO2 decreased when cardiac output decreased. A decrease in PACO2 explained the decrease in PETCO2 better than an increase in VD/VT did. Decreased cardiac output might cause hypocapnia through decreased CO2 delivery to the lung, decreased CO2 production and/or increased ventilation-to-perfusion ratio.

Adult↗

Portal blood flow in beef steers: comparison of techniques and relation to hepatic blood flow, cardiac output and oxygen uptake.

We compared two techniques for measuring blood flow through portal-drained viscera (PDV) of beef steers and measured portions of cardiac output and total oxygen uptake attributable to PDV and hepatic tissues. Four steers (198 +/- 2 kg), equipped with chronic catheters in appropriate vessels, a transit-time ultrasound probe around the hepatic portal vein and a temporary cardiac output thermodilution catheter, were fed a 60:40 hay: concentrate diet. Treatments, designed to alter blood flow, were: 12 equal meals every 2 h (CNTL); CNTL plus 2 mg clenbuterol in one meal (CLEN); and a 65-h fast (FAST). Blood flow through PDV was measured by dilution of p-aminohippurate (PAH) and transit-time ultrasound. Hepatic blood flow was measured by PAH dilution and cardiac output was measured by thermodilution. Blood flow measured by transit-time ultrasound was consistently slower (45%, P less than .01) than blood flow measured by PAH dilution. Necropsy revealed anatomical constraints that precluded proper placement and function of the flow probes. Cardiac output (liters/h) was greater (P less than .05) for CLEN (3,082) than for CNTL (1,655) or FAST (1,047). Percentage of cardiac output flowing through PDV and hepatic tissues was less (P less than .05) for CLEN (23 and 24%) than for CNTL (31 and 38%) or FAST (32 and 38%). Whole body oxygen uptake (mmol/h) was greatest (P less than .05) for CLEN (4,220), intermediate for CNTL (2,999) and least for FAST (1,965). Percentage of oxygen uptake attributable to hepatic tissues was greater (P less than .05) for FAST (31%) than for CLEN (18%), with CNTL intermediate (24%). Percentage of oxygen uptake attributable to PDV (22%) was not affected (P greater than .05) by treatments.

Animals↗

Continuous cardiac output measurements in the perioperative period.

Management of critically ill patients is based on knowledge of fundamental physiologic variables. Automatized and continuous measurement of these variables is preferable. A new system based upon the thermodilution method has been developed to measure cardiac output automatically and continuously. We evaluated the system in the potentially unstable perioperative period with possible great and rapid changes in cardiac output. Twenty patients, scheduled for open heart or abdominal aortic aneurysm surgery, were included in the study, which was approved by the local ethical committee. The patients were monitored up to 30 hours. At random intervals five, iced, bolus thermodilution cardiac output (BCO) determinations were made and compared to the continuous cardiac output measurements (CCO). Two hundred and thirty-one pairs of data were obtained. The cardiac outputs ranged from 2.5-14.9 l.min-1. The absolute bias was 0.31 l.min-1 (95% limits of agreement -14 l.min-1 to 2.0 l.min-1). The mean relative error was 4.7% with a standard deviation of the relative error of 15.4%. The linear regression was represented by: CCO = 1,1352.BCO-0.36. The correlation coefficient R was 0.90 (P < 0.001). In conclusion, the CCO measurement technique is a promising clinical method. The method is straightforward, requires no calibration, is independent of vascular geometry and measures with its limitations volumetric flow. Finally automatic and continuous patient monitoring provides more information and has potential to reveal previously undetected haemodynamic events.

Aged↗

Maternal organ distribution of cardiac output in the diet-restricted pregnant rat.

Maternal organ distribution of cardiac output was measured with 15-micron diameter, radioactively labeled microspheres in ad libitum-fed or 50% diet-restricted, term pregnant rats, and in ad libitum-fed nonpregnant rats. The diet-restricted dams had a 33% lower total cardiac output than the ad libitum-fed dams, but it was not significantly different from that of the nonpregnant rats. Placental blood flow in the diet-restricted rats was 30% lower than that in the ad libitum-fed rats. Except for a higher blood flow to the pancreas and a lower blood flow to the uterine tissue, blood flows to the other organs of the diet-restricted dams were not significantly different from those of ad libitum-fed pregnant dams. Blood flows to the lungs, small intestine and ovaries of the diet-restricted pregnant rats were higher than those in the nonpregnant rats. Dietary restriction resulted in a decreased percentage of the cardiac output being distributed to the pregnant uterus and an increased percentage to the hepatic portal circulation, thus maintaining a liver blood flow similar to that in nonpregnant rats. Thus, maternal liver blood flow, rather than that to the placentas, is protected during malnutrition.

Animals↗

Central hemodynamics and cardiac output control in essential hypertensive patients.

Central hemodynamics were determined in 202 men including 101 normotensive and 101 permanent essential hypertensive patients of the same age. Cardiac output was identical in the two groups while blood pressure and total peripheral resistance were significantly different. Strong differences between the two groups are revealed by a systematic correlation study: (i) correlations of blood pressure (with respectively heart rate and total blood volume) were significant in the normotensive group but not in the hypertensive group; (ii) correlations of cardiac output (with respectively heart rate and total blood volume) were significant in both groups; (iii) correlations of renal blood flow (with respectively cardiac output and blood pressure) were significant in the hypertensive group but not in the normo tensive group. This study provided evidence that the volume and neural pressure controls are impaired in hypertensive patients while the cardiac output control is maintained and, suggested the existence of adaptive mechanisms involving the kidney in the maintenance of normal cardiac output in permanent essential hypertensive patients.

Adaptation, Physiological↗