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Reservoir and conduit function of right atrium: impact on right ventricular filling and cardiac output.

The purpose of this study was to investigate the relationship between right atrial (RA) reservoir and conduit function and to determine how hemodynamic changes influence this relationship and its impact on cardiac output. In 11 open-chest sheep, RA reservoir and conduit function were quantified as RA inflow with the tricuspid valve closed versus open, respectively. Conduit function was separated into early (before A wave) and late (after A wave) components. The effects of inotropic stimulation, partial pulmonary artery occlusion, and pericardiotomy were tested. At baseline with the pericardium intact, reservoir function accounted for 0.56 (SD 0.13) of RA inflow, early conduit for 0.29 (SD 0.07), and late conduit (during RA contraction) for 0.16 (SD 0.11). Inotropic stimulation decreased conduit function and increased reservoir function, but these effects did not reach statistical significance. With partial pulmonary artery occlusion, early conduit function fell to 0.20 (SD 0.11) (P < 0.04), and the conduit-to-reservoir ratio decreased by 41% (P < 0.03). Similarly, after pericardiotomy, early conduit function fell to 0.14 (SD 0.09) (P < 0.004), reservoir function increased to 0.72 (SD 0.08) (P < 0.04), and, consequently, the early conduit-to-reservoir ratio decreased by 63% (P < 0.006). Cardiac output was inversely related to the conduit-to-reservoir ratio (r = 0.39, P < 0.001). This study demonstrated that the right atrium adjusts its ability to act more as a reservoir than a conduit in a dynamic manner. The RA conduit-to-reservoir ratio was directly related to the right ventricular pressure-RA pressure gradient at the time of maximum RA volume, with increased ventricular pressures favoring conduit function, but it was inversely related to cardiac output, with an increase in the reservoir contribution favoring improved cardiac output.

Acute Disease↗

[The Göttinger minipig as a laboratory animal. 5. Communication: cardiac output, its regional distribution and organ blood flow (author's transl)].

In 16 juvenile minipigs weighing 3.08 kg an average cardiac output of 23 ml/100 g body weight was measured with the dye-dilution method. The microsphere technique was used to assess distribution of cardiac output and organ blood flow. In 12 adult minipigs with a mean body weight of 21.5 kg the cardiac output of 14 ml/100 g body weight was measured with an electromagnetic flowmeter. The values of total systemic and organic blood flow correlated well with those of man and partly with those of other laboratory animals.

Animals↗

Cardiac output and organ blood flow in experimental septic shock: effect of treatment with antibiotics, corticosteroids, and fluid infusion.

Septic shock from intraperitoneal (i.p.) injection of live Escherichia coli bacteria in rats induces marked pathophysiological changes, including 40% decrease in plasma volume (PV), cardiac output, and oxygen consumption with 100% mortality within 24 hr. The present study evaluates cardiac output and organ blood flow before and after treatment of septic shock with an effective antibiotic (AB), plasma volume (PV) expansion, and corticosteroids (CS), alone and in combination. Treatment was initiated at 5.5 hr after bacterial injection, at a time when AB therapy did not improve 24 hr survival rate. Cardiac output decreased from 28.6 +/- 3.1 (SD) to 15.4 +/- 2.8 ml/min/kg (P less than .01) in septic rats concomitant with redistribution of blood flow from carcass to the heart, brain, intestines, liver, and adrenal glands. Absolute arterial blood flow increased only to the adrenal glands and the liver to 158% (P less than .01) and 167% (P less than .01) of control values, respectively. AB, CS, and Ringer's lactate (RL) alone or in combination did not significantly improve any organ blood flow compared to untreated septic animals but increased survival significantly to about 60% (P less than .01). Albumin (ALB) and CS in combination expanded PV to 138% (P less than .01), restored cardiac output to 100%, and achieved supranormal blood flow values to the brain (109%), liver (125%), small intestine (147%) (P less than .01), and kidneys (190%) (P less than .01) of preshock levels. More importantly, survival at 24 hr was 90% (9/10) (P less than .001). It is concluded that a colloid diluted in an electrolyte solution, combined with CS, and an effective antibiotic agent are necessary therapeutic ingredients for the successful recovery of experimental E. coli sepsis.

Adrenal Cortex Hormones↗

The distribution of cardiac output in the anaesthetized spontaneously hypertensive rat.

1. Radioactive 15 micrometer and 50 micrometer diameter microspheres were used to determine cardiac output, its regional distribution and tissue blood flow in adult normotensive Wistar and Okamoto spontaneously hypertensive rats. 2. Cardiac output in the spontaneously hypertensive rats was the same as in Wistar normotensive rats, but its distribution in the hypertensive rats appeared to differ: there was a significant increase in the proportion of microspheres trapped in the liver whereas fewer were found in the gastrointestinal tract. This indicates that a greater fraction of the cardiac output passes along the hepatic artery and less through the splanchnic bed. 3. Blood flow in skin and skeletal muscle in spontaneously hypertensive rats was approximately 50% of that in Wistar normotensive rats.

Animals↗

Determination of cardiac output and other reference physiology parameters in lightly anesthetized dogs.

1. Cardiac output; arterial, pulmonary artery, central venous and pulmonary wedge pressures; heart rate, hematocrit, and plasma sodium and potassium; arterial and mixed venous blood gases; and respiratory rates were measured in 45 mixed sex, non-pregnant, clinically normal mongrel dogs of 8-30 kilograms body weight following light anesthesia with halothane/50% N20-02. 2. Arithmetic means and standard deviations were calculated to develop tables of reference values. 3. Mean measured cardiac outputs were found to be 31-59% higher in these dogs than the values indicated by published standards; cardiac indices were 30-44% higher; heart rates were 16-30% lower; calculated stroke volumes were 60-112% greater; and total peripheral resistances were 35-57% less than the standard published values. 4. All other measured or calculated parameters fell within previously published canine or human reference limits.

Anesthesia, General↗

Prostaglandins and fetal cardiac output distribution in the lamb.

With the use of a triple thermodilution technique in 17 fetal lambs, combined with microsphere estimations in 7, the effects of indomethacin prostaglandin (PG) I2 and PGE2 on cardiac output and its distribution were measured. Indomethacin (0.2 mg/kg) induced a main pulmonary artery-to-aorta pressure gradient, which peaked within 45-60 min and persisted for 2-3 h. PGE2 abolished this gradient (threshold 50 ng X kg-1 X min-1), while PGI2 in doses up to 100 ng X kg-1 X min-1 increased it. Indomethacin did not change total cardiac output but altered its distribution (right ventricular output, left ventricular output) and increased the percentage of right ventricular output flowing to the lungs. Ductal flow decreased concomitantly. After indomethacin, PGI2 further decreased ductal flow, increased pulmonary flow, and decreased pulmonary vascular resistance. PGE2 restored the original right ventricular-to-total cardiac output ratio, although ductus flow did not return to base-line levels. Pulmonary resistance increased slightly, reflecting decreased pulmonary flow, associated with decreased right ventricular output. Thus PGE2 was more effective on the ductus than on the pulmonary circulation. PGI2 did not relax the ductus but was a potent pulmonary vasodilator. Neither PGI2 nor PGE2 nor indomethacin changed total cardiac output but all altered its distribution.

Animals↗

Cardiac output requirements and maximum dimensions for a neonate total artificial heart.

Two equally important issues need to be addressed during the early stages of the design of an implantable total artificial heart (TAH): proper anatomical fit and cardiac output capacity. As part of a first-time feasibility study to develop a neonate-size TAH, two studies were conducted to establish useful anatomical and physiological standards. The first (Study A) was conducted to determine the maximum dimensions of a neonate-size TAH. Twelve preserved hearts from full-term neonates with the hypoplastic left heart syndrome were examined. A second study (Study B) was designed to determine the acceptable minimum stroke volume compatible with minimum neonate cardiac output requirements. This study was based on a combination of: a) reported cardiac output studies in healthy term neonates, and term neonates with heart failure, b) body weight range, and c) limiting factors of TAH technology, e.g., valvular regurgitation and leveling off of the maximum cardiac output value at a specific heart rate and filling pressure. The proposed neonatal standards for TAH technology are presented.

Cardiac Output↗

Aortic flow velocity indices during upright exercise: reliability and relationship to cardiac output.

OBJECTIVE: To determine the intra- and interobserver reproducibility of Doppler-derived ascending aortic flow velocity measurements at rest and during upright exercise of increasing intensity; and to determine the relationship between Doppler-derived measurements and cardiac output obtained by the indirect Fick carbon dioxide rebreathing method in the same conditions. SUBJECTS: Twenty young healthy adults participated in the study; eight participated in the first part and 12 in the second. DESIGN: For the intra-observer study, subjects were submitted to three workloads (50, 100 and 150 W) of 5 mins duration on two occasions, seven days apart. The intra-observer reproducibility was determined by two technicians taking the Doppler measurements within 90 s during the steady state of each workload during the first session. The relationship between cardiac output and aortic flow velocities was studied by measuring cardiac output by carbon dioxide rebreathing and flow velocities by continuous wave Doppler ultrasound simultaneously at rest as well as during the last minute of the three workloads (50, 100 and 150 W) of 5 mins duration. RESULTS: The interobserver reproducibility was very good, with r values of 0.87 for peak velocity (PV) and 0.97 for peak acceleration (PA). The intra-observer reproducibility at the seventh day interval showed r values of 0.93 for PV and 0.96 for PA for one of the technicians. PV and PA of the ascending aortic flow correlated well with cardiac output (r = 0.85 and 0.82, respectively, P < 0.01). ANOVA showed that PV and PA increase proportionately with exercise intensity. CONCLUSION: PV and PA of ascending aortic flow are reproducible and reflect changes in left ventricular function during exercise.

Adolescent↗

Changes of organ blood flow and cardiac output after imidazole administration.

Effects of imidazole, an inhibitor of thromboxane synthesis (10 mg/kg bw., iv.) on the distribution of cardiac output and intrarenal hemodynamics were investigated in normovolemic (free water and salt uptake before the experiment) narcotized rats. The cardiac output was measured on the basis of the Stewart-Hamilton principle, the blood flow of the organs by the Sapirstein method. 86Rb was used as indicator. One hour following the imidazole administration while mean arterial blood pressure remained constant a slight drop in the cardiac output (CO) was observed (CO-control: 24.1 +/- 4.77; CO-imidazole: 20.6 +/- 2.40 ml/min/100 g; p < 0.05) and total peripheral resistance increased (TPR-control: 42.3 +/- 9.27; TPR-imidazole: 48.3 +/- 7.05 R; p < 0.05). The vascular resistance in the heart, lungs (bronchial fraction), liver, spleen, intestine and adrenal glands remained unchanged. The blood flow of the skin and skeletal muscle decreased moderately, their vascular resistance increased following imidazole treatment. Inhibition of the thromboxane synthesis did not influence the renal and intrarenal (cortex and medulla) circulation, the percentile distribution of the intrarenal blood flow remained unchanged. The results suggest that TXA2 does not play a definite role in maintaining the a) vascular tone (blood flow) of different organs b) intrarenal hemodynamics (salt and water excretion) in normovolemic rats.

Animals↗

High Doppler-derived cardiac output in the cerebral arteriovenous fistula measured by pulsed Doppler ultrasound.

Cerebral arteriovenous fistula may cause a significant increase in cardiac output. So far, the right ventricular output measurement with conventional cardiac output methods has been difficult in newborn infants because of the shunts through the foramen ovale and patent ductus arteriosus. This difficulty can be avoided by measuring left ventricular output with the pulsed Doppler ultrasound method. In our case, the patient was a newborn infant with large patent ductus arteriosus and an arteriovenous malformation of the great cerebral vein of Galen. The malformation was found by noticing a loud murmur from the infant's head. The diagnosis was later confirmed by ultrasound scanning and a computer tomography. Left ventricular output was enormous with values from 740 to 830 ml/min/kg, when the normal value for the newborn infant at this age is 260 ml/min/kg. Because of constant cardiac failure, the malformation was operated on. The infant died of cardiac failure during this operation. An enormous left ventricle output in an infant with arteriovenous fistula and patent ductus arteriosus predisposes to cardiac failure. The Doppler ultrasound method in newborn infants seems to be a useful tool to determine cardiac function.

Blood Flow Velocity↗

Recurrence of hypertension in primary aldosteronism after discontinuation of spironolactone. Time course of changes in cardiac output and body fluid volumes.

Hemodynamic mechanisms underlying the hypertensive action of long-standing sodium overload were studied in ten subjects with aldosterone-producing adenoma. Arterial pressure was 129+/-4/91+/-4 mm Hg (mean+/-SEM) during spironolactone treatment, 177+/-5/114+/-3 mm Hg six weeks after the drug had been stopped, and 136+/-4/94+/-3 mm Hg two months after operation. In the six weeks following cessation of spironolactone, cardiac output, stroke volume, blood volume and sodium space were determined at weekly intervals. In each subject the biochemical syndrome of aldosterone-excess had been fully developed in two weeks. The hemodynamic changes in that period were also uniform. Mean arterial pressure in week 2 was increased by 20+/-3% with parallel increments of cardiac output and stroke volume of 22+/-5 and 30+/-6%. Blood volume and sodium space were increased by 11+/-2 and 29+/-4%. The patterns in weeks 2-6 were not uniform. In five subjects (age 33-49 yr) the hypertension was maintained through increased cardiac output; in week 6 it was 34+/-7% above its initial value, and stroke volume and blood volume were 37+/-4 and 16+/-4% above control. In the remaining five subjects (age 50-60 yr) cardiac output, stroke volume and blood volume returned to their initial values, and total peripheral resistance in week 6 was 36+/-13% above control. Sodium space remained expanded in both groups. The measurements after surgery confirmed the existence of the high-flow and high-resistance patterns; there was a decrease in cardiac output in the former group of subjects and a decrease in resistance in the latter. Apparently, increased resistance is not a direct consequence of increased flow. The observed age-related differences in hemodynamic patterns of sodium overload bear some resemblance to essential hypertension where a high-flow state of long duration may precede the ultimate phase of low vascular capacitance and high resistance.

Aldosterone↗

Measurement of cardiac output by thermodilution in pediatric patients.

Thermodilution systems for the measurement of cardiac output constitute a reliable and relatively noninvasive method which is ideal for small patients, particularly infants and small children. Thermodilution is an important new advance in the monitoring of critically ill children in that it measures cardiac output directly.

Adolescent↗

Automatic cardiac output measurement (ACOM): clinical applications of a new noninvasive tool.

This study sought to validate a new noninvasive method to measure cardiac output, in the clinical setting, using color Doppler flow integration. This method, the automatic cardiac output measurement (ACOM), using color Doppler was recently developed and validated in vitro. ACOM was performed at the aortic valve and in the left ventricular outflow tract in 106 subjects (60 men, mean age 52 +/- 18) and compared with the echocardiographic pulsed-wave Doppler and a 2-D volume method. In 14 patients the noninvasive methods were correlated with the thermodilution technique. ACOM was feasible in 101 subjects (95%). The correlation factor between the values obtained with ACOM in the apical 5-chamber view and apical long-axis view was 0.75 at the aortic valve and 0.74 in the left ventricular outflow tract. Interoperator variability for ACOM in the apical 5-chamber and apical long-axis views were 0.93 and 0.75, respectively. The best comparison of ACOM with the pulsed-wave echo-Doppler technique occurred in the apical long-axis view (n = 79, r = 0.62), whereas the correlation with the 2-D volume method was poor. The most favorable comparison of ACOM with the thermodilution technique (n = 14) was also obtained in the apical long-axis view (5.408 +/- 1.72 vs. 3.356 +/- 1.281/min. [mean +/- SD], r = 0.71). Assuming the thermodilution technique as 'gold standard', the pulsed-wave echo-Doppler technique showed a better correlation (5.408 +/- 1.72 vs. 4.664 +/- 1.281/min., r = 0.84). ACOM is a useful, reproducible, noninvasive tool for rapid automated measurements of cardiac output. There is, however, an underestimation when compared with the pulsed-wave Doppler echocardiography and the thermodilution techniques. Good 2-D echocardiographic images, adequate color filling of the outflow tract and high frame rates are prerequisites for accurate values. Further refinements of this new technique are needed to enhance its clinical value in the future.

Cardiac Output↗

Effect of acute blood volume expansion on cardiac output, plasma dopamine beta-hydroxylase, and renal function in rats with chronic constriction of the ascending aorta.

To examine the effect of raised left atrial pressure (AP) on the relationship of cardiac output to renal function, we constricted the ascending aorta in rats (AC) and 1-6 months later tested their response to acute volume expansion (VE) with blood (2% body weight, iv). Sham-operated (SH) rats were controls. In AC rats heart weight increased 38%, but cardiac output was 47% lower. Statistically significant differences in the initial clearance periods were (AC vs. SH): venous pressure (VP) 8 +/- 2 vs. 3+/- 1 cm H2O; inulin clearance (CIN) 0.61 +/- 0.06 vs. 0.84 +/- 0.04 ml/min; sodium excretion (UNAV) 1.2 +/- 0.2 vs. 2.1 +/- 0.3 muequiv./min. Filtration fraction, fractional UNaV, mean arterial pressure (MAP), and plasma dopamine beta-hydroxylase (DBH) were the same in both groups. After VE, cardiac output increased proportionately more in AC (69% vs. 27%); however, the absolute increases were not different. UNaV increased proportionately more in AC rats, but the absolute increase was less (5.1 vs. 7.5 muequiv./min). Multiple variable regression analysis showed that UNaV correlated with CIN, MAP, and VP, with no difference between AC and SH animals. Cardiovascular-renal relationships were indistinguishable from previous descriptions of dogs and rats with chronic vena caval constriction. Modulation of renal function by left AP was not apparent. In both groups after the peak response to VE, UNaV decreased in association with decreased cardiac output and increased sympathetic nervous activity as indicated by raised DBH levels. After VE, VP remained high in AC but not in SH animals.

Animals↗

Regulation of cardiac output during aldosterone-induced hypertension.

The classical haemodynamic transients of volume-loading hypertension have been difficult to demonstrate in aldosterone-induced hypertension. Because recent studies have shown that continuous whole-day measurements of cardiac output are superior to short-term recordings, we studied the transient haemodynamic effects of aldosterone-induced hypertension while monitoring arterial pressure and cardiac output (electromagnetic flow probe) continuously for 20 h a day. In six dogs maintained on a fixed sodium intake of 150 mmol/day, we infused aldosterone (12 micrograms/kg per day, intravenously) for 10 days. The aldosterone induced a progressive increase in mean arterial pressure, from a control value of 88 +/- 1 to 107 +/- 2 mmHg. Cardiac output increased progressively, reaching a peak average value on the 4th day of infusion of +14 +/- 5% above control, and remained slightly elevated throughout the infusion period. Total peripheral resistance increased slowly to a value averaging +13 +/- 4% above control. Therefore, our experiments show that aldosterone induces a primary increase in cardiac output followed by a secondary vasoconstriction, which is consistent with the classical transient haemodynamic effects of volume-loading hypertension.

Aldosterone↗

Comparison of cardiac output determined by a carbon dioxide-rebreathing and direct Fick method at rest and during exercise.

1. To study the validity of a CO2-rebreathing method at rest and during graded exercise, cardiac output was measured simultaneously on 59 occasions in 16 subjects with normal pulmonary function with the CO2-rebreathing method and the direct Fick method for oxygen. The correlation coefficient between the results of both methods was significantly higher during exercise than at rest. 2. No systematic difference was shown between (a-v)CO2 content difference determined on whole blood and end-tidal gas, which justified the exclusion of a correction factor for blood to alveolar gas PCO2 gradients. 3. In the calculation of cardiac output by the direct Fick method for CO2 and by CO2 rebreathing, a standard CO2 dissociation curve was preferred to a synthetic CO2 dissociation curve, constructed by allowance for changes in haemoglobin concentration, pH and oxygen saturation. The latter curve tended to increase values for cardiac output and induced a large dispersion around the line of identity, when compared with simultaneous cardiac output estimates by the direct Fick method for oxygen.

Adult↗

The measurement of cardiac output by electrical impedance plethysmography in pregnancy. Are the assumptions valid?

The assumptions of the Kubicek technique for measurement of cardiac output by detection of changes in the chest wall electrical impedance have been re-examined. The fall in cardiac output in the latter half of pregnancy which Crawford's group calculated using the Kubicek technique can be almost entirely accounted for by a fall in the term dZ/dT of the Kubicek equation, as pregnancy progress. One key assumption of the Kubicek technique is a constant ejection flow rate equal to the initial flow as the pulmonary valve opens, which is multiplied by the estimated ejection time to obtain stroke volume. Initial flow rate is represented by the term dZ/dT in the Kubicek equation. Although this assumption has been shown to give a reasonable correlation with other techniques for measurement of cardiac output in the non-pregnant state, this may not be so for longitudinal studies in pregnancy because of the changes in lung mechanics and in the circulation which occur in this state. Crawford's data emphasizes the necessity for validating the Kubicek technique very critically during pregnancy.

Cardiac Output↗