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Determination of cardiac output by first passage radiocardiography: theoretical considerations and phantom studies.

Non-invasive determination of cardiac output by aid of precordial first passage radiocardiography may prove a useful tool in the management of cardiac disorders. The basic concepts of a method together with theoretical assumptions necessary for the clinical application of the method are described. The principle of the technique was tested in a cardiac phantom model with adjustable stroke volume and heart rate, in which background problems were avoided. First passage radiocardiography gave highly accurate cardiac output determinations compared with the 'true' phantom values, r = 0.998 (p less than 0.001).

Cardiac Output↗

Noninvasive cardiac output determined with a new method based on gas exchange measurements and carbon dioxide rebreathing: a study in animals/pigs.

A system has been designed to determine cardiac output noninvasively. The system's main component is a closed breathing circuit and it measures oxygen uptake (VO2), carbon dioxide elimination (VCO2), and end-tidal CO2 partial pressure (PET). As an integral part of the system, periods of CO2 rebreathing can be automatically implemented. The CO2 partial pressure of oxygenated mixed venous blood (Pv) is obtained from the measured exponential rise of the PET value during such a CO2 rebreathing maneuver. A new method is described for estimating the pulmonary blood flow, alveolar ventilation, cardiac output (CO), and mixed venous oxygen saturation (SVO2) from PV, PET, VO2, VCO2, tidal volume, and arterial oxygen saturation. The method was evaluated in 6 anesthetized and mechanically ventilated pigs. A wide range of cardiac output, shunt fractions, and dead space to tidal volume ratios were induced by combinations of bronchoalveolar lavage, hypervolemia, hypovolemia, and variable levels of positive end-expiratory pressure (PEEP). The bias between the CO obtained with the noninvasive technique (CO L/min) and the thermodilution CO (Qt L/min) was 0.13 L/min (SD = 0.78 L/min) and the correlation was N = 64; R = 0.92; CO = 0.95*Qt + 0.38. The bias obtained for double determinations with the noninvasive CO technique was 0.3 L/min (SD = 0.5 L/min). The bias between the noninvasive estimates of Svo2 and the directly measured values was 1.1% (SD = 9.3%). For double determination with the noninvasive technique the bias was -0.9% (SD = 4.7%). It is concluded that in mechanically ventilated pigs the proposed method produces good estimates of CO and SVO2 also in the presence of significant ventilation/perfusion mismatch.

Anesthesia, Closed-Circuit↗

Different response of oxygen consumption and cardiac output to various endogenous and synthetic catecholamines in awake dogs.

OBJECTIVE: To determine whether catecholamines with different adrenergic receptor affinities are characterized by individual relationships between cardiac output (Q) and oxygen consumption (VO2). DESIGN: Comparison of the dose-effect relationships and Q/VO2 relationships of four different catecholamines in the same awake dogs. SETTING: University research department of experimental anesthesiology. SUBJECTS: Ten trained, healthy dogs in the basal metabolic state with chronically implanted ultrasonic flow transducers around the pulmonary artery for the continuous measurement of cardiac output. INTERVENTIONS: Increasing doses of norepinephrine, epinephrine, dobutamine, or dopexamine were infused in a randomly varied sequence on separate days until VO2 and Q reached a maximum. MEASUREMENTS AND MAIN RESULTS: VO2 was measured by indirect calorimetry, and Q was measured via the pulmonary artery by ultrasonic flowmetry. In healthy dogs, catecholamines increased both VO2 and Q in a dose-dependent manner until a plateau was reached when VO2 had doubled and Q had quadrupled compared with baseline conditions. Regardless of the catecholamine, the resulting Q/VO2 relationships were linear up to the maximal effects, but their slopes (s) differed significantly between agents (p < .05, paired sign test) and increased approximately three-fold in the order norepinephrine (s = 34), epinephrine (s = 54), dobutamine (s = 86), and dopexamine (s = 105). Except for norepinephrine, the catecholamines also increased oxygen delivery more than VO2, so that O2 extraction decreased to 40% below baseline. CONCLUSIONS: Catecholamines are characterized by linear Q/VO2 relationships with drug-specific slopes. All agents (except norepinephrine) increased oxygen delivery more than oxygen demand. For the practice of catecholamine therapy, our experiments imply that synthetic agents such as dobutamine and particularly dopexamine may be preferred in the treatment of low cardiac output states because they increase Q with the least metabolic effects.

Adrenergic Agonists↗

Low cardiac output abolishes cardiovascular responses to infra-renal aortic cross-clamping in the pig.

BACKGROUND: Previous data suggest that preoperative myocardial dysfunction is associated with an altered cardiac response to infra-renal aortic cross-clamping (AXC). This study was designed to further explore how acute reductions in stroke volume and cardiac output influence the systemic, preportal and renal circulatory responses to AXC. METHODS: In chloralose-anesthetized normoventilated pigs, graded increases in pericardial pressure (PPERICARD) were obtained by local infusions of dextran. Measurements included cardiac output (CO, thermodilution), mean blood pressure proximal to the aortic clamping site (MAPPROX) and ultrasonic flowmetry for portal (QPORT) and renal (QREN) blood flows. In all animals, measurements were made a) prior to AXC, b) at the end of a 5 min AXC period and, c) 5 min following declamping. These recordings were repeated during control (PPERICARD 0 cmH2O) and during stages with increased PPERICARD (4 and 8 cmH2O, respectively). RESULTS: Pericardial infusions of dextran produced hemodynamic responses that in magnitude were proportional to PPERICARD levels. Stroke volume, CO and mean arterial pressure decreased, while systemic vascular resistance (SVR) increased. In the preportal tissues, vascular resistance increased and QPORT decreased. Similarly, in the kidney, vascular resistance and QREN decreased, but only at a PPERICARD of 8 cmH2O. At control, AXC increased SVR, MAPPROX, QPORT and both renal and preportal vascular resistances. When PPERICARD was increased to 4 cm H2O, the responses to AXC concerning SVR and MAPPROX were not significantly altered, while renal and preportal circulatory responses were blunted. At stages with a PPERICARD of 8 cmH2O, we could not demonstrate any circulatory responses to AXC. CONCLUSIONS: AXC-induced systemic, preportal and renal circulatory responses are inhibited during a condition of acutely lowered cardiac output.

Animals↗

Hyperpyrexia complicating low fixed cardiac output.

A 41-year-old woman with end-stage mitral and aortic stenosis developed the cycle of low cardiac output, peripheral vasoconstriction, increased core temperature, and cardiac decompensation. This was interrupted by core cooling utilizing iced gastric lavage. We propose that her severe hyperthermia was caused or abetted by her low cardiac output.

Adult↗

Effect of an increase in cardiac output on the in vivo C02 titration curve of mixed venous blood.

The slope of the in vivo CO2 titration curve of blood (pH-[HCO3-]p relationship, in vivo slope, unit: slyke) expresses the buffering capacity of blood for CO2 in vivo or the buffering capacity of extracellular fluid for CO2. It depends on the extent of contributions by chemical and physiological buffering processes for CO2 occurring during CO2 titration. Theoretically, the in vivo slope obtained for mixed venous blood is independent of cardiac output during CO2 titration. The present study was attempted to confirm this theoretical concept experimentally. Anesthetized dogs were allowed to breathe air and then 10% CO2-25% 02 in N2 for 60 min for the titration in vivo. During the CO2 breathing period the legs were exercised through direct electrical stimulation of the muscles; this also induced an increase in cardiac output 130% above the air breathing period. The in vivo slope (delta[HCO3-]p/delta/pH-]p/"pH) of the mixed venous blood at an apparent steady state in the CO2 breathing period was 16 slyke, which was 5 slyke higher than in other dogs breathing CO2 at rest with a 60% increase in cardiac output observed in our previous study. This finding was discussed in relation to a greater contribution of tissue fluid for buffering of CO2. The present study suggests that cardiac output is a significant determinant of the buffering capacity of extracellular fluid.

Acid-Base Equilibrium↗

Role of the Frank-Starling mechanism in maintaining cardiac output during increasing levels of treadmill exercise in beta-blocked normal men.

To determine the effects of beta blockade on hemodynamics during increasing levels of treadmill exercise, 10 healthy volunteers were studied after 1 week of placebo, and then after 1 week of treatment with oral propranolol, 80 mg twice daily, or dilevalol, 400 mg once daily. The study was randomized and double-blind, with a crossover sequence. Hemodynamics were measured by CO2 rebreathing at rest and at 25, 50, 75 and 100% of VO2 max. After placebo, cardiac output increased from 5.8 +/- 2.1 (rest), to 19.4 +/- 6.4 liters/min (100% VO2 max), mainly due to an increase in heart rate from 84 +/- 6 to 169 +/- 15 beats/min. Stroke volume increased from 70 +/- 27 (rest), to 137 +/- 65 ml (25% VO2 max), and then leveled off to 116 +/- 41 at 100% VO2 max. After both beta blockers, exercise cardiac output was maintained at 100% VO2 max: 20.1 +/- 9.3 liters/min with propranolol and 19.1 +/- 8.6 with dilevalol. However, a significant reduction versus placebo values was observed for cardiac output at 25% VO2 max, from 13.7 +/- 5.9 during placebo, to 9.4 +/- 2.5 during propranolol, and to 9.6 +/- 2.3 during dilevalol (both p less than 0.01 vs placebo). Maintenance of cardiac output with both beta blockers at higher levels of exercise came from an increased stroke volume (p less than 0.05 vs placebo), while heart rate (in beats/min) was greatly reduced (propranolol 61.6 +/- 9.4 rest, 90.1 +/- 10.7 at 100% VO2 max; dilevalol 70.8 +/- 6.4 rest, 99.2 +/- 11.8 at 100% VO2 max, p less than 0.01 vs placebo for each).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗

Decreased cardiac output in infants of mothers who abused cocaine.

Cocaine increases the level of circulating catecholamines by blocking the catecholamine reuptake receptors. The effect of intrauterine cocaine exposure on cardiac output was studied in 15 full-term newborn infants whose mothers used cocaine during pregnancy. A total of 22 healthy nonexposed full-term infants served as a control group. On the first day of life, cardiac output (183 +/- 12 vs 235 +/- 13 mL/kg per minute, mean +/- SD; P less than .05) and stroke volume (1.3 +/- 0.1 vs 1.9 +/- 0.1 mL/kg, mean +/- SD; P less than .005) were lower and arterial blood pressure (60 +/- 2 vs 41 +/- 2 mmHg, mean +/- SD; P less than .001) higher in the infants exposed to cocaine. On day 2, cardiac output, stroke volume, and mean arterial blood pressure were similar, probably because of the gradual excretion of cocaine and its metabolites by the infant. It was speculated that an increase in plasma norepinephrine levels is responsible for the cardiovascular effects of intrauterine cocaine exposure.

Blood Pressure↗

Attenuation correction of equilibrium radionuclide angiography for noninvasive quantitation of cardiac output and ventricular volumes.

Gated equilibrium radionuclide angiography (RNA) provides count information which is proportional to ventricular volumes. In order to convert ventricular count data directly to accurate absolute volumes, we performed attenuation correction on equilibrium radionuclide angiograms by means of a simple geometric method of attenuation distance quantitation. Attenuation distance defined during imaging agreed with similar measurements obtained during fluoroscopy (r = 0.86). In seven patients, 23 simultaneous cardiac output determinations by Fick and radionuclide imaging techniques showed excellent correlation over a wide range of cardiac outputs (r = 0.91). Radionuclide angiographic ventricular volumes correlated with contrast angiographic ventricular volumes in 28 patients (r = 0.80). The weaker correlation found for ventricular volume data may be due to inaccuracies in ventricular volume calculation when single-plane contrast angiography is applied to patients with wall motion abnormalities. We conclude that attenuation-corrected RNA allows direct calculation of cardiac output and ventricular volumes in individual patients without use of regression equations.

Cardiac Catheterization↗

Body, eye, and chorioallantoic vessel growth are not dependent on cardiac output level in day 3-4 chicken embryos.

Normal aerobic metabolic rates persist in the early chicken embryo after elimination of cardiac output, but the dependence of tissue growth and differentiation on blood flow is unknown in these early stages. We partially ligated (25-50% occlusion) the ventricular outflow tract of Hamburger-Hamilton stage (HH) 16-18 embryos, producing a wide range of cardiac output. For the next approximately 48 h (to HH 24), we measured heart rate (HR), stroke volume (SV), and cardiac output (CO), as well as these growth indicators: eye diameter, chorioallantoic vessel density, and body mass. Acutely, HR declined with partial ligation (from 108 to 98 beats/min). Paradoxically, SV and CO decreased sharply in most embryos but increased in others, collectively producing the desired large variation (up to 25-fold) in CO and permitting assessment of tissue growth over a very large range of blood perfusion. Eye diameter doubled (from 0.6 to 1.2 mm) with development from HH 16 to HH 24, but within a developmental cohort there was no significant correlation between eye diameter and CO over a 25-fold range of CO. Similarly, chorioallantoic membrane vessel index was independent of CO over the CO range at all stages. Finally, body mass increase during development was not significantly affected by partial conal truncal ligation. Collectively, these data suggest that normal eye and vessel growth and body mass accumulation occur independent of their rate of blood perfusion, supporting the hypothesis of prosynchronotropy-that the heart begins to beat and generate blood flow in advance of the actual need for convective blood flow to tissues.

Allantois↗

Atrial natriuretic peptide, plasma renin activity, plasma volume, systemic vascular resistance and cardiac output in patients with cirrhosis.

The present study aimed to assess relationships between plasma levels of atrial natriuretic peptide (ANP) and plasma volume, systemic vascular resistances, cardiac output and plasma renin activity in patients with cirrhosis. Thirty patients were included: eight with no history of liver disease were used as controls; 22 patients had biopsy-proven alcoholic cirrhosis without ascites (n = 11) and with ascites (n = 11). Mean ANP plasma level was significantly higher in both groups of cirrhotic patients than in controls (P less than 0.05). In the control group, ANP and plasma renin activity were inversely correlated (P less than 0.05) but no correlation was found in cirrhotic patients. In the group of patients with ascites, ANP plasma levels were inversely correlated to plasma volume (P less than 0.05) and to cardiac output (P less than 0.01) and directly correlated to systemic vascular resistances (P less than 0.01). Using multiple regression analysis, ANP remained correlated only with systemic vascular resistances (P less than 0.05). These results suggest that cirrhotic patients have high plasma levels of ANP whether or not they have ascites. In the light of current knowledge of ANP actions, the relationships between ANP plasma levels and plasma volume, cardiac output, and systemic vascular resistances are paradoxical in cirrhotic patients with ascites. ANP does not seem to play a critical role in the pathogenesis of sodium and water retention observed in these patients.

Ascites↗

Oscillations in stroke volume and cardiac output arising from oscillatory ventilation in humans.

Oscillations in the cardiovascular system have been observed in patients with periodic breathing. It is not clear whether these are driven by primary oscillations in the respiratory system or whether an intrinsic cardiovascular instability is required, as previous studies with subjects performing voluntary periodic breathing have failed to produce the cardiovascular oscillations. We investigated whether cardiovascular oscillations occurred in healthy controls performing voluntary periodic breathing. Six healthy subjects performed voluntary periodic breathing with guidance from a real-time computer display. We measured ventilation, end-tidal partial pressures of O2 (PO2) and CO2 (PCO2), heart rate, blood pressure (BP), arterial oxygen saturation and stroke volume and cardiac output by transthoracic impedance cardiography. Fourier analysis was used to quantify the size and phase of the periodic breathing-induced oscillations in these parameters. Periodic breathing (amplitude 30% of mean ventilation) induced oscillations in end-tidal PO2 (amplitude 0.8 kPa), end-tidal PCO2 (amplitude 0.3 kPa), R-R interval (amplitude 32.6 ms), systolic BP (amplitude 3 mmHg), diastolic BP (amplitude 3 mmHg), stroke volume (amplitude 8.0 ml, mean 79.5 ml) and cardiac output (amplitude 0.6 1, mean 5.9 l x min(-1)). The oscillations in stroke volume and cardiac output were nearly in phase with ventilation, with their peaks occurring 5.6 and 6.1 s, respectively, after the peak in ventilation. An oscillatory ventilatory pattern entrains the cardiovascular system in healthy controls into fluctuations, not only in heart rate and BP, but also in stroke volume and cardiac output.

Adult↗

Evaluation using dogs of a method for estimating cardiac output from a single breath.

We have evaluated the single-breath method of Kim, Rahn, and Fahri (J. Appl. Physiol. 21: 1338, 1966) using anesthetized dogs (avg wt 26 kg). The systematic error was determined by comparing the single-breath estimates of cardiac output with values obtained by the dye-dilution method. In some dogs the effects of moderate exercise were stimulated by joining the circulations of two dogs. From paired estimates, the random error of the single-breath method was +/- 12% (95% tolerance limits; 23 pairs) over a range of outputs 1.1-5.0 l/min. There was no significant difference between values of cardiac output by the single-breath method and by dye dilution, and in four dogs the dye-dilution values were not significantly different from values of pulmonary blood flow controlled by perfusion. These results indicate that under carefully controlled conditions the single-breath method is capable of providing reliable estimates of cardiac output.

Animals↗

[The low cardiac output syndrome after valve-conserving operations under hypothermia without perfusion].

Under study were the frequency of occurrence and causes of development of the syndrome of low cardiac output after the saving correction of mitral defects under conditions of cranio-cerebral (1st group-80 patients), general moderate (2nd group-130 patients) and deep hypothermia (open mitral commissurotomy-3rd group of 134 patients and reconstructive operations on the mitral valve-4th group of 104 patients). Frequency of development of the complication was reliably higher in groups with deep hypothermia (1.25% of patients in the 1st group, 9.2% in the 2nd group, 27.6% in the 3rd group, 25% in the 4th group). Factors influencing the development of the low cardiac output syndrome in patients of the 2nd group was duration of the disease, in the 3rd group patients-the class according to the classification of the New York cardiological association and age of the patient, in operated patients of the 4th group it was the value of the cardio-pulmonary coefficient. Pharmaco-ice-chip cardioplegia used in patients of the 3rd and 4th groups failed to decrease frequency of the development of the low cardiac output syndrome in the postoperative period.

Adult↗

Measurement of cardiac output by computed transmission tomography.

The capability of computed tomography (CT) scanning to measure cardiac output was explored using ten anesthetized dogs, and the results were compared with those obtained by thermodilution. Dynamic CT scans were performed at the level of the aortic root while small peripheral intravenous boluses of contrast medium were injected. Time/density curves were generated using a gamma variate fitting program. These were used to estimate cardiac output by applying indicator dilution principles. CT results correlated favorably (r = 0.86) with those of thermodilution. This feasibility study indicates the utility of CT for obtaining physiologic measurements of cardiac function and should encourage further studies to develop the potential of CT for cardiovascular diagnostic purposes.

Animals↗

Influence of cardiac output, injection time and injection volume on the initial mixing of drugs with venous blood after i.v. bolus administration to sheep.

The aim of this study was to quantitate factors affecting the initial "peak" of the pulmonary artery (PA) drug concentrations after i.v. bolus drug administration, which is a determinant of the subsequent drug uptake into both the lungs and other well-perfused organs. Indocyanine green (ICG) was used as a marker drug in anaesthetized (1.5% halothane) sheep prepared with an inferior vena cava injection catheter and a large-gauge pulmonary artery blood sampling catheter. For three ranges of cardiac output, 2.5-mg doses of ICG were injected in the following combinations: 10 ml injected over 1, 5 or 10 s; 5 or 25 ml injected over 1 s. On-line PA ICG concentrations were recorded for approximately 60 s using a densitometer. The mean maximum PA ICG concentrations (2-8 mg litre-1), the mean times at which they occurred (7-18 s after injection) and the time lags before ICG was detected in the PA (4-9 s), were inversely related to cardiac output, but linearly related to the time over which the injection was made. The area under the curve of the peak was related inversely to cardiac output only, while the aspect ratio of the peak was related inversely to the time over which the injection was made only. The injectate volume had no effect on any of the measured values. We conclude that, in some circumstances, the rate of injection of drugs with narrow margins of safety should be tailored to the cardiac output of an individual.

Animals↗

Comparative responses to dobutamine and nitroprusside in patients with chronic low output cardiac failure.

The acute hemodynamic effects of dobutamine and nitroprusside were compared in 19 patients with low output cardiac failure. At dosage levels yielding similar increases in cardiac index (12 patients), nitroprusside resulted in significantly lower arterial systolic and wedge pressures and did not increase heart rate suggesting advantages over dobutamine when reduction in myocardial oxygen requirement or pulmonary congestion is a major goal. Systemic arterial mean and diastolic pressures were minimally changed with dobutamine, but fell significantly with nitroprusside suggesting advantages of dobutamine over nitroprusside in patients where hypotension could limit coronary blood flow or perfusion of other vital organs. Reduction in pulmonary arteriolar resistance occurred only with nitroprusside. Arterial hypoxemia developed in three patients during nitroprusside infusion suggesting the possibility of increased right-to-left intrapulmonary shunting resulting from a direct vasodilating effect of nitroprusside on pulmonary arteriole smooth muscle. Although both inotropic and vasodilator drugs can result in hemodynamic improvement when administered to patients with chronic low output cardiac failure, significant differences of potential clinical importance exist between these two modes of therapy.

Adult↗

Pulmonary blood flow (cardiac output) and the effective lung volume determined from a short breath hold using the differential Fick method.

OBJECTIVES: This work attempts to show how pulmonary blood flow (Qp), cardiac output (CO(Fick)) and the lung volume of effective gas exchange (ELV) can be determined from breath-by-breath measurements of the tidal exhaled CO2 elimination V (litre/min) and the end tidal CO2 concentration P (%) using the differential Fick method. The measurements are made during steady state ventilation and when the CO2 balance in the lungs changes subsequent to a perturbation of the gas exchange conditions. METHODS: A short breath hold is used to implement such a perturbation. V and P were measured in patients on mechanical ventilation. When the end tidal CO2 values were stable, the end inspiratory pause of a single breath was prolonged 3 seconds as compared to the normal ventilation pattern. From the changes induced in P and V, Qp, CO(Fick) and ELV are obtained. RESULTS: Cardiac output values were measured in 18 patients after CABG. CO(Fick) was found to be in good agreement with the thermodilution cardiac output reference COth. (n = 51 and (COth-CO(Fick)) with Mean = -0.17 litre/ minute and SI) = 0.62 litre/minute). CONCLUSIONS: With a single breath perturbation, the differential Fick method can yield cardiopulmonary information using 2-3 breaths only and with a minimum of interference with the patient. Complete data analysis results in multiple determinations of the Qp and ELV values which improve the attainable precision. Our investigation points to the possibility to determine Qp, CO(Fick) and ELV also during spontaneous breathing, by using the natural tidal variations of V and P.

Aged↗