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Dobutamine is a newly developed catecholamine reported to have minimal direct vascular effects relative to its inotropic activity and to have less chronotropic and arrhythmogenic properties than other catecholamines used in the treatment of low output states. In this study, the acute hemodynamic effects of dobutamine were compared to those of dopamine in 13 patients with chronic low output cardiac failure. At dosages adjusted to achieve similar increments in cardiac output, dobutamine reduced left ventricular filling pressure (LVEP) from 24 +/- 2 mm Hg (SEM) to 17+/- 2 mm Hg, while dopamine increased LVEP to 30 +/- 3 mm Hg and in six patients caused arterial O2 saturation to fall below 90%. This poor response to dopamine was probably the result of its vasoconstrictive effects and illustrates the potential advantages of using a cardioselective agent such as dobutamine when the desired goal of therapy is to improve ventricular function by direct inotropic stimulation.
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Cardiac output estimation by thermodilution is carried out using room temperature or iced injectate, but the accuracy and variability of the two methods is not well documented. Room temperature and iced injectate were compared in 21 patients undergoing diagnostic cardiac catheterization. Dextrose injectate (10 ml) was administered in prefilled syringes left to stand either in iced water or in room air. Four injections were made sequentially with room temperature and iced injectate. Cardiac output by room temperature and iced injectate were not significantly different (4.70 +/- 1.22 for room temperature and 4.90 +/- 1.37 for iced injectate, n = 21, P = 0.155). There was a significant difference in the variance of the estimations by the two methods (room temperature = 0.296, iced = 0.120, P less than 0.005). From this variance the calculated number of measurements needed to estimate cardiac output to +/- 0.5 L/min with 95% confidence is seven for room temperature and four for iced injectate. For five patients with cardiac output less than 4.00 L/min with room temperature injectate, cardiac output with iced injectate was significantly higher (3.33 +/- 0.34 for room temperature vs. 3.69 +/- 0.49 for iced injectate, P = 0.05). Thus room temperature injectate generally gives a satisfactory cardiac output estimation but with significantly greater variability than iced injectate. Sample size for accurate cardiac output estimation must be greater with room temperature injectate. Iced injectate may over-estimate output when cardiac output is low.
Cardiac output was measured by two-dimensional echocardiographic Doppler technique in 55 adult patients in the intensive care unit. Doppler cardiac output determinations were measured from four sites (suprasternal long axis of the ascending aorta, suprasternal long axis of the descending aortic, apical left ventricular outflow tract, and parasternal long axis of the main pulmonary artery) and were compared to cardiac output determined by thermodilution for a total of 101 observations (r = 0.84). Mean cardiac output was 5.3 L/min (range 1.8 to 9.5 L/min) by Doppler technique and 5.1 L/min (range 1.6 to 8.9 L/min) as measured by thermodilution. Correlation of Doppler cardiac output with thermodilution cardiac output gave r values of 0.85, 0.83, 0.90, and 0.81 from the ascending aorta, descending aorta, left ventricular outflow tract, and pulmonary artery, respectively. Averaging of data in patients in whom more than one determination was possible resulted in improved correlation (r = 0.94). Thus, cardiac output can be measured with reasonable accuracy by Doppler from a variety of sampling sites and averaging of data from more than one site may improve these results.
Cardiac output estimation is an important and much needed measurement for assessing patients in heart failure. In hypertension, it is vital for understanding the haemodynamic basis of the disease and the mode of action of drugs. Measurements of blood pressure and cardiac output provide the only means of estimating peripheral resistance. Of the available methods to determine cardiac output, thermodilution is the most practical, although it has its difficulties and care has to be exercised in its use. When intra-arterial blood pressure measurements are needed, the dye-dilution method is equally valid, and if respiratory techniques are available the Fick principle may also be used. Of the non-invasive methods, none is yet developed to a stage suitable for general clinical use. Doppler velocimetry is the most promising technique, but it requires complex computer analysis and, as yet, can reliably be used only to measure changes in cardiac output in an individual. The technique has been assessed against the electromagnetic flowmeter in man and gives reasonable accuracy and repeatability. Echocardiography and impedance cardiography are not yet satisfactory for clinical use; neither are the radionuclide methods, apart from the 'first pass' method, but this also needs further verification.
Cardiac output is determined by the interaction of cardiac pump function and the mechanical properties of the peripheral circulation that govern venous return. Increasing pleural pressure impedes peripheral venous return but aids cardiac ejection; on the other hand, decreasing pleural pressure can augment venous return but impedes the emptying of the left ventricle, creating an increase in aortic pressure. Whether a fall in pleural pressure leads to an increase or decrease in cardiac output depends upon the functional state of the heart and its sensitivity to changes in afterload. Understanding the effect of pleural pressure on cardiac output may lead to the development of therapeutic or diagnostic techniques using altered pleural pressure.
Cardiac output was measured in 89 patients using transthoracic continuous-wave echo Doppler comparing right ventricular outflow tract pacing with the right ventricular apex at the time of permanent pacemaker implantation. Overall, cardiac output improved 18.8% (p <0.0001) and cardiac index 21.0% (p <0.0001) with outflow tract placement; patients with a lower baseline cardiac index had a greater percent improvement with outflow tract placement.
Cardiac output was determined by means of radioactive microspheres, 15 +/- 5 microns in diameter. Blood flow in the ascending aorta was measured by an electromagnetic flowmeter. In eight cats thirty-eight simultaneous measurements were made of cardiac output and aortic flow. The observations correlated well (r = 0.89), with a mean difference of 5.2%, probably corresponding to coronary blood flow. Continuous flow recordings showed no alterations in aortic flow during the injections of microspheres; arterial blood pressure and heart rate remained unchanged even after six injections, each consisting of about 2 x 10(5) spheres per kg body weight. Tests for shunting of microspheres were performed and revealed shunt fractions in the systemic circulation of about 8%, with no significant shunting through the lungs. The microsphere method for determining cardiac output is thought to be an accurate method, suitable for small and medium sized animals.
We studied 99 adult patients after elective cardiac surgery who had low cardiac output (cardiac index less than 2.5 L/min/m2) in spite of adequate cardiac filling pressure (pulmonary capillary wedge pressure less than 8 mm Hg). Patients received milrinone by loading dose (50 micrograms/kg over a 10-minute period), followed by a continuous infusion of either 0.375, 0.5, or 0.75 micrograms/kg/min (low-, middle-, and high-dose groups, respectively) given for a minimum of 12 hours. Patients were allocated to each dosage group sequentially, not randomly. Hemodynamic measurements were made before the loading dose and at 15, 30, 45, and 60 minutes, 3, 6, and 12 hours after the start of milrinone therapy. Further measurements were made at 2 and 4 hours after treatment was stopped. Milrinone therapy was associated with a rapid, well-sustained, and highly significant increase in cardiac index in all three dose groups (p less than 0.001), and a similar fall occurred in pulmonary capillary wedge pressure in all groups (p less than 0.001). Significant increases occurred in heart rate in all three groups (p less than 0.001). Systemic and pulmonary vascular resistance also fell significantly, although changes in this latter parameter were less predictable and more dose dependent. Few serious treatment-related adverse effects were seen. We conclude that intravenous milrinone is an effective and safe therapy for the treatment of low output states after cardiac surgery.
Cardiac output is determined by heart rate, by contractility (maximum systolic elastance, Emax) and afterload, and by diastolic ventricular compliance and preload. These relationships are illustrated using the pressure-volume loop. Diastolic compliance and Emax place limits determined by the heart within which the pressure-volume loop must lie. End-diastolic and end-systolic pressures and hence the exact position of the loop within these limits are determined by the peripheral circulation. In the presence of minimal sympathetic tone, some 60% of total blood volume is hemodynamically inactive and constitutes a blood volume reserve (the unstressed volume). The remainder of the blood volume (the stressed volume) and the compliance of the venous system determine the venous pressure. This venous pressure together with venous resistance determines venous return, right atrial pressure, cardiac preload, and hence cardiac output. Venoconstriction causes conversion of unstressed volume to the stressed volume, the blood volume reserve is converted into hemodynamically active blood volume. After hemorrhage this replaces the lost stressed volume, while in other situations where total blood volume is not reduced, it allows a sustained increase in cardiac output. The major blood volume reserve is in the splanchnic bed: the liver and intestine, and in animals but not man, the spleen. A major unsolved problem is how the conversion of unstressed volume to stressed volume by venoconstriction is reflexly controlled.
We have studied the haemodynamic effects of i.v. milrinone, a new phosphodiesterase inhibitor, in patients with low cardiac output after cardiac surgery. Thirty-five patients with a cardiac index (Cl) less than 2.5 litre min-1 m-2 and a pulmonary capillary wedge pressure (PCWP) greater than 8 mm Hg were given a loading dose of milrinone 50 micrograms kg-1 followed by an infusion at one of three rates: 0.375 micrograms kg-1 min-1, 0.5 micrograms kg-1 min-1 or 0.75 micrograms kg-1 min-1 for 12 h. After 1 h there were increases in Cl (35%) (P less than 0.001), heart rate (13%) (P less than 0.01) and stroke volume index (19%) (P less than 0.005). There were decreases in mean arterial pressure (12%) (P less than 0.01), systemic vascular resistance (35%) (P less than 0.001) and PCWP (24%) (P less than 0.05). Pulmonary vascular resistance was unchanged or reduced and left ventricular stroke work index was unchanged or increased. The haemodynamic improvements were sustained throughout the infusion period. Milrinone was tolerated well: three patients developed tachycardia greater than 125 beat min-1, one patient developed atrial fibrillation and one patient had a short run of atrial bigemini. We conclude that milrinone is a useful agent in the treatment of patients with a reduced cardiac output after cardiac surgery.
Patients often experience low cardiac output following cardiac surgery and as many as 90% of patients experience a decreased left ventricular ejection fraction (LVEF) and cardiac index (CI). Causes may vary from volume depletion to global myocardial dysfunction. Critical thinking skills, combined with diligent patient monitoring and a knowledge of cardiovascular physiology and pharmacology are required for prompt recognition and treatment of low cardiac output following cardiac surgery.
Cardiac output was measured 120 times in 27 critically ill patients using the thermodilution and transthoracic electrical impedance methods. Both the minimum and mean values for the distance between the inner electrodes, and a variety of values for the resistivity of blood (rho) were substituted in the Kubicek's empiric formula for calculating cardiac output by transthoracic electrical impedance. Using the mean distance between the inner electrodes and a rho-value of 150 ohm X cm gave the best agreement between the methods (mean difference 0.17 +/- 2.4 L/min). Ventilation alone or with positive end-expiratory pressure did not significantly affect the bias of the estimate, but both affected its precision when compared with measurements in spontaneously breathing patients (SD of mean difference 2.4 and 3.2 L/min, respectively, vs. 1.5 L/min). The pulmonary artery wedge pressure was significantly higher in patients with an abnormal diastolic impedance waveform (zero-wave), but there was no relationship between wedge pressure and base impedance per unit length between the measuring electrodes.
Cardiac output (CO) was measured in 10 young, healthy male subjects during rest and submaximal exercise on a bicycle ergometer by rebreathing a 2.0-2.8 l (ATPS) gas mixture of acetylene (0.7-1.2%), freon-22 (3-4.2%), argon (6-7%), and oxygen (ca. 40%) in nitrogen. End tidal gas fractions were measured by a mass spectrometer. Argon was used as an inert, insoluble gas for corrections of end tidal acetylene-, freon-, and oxygen fractions. The acetylene results corresponded to cardiac outputs found in literature (6.06 +/- 0.20 l/min, at rest and 15.05 +/- 0.44 l/min at 150 W). The freon values followed those of acetylene but were systematically lower by 0.74 l/min at rest and 1.20 l/min at 150 W. A forced respiratory rate (30-32/min) increased CO and VO2 during rebreathing at rest and lower exercise levels, while a spontaneous respiratory rate (14/min at rest and 22/min at 150 W) did not change VO2 during rebreathing compared to Douglas measurements at steady state. We conclude that freon can be used as the inert, soluble gas in the rebreathing procedure and recommend a spontaneous respiratory rate.