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The cardiac output has been measured in 40 elderly patients by impedance cardiography and an isotopic indicator-dilution method. There was no significant systemic difference between the results obtained by the two methods. The mean difference between paired values was 0.76 1/min (approximately 16%). The value and limitations of impedance cardiography in the study of the circulation in the elderly are discussed.
OBJECTIVE: To compare the pH and PCO2 values determined from of simultaneously corrected samples of central venous and intraosseous blood during sequential changes in cardiac output. DESIGN: Prospective, descriptive study. SETTING: An animal laboratory in a university medical center. SUBJECTS: Fourteen mixed breed 4-wk-old piglets. INTERVENTIONS: Animals were anesthetized with ketamine hydrochloride and neuromuscular blockade was induced by the administration of pancuronium bromide. After endotracheal intubation and the institution of mechanical ventilation, a 4-Fr pulmonary artery catheter and a carotid artery cannula were inserted via a cutdown into the right neck of each piglet. A 16-gauge intraosseous needle was inserted into the anteromedial surface of the right tibia. MEASUREMENTS AND MAIN RESULTS: Central venous and intraosseous blood gas samples were obtained simultaneously with thermodilution cardiac output measurements. Cardiac output measurements were as follows: during steady state (0.80 +/- 0.14 L/min), after volume loading of 15 mL/kg (1.00 +/- 0.25 L/min), after three successive bleeds of 15 mL/kg each at 30-min intervals (0.70 +/- 0.28, 0.54 +/- 0.22, and 0.43 +/- 0.16 L/min, respectively) and at exsanguination (unrecordable). Paired t-tests demonstrated no significant differences in pH and PCO2 values between intraosseous and central venous samples under all study conditions. Limits of agreement for difference in PCO2 between sites, within the range of cardiac outputs studied, were -12.86 to 11.38 torr (-1.71 to 1.46 kPa) and for pH were -0.09 to 0.15. CONCLUSIONS: Intraosseous blood samples can be obtained without difficulty even during extreme hypovolemia. The pH and PCO2 values of intraosseous and central venous blood samples were similar under all study conditions. Intraosseous blood may be a useful alternative to central venous blood to assess tissue acid-base status during hemorrhagic shock and other low-flow states.
To measure fetal cardiac output by thermodilution, we injected 2.5 ml of iced 5% glucose rapidly into the superior vena cava and recorded areas of temperature-time curves in the brachiocephalic artery (AS) and descending aorta (BS). One minute later we repeated the injection into the inferior vena cava and recorded areas under two curves (AI and BI). Cardiac output was calculated as Qco = H (AS + BI - AI - BS) (ASBI - AIBS), where H is the change in caloric content of the blood. In a mechanical model we found thermal results correlated well with timed collections (r = 0.98) with a slope of 0.995. In 7 acutely prepared fetal lambs, electromagnetic flow probe measurements of total cardiac output (descending aorta + brachiocephalic artery) correlated well (0.90) with thermal measurements. The slope (1.16) was significantly greater than 1.0, reflecting the inclusion of coronary and pulmonary flows in thermal, but not in flow probe, measurements. In 11 acutely and chronically prepared fetal lambs, the correlation between microsphere and thermal measurements was 0.81 with a slope of 1.09, not significantly different from 1.0. Hence, thermodilution gives results comparable to other methods and is convenient, indefinitely repeatable, inexpensive, and nonradioactive.
Cardiac output was measured by thermodilution and ear densitometry in surgical ICU patients who had pulmonary arterial catheters. Overall comparison based on 56 sets of triplicate measurements revealed a correlation coefficient (r) of 0.76 between the two techniques. Although ear densitometry was more accurate with injection via the antecubital vein (r = 0.88) vs. more distal injection (r = 0.67), these data suggest that this technique lacks the accuracy for clinical application.
We tested the hypotheses that, in hypoxic young pigs, reductions in cardiac output restrict systemic oxygen transport to a greater extent than does hypoxia alone and that compensatory responses to this restriction are more effective in higher than in lower priority vasculatures. To study this, 10- to 14-day-old instrumented awake hypoxic (arterial oxygen tension = 39 Torr) pigs were exposed to reduced venous return by inflation of a right atrial balloon-tipped catheter. Blood flow was measured with radionuclide-labeled microspheres, and oxygen metabolism was determined with arterial and venous oxygen contents from appropriate vessels. Hypoxia resulted in a reduction in oxygen tension; increases in cardiac output and perfusion to brain (72% over baseline), heart, adrenal glands, and liver without reductions to other organs except for the spleen; reductions in systemic and intestinal oxygen delivery; and increases in systemic and intestinal oxygen extraction without changes in systemic, cerebral, or intestinal oxygen uptake. During hypoxia, decreasing venous return was associated with increases in arterial lactic acid concentration and central venous pressure; attenuation of the hypoxia-related increase in cardiac output; sustained increases in brain (72% over baseline) and heart perfusion; reductions in lung (bronchial artery), pancreatic, renal, splenic, and intestinal (-50% below baseline) perfusion; decreases in systemic and gastrointestinal oxygen delivery; sustained increases in systemic and intestinal oxygen extraction; and decreases in intestinal oxygen uptake, without changes in cerebral oxygen metabolism. We conclude that when venous return to the heart is reduced in hypoxic young pigs, the hypoxia-related increase in cardiac output was attenuated and the relative reduction in cardiac output was associated with preserved cerebral oxygen uptake and compromised intestinal oxygen uptake. Regional responses to hypoxia combined with relative reductions in cardiac output differ from that of hypoxia alone, with the greatest effects on lower priority organs such as the gastrointestinal tract.
A modification of the Farhi one-step rebreathing technique (1) is described for determining submaximal exercise cardiac output (Q). Factors critical in the estimation of Q are initial rebreathing bag volume and constant bag volume during the maneuver. By substituting a high flow rate analyzer (500 ml.min-1) for the recommended low flow rate mass spectrometer (60 ml.min-1), adding a recirculation circuit from the outlet of the analyzer to an inlet at the base of the rebreathing bag, and reducing the length of sample tubing to the analyzer, we were able to recirculate the subject's expired gas and achieve no loss of bag volume. No statistically significant differences in estimate of cardiac output were noted between the mass spectrometer and LB-2 analyzer with recirculation circuit during submaximal cycling. Heart rate and oxygen uptake were highly correlated with cardiac output and agreed well with the literature, irrespective of the CO2 analyzer system used. A unique feature of our method is that the subject's tidal volume is measured prior to the maneuver and then used as the initial rebreathing bag volume. Varying the bag volume by +/- 0.2 L from the tidal volume had no significant effect on the estimate of cardiac output during exercise. Now quick, reliable, and noninvasive measurements of cardiac output are feasible in subjects--not only in the laboratory but also in the field where a mass spectrometer is not readily portable.
1. In published studies of the effects of acute blood loss in conscious rabbits, the rates of haemorrhage have ranged for 3-9% of blood volume/min. This is potentially a confounding factor when it comes to comparing the results of different studies. We have therefore tested whether the haemodynamic response to acute central hypovolaemia depends on the rate of fall of cardiac output. 2. Cardiac output in six conscious rabbits was reduced by 4, 8 and 12% of baseline levels per min by gradual inflation of a cuff around the thoracic inferior vena cava. These rates correspond approximately to blood loss at rates of 3, 6 and 9% of blood volume/min. 3. The haemodynamic responses were biphasic. In Phase I (compensatory) there was progressive systemic vasoconstriction and tachycardia, and only a small fall in blood pressure. In Phase II (decompensatory), systemic vasoconstriction failed abruptly, arterial pressure plummeted and heart rate declined. 4. We could detect no effect of rate of fall of cardiac output on the pattern of the haemodynamic responses in either Phase I or Phase II. 5. We conclude that the rate of blood loss in different studies of haemorrhage in conscious rabbits, within the range 3 to 9 per cent of blood volume per minute, need not be regarded as a confounding factor when it comes to interpreting the results. It is likely that this conclusion can be generalized to studies of haemorrhage in other mammalian species.
OBJECTIVE: We sought to evaluate the capacity of a new thoracic electric bioimpedance system to estimate cardiac output in patients with preeclampsia. STUDY DESIGN: We performed a prospective comparison of thoracic electric bioimpedance and echocardiographic M-mode volumetric estimates of cardiac output (in liters per minute) in preeclampsia. Subjects with preeclampsia who were chosen by means of strict criteria (either a systolic blood pressure >/=140 mm Hg or a diastolic blood pressure 90 mm Hg, or both, and proteinuria >/=300 mg in 24 hours or >/=+1 on repeat dipstick measurement 6 hours apart) were asked to participate in an institutional review board-approved study. Thoracic electric bioimpedance and echocardiography were performed with the patients in the left lateral recumbent position. Thoracic electric bioimpedance estimates were recorded at bedside; investigators were blinded to 3 simultaneously obtained echocardiographic M-mode estimates of cardiac output. Means were entered as the estimate for each patient. To satisfy the assumption of independent samples, only 1 estimate from each technique was used for each patient. Data were analyzed by Bland-Altman comparison. Hemodynamic and demographic variables are presented as mean +/- SD. RESULTS: Fifteen patients were enrolled. Mean maternal age was 25.9 +/- 4.8 years, and mean gestational age was 34.0 +/- 3.5 weeks. Mean arterial pressure was 112 +/- 14 mm Hg. There was good agreement of thoracic electric bioimpedance-derived and M-mode-derived cardiac output estimates. CONCLUSIONS: In patients with preeclampsia, thoracic electric bioimpedance estimates of cardiac output compare well with echocardiographic M-mode estimates.
Female broilers were evaluated at 4, 5, and 6 wk of age (1.2, 1.8, and 2.3 kg BW, respectively) to assess changes in cardiac output and related hemodynamics associated with BW gain, and to evaluate cardiopulmonary hemodynamic adjustments occurring secondary to i.v. injections of epinephrine (0.1 mg/ kg BW). Cardiac output increased with BW (253, 348, and 434 mL/min at 4, 5, and 6 wk, respectively) due to increases in stroke volume (0.70, 1.03, and 1.33 mL/beat) that more than compensated for reductions in heart rate (362, 337, and 328 bpm). Normalization for BW eliminated the differences in cardiac output and stroke volume. Increases in cardiac output were not associated with age- or BW-related increases in mean systemic arterial pressure (101.5, 108.6, and 108.0 mm Hg) due to corresponding reductions in total peripheral resistance (0.41, 0.32, and 0.26 relative resistance units). Epinephrine initially triggered immediate (within 90 s) threefold increases in total peripheral resistance and pulmonary vascular resistance, which, in turn, increased the systemic arterial pressure and pulmonary arterial pressure in spite of concurrent reductions in cardiac output that were associated with diminished venous return and dependent reductions in stroke volume and heart rate. Within 150 s after epinephrine injection, the systemic and pulmonary vascular resistances returned to preinjection control levels. By 300 s postinjection, stroke volume and heart rate increased, causing cardiac output to rise above preinjection control levels, which, in turn, elicited variable pulmonary arterial pressure responses apparently reflecting individual variability in the capacity for flow-dependent pulmonary vasodilation. These studies demonstrate that chronic (age- and BW-related) and acute (epinephrine-induced) changes in cardiac output in broilers reflect complex interactions among hemodynamic variables that include stroke volume, heart rate, and systemic and pulmonary vascular resistances.
It is well established that the improvement in gas exchange that occurs with positive pressure ventilation may come at the expense of a decrease in cardiac output and oxygen delivery. Clinical observation suggests that children and infants may be more resistant than adults to the falls in cardiac output induced by positive airway pressure. The aims of this study were to quantify the effect of a sustained increase in intrathoracic pressure on cardiac output and stroke volume, and to determine whether this change is age-related. Twenty-eight children undergoing general anaesthesia were studied. Cardiac output was derived using pulsed wave Doppler techniques at four different levels of sustained positive airway pressure, and stroke volume was calculated. The relationship between airway pressure and both cardiac output and stroke volume was examined using a general linear model which included age as a continuous variable. Cardiac output decreased with increasing levels of sustained positive airway pressure (P = 0.001). The fall in SV for a given airway pressure increased with increasing age (P = 0.02). The mechanisms responsible for the increase of the magnitude of the fall in stroke volume with age remain to be elucidated.
OBJECTIVE: Previous work from our laboratory has demonstrated that optimization of biventricular pacing is load dependent. Cardiac output was maximized with a ventricular-ventricular delay of +40 milliseconds (right ventricle-first pacing) during right ventricular pressure overload and with a ventricular-ventricular delay of -40 milliseconds (left ventricle-first pacing) during right ventricular volume overload. We hypothesized that a model of left ventricular volume overload would also have specific timing requirements during biventricular pacing for optimization of cardiac output. METHODS: After median sternotomy in 6 anesthetized pigs, complete heart block was induced by ethanol ablation. A conduit was grafted from the left ventricle to the left atrium to produce left ventricular volume overload. An ultrasonic flow probe was placed around the conduit to measure retrograde flow that averaged 50% of cardiac output. During epicardial atrial tracking DDD biventricular pacing, atrioventricular delay was varied between 60 and 270 milliseconds in 30-millisescond increments for 20-second intervals. After determination of optimum atrioventricular delay, ventricular-ventricular delay was varied in 20-millisecond increments from +80 to -80 milliseconds for 20-second intervals. RESULTS: Ventricular-ventricular delays had no significant effect on cardiac output with the graft clamped (control). With the graft unclamped, however, there was a statistically significant (P = .0001 by repeated-measures analysis of variance) trend toward higher cardiac output with right ventricle-first pacing. CONCLUSIONS: Right ventricle-first pacing in swine significantly increased cardiac output during acute left ventricular volume overload, but not during the control state. Understanding load-specific pacing requirements will facilitate the development of perioperative temporary biventricular pacing for acute heart failure.
This study was undertaken to determine the optimum number of Doppler velocity waveforms required to calculate cardiac output in atrial fibrillation with the same degree of accuracy as that for sinus rhythm. Twenty-one patients in atrial fibrillation underwent calculations of cardiac output derived from aortic Doppler waveform velocity time integrals and RR intervals. The variability in estimates of the cardiac output was calculated with the successive addition of sequential beats and compared with that determined in a control group of 12 subjects in sinus rhythm. For the group in atrial fibrillation, a mean of 13 beats (range 4 to 17 beats) was required to achieve an estimation of cardiac output with a variability of less than 2%, compared with a mean of four beats in sinus rhythm. In atrial fibrillation, the mean number of beats required to determine cardiac output was approximately three times that necessary in sinus rhythm.
We have been comparing cardiac output measured with a novel Doppler pulmonary artery catheter to that measured by thermodilution and aortic electromagnetometry in cardiac surgical patients. We report here our observation of a nearly twofold increase in thermodilution cardiac output after the acute intraoperative onset of tricuspid regurgitation that was not confirmed by the novel catheter or direct measurement of aortic blood flow. We conclude that in some patients, acute tricuspid regurgitation may lessen the reliability of thermodilution cardiac output.
We have analysed the clinical agreement between two methods of continuous cardiac output measurement pulse contour analysis (PCCO) and a continuous thermodilution technique (CCO), were both compared with the intermittent bolus thermodilution technique (BCO). Measurements were performed in 26 cardiac surgical patients (groups 1 and 2, 13 patients each, with an ejection fraction > 45% and < 45%, respectively) at 12 selected times. During operation, mean differences (bias) between PCCO-BCO and CCO-BCO did not differ in either group. However, phenylephrine-induced increases in systemic vascular resistance (SVR) by approximately 60% resulted in significant differences. Significantly higher absolute bias values of PCCO-BCO compared with CCO-BCO were also found early after operation in the ICU. Thus PCCO and CCO provided comparable measurements during coronary bypass surgery. After marked changes in SVR, further calibration of the PCCO device is necessary.
PURPOSE: The purpose of this study was to determine whether the pattern of respiratory variation in right atrial pressure (Pra) predicts the cardiac output response to positive end-expiratory pressure (PEEP). MATERIALS AND METHODS: We studied 18 patients with a variety of cardiac and pulmonary disorders requiring ventilatory support. A pulmonary artery flotation catheter was in place as part of their routine management. Changes in PEEP were made from 0 to 14 cm H2O to determine the level of PEEP, which increased PO(2) without decreasing cardiac output (ie, assessment of best PEEP). Static lung compliance and auto-PEEP were obtained from the pressure signal on the ventilator. The change in Pra with a spontaneous inspiratory effort (ie, triggered breath) was used to determine whether patients had a restrictive (ie, operating on the flat part of the Starling curve), or nonrestrictive pattern (acting on the ascending part of the Starling curve) as previously described. RESULTS: Cardiac output decreased 0.7 +/- 0.8 L/min (change from baseline P <.05) in the group with an inspiratory decrease in Pra and -0.04 +/- 1.50 L/min (P = NS) in the group without an inspiratory decrease in Pra. The groups were not significantly different. However, the variance in cardiac output was large and, in contrast to our hypothesis, two patients in the group with an inspiratory decrease in Pra did not have a decrease in cardiac output. Pra and pulmonary artery occlusion pressure after the PEEP trial were greater than before, indicating that reflex circulatory adjustments occurred in response to the PEEP. CONCLUSIONS: The inspiratory pattern in Pra does not predict the response to cardiac output to PEEP in individual patients. This is most likely because of reflex adaptations in the circuit that occur with the application of PEEP. The response of a patient to PEEP is affected by the patient's volume reserves, filling status of the right atrium, and neurosympathetic activity.
This article reviews the available literature on the validity and reliability of the non-invasive techniques, commonly known as CO2 rebreathing, for estimating cardiac output. The differing indirect methodologies are described and illustrated. A table, constructed from the available literature, comparing criterion versus estimated cardiac outputs is presented. The varying combinations of methods employed, differing measurement conditions, i.e. rest and exercise, and divergent populations are illustrated and discussed. The correlation between criterion and estimated cardiac output for these studies ranged from r = 0.09 to 0.96, with a % standard deviation of the differences of 1.5 to 176.8%. The Collier and end-tidal methods, in conjunction with either the Comroe or McHardy CO2 dissociation curve appears to be the most established, valid and reliable combination of methods for estimating resting cardiac output. These methods appear to be comparable to the combination of the Defares, end-tidal and Comroe curve methods for estimating cardiac output during exercise. Because of the potential for large errors, caution is urged when interpreting cardiac output results based on indirect estimation for individual assessment, or for subjects with certain types of pulmonary or heart diseases.
The ability to predict cardiac output (CO) before termination of cardiopulmonary bypass (CPB) allows identification of potential complications once the patient is off bypass. We have previously demonstrated that CO early after CPB can be reliably predicted by a plot of venous oxygen saturation at various flow rates on CPB, based on in-line monitoring of venous oxygen saturation. In this study, we evaluated a simplified technique for predicting CO with a series of 50 patients on CPB. When CPB weaning began, patients were normothermic, anesthetized, and paralyzed. Venous oxygen saturation and arterial blood flow were recorded. At low pump flow just before termination of CPB, the final venous oxygen saturation was recorded. Assuming a proportional relationship between venous oxygen saturation and arterial blood flow, CO early after CPB was predicted. The simplified CO prediction was compared with the thermodilution CO immediately after CPB. The simplified technique reliably predicted CO early after CPB compared with the thermodilution technique. The simplicity and reliability increase the clinical value of the CO prediction.
Cardiac output (CO) and the blood flow to the heart, cerebellum, kidney, pancreas, spleen and skeletal muscle were studied in 20 pigs during spontaneous breathing (SB) and intermittent positive pressure ventilation (IPPV) with a positive end-expiratory pressure (PEEP) of 0, 8, 16 or 24 cmH2O. Microspheres (15 micrometers) labelled with either 85-sr or 141-Ce were used. Injection of microspheres labelled with one of the isotopes was given during SB (all pigs) and with the other isotope during IPPV with PEEP of 0, 8, 16 or 24 cmH2O (five pigs at each level). CO decreased by 11% during IPPV with PEEP of 0 and 31%, 53% and 66% during PEEP of 8, 16 or 24 cmH2O, respectively. Mean arterial blood pressure was fairly well maintained in all groups except the group with PEEP of 24 cmH2O. The perfusion of the six organs deteriorated, but when taken as fractions of CO measured at the same time, the blood flow to the heart, cerebellum and kidney increased with increasing airway pressure, while that to the pancreas, spleen and skeletal muscle decreased. The vascular resistance of the three former organs did not change, while in the latter it increased markedly. It is concluded that when CO decreases as a result of positive pressure ventilation, a redistribution takes place, mainly due to vascular constriction in skeletal muscle, which acts to preserve the blood flow to vital organs.