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PubMed2002

Clinical evaluation of a partial CO2 rebreathing technique for cardiac output monitoring in critically ill patients.

BACKGROUND: Monitoring central hemodynamics is essential in critically ill patients and less invasive techniques are needed. In this study, the clinical and technical performance of a new non-invasive cardiac output monitor (NICO) based on partial CO2 rebreathing technique and a modified Fick equation were evaluated. The various sources of possible errors in measurement of cardiac output (CO), carbon dioxide production (VCO2) and pulmonary shunt were also assessed. METHODS: Simultaneous measurements of CO with partial CO2 rebreathing technique (CO(nico)) and thermodilution (CO(td)) were performed in 15 patients during major surgery or in the ICU. Pulmonary shunt was estimated from this device and compared to values obtained by standard shunt formula. The accuracy of VCO2 measurements was assessed in a mechanical lung model. RESULTS: A good correlation was found between CO(nico) and CO(td) (r = 0.96, within-subject correlation r = 0.88) with a small underestimation of cardiac output by the NICO of 0.04 L/min, limits of agreement (+/- 2 SD) being - 1.68 and 1.76 L/min. In hemodynamic unstable patients the method closely tracked changes in CO. Pulmonary shunt was underestimated by approximately 11%-units compared to standard shunt calculations using arterial and mixed venous blood gases. We also observed an underestimation in VCO2 measurements. CONCLUSION: Clinical evaluation shows that partial CO2 rebreathing technique provides a useful and accurate non-invasive estimate of cardiac output. Although this technique cannot fully replace the pulmonary artery catheter, it may be used to monitor central hemodynamics in a large number of critically ill patients.

Adult↗
PubMed1990

Cardiac output effects of endothelin-1, -2 and -3 and sarafotoxin S6b in conscious rats.

Conscious, Long-Evans rats, chronically-instrumented for the direct measurement of intra-arterial and central venous pressures and ascending aortic blood flow (i.e. cardiac output), were given bolus, intravenous doses (4 and 40 pmol) of endothelin-1, -2, or -3 or sarafotoxin S6b in random order. The lower dose of endothelin-1 and -3 and sarafotoxin S6b caused a significant increase in cardiac output. The higher bolus dose of the same three peptides caused initial hypotension and increases in cardiac output, stroke volume and total peripheral conductance. Endothelin-2 did not have these initial effects in all animals. Subsequently, all peptides increased mean arterial blood pressure and decreased cardiac output and total peripheral conductance. Overall the effects of endothelin-1 and sarafotoxin S6b were very similar, consistent with them acting at the same site.

Animals↗
PubMed2000

[Continuous recording of cardiac output volume with the OptiQ system--experiences with clinical application].

This report discusses initial experiences with the clinical application of continuous cardiac output measurement (OptiQ SvO2/CCO-System). The system was used in 9 intensive care patients suffering either global cardiac insufficiency or systemic inflammatory response syndrome. Continuous cardiac output measurement was recorded during a period of stable blood pressure conditions and compared with the results of the conventional thermodilution method (bolus technique) in these patients. Regression analyses yielded r = 0.523 (r2 = 0.274) for the "urgent" mode, r = 0.943 (r2 = 0.889) for the "fast" mode, r = 0.953 (r2 = 0.907) for the "fast filter" mode and r = 0.990 (r2 = 0.980) for the "normal" mode. Mean differences between the continuous and the bolus technique were calculated as -0.13 +/- 1.81 l/min for the "urgent" mode, -0.42 +/- 0.51 l/min for the "fast" mode, -0.14 +/- 0.48 l/min for the "fast filter" mode and -0.08 +/- 0.19 l/min for the "normal" mode. After a period of two days, the costs of the conventional bolus technique significantly exceeded those of continuous measurement. The expenses for the conventional thermodilution technique are largely determined by the frequency of application and, hence, by the personnel and laboratory costs. In our experience, easy component handling and stable measuring properties make this new method of continuous cardiac output monitoring a valuable method in the diagnose and care of patients who are critically ill.

Cardiac Output↗
PubMed1986

Dobutamine-induced augmentation of cardiac output does not enhance respiratory gas exchange in anesthetized recumbent healthy horses.

The influence of pharmacologic enhancement of cardiac output on the alveolar-to-arterial oxygen tension (difference (P[A-a]O2), physiologic right-to-left shunt fraction (Qs/Qt), and physiologic dead space-to-tidal volume ratio (VD/VT) ws studied in halothane-anesthetized horses in left lateral, right lateral, and dorsal recumbencies. Adult horses were anesthetized, using xylazine (2.2 mg/kg, IM), guaifenesin (50 mg/kg, IV), thiamylal (4.4 mg/kg, IV), and halothane (1.5% to 2% inspired) in 100% O2. Mechanical ventilation was controlled to maintain arterial eucapnia (PaCO2) 35 to 45 mm of Hg) for a period lasting at least 1 hour. Dobutamine was administered at dosages of 1, 3, and 5 micrograms/kg/min, IV, on a randomized basis. The P(A-a)O2, Qs/Qt, and VD/VT were calculated during equilibration and after each dobutamine infusion was given. The P(A-a)O2 and Qs/Qt were significantly (P less than 0.05) greater and VD/VT tended to be greater in horses in dorsal recumbency, compared with those values in horses in left lateral or right lateral recumbency. Cardiac output was similar in all horses, regardless of body position (recumbency). The qualitative relationship between horses in the 3 recumbent positions were not altered by dobutamine. Cardiac output was significantly (P less than 0.05) increased by 3 or 5 micrograms of dobutamine/kg/min in all horses, whereas P(A-a)O2, Qs/Qt, and VD/VT were not significantly altered by dobutamine. The results of the present study failed to substantiate our clinical observations of decreased P(A-a)O2 and Qs/Qt in anesthetized compromised horses given dobutamine.

Anesthesia, General↗
PubMed1977

Changes in cardiac output distribution after liver dearterialization in the rat.

The changes in cardiac output distribution in rats have been studied after hepatic artery ligation and additional ligament division. These procedures resulted initially in a marked decrease in the arterial blood supply to the liver and this effect was pronounced still four weeks after the operation. Evidence was found that the decrease in liver blood supply induced by the procedure was in part counterbalanced by arteriovenous shunting in the preportal region. Furthermore, a temporary redistribution of cardiac output with reduced fractions to colon and spleen was found two weeks after these operations.

Animals↗
PubMed1984

Effects of cardiac output on the clearance of air emboli from the superior vena cava.

The authors assessed the effect of cardiac output on the rate of clearance of air emboli from the superior vena cava (SVC) in 11 dogs placed in a supine 30 degrees head-up inclined position. Venous air emboli were produced by infusing 4 ml of air into the dorsal sagittal sinus. Air emboli appearance and clearance from the SVC were determined from the analog record produced by a transesophageal Doppler ultrasound monitor. Cardiac output was altered by changing the level of anesthesia and the administration of intravenous fluid. Eighty-eight per cent of air infusions resulted in an analog response of consistent amplitude indicating that all or a similar fraction of the infused air arrived consistently at the ensonified region of the SVC. In this group, air emboli passed from the SVC with a clearance time (CT) that was related inversely to the cardiac index (CI). CT = 24 CI-1.3 with a correlation coefficient = 0.57. Following 12% of the air infusions, there was evidence that a part of the air became detained in vascular sites cranial to the ensonified portion of the SVC. This evidence consisted of the following observations: analog responses were diminished in amplitude; subsequent air injections evoked responses that sometimes were exaggerated; and/or subsequent increases in cardiac output alone, produced spontaneous analog responses characteristic of air emboli. The authors postulate that air similarly may be detained in clinical settings and may explain such phenomenon as persistent precordial Doppler sounds of air emboli after pulmonary artery pressure has returned to normal following symptomatic air embolism and occurrence of air emboli after scalp closure.

Animals↗
PubMed1987

Role of the alpha agonist activity of dobutamine in mediating cardiac output: effects of prolonged isoproterenol infusion.

Hemodynamic activities of dobutamine enantiomers were studied in either control rats or those infused with isoproterenol (400 micrograms/kg/hr) for 4 days. In control animals prazosin attenuated the effects of (+/-)-dobutamine on cardiac output by approximately 50%; remaining activity was blocked by propranolol. After isoproterenol infusion (+/-)-dobutamine was less efficacious and the blocking effects of prazosin were greater than 90%. Isoproterenol infusion had no effect on (-)-dobutamine-mediated (alpha-1 adrenoceptor agonist) increases in cardiac output and these actions were blocked by prazosin. By contrast, compared to (+/-)- and (-)-dobutamine, effects of (+)-dobutamine (beta adrenoceptor agonist) on cardiac output were modest, not altered by prazosin and were blocked by propranolol; (+)-dobutamine was inactive after isoproterenol infusion. (-)-Dobutamine increased systemic vascular resistance in both control and isoproterenol infused rats, whereas (+)-dobutamine was inactive. (+/-)-Dobutamine increased systemic vascular resistance only in isoproterenol-infused rats. All increases in systemic vascular resistance were blocked by prazosin. Neither (+/-)- nor (+)-dobutamine significantly altered stroke volume. By contrast, (-)-dobutamine resulted in prazosin-sensitive increases in stroke volume in both control and isoproterenol-infused rats. In control animals, (+/-)-, (+)- and (-)-dobutamine increased heart rate in a dose-dependent manner; chronotropic effects of (-)-dobutamine were less than those of either (+/-)- or (+)-dobutamine. Chronotropic effects were not demonstrable in isoproterenol-infused animals. These data support the notion that in control rats cardiac output may be increased by either alpha or beta adrenoceptor stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Agonists↗
PubMed1986

[Monitoring of cardiac output during use of bupivacaine 0.75% by ventriculography (99mTC)].

Fifteen patients undergoing orthopaedic surgery on the lower limbs were give continuous epidural anaesthesia with bupivacaine 0.75%. It was looked after changes in heart frequency, beat volume and changes in heart rhythm. Changes in cardiac output were investigated by ventriculography with 99mTC during 4 periods--10 min before and 10, 20 and 30 min after epidural blockade--the cardiac output was measured by a computer mathematically. Each patient received 2 mg/kg body weight of bupivacaine 0.75%. Besides the observation of blood pressure, heart rate and electrocardiogram the venous plasma levels of bupivacaine were measured up to 60 min after blockade. The results showed no changed in cardiac output. Except for one case with bradycardia--which could be treated with atropine--no changes in heart frequency occurred. Tachy- or bradycardia was not seen at all. Besides rare respiratory sinus arrhythmia no arrhythmia could be detected. The venous plasma levels of bupivacaine increased after 30 min up to 0.81 microgram/ml. The highest concentration measured was 1.45 microgram/ml 10 min after injection of bupivacaine. According to the results of the study the following statement can be given: Following bupivacaine 0.75% (2 mg/kg) given epidurally no changes in cardiac output, no changes in beat frequency, no pathological changes in cardiac rhythm and no specific cardiac toxicity related to bupivacaine 0.75% could be found in this study.

Adult↗
PubMed1998

[Retrospective analysis of transpulmonary and pulmonary arterial measurement of cardiac output in ARDS patients].

OBJECTIVES: To investigate the agreement (and its potential dependency on extra-vascular lung water) between transpulmonary (TPID) and standard pulmonary artery (PAID) thermodilution cardiac output measurements. METHODS: One hundred and sixty simultaneous cardiac output measurements using transpulmonary and pulmonary artery thermodilution techniques were retrospectively compared in 18 patients with acute respiratory distress syndrome. In addition, extravascular lung water was determined using a double indicator technique (temperature and indocyanine green). RESULTS: Mean (+/- SD) difference ("bias") was 0.03 L/min (+/- 1.04 L/min), linear regression analysis resulted in TPID = 0.87 PAID + 1.16 (r = 0.91). Mean extra vascular lung water was 1625 mL (minimum-maximum: 403-3266 mL) and therefore markedly elevated as could have been expected in patients with ARDS. Bias (PAID-TPID) was not dependent on extravascular lung water. CONCLUSIONS: Transpulmonary and pulmonary artery thermodilution methods can be used interchangeably. The results demonstrate for the first time in humans that transpulmonary thermodilution provides valid cardiac output values in patients with markedly increased fluid content of the lungs.

Adult↗
PubMed1985

Cardiac output in infants of insulin-dependent diabetic mothers.

The purpose of our study was to quantitate left ventricular outflow obstruction in the infant of the diabetic mother (IDM) through estimation of cardiac output by pulsed Doppler ultrasound. We evaluated 42 IDMs (White class B, C, or D) and compared them with two control groups, one similar in birth weight and the other similar in gestational age. Ventricular septal hypertrophy was found in 18 (43%) of 42 of the IDMs, but in none of the control infants. Morbidity increased with advancing septal thickness. None had hyaline membrane disease. Twenty-nine IDMs were asymptomatic, 11 of whom had septal hypertrophy. Thirteen IDMs developed congestive heart failure, seven of whom had septal hypertrophy. Cardiac output per kilogram diminished linearly with increasing septal thickness (r = -0.78, P less than 0.001) secondary to reduced stroke volumes at comparable heart rates. The IDMs had higher left atrial/aortic ratios and greater right ventricular systolic time intervals than the control infants. We conclude that cardiac output is significantly reduced in IDMs with septal hypertrophy. This reduction is secondary to reduced stroke volume and is directly related to the degree of septal hypertrophy.

Birth Weight↗
PubMed1989

Cardiac output at rest and in exercise in elderly subjects.

We measured cardiac output (Q), at rest and during graded exercise, in 68 women and 41 men over the age of 55 yr, using a CO2 rebreathing method. Mean (+/- SD) age was 66 +/- 5 yr in women and 66 +/- 6 yr in men. Only subjects with no history or physical examination findings of pulmonary, cardiac, neuromuscular, or endocrine disease and normal electrocardiography and spirometry were studied. We found a linear relationship between Q and oxygen uptake (VO2) in males and females. The regression equation expressing this relationship in males was Q = 2.9 + 5 VO2 1.min-1 (SEE 2.8) and, in females, Q = 2.9 + 4.6 VO2 1.min-1 (SEE 2.8). This is similar to the relationship previously estimated for elderly males using the direct Fick method and concurs with other reports in the literature which show that, while the Q-VO2 relationship in the elderly has a slope similar to that in younger groups, the Q-VO2 intercept is lower. This means that the absolute level of cardiac output for a given level of work is lower in the elderly than in younger populations. This may reflect an age-related decrease in active metabolic tissue in the elderly and/or altered metabolic regulation with increased oxygen extraction from blood.

Aged↗
PubMedDate not supplied

Validation of the saline-dilution method for measuring cardiac output by simultaneous measurement with a perivascular electromagnetic flowprobe.

The validity of measurements of right heart output obtained by the saline-indicator method with a catheter-mounted, tetrapolar resistivity sensor placed in the pulmonary artery was assessed. In ten anesthetized dogs, cardiac output was measured simultaneously by the saline-indicator method, using 5 ml of 3 per cent saline as the indicator, and by a perivascular electromagnetic flowprobe placed around the trunk of the pulmonary artery. Cardiac output was altered over a wide range by increasing the depth of halothane anesthesia and by bolus injections of isoproterenol. Linear regression analysis of cardiac output determined from 455 saline-indicator curves and from simultaneous recordings of the electromagnetic flow signal yielded a slope of 0.973, a Y intercept of -0.0047 1/minute, and a correlation coefficient of 0.965. Hence, this method provides accurate and precise measurement of cardiac output. The saline-indicator method with the catheter-mounted resistivity sensor is simple to use and eliminates or minimizes the disadvantages of other indicator-dilution techniques.

Animals↗
PubMed1994

[Simple method to estimate cardiac output using first-pass data on RI angiography].

In order to estimate cardiac output (CO) without using data equilibrium state, a simple index (cardiac output index, COI) was developed from the first-pass data as a ratio of the integrated radioactivity on the right ventricle to the total injected radioactivity. COI was well correlated with CO calculated by the conventional Stewart-Hamilton method (r = 0.894, p < 0.01), and thus, CO could be readily estimated from COI. This index might be useful to estimate CO since it can be obtained even with the agents which distribute to organs.

3-Iodobenzylguanidine↗
PubMed1998

L-arginine restores the depressed cardiac output and regional perfusion after trauma-hemorrhage.

BACKGROUND: Previous studies indicate that vascular endothelial cell dysfunction occurs early after trauma-hemorrhage and may contribute to further alteration in tissue perfusion and cellular function. Because endothelial cell dysfunction is characterized by the reduced release of nitric oxide (NO) by endothelial constitutive NO synthase (cNOS), we tested the hypothesis that administration of L-arginine (ie, the substrate for cNOS) after trauma and hemorrhage should have beneficial effects on depressed cardiac output and organ blood flow under those conditions. METHODS: Rats underwent a laparotomy (ie, trauma induced) and were bled to and maintained at a mean arterial pressure of 40 mm Hg until 40% of maximal shed blood volume was returned in the form of Ringer's lactate solution. The animals were than resuscitated with 4 times the volume of the shed blood in the form of Ringer's lactate solution over 1 hour. L-arginine (300 mg/kg body wt) or saline solution was infused intravenously during the first 15 minutes of resuscitation. Cardiac output and organ blood flow were determined by 85Sr-microspheres at 1.5 and 4 hours after the completion of resuscitation. Plasma interleukin-6 (IL-6) was determined by bioassay at 4 hours after resuscitation. RESULTS: Cardiac output and blood flow in the kidneys, small intestine, and lungs decreased significantly after hemorrhage and resuscitation. In addition, portal blood flow and total hepatic perfusion were also significantly reduced. Administration of L-arginine at the onset of fluid resuscitation, however, restored the depressed cardiac output and tissue perfusion. Moreover, the up-regulated plasma levels of IL-6 were also attenuated by L-arginine administration. CONCLUSIONS: Because the adjuvant use of L-arginine restored the depressed cardiac output and organ blood flow and decreased plasma levels of IL-6, administration of this essential amino acid should be considered as a useful adjunct to fluid resuscitation for improving cardiovascular function in trauma victims.

Animals↗
PubMed1990

Unilateral megalencephaly associated with neonatal high output cardiac failure.

High-flow cerebral arteriovenous fistulae are well known to present in the neonatal period with macrocephaly, cranial bruits and high-output cardiac failure. This report describes a newborn infant with such a clinical presentation, who had unilateral megalencephaly without macroscopic arteriovenous shunts. Ultrasound Doppler examination of the carotid and cerebral vessels showed diastolic flow, or a decreased pulsatility index, consistent with decreased intracranial vascular resistance. The ipsilateral cerebral arteries and veins were markedly enlarged at angiography and at post-mortem examination, but there was no arteriovenous malformation. The infant expired from high-output cardiac failure and hypoglycemia. It is postulated that the high-output cardiac failure was due to increased blood flow through the enlarged, dysplastic cerebral hemisphere.

Brain↗
PubMed1963

Cardiac output during cardiopulmonary bypass. Animal experiments as a guide to flow rate.

Superior total body perfusion during cardiopulmonary bypass in dogs is achieved by duplicating, in each individual case, the actual operative cardiac output, rather than by relying on the currently recommended perfusion flow rates.A highly accurate method of measuring the cardiac output is presented using the gated sinewave electromagnetic flowmeter. Simplicity and sensitivity of the method enable the operator to measure the flow in situ (in the intact canine ascending aorta) and thus to determine a truly representative cardiac output before the cardiopulmonary bypass is effected. An adjustable hydraulic pump in conjunction with the electromagnetic flowmeter is used to substitute the natural cardiac action in order to maintain the normal hemodynamic state by providing a pulsatile flow of proper magnitude. The procedure is technically simple and, supported by favorable experimental evidence, is recommended for clinical use in open heart operations.

Animal Experimentation↗
PubMed1982

Effects of chronic exercise on cardiac output and its determinants.

A protocol which combines the noninvasive measurement of cardiac output (Q), systolic time intervals (STIs), and blood pressure was used to evaluate the effects of jogging on cardiac function. Studies were conducted during levels of steady-state cycle ergometer exercise which represented approximately 35, 55, and 75% of aerobic capacity. Subjects were 15 healthy men (mean age = 37.2 years) and 13 healthy controls. Predicted aerobic capacity (pred VO2max) increased 15 and 17% in the training group after 3 and 6 months of training; the control group displayed a small detraining effect. Changes in the training group versus control group included significant increases in exercise Q, stroke volume (SV), mean systolic ejection rate (MSER), and systolic blood pressure (SBP). Changes in STIs were small and usually nonsignificant. The findings, considered in relation to echocardiographic measurements from the same subjects (L. A. Wolfe, D. A. Cunningham, P. A. Rechnitzer, and P. M. Nichol. 1979 J. Appl. Physiol. 47: 207-212.), suggested that changes in cardiac output were due to an increased preload, rather than a change in exercise heart rate, reduced afterload, enhanced contractile state, or myocardial enlargement.

Adult↗