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The validity of a CO2 rebreathing (exponential) method to determine cardiac output was acceptable during exercise, but not at rest. The reproducibility during exercise of the measurement of cardiac output was similar to data published for the dye dilution method.
A new indicator dilution technique is described for measuring cardiac output and shunt fraction in patients undergoing venovenous extracorporeal membrane oxygenation (ECMO). Shunt fraction is the proportion of the ECMO pump flow which recirculates through the ECMO circuit (passing directly from the inflow cannula to the outflow cannula) instead of flowing through the pulmonary and systemic circulations. The indicator is an isotonic (150 mmol/l) solution of lithium chloride which is injected into the ECMO flow returning to the patient. Two lithium sensors are used simultaneously to record the resulting lithium dilution curves in arterial blood and in the blood in the ECMO circuit. Cardiac output and shunt fraction are derived from these curves. The techniques, which is simple and safe, provides measurements that allow optimal adjustment of ECMO flow and cardiovascular support.
BACKGROUND: Laparoscopic Nissen fundoplication (LNF) is gaining popularity. Although the hemodynamic effects of the typical pneumoperitoneum have been studied, the additional consequences of the hiatal dissection necessary for LNF have not. METHODS: Seven female pigs were anesthetized, intubated, and ventilated with a volume ventilator and hemodynamic and mechanical pressure monitoring devices were placed. Pressures were recorded every 15 minutes for 1 hour after each of four interventions: (1) anesthesia induction, (2) CO2 pneumoperitoneum (15 mm Hg), (3) LNF, and (4) release of pneumoperitoneum (and removal of ports). RESULTS: Right atrial, inferior vena caval, mediastinal, pleural, airway, and pulmonary capillary wedge pressures all increased after pneumoperitoneum (p < 0.05). Only mediastinal pressure (8.6 vs 13.7 mm Hg, pneumoperitoneum vs LNF; p < 0.05) and pleural pressure (2.6 vs 3.5 mm Hg, pneumoperitoneum vs LNF; p < 0.05) showed a further significant increase after LNF. In addition, cardiac output fell significantly after LNF (5.9 vs. 4.6 L/min; p < 0.05). Mediastinal pressure and cardiac output remained significantly altered after the release of pneumoperitoneum. CONCLUSIONS: Surgical disruption of the esophageal hiatus during LNF causes both increased mediastinal and pleural pressure and a significant reduction in cardiac output. These findings uncover a previously unsuspected physiologic detriment that may occur during LNF.
To determine the individual contributions of variables in the Fick equation to cardiac output, we simultaneously measured oxygen uptake (VO2), carbon dioxide production (VCO2), venous oxygen saturation (SvO2) and thermodilution cardiac output (Qth) in 28 medical and surgical ICU patients. Patients were intubated and ventilated with the intermittent mandatory ventilation mode. VO2 and VCO2 (averaged over 3 min) were obtained from a metabolic cart. SvO2 was measured with fiberoptic reflectance oximetry (and COoximetry). Thirty-nine studies (average duration, 4.3 h) with 151 Qth measurements were performed. The relationships between Qth and VO2, Qth and VCO2, Qth and SvO2, and 1/Qth and SvO2, as well as between the sequential changes in these variables were analyzed by least squares linear regression. The ability of changes in the variables VO2, VCO2, and SvO2 to predict changes in Qth were analyzed by receiver operating characteristic (ROC) curves. Qth was weakly related to VO2 (r = 0.45), VCO2 (r = 0.45), or SvO2 (r = 0.36). Changes in Qth were weakly related to changes in VCO2 (r = 0.40), and even less to changes in VO2 (r = 0.18) and SvO2 (r = 0.13). The areas under the ROC curves for increases in Qth > 10 percent were as follows: 0.66 for VCO2, 0.50 for VO2, and 0.55 for SvO2. The areas for decreases in Qth < 10 percent were as follows: 0.78 for VCO2, 0.65 for VO2, and 0.49 for SvO2. None of the above oximetry relationships were substantially altered by use of COoximetry venous oxygen saturations. We conclude that Qth cannot be predicted well solely from VO2, VCO2, or SvO2 nor can changes in Qth be predicted well solely from changes in VO2, VCO2, or SvO2. Of the metabolic variables, changes in VCO2 best predicted changes in Qth.
Recent studies have been conducted to evaluate the relationship between plasma beta-endorphin (END) levels and the hemodynamic changes that occur in severely stressed animals. Using our canine hypovolemic shock model, END levels were analyzed during the baseline period, at the beginning of treatment (after a period of fixed-pressure hypovolemic shock), and at the end of treatment. Mean arterial pressure (MAP) and cardiac output were also measured at these intervals. Animals were given iv 5 ml of 0.9% NaCl, 4 mg/kg of naloxone (NAL), 30 mg/kg of methylprednisolone (MP), or 4 mg/kg of NAL and 30 mg/kg of MP. A fifth group was composed of nonsteroid-treated animals. Scatterplots were generated and linear regression lines were drawn comparing END with cardiac output and MAP. In the nonsteroid-treated animals, a significant correlation was found between decreases in both MAP and cardiac output and increasing levels of END. The addition of MP did not seem to alter the relationship, suggesting that MP did not affect END release.
A study was made of the hemodynamic effects of levarterenol and phentolamine in patients in whom low cardiac output developed following open-heart operation. After the patients were weaned from cardiopulmonary bypass, the inotropic agents were infused into an external or internal jugular vein through an IVAC pump. Levarterenol was administered first until systolic arterial pressure rose 20 to 30% above the higest recorded preoperative pressure. After stabilization, phentolamine was administered, and infusion rates were adjusted so that arterial blood pressure was returned to levels measured before bypass. After infusion, all patients showed an increase in cardiac index, mean arterial pressure, mean stroke volume index, and left ventricular stroke work index. Mean pulmonary artery pressure, pulmonary vascular resistance, and left atrial pressure decreased in all patients. This study demonstrates that hemodynamic improvement occurs in humans in low cardiac output state with simultaneous infusion of levarterenol and phentolamine. We recommend these agents for use in patients with low output, unless they continue to receive propranolol during and after operation. Patients on a regimen of propranolol should not be given levarterenol and phentolamine.
PURPOSE: Clonidine is a classical sympatholytic drug that is widely used for the treatment of hypertension. Experimental and clinical studies suggest that Clonidine may activate baroreflex. The aim of this study was to determine the hemodynamic response to Clonidine under physiological conditions and to test the hypothesis that Clonidine would reduce cardiac output and blood pressure resulting in an increase in total peripheral resistance. METHODS: Clonidine's hemodynamic effect was evaluated in 28 young, healthy subjects after a single i.v. dose of 1 microg x kg(- 1). Impedance cardiography, systolic time intervals and pulse wave analysis were used to characterize myocardial and vascular function. RESULTS: Clonidine lowered blood pressure, heart rate, left ventricular ejection time, and pulse wave velocity and increased pre-ejection period. Stroke volume and cardiac output decreased gradually over the investigation time of 240 min. Central systolic blood pressure (SBP) was lowered to a larger extent than peripheral SBP. Total peripheral resistance was characterized by an immediate fall of short duration followed by a continuous rise above baseline after 120 min. Placebo did not have any significant effect on hemodynamic parameters. CONCLUSIONS: Clonidine's blood pressure lowering effect is mediated by both an immediate decrease in vascular resistance and a prolonged decrease in cardiac output, and Clonidine lowers central SBP more than peripheral SBP.
Continuous positive airway pressure (CPAP) is used to treat congestive heart failure (CHF). Mechanisms for improved cardiac output (CO) include increased left ventricular (LV) surface pressure, changes in sympathoadrenal tone, nonadrenergic vasodilation, or shifting blood volume from intra- to extrathoracic compartments. At CPAP = 0 and CPAP = 5 cm H2O we measured CO, LV surface pressure, plasma norepinephrine (PNE), and systemic vascular resistance (SVR) in normal and hypervolemic pigs and pigs with CHF (rapid ventricular pacing). In normovolemia CPAP led to no change in CO. With both hypervolemia and CHF. CPAP led to increased CO (10-20%). With CPAP, LV surface pressure increased slightly in normovolemia, but did not increase, or even decreased, in hypervolemia. With CPAP, PNE did not change in normovolemia, increased in hypervolemia, and decreased in CHF, SVR always decreased when cardiac output increased with CPAP. We conclude that changes in cardiac surface pressure and overall sympathoadrenal tone cannot explain changes in CO with CPAP. Non-adrenergic mediated vasodilation could lead to unloading the LV. Alternatively, volume shift from intra- to extrathoracic compartments could lead to greater decreases in systolic than diastolic volume, thus increasing stroke volume. CPAP increases CO in the presence of cardiac distension whether or not myocardial function is impaired.
Previous experiments in the dog have shown that static contractions of the muscles of one limb elicit a reflex increase of resistance in the vessels of the opposite limb, along with an increase of systemic blood pressure. The aim of the present experiments was to examine whether this reflex can cause a redistribution of cardiac output from the resting areas, in favor of the working parts. In 17 anesthetized and ventilated dogs, static contraction of the muscles of the right thigh was elicited with electrodes inserted into these muscles. The carotid sinuses were kept at constant pressure and the vagi cut. During static contractions systemic blood pressure and cardiac output increased by 17.7 +/- 3.1 and 24.2 +/- 5.5%, respectively. The blood flow measured with an electromagnetic flowmeter decreased by 21.9 +/- 5.3% in the femoral artery of the resting limb and increased by 101 +/- 21% in the femoral artery of the "active limb". Data obtained in six dogs with injection of radioactive microspheres during stimulations show that blood flow decreased not only in the muscles of the rising limb (34 +/- 10%), but also in several other resting areas, such as skin (38 +/- 8%), kidney (24 +/- 8%), gut (38 +/- 6%), and tongue (23 +/- 3%). The results show that the reflex under study causes a redistribution of the cardiac output during static muscular contractions.
To assess the value of impedance cardiography in pregnancy, simultaneous measurements of cardiac output were made with impedance and thermodilution techniques in 10 patients who required pulmonary artery catheterization. The methods correlated poorly (r = 0.17). The discrepancy between methods was particularly pronounced in hypertensive patients. Impedance cardiography does not measure cardiac output accurately in hypertensive pregnant women.
Bioimpedance offers a simple non-invasive means of measuring systolic ejection volume and heart rate and thus cardiac output. Four pairs of electrodes are placed on precise locations on the chest and stroke volume is calculated according to the equation developed by Kubicek in 1966 and modified by Sramek in 1980. The aim of this work was to evaluate this method in patients with heart disease. In a series of 50 patients, the coefficient of correlation for cardiac index between impedance values (2.52 +/- 0.71 ml/min/m2) and thermodilution values (2.74 +/- 0.69 ml/min/m2) was 0.63 (p < 0.01). The mean difference was -0.2 l/min/m2 (confidence interval +1 l/min/m2 to -1.4 l/min/m2). There was no statistical correlation in patients with complete left bundle branch block, severe mitral or aortic regurgitation or dilatation of the aorta. In a group of 11 healthy volunteers, there was a good correlation between two measures taken at a 2 day interval (r = 0.95). The coefficient of variation ranged from 1.2 to 7% for ejection volume. Bioimpedance is reproducible and simple, authorizing its use for non-invasive monitoring of cardiac output in a given patient in various clinical situations.
BACKGROUND: The efficacy of ACE-inhibitor therapy is well documented in the treatment of chronic heart failure. As pharmacological mechanisms of ACE-inhibition and angiotensin II AT1-receptor-antagonists differ, an additional positive effect concerning left ventricular function can be expected in combining both classes of drugs. METHODS: Twenty patients (64.9+/-8.5 years) with advanced chronic heart failure (NYHA class III) receiving long-term medication with digitalis, diuretics and ACE-inhibitors were randomized to either eprosartan (540+/-96 mg/day) or placebo, according to a blinded protocol. Hemodynamic measurements by impedance cardiography were performed at baseline and after 8.85+/-1. 5 days of study medication treatment. RESULTS: Additional treatment with eprosartan resulted in a higher cardiac output than in the control group (P<0.05). While in the active treatment group cardiac output increased significantly from baseline (2.27-3.24 l/min, P=0. 039), there was no change in the control group. CONCLUSIONS: The additional treatment with the AT1-receptor antagonist eprosartan, given to severe heart failure patients, who received digitalis, diuretics and ACE-inhibitors, resulted in a beneficial effect by increasing cardiac output. This effect may be due to eprosartan's additional property of blocking the autocrine interaction of locally and not ACE-generated angiotensin II with their respective vascular and myocardial AT1-receptors as well as the influence on prejunctional AT1-receptors located on sympathetic nerve terminals.
Simultaneous estimates of cardiac output were made during graded upright maximal exercise in 10 male subjects by means of Doppler velocity spectrum of ascending aortic flow, apical two-dimensional echocardiograms, thermodilution, and Fick oximetry. In 15 subjects, aortic annular and root diameters were measured during similar exercise from parasternal two-dimensional echocardiograms. The linear correlation between Doppler, two-dimensional echocardiography, and the invasive estimates ranged from r = .78 to r = .92. Both echocardiographic techniques were able to predict changes in invasive flow estimates with reasonable accuracy. Two-dimensional echocardiographic flow estimates underestimated invasive values by about 60%. The accuracy of Doppler flow estimates varied with the method of estimating aortic cross-sectional area. Greatest accuracy was obtained with areas calculated from diameters measured at the aortic value anulus with the leading edge-to-leading edge method of measurement. Correlation coefficients comparing Doppler and thermodilution flow estimates were generally higher (r = .75 to .96, mean .86) for individuals than for the group, but accuracy of the Doppler estimates in single subjects was quite variable. Aortic diameters did not increase from rest to moderate levels of upright exercise. A 3% to 5% increase in resting aortic diameter was noted in the upright posture as compared with the supine. Doppler flow estimates were obtained in all subjects to maximal exertion but in only a minority of subjects with two-dimensional echocardiography or thermodilution. Thus two-dimensional and Doppler echocardiography offer a noninvasive means of estimating cardiac output during vigorous exercise. The Doppler technique is technically more suitable to the study of exercise than two-dimensional echocardiography.(ABSTRACT TRUNCATED AT 250 WORDS)
We compared the hemodynamic effects of high-frequency oscillatory ventilation (HFOV) with conventional continuous positive pressure ventilation (CPPV). Six mongrel dogs were anesthetized with chloralose and evaluated over a range of mean airway pressures (Pao) during CPPV and HFOV. Pao during HFOV was measured by allowing alveolar pressure to come into equilibrium with airway opening pressure and was set to equal mean Pao during CPPV. Pao during CPPV was set by adding positive end-expiratory pressure (PEEP) of 0, 5, 10, and 15 cm H2O. Transmural pulmonary capillary wedge pressures (Pwp) were maintained at near 11 mm Hg in both groups during all four ventilatory periods. Cardiac output as measured in triplicate by thermal dilution was similar between HFOV and CPPV at each level of mean airway pressure. After matching mean airway pressure and transmural Pwp we were unable to find any sparing effect of HFOV on cardiac output over a wide range of airway pressures. We conclude that there is not an independent effect of HFOV on cardiac output.
The response of the fetal circulation to beta adrenergic stimulation with ritodrine hydrochloride has been investigated by long-term monitoring of the fetal lamb in utero. Ritodrine was infused intravenously either into the ewe or directly into the fetus, and cardiovascular and acid-base responses were measured. Fetal cardiac output and its distribution were measured with the use of radionuclide-labeled microspheres. The output of each ventricle also was measured by means of long-standing implanted electromagnetic flow transducers around the ascending aorta or pulmonary trunk during infusion of ritodrine at various rates into the fetus. Infusion of ritodrine (1.9 mcg. per kilogram per minute) into the ewe caused no change in fetal heart rate, blood pressure, cardiac output, or umbilical blood flow, but did cause an increase in fetal adrenal and myocardial blood flow. Ritodrine infused directly into the fetus produced a marked increase in fetal heart rate and a minimal change in cardiac output. There were no significant changes in fetal or maternal acid-base balance during the ritodrine infusions.
In 12 patients requiring pulmonary artery catheterization, cardiac output was measured using Doppler and thermodilution techniques. The Doppler technique accurately predicted measurements made by thermodilution (r = 0.91; P less than .001). Eighteen normal patients in the third trimester and 36 preeclamptics who had not been treated with medications other than magnesium sulfate were evaluated with Doppler alone. Of note was the heterogeneity among preeclamptics. Although their mean systemic vascular resistance was elevated, it ranged from 2256-648 dyne X sec X cm-5. Cardiac output ranged from 13.2-3.9 L/minute.
The suitability of impedance cardiography as a method to follow changes in cardiac output (CO) was investigated by comparing it with thermodilution and by measurements in conditions with predictable effects on CO. The correlation between absolute CO values obtained by impedance and thermodilution techniques was moderate (r = 0.61), but the percentage changes showed a good correlation (r = 0.84). Head-up tilting decreased CO by 25% in 5 normal subjects. Bloodletting in three subjects caused a 20% decrease, reinfusion in one subject a 16% increase. Occlusion of artificial large flow arteriovenous shunts in 6 dialysis patients caused a 12% decrease in CO, whereas the effect was less with moderate and absent with small flow shunts. Ultrafiltration caused a 28% decrease in two dialysis patients. In 20 hypertensive patients CO dropped 25% after salt depletion; propranolol administered intravenously gave a 15% decrease (n = 13), diazoxide intravenously a 30% increase (n = 6). It is concluded that, provided conditions are strictly defined, impedance cardiography is a reproducible method and suitable for the measurement of intrapatient changes in cardiac output.
Two methods of measuring stroke volume and cardiac output with pulsed Doppler two-dimensional echocardiography were developed and validated against the thermodilution technique in 39 patients, 33 of which were in an intensive care unit. With the use of the apical four-chamber view, a mitral inflow method combined the velocity of left ventricular inflow at the mitral anulus with the cross-sectional area of the anulus calculated from its diameter at middiastole (area = pi r2). From the apical five-chamber view a left ventricular outflow method combined the velocity of left ventricular outflow with the cross-sectional area of the aortic anulus calculated from its diameter during early systole (parasternal long-axis view). Measurements with the mitral inflow and left ventricular outflow methods were obtained in 35 of 39 (90%) and 39 of 39 (100%) patients, respectively. Validation of the mitral method excluded patients with mitral regurgitation (n = 11) and validation of the left ventricular outflow method excluded those with aortic regurgitation (n = 4). Good correlations were observed between thermodilution and Doppler measurements of stroke volume and cardiac output for both the mitral anulus method (R = .96 and .87, respectively) and the left ventricular outflow method (R = .95 and .91, respectively). The results of the two methods correlated well with each other in patients without regurgitant valve lesions. A greater interobserver variability was observed with the mitral anulus method, which was related solely to greater variability in measuring the annular diameter.(ABSTRACT TRUNCATED AT 250 WORDS)