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Plasmodium berghei: malaria infection causes increased cardiac output in rats, Rattus rattus.

Thirty-two 4-week-old male Wistar rats were infected with Plasmodium berghei malaria. On Days 12 through 14, blood volume, arterial blood pressure, right ventricular pressure, heart rate, cardiac output, stroke volume, hematocrit, and vascular resistances were determined. All of the cardiovascular parameters measured, with the exception of calculated pulmonary vascular resistance, changed progressively as the peripheral blood parasitemia increased. With a rising parasitemia, cardiac output increased, despite a reduced heart rate. The highest parasitemia of 63% was accompanied by a doubling of the normal cardiac output. The relationship between parasitemia and cardiac output can be described by the equation, cardiac output = (6.14) x % parasitemia + 452 ml/min/kg. The mean arterial blood pressure was lower than controls when parasitemia exceeded 20%, whereas systolic right ventricular pressure was elevated only at the highest parasitemias. When noninfected control rats were compared with those animals having parasitemias greater than 40%, in the infected animals, mean arterial pressure was 28% lower (P less than 0.01) and systolic right ventricular pressure rose by 21% (P less than 0.02). A 50% decline was observed in the total peripheral vascular resistance (P less than 0.01), although the pulmonary resistance was apparently unchanged. With P. berghei infection, there is also a marked anemia, an increase in plasma volume, and a 16% increase in blood volume (% body weight). It is concluded from these results that although the hemodynamic changes previously reported in the literature indicate that infection with malaria may result in focal blockages in microvessels and poor tissue perfusion, the total systemic effect, in the rat, is an increase in cardiac output secondary to a reduced peripheral resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Neither the accuracy nor the precision of thermal dilution cardiac output measurements is altered by acute tricuspid regurgitation in pigs.

UNLABELLED: Whether measurement of cardiac output using the thermal dilution technique (TDCO) is valid in the presence of tricuspid regurgitation (TR) is controversial. We assessed the accuracy and precision of the technique in pigs by comparison with data from an electromagnetic flowmeter on the aorta (EMCO). TR was created with sutures that immobilized the free-wall leaflets of the tricuspid valve, and cardiac output was adjusted with dobutamine to give values comparable to control measurements. TR reduced forward stroke volume from 17.2 to 12.6 mL/beat and caused the right atrium to dilate and pulse in synchrony with the right ventricle. Acute TR did not affect the linear regression relation between TDCO and EMCO and did not alter the correlation coefficient (r = 0.94 during both control and TR). These data demonstrate that acute TR does not affect the accuracy or precision of TDCO in pigs. IMPLICATIONS: Cardiac output is a valuable measurement that guides the medical care of patients with heart and lung disease. This study demonstrates that the thermal dilution technique of determining cardiac output is valid when acute tricuspid valve regurgitation is present in pigs.

Anesthesia, Inhalation↗

Reproducibility of cardiac output measurement by cross sectional and Doppler echocardiography.

The variability of Doppler echocardiographic estimation of cardiac output at the aortic orifice was investigated in eight healthy subjects. Cross sectional echocardiograms of the aortic orifice and aortic Doppler velocities were recorded and measured by four echocardiographers. Between subject variability was significantly larger than within subject variability for all variables. Variability owing to different echocardiographers and different measurement times was small compared with total variability. Coefficients of variation for aortic annular diameter, aortic velocity integral, and heart rate were 4.1%, 6.4%, and 5.0% respectively. The coefficient of variation for cardiac output was 8.8% and the 95% confidence interval for measurement of cardiac output by the Doppler method was 4.45 to 6.35 l/min. One echocardiographer reanalysed all the recordings and the results showed that recording the echocardiograms introduces a significantly larger source of error than measuring them. Thus serial measurements of cardiac output by the Doppler method can be performed with acceptable reproducibility; this indicates that the technique can be accurately applied in clinical practice.

Adult↗

A new closed-system using partially frozen injectate for thermodilution cardiac output determinations.

The FI (partially frozen injectate) system, a new closed-system devised by the authors for thermodilution cardiac output determinations, has two major features: 1) it needs no ice-filled receptacle to keep injectate cold because it uses partially frozen injectate, and 2) it can go without monitoring the injectate temperatures during the whole process of cardiac output determinations. The author evaluated the accuracy and reproducibility of cardiac output determinations with the FI system in 10 critically ill patients, as compared with another closed-system (which is commercially available) and the standard open method. The injectate temperatures in the FI system were also measured in vitro. The mean injectate temperature in the FI system was 0.71 +/- 0.26 degrees C and 80% of the injectate temperatures were lower than 1.0 degrees C. Even when no monitoring of injectate temperatures was made, the predicated error in the calculated cardiac output resulted as low as 2% with the FI system. The mean cardiac output values were not statistically different between the FI system and the other two systems.

Journal Article↗

Measurement of cardiac output and its distribution in rats under various sodium intakes, using 15 and 10 micron spheres.

We estimated cardiac output and its distribution to organs using simultaneously injected 15 micrometers and 10 micrometers radioactive microspheres. This study was carried out in anaesthetised rats with high cardiac output induced by sodium loading and low cardiac output by sodium restriction. In neither group were the values of cardiac output and blood flow to kidneys, brain, heart and spleen affected by microsphere size. However, the ratio of blood flow estimated with 15 micrometer to that with 10 micrometer microspheres averaged 0.67: 0.60 for liver, 1.09: 1.10 for duodenum, 3.51: 3.52 for testes, and 1.19: 1.07 for adrenals in high and low sodium rats respectively. A significant escape of 10 micrometer microspheres from testicular, adrenal, and gastrointestinal vasculatures may explain such finding. With regard to the liver, this view was reinforced by the finding of comparable hepatic blood flow values with either bead size after clamping of the portal vein. Additional preferential losses of 10 micrometer microspheres from muscular vasculature seemed to contribute to the fractions of injected radioactivities recovered in lungs (that is 6 and 2% for 10 micrometer and 15 micrometer spheres respectively). These results suggest that in the rat blood flow data provided by 10 micrometer microspheres should be carefully analysed according to the organ(s) studied.

Animals↗

Effects of long-term, high-altitude hypoxemia on ovine fetal cardiac output and blood flow distribution.

OBJECTIVE: We sought to determine the effects of long-term hypoxemia on fetal cardiac output and flow distribution. STUDY DESIGN: We exposed six pregnant sheep to high altitude (3820 m) hypoxia from 30 to 135 days' gestation (term 146 days). Ten to 14 days after surgery we determined fetal cardiac output and organ blood flows by means of the radiolabeled microsphere technique during a baseline period and also during an additional 30-minute period of more severe added acute hypoxemia. RESULTS: Baseline maternal arterial PO2 was 60.7 +/- 1.7 torr and fell to 35.1 +/- 3.0 torr during the added acute hypoxemia. Fetal arterial PO2 decreased from 18.5 +/- 1.1 to 11.4 +/- 1.5 torr during added acute hypoxemia. Baseline fetal cardiac output was 351 +/- 55 ml/min/kg, which was significantly lower than previously reported values in low-altitude fetuses. Blood flow to critical organs such as the heart and brain was maintained at levels found in low-altitude fetuses, but flow to the carcass was significantly lower (-49%) than the mean value reported in the literature for low-altitude fetuses. Oxygen delivery was also maintained at normal levels to the brain and heart but was reduced in the kidneys (-31%), gastrointestinal tract (51%), and carcass (-58%). During added acute hypoxemia cardiac output did not change significantly; however, blood flow to the brain, heart, and adrenal glands increased 112%, 135%, and 156% (p < 0.05), respectively. CONCLUSION: We conclude that during long-term hypoxemia redistribution of fetal cardiac output is maintained favoring the brain and heart.

Adrenal Glands↗

Increased cardiac output by downstream pumping with a reversed unidirectional intra-aortic balloon.

Downstream and upstream pumping with unidirectional intra-aortic balloons was compared in 8 open-chest normal mongrel dogs anesthetized with pentobarbital. Downstream pumping effect a 32 per cent increase in cardiac index, a 24 per cent decrease in systemic resistance, and a 2 per cent decrease in heart rate. Upstream pumping did not significantly affect these parameters. Mean aorta pressure proximal and distal to the balloon was not altered significantly by pumping in either direction. This unique observation of increased cardiac output may have important implications for the treatment of low output cardiac failure. Preliminary studies including baroreceptor denervation suggest that a reflex mechanism may be involved.

Animals↗

Cardiac output and peripheral resistance in strains of rats sensitive and resistant to NaCl hypertension.

The interrelationship of blood pressure, cardiac output, and peripheral resistance was studied in Dahl "S" and "R" rats after 3 days on a high (8%) NaCl diet. Both "S" and "R" rats were normotensive when fed a normal (0.3%) NaCl diet. After 3 days of the high NaCl diet, the "R" rats remained normotensive (BP 112 mm Hg), while the "S" rats had an elevation of arterial pressure (BP 133 mm Hg) (p less than 0.001). The cardiac outputs of both "S" and "R" rats were similar on the low NaCl diet. After 3 days of high NaCl feeding, the cardiac output of the "R" rats rose 18% above the "R" control level (p less than 0.0001), while the peripheral resistance declined 14% below the "R" control level (p less than 0.005), and the blood pressure (BP) did not change, a pattern quite contrary to the concept of "whole-body" autoregulation. With a similar 3-day high NaCl feeding in "S" rats, cardiac output (p less than 0.005) and peripheral resistance (p less than 0.05) both increased 10%, while BP rose 20%. After 7 days of high NaCl feeding, the cardiac output of the "S" rats had returned to normal, while blood pressure and peripheral resistance both continued to be elevated. This pattern of response in "S" rats could be compatible with the concept of "whole-body" autoregulation. However, since both NaCl hypertension and Goldblatt hypertension can occur in settings in which "whole-body" autoregulation appears not be to causally related, one cannot be certain whether "whole-body" autoregulation is playing a causal role in the mechanism of NaCl-induced hypertension in "S" rats. It is a striking dichotomy that 3 days of high salt feeding produces vasoconstriction in "S" rats and vasodilation in "R" rats.

Animals↗

Effect of increased oxygen affinity and anemia on cardiac output and its distribution.

Effect of increased blood O2 affinity on cardiac output and its distribution was studied in conscious sedated rats by the microsphere-reference sample method. After a preliminary measurement of cardiac output and its distribution, rats were exchange transfused with normal blood or low-P50 (PO2 at which hemoglobin is half-saturated with O2) blood; other groups were made anemic with and without a simultaneous reduction in P50. Reduction in P50 from 38 to 17 Torr did not change cardiac output, pulse, or blood pressure but caused, after allowance for changes in controls, a 102% increase in coronary blood flow and an 88% increase in cerebral blood flow. Anemia (hematocrit = 22%) produced similar changes in coronary and cerebral flow. When anemia was combined with a 12-Torr reduction in P50, coronary and cerebral flow increased by 297 and 209%, respectively. These increases in coronary and cerebral flow were not attributable to increased cardiac work or hypercapnia. It is concluded that a left shift of the O2 dissociation curve induces increased blood flow to brain and heart, probably in compensation for decreased tissue O2 pressure.

Anemia↗

Positional effects on maternal cardiac output during labor with epidural analgesia.

OBJECTIVE: Our purpose was to test the hypothesis that the supine versus the lateral position is associated with a greater decrement in cardiac output after epidural analgesia in labor. STUDY DESIGN: Twenty-one normal term subjects were randomized to the left lateral or supine position in early labor. Cardiac output measured by the acetylene rebreathing method, stroke volume, heart rate, mean arterial pressure, and systemic vascular resistance were obtained at 5-minute intervals, beginning before a 500 ml intravenous fluid bolus (baseline) and ending 45 minutes after epidural injection. RESULTS: Mean baseline supine versus lateral group differences were significant for 21% lower cardiac output, 21% lower stroke volume, 19% higher mean arterial pressure, 50% higher systemic vascular resistance, and equivalent heart rate. In the supine group fluid bolus resulted in significantly increased cardiac output and stroke volume, decreased mean arterial pressure and systemic vascular resistance, and unchanged heart rate. In the supine group cardiac output and stroke volume decreased significantly after epidural injection. The lateral position group exhibited no hemodynamic alterations after fluid bolus or epidural. CONCLUSIONS: In contrast to the lateral position, the supine position is associated with a significant postepidural decrement in cardiac output, not identified by a change in heart rate. This likely reflects an inability to maintain stable preload volume in the supine position.

Adult↗

The effects of spread of block and adrenaline on cardiac output after epidural anesthesia in young children: a randomized, double-blind, prospective study.

UNLABELLED: Epidural anesthesia is considered to be without significant hemodynamic consequence in young children. However, conversely to adults, few studies have investigated cardiac output. Using transesophageal Doppler monitoring of cardiac output, we prospectively investigated hemodynamic alterations in 48 children (median age, 22.5 mo) receiving sevoflurane general anesthesia combined with caudal or thoracolumbar epidural anesthesia. They were randomly assigned to receive 0.8 mL/kg of plain local anesthetic mixture (lidocaine 1% + bupivacaine 0.25% (50/50) + 1 microg/mL of fentanyl) or 1 mL/kg of the same mixture with 5 microg/mL of adrenaline. No significant hemodynamic alteration was elicited in caudal and thoracolumbar groups receiving the plain mixture except a moderate decrease in heart rate. Conversely, a mixture with adrenaline added provoked a significant decrease in mean arterial blood pressure by 14% and 17%, in systemic vascular resistance by 24% and 40%, and an increase in cardiac output by 20% and 34% in caudal and thoracolumbar groups, respectively. The adrenaline effect was greater by the thoracolumbar than the caudal approach. In young children, epidural anesthesia induces an increase in cardiac output only when adrenaline is added to local anesthetics, probably through its systemic absorption from the epidural space. IMPLICATIONS: Epidural anesthesia may induce significant hemodynamic changes, well documented in adults. Using noninvasive hemodynamic monitoring in children, we reported an increase in cardiac output and a decrease in arterial blood pressure only when epinephrine was added to epidurally-injected local anesthetics.

Algorithms↗

Failure of continuous cardiac output measurement using the PiCCO Device during induced hypothermia: a case report.

Continuous cardiac output measurement using pulse contour analysis is a technique gaining widespread acceptance in intensive care units. We report a case where a pulse contour analysis computer (PiCCO, Pulsion Medical Systems, Munich, Germany) failed to calibrate in a patient who was undergoing induced hypothermia for anoxic brain injury. Despite several attempts to calibrate, using increased cold injectate volumes and exchanging both the PiCCO device and the arterial catheter, we were unable to correct the calibration problem and hence were unable to monitor cardiac output. Subsequent rewarming of the patient allowed calibration of the arterial waveform and continuous cardiac output measurement. We were unable to find any previous reports of this problem using a PiCCO device, although similar problems with thermodilution cardiac output estimation using the pulmonary artery catheter during hypothermic cardiopulmonary bypass have been documented.

Journal Article↗

Changes of cardiac output during treadmill exercise by impedance cardiography.

Nine athletes and ten nonathletes were selected randomly to study the changes of cardiac function during exercise by impedance cardiography. The speed of the treadmill was maintained at 3.4 mph, and its grade was increased by 1% (Balke protocol). The exercise was continued until the target heart rate (THR), 85% of maximum oxygen uptake (VO2max). The measured parameters for pre- and post-exercise were stroke volume (SV), heart rate (HR), and cardiac output (CO). Average stroke volume of athletes at pre-exercise, 71.1 ml, was higher than that of nonathletes, 64.6 ml, and stroke volume of the former at post-exercise, 97.0 ml, was also higher than that of the latter, 85.2 ml. Therefore, despite the lower heart rate, cardiac outputs of athletes at pre- and post-exercise, 4.98 and 16.3 L/min, were higher than those of nonathletes, 4.87 and 14.2 L/min. For the second phase of the study, cardiac outputs of three subjects were measured during the continuous treadmill exercise with newly developed electrodes and shoes for minimizing motion artifact. Though there were several studies measuring cardiac output during continuous bicycle exercise, this is thought to be the first study in the world measuring cardiac output during continuous treadmill exercise without aid of ensemble averaging.

Adult↗

A continuous cardiac output computer based on thermodilution principles.

A totally self-contained instrument for the measurement of cardiac output is described. The microcomputer controlled instrument is based upon the principles of thermodilution and is capable of making cardiac output determinations on a minute by minute basis. A bolus of heat is delivered to the blood via a resistive heating element wound on the surface of a conventional thermodilution catheter, and the resulting transient pulmonary artery blood temperature increases is monitored with the thermistor located near the tip of the catheter. The performance of the instrument was tested in a mock circulatory loop and in dogs for periods of up to 13 hours. The accuracy and reproducibility of flow determinations made with the system compare favorably with those made with a conventional cardiac output monitor. This study demonstrates the feasibility of a stand-alone cardiac output computer that can provide virtually continuous measurements of blood flow without the intervention of a technician.

Animals↗

The effects of aging after coronary arterial bypass grafting on the regulation of cardiac output during upright exercise.

We examined the effects of age on cardiac performance and the mechanisms that regulate cardiac output during upright exercise in patients free of myocardial ischemia after coronary revascularization. There were 90 subjects, aged 36 to 75 years, of whom 27 were greater than or equal to 60 years. There were no age-related changes in resting heart rate, systolic blood pressure, left ventricular end-diastolic volume index, left ventricular end-systolic volume index, stroke volume index, cardiac index and left ventricular ejection fraction. There were, however, age-related changes in exercise capacity (y = 20 - 0.21x, r = -0.52, P less than 0.001); exercise heart rate (y = 185 - 1x, r = -0.42, P less than 0.001); exercise end-systolic volume index (y = 11 + 0.46x, r = 0.28, P less than 0.01) and exercise ejection fraction (y = 81 - 0.31x, r = -0.28, P less than 0.01). In a subgroup of 54 patients with comparable exercise workload (27 aged less than 60 and 27 greater than or equal to 60 years), the age-related differences in exercise end-systolic volume index, exercise ejection fraction and exercise cardiac index were not observed, but the exercise heart rate was still higher in the younger patients (y = 168 - 0.76x, r = -0.34, P less than 0.01). Thus, age modifies the compensatory mechanisms that regulate the cardiac output during exercise. Young and old patients alike show increases in end-diastolic volume and ejection fraction to maintain exercise cardiac output. The higher exercise heart rate in the younger subjects suggests a decrease in cardiac responsiveness to adrenergic stimulation associated with aging.

Adult↗

Distribution of the increased cardiac output secondary to the vasodilating and inotropic effects of secretin.

Infusion of the peptide secretin augments cardiac output due to vasodilating and inotropic properties. The aim of this investigation was to study how the increased cardiac output is distributed in the peripheral circulation. Before, during and after 15 min infusion of secretin 64 CU kg-1 h-1 flow changes in renal, carotid, femoral and the superior mesenteric arteries were measured by means of electromagnetic flowmetry in anaesthetized dogs. Cardiac output and stroke volume increased by 41 and 27%, respectively, whereas the total systemic resistance fell 35%. The LVdP/dt increased by 35%. After 5 min infusion, renal and carotid flows increased by 62 and 50%, respectively, whereas the femoral flow was only slightly elevated and the superior mesenteric flow unchanged. Both the femoral and the superior mesenteric flow gradually augmented and at the end of the infusion flow was substantially elevated in all four arteries. The study demonstrated that the increased cardiac output by secretin was distributed to all the four arteries, although a preponderance of flow to the renal circulation was indicated. This flow profile may be regarded as favourable in the management of low output conditions.

Animals↗

Relationship between ventricular rate and cardiac output in mimic experimental atrial fibrillation.

In treating atrial fibrillation (AF) the goal of ventricular rate reduction is still not determined. An animal model of AF was developed in which the relationship between ventricular rate and the parameters of cardiac function in AF can be studied. To simulate AF, complete heart block was chemically produced on open-chest dogs. Then, assisted by a portable computer, the ventricles were paced with a series of grossly irregular stimuli of predetermined rates, while atria were paced rapidly (500 beats/min). The resulting electrocardiogram and pressure were indistinguishable from the naturally occurring AF. It was found that in AF with ventricular rates that were lower than that of the control state, cardiac output was decreased. Cardiac output increased and reached a plateau when the ventricular rate increased to the level of the control state and then kept stable up to a rate of 320 beats/min. There was a discrepancy between the effective ventricular rate (rate of beats with pulse pressures > or = 25 mmHg in the femoral artery) and the electrical ventricular rate. When the electrical ventricular rate increased over the control ventricular rate the effective ventricular rate did not increase in a parallel manner. Rather, the effective ventricular rate leveled off at the control ventricular rate. This discrepancy may explain the parallel relationship between the effective ventricular rate and cardiac output.

Animals↗

A longitudinal study of cardiac output in normal human pregnancy.

OBJECTIVE: Our purpose was to investigate the maternal hemodynamic and cardiac structural changes that occur during pregnancy. STUDY DESIGN: Eighteen women underwent serial echocardiography beginning at 8 to 11 weeks' gestation, then at monthly intervals throughout pregnancy and at 6 and 12 weeks post partum. Cardiac output was measured by pulsed- and continuous-wave Doppler at the aortic valve. Left ventricular chamber size, wall thickness, and mass were determined by M-mode echocardiography. Ventricular diastolic function was assessed by Doppler recording of mitral inflow. RESULTS: Cardiac output by pulsed Doppler increased from 6.7 +/- 0.6 L/min at 8 to 11 weeks' gestation to 8.7 +/- 1.4 L/min at 36 to 39 weeks' gestation before falling to 5.7 +/- 0.7 L/min 12 weeks post partum. Heart rate increased 29%, and stroke volume increased 18%. Left ventricular mass increased because of an increase in wall thickness. Peak mitral A wave velocity increased in late pregnancy. Cardiac output by pulsed and continuous-wave Doppler was similar. CONCLUSION: Cardiac output continues to increase even in late pregnancy. Left ventricular mass increases because of increased wall thickness. The mitral flow velocity findings suggested decreased ventricular compliance or increased preload.

Adult↗