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PubMed2003

Validity and reliability of cardiac output by arterial thermodilution and arterial pulse contour analysis compared with pulmonary artery thermodilution in intensive care unit.

Cardiac output measurement has a significat role in the critical care setting. The standard of measurement currently is via pulmonary arterial catheter but it has some technical difficulties and serious complications. The authors performed a new method of measurement that used a catheter in a femoral artery. The results of both methods performed simultaneously in 10 surgical intensive care patients every 2 hours for 24 hours were compared. There was high correlation between the two methods, r = 0.97. The average difference of the cardiac output values was 0.46 l/min with standard deviation 0.56 l/min.

Adult↗
PubMed1977

The contribution of alterations in cardiac output to changes in arterial pressure reflexly evoked from the carotid sinus in the rabbit.

1. The reflex cardiovascular effects of changes in pressure within the vascularly isolated carotid sinus were examined in seventeen anaesthetized rabbits. The opposite sinus was denervated and both aortic nerves were divided, 2. Comparison of the mean values at sinus pressures of 40 and 200 mmHg showed a large reduction in systemic arterial pressure from 126 to 58 mmHg and a moderate reduction in heart rate, from 287 to 253 beats min-1. Cardiac output, measured by thermal dilution, showed only a small change, a fall from 160 to 148 ml. min-1 kg-1. 3. By contrast with this reduction in cardiac output of just over 7%, total peripheral resistance, derived by dividing mean arterial pressure by cardiac output, was halved, falling from 0-48 to 0-41 mmHg ml.-1 min kg. 4. Thus in the anaesthetized rabbit changes in cardiac output make only a small contribution to the changes in systemic pressure evoked by alterations in carotid sinus pressure. Changes in total peripheral resistance are principally responsible for the effect on systemic pressure. 5. Though the changes in output of the heart were small, there were considerable changes in the work done by the left ventricle which was approximately halved when carotid sinus pressure was raised from 40 to 200 mmHg.

Animals↗
PubMed2002

Noninvasive cardiac output assessment during heart surgery.

OBJECTIVE: To evaluate the reliability of a new noninvasive method for the assessment of cardiac output with the partial carbon dioxide rebreathing technique. METHODS: This technique was applied to patients undergoing heart surgery. Values of cardiac index obtained with this equipment were compared with the artero-venous CO2 gradient, a reliable index of cardiovascular status. Positive and negative predictive values of the test were assessed. RESULTS: A total of 21 simultaneous measurement of the cardiac index and of the artero-venous CO2 gradient were obtained. The positive predictive value of the test was 67% while the negative predictive value was 100%, indicating that a normal value of cardiac index recorded with the rebreathing technique predicts with a good reliability a normal cardiovascular state. CONCLUSIONS: Working through a series of mathematical algorithms, accuracy in the computation of cardiac output can be decreased with this equipment; however, this limitation seems to be outweighed by the simplicity and noninvasive nature of the methods.

Algorithms↗
PubMed1998

Liquid ventilation improves pulmonary function and cardiac output in a neonatal swine model of cardiopulmonary bypass.

OBJECTIVE: Neonatal and infant cardiopulmonary bypass results in multiorgan system dysfunction. Organ protective strategies have traditionally been directed at the myocardium and brain while neglecting the sometimes severe injury to the lungs. We hypothesized that liquid ventilation would improve pulmonary function and cardiac output in neonates after cardiopulmonary bypass. METHODS: Twenty neonatal swine were randomized to receive cardiopulmonary bypass with or without liquid ventilation. In the liquid-ventilated group, a single dose of perflubron was administered before bypass. The control group was conventionally ventilated. Each animal was placed on nonpulsatile, hypothermic bypass. Low-flow cardiopulmonary bypass was performed for 60 minutes. The flow rate was returned to 125 ml/kg per minute, and after warming to 37 degrees C, the animals were removed from bypass. Hemodynamic and ventilatory data were obtained after bypass to assess the effects of liquid ventilation. RESULTS: Without liquid ventilation, cardiopulmonary bypass resulted in a significant decrease in cardiac output, oxygen delivery, and static pulmonary compliance compared with prebypass values. Input pulmonary resistance and characteristic impedance increased in these control animals. At 30, 60, and 90 minutes after bypass, the animals receiving liquid ventilation showed significantly increased cardiac output and static compliance and significantly decreased input pulmonary resistance and characteristic impedance compared with control animals not receiving liquid ventilation. CONCLUSIONS: Liquid ventilation improved pulmonary function after neonatal cardiopulmonary bypass while increasing cardiac output. The morbidity associated with cardiopulmonary bypass may be significantly reduced if the adverse pulmonary sequelae of bypass can be diminished. Liquid ventilation may become an important technique to protect the lungs from the deleterious effects of cardiopulmonary bypass.

Animals↗
PubMed1996

Comparison of Doppler echocardiography with thermodilution for assessing cardiac output in advanced congestive heart failure.

Noninvasive cardiac output estimation by Doppler echocardiography was compared with thermodilution and Fick oxygen methods in 73 patients with advanced chronic congestive heart failure due to dilated cardiomyopathy. In these patients, Doppler echocardiographic measurements showed a closer agreement with Fick measurements than that of thermodilution.

Cardiac Output↗
PubMedDate not supplied

Doppler flowmetry in the lower thoracic aorta. An indirect estimation of cardiac output.

Duplex scanning of the lower thoracic aorta was performed on 67 patients subjected to routine left and right heart catheterization with estimation of cardiac output ad modum Fick. Adequate Doppler signals from the lower thoracic aorta were obtained in 59 patients (88%), 26 of whom had aortic valve abnormality. A high correlation was found between the Doppler and Fick findings (r=0.89), with a regression line intercepting close to zero (cardiac output = 1.76 X Doppler flow +0.05). The presence of aortic valve abnormality did not seem to influence the accuracy of the Doppler flow results. It is concluded that Doppler flowmetry in the lower thoracic aorta is a useful method in estimation of resting cardiac output, especially in patients with aortic valve lesions making Doppler flowmetry in the ascending aorta impossible.

Adult↗
PubMed1997

Cold stress provokes sympathoinhibitory presyncope in healthy subjects and hemodialysis patients with low cardiac output.

BACKGROUND: Sudden hypotension in progressive hypovolemia or during hemodialysis is attributed to sudden inhibition of sympathetic activity. Critical ventricular underfilling seems responsible for this paradox, but it is unknown why the transition from sympathoactivation accompanying hypovolemia to sympathoinhibition is so abrupt. We studied whether brief fluctuation of sympathetic activity induced by cold pressor test (CPT) evokes sympathoinhibition if applied during low cardiac output. METHODS AND RESULTS: Fourteen healthy subjects underwent CPT, lower-body negative pressure (LBNP; -45 mm Hg for 60 minutes), or the combination thereof. CPT alone caused vasoconstriction and increased muscle sympathetic nerve activity, followed by uneventful relaxation. When applied during reduced cardiac output, tachycardia, and vasoconstriction induced by prior LBNP for 6 minutes, CPT again caused vasoconstriction, now followed by acute hypotension in 10 subjects, and was associated with vasorelaxation, relative bradycardia, and fall in muscle sympathetic nerve activity. Eight subjects also experienced acute LBNP-induced hypotension in the absence of CPT, but not until 17 +/- 6 minutes of LBNP. We also performed CPT before and in the final phase of hemodialysis in 8 patients. Before dialysis, the patients tolerated CPT uneventfully, but during hemodialysis, CPT provoked acute hypotension in 5 cases, showing similar withdrawal of vasoconstriction. CONCLUSIONS: This is the first study showing that brief cold stress, tolerated well in normal circulatory conditions, can provoke sudden sympathoinhibition and hypotension when applied during decreased cardiac output induced by LBNP or hemodialysis. We suggest that during conditions of a decreased cardiac output, subtle sympathetic relaxation such as follows cold stress triggers self-enhancing relaxation that cannot be controlled.

Adult↗
PubMed1993

Cocaine-induced myocardial ultrastructural alterations and cardiac output responses in rats.

Cocaine use has been associated with profound functional and pathological myocardial responses in otherwise asymptomatic humans, yet a number of individuals appear to tolerate large doses of the drug. This study was designed to determine whether there is a relationship between the differential effects of cocaine administration on cardiovascular responses and on the development of cardiomyopathies in rats. After instrumentation for determination of cardiac output, conscious, freely moving rats were treated with cocaine (5 mg/kg) or saline intravenously twice daily for 14 days before removing the myocardium for analysis. Although most cardiovascular responses were similar, cocaine administration elicited consistent decreases in cardiac output in some rats, whereas others showed little change or an increase. While little change was evident at low magnification, electron microscopy revealed diffusely distributed myocardial lesions including focally dilated sarcoplasmic reticulum and myofibrillar derangement, early signs of mitochondrial alterations, and foci of myocardial fibrosis. The incidence of these alterations was greater in rats with a decrease in cardiac output. We also observed these lesions in a subset of rats treated with cocaine without cardiac output instrumentation. These data represent the first evidence that there is a relationship between cocaine-induced functional and pathological alterations and that rats, like humans, may be differentially sensitive to these effects.

Animals↗
PubMed1991

Low oxygen delivery produced by anemia, hypoxia, and low cardiac output.

In pentobarbital-anesthetized dogs, oxygen delivery (DO2) was measured by thermodilution cardiac output and cooximeter determined oxygen content, while oxygen consumption (VO2) was measured independently by spirometry. Oxygen delivery was decreased by isovolemic dilutional anemia, breathing hypoxic gas mixtures, or cardiac tamponade to reduce cardiac output. Baseline VO2 (cc/kg/min) for the three groups was 5.9 +/- 0.7 (anemia), 5.4 +/- 0.4 (hypoxia), and 5.6 +/- 0.1 (low C.O.) (NS). A critical level of oxygen delivery (DO2crit) was found at 9-10 cc/kg/min (anemia), 10-11 cc/kg/min (hypoxia), and 9-10 cc/kg/min (low C.O.) (NS.). Below this level, VO2 fell (became supply dependent) and lactic acidosis occurred, regardless of the mechanism of impaired oxygen delivery.

Anemia↗
PubMed1997

Dissociation between the increase in systemic vascular resistance induced by acute nitric oxide synthesis inhibition and the decrease in cardiac output in anesthetized dogs.

The decrease in cardiac output (CO) that follows nitric oxide (NO) synthesis inhibition is thought to be the result of an increase in systemic vascular resistance (SVR). We investigated whether sodium nitroprusside (SNP) and iloprost prevent the decrease in CO induced by short-term administration of N omega-nitro-L-arginine methyl ester (L-NAME) in anesthetized dogs. The left femoral artery and vein were cannulated for mean arterial blood pressure (MABP) measurement and drug administration, respectively. A Swan-Ganz thermodilution catheter was inserted into the right femoral vein and allowed the determination of CO and the calculation of SVR, expressed as the cardiac index (CI) and the index of systemic vascular resistance (ISVR), respectively. L-NAME (0.01-10.0 mg/kg; n = 13) induced dose-dependent increases in MABP and in the ISVR. These changes were accompanied by significant decreases in both the CI and the heart rate. SNP (1 microgram/kg/min; n = 6) virtually abolished L-NAME-induced hypertension and significantly attenuated both the increase in the ISVR (< 3.0 mg/kg) and the decrease in CO. Iloprost (50 ng/kg/min; n = 6) also abolished L-NAME-induced hypertension and markedly attenuated the increase in SVR. However, the decrease in CO was not prevented by this vasodilator. These results clearly demonstrate that the increase in SVR is not the major factor accounting for the decrease in CO after short-term NO synthesis inhibition in anesthetized dogs.

Anesthesia↗
PubMed2000

[Relation between oxygen consumption and cardiac output during inhalation anesthesia under the influence of catecholamines. A study in dogs].

OBJECTIVE: The metabolic regulation of tissue blood flow manifests itself in a linear relation between blood flow and oxygen consumption (VO2). It is unknown, however, if this fundamental physiological principle operates also during inhalation anaesthesia and catecholamine therapy, both known to be associated with changes of cardiac output (Q) and VO2 in opposite directions. METHODS: On different days, 17 trained, healthy dogs (26-33 kg) with chronically implanted flow probes around the pulmonary artery were either anaesthetized with halothane, enflurane, isoflurane, sevoflurane, and desflurane at increasing minimum alveolar concentrations (1-3 MAC) or treated with one of the endogenous catecholamines epinephrine and norepinephrine or the synthetic ones dobutamine and dopexamine (a total of 186 experiments). Cardiac Output (ultrasound transit-time flowmeter) and VO2 (indirect calorimetry) were measured continuously and the relations between both variables (Q/VO2 relations) analyzed. MAIN RESULTS: In awake dogs under basal metabolic conditions, VO2 was 4.6 +/- 0.1 ml x kg-1 x min-1 and Q 105 +/- 3 ml x kg-1 x min-1 (mean +/- SEM). During inhalation anaesthesia, VO2 and Q decreased in parallel, yielding a uniform Q/VO2 relation, which was nearly linear. Above 2 MAC, O2 extraction increased by 50%, indicating compromised oxygen delivery (DO2). Imposed increases in Q and thus DO2 during anaesthesia to rates comparable to that in the awake state did not restore VO2 to baseline. Catecholamines increased both VO2 and Q in a dose-dependent manner, albeit to a different extent. The resulting Q/VO2 relations were linear up to the maximum effects, but their slopes increased about threefold in the order norepinephrine (34), epinephrine (54), dobutamine (86), and dopexamine (105). Despite these differences, VO2 and Q correlated linearly over the whole range studied, which covered a doubling of VO2 and an up to fourfold increase in Q. CONCLUSIONS: The metabolic regulation of blood flow apparently also operates during inhalation anaesthesia, regardless of the anaesthetic. Catecholamines (except norepinephrine) preferentially stimulated Q rather than VO2 (excess perfusion), so that agents like dopexamine might be preferred in the treatment of low cardiac output states because of its low metabolic costs. Our observations imply that cardiac output alone provides little information on the function of the circulation during inhalation anaesthesia and catecholamine therapy unless related to metabolic demands, i.e. to VO2.

Adrenergic alpha-Agonists↗
PubMed2003

Effects of endothelin-1 and endothelin-1 receptor blockade on cardiac output, aortic pressure, and pulse wave velocity in humans.

Endothelin-1 (ET-1) is a potent vasoconstrictor. Its effect on arterial wave reflections and central pressure augmentation is unknown. We studied whether ET-1, in plasma concentrations present in disease, increases pulse wave velocity (PWV) and augmentation index (AIx) and therefore compromises cardiac output, and whether the ET-1 receptor blocker VML-588 (previously AXV-034343 and Ro 61-1790) prevents such effects. Nine healthy men received a 2-hour infusion with ET-1 (2.5 ng x kg(-1) x min(-1)) superimposed on vehicle or VML-588 (0.05, 0.20, or 0.40 mg x kg(-1) x h(-1)) (randomized order). Arterial tonometry and pulse wave contour analysis were used to assess aortic PWV and central aortic pressures and impedance cardiography for cardiac output. ET-1 slightly increased mean arterial pressure and peripheral resistance but had no significant effect on systolic blood pressure and pulse pressure. PWV increased from 5.4+/-0.2 to 5.7+/-0.3 m/s (P<0.05), AIx from 9.9+/-3.3 to 17.2+/-3.8 (P<0.05), central systolic blood pressure by 8.7+/-1.7 mm Hg (P<0.05), and central pulse pressure by 5.1+/-1.9 mm Hg (P<0.05). This was associated with a fall in cardiac output by approximately 18% (P<0.05). VML-588 caused a slight decrease in brachial mean arterial pressure, PWV, and AIx, and prevented the effects of ET-1 on central hemodynamics without a clear dose-response effect. In summary, ET-1 in plasma concentrations as found in renal failure and heart failure accelerates PWV, causes a disproportionate increase in central aortic systolic blood pressure and pulse pressure, and decreases cardiac output. These effects can be prevented with an ET-1 receptor blocker such as VML-588. This makes it worthwhile to focus on endothelin as a target to prevent ventricular hypertrophy and to maintain cardiac function in diseases associated with high ET-1.

Adolescent↗
PubMed1977

[Physiopathology of low cardiac outputs after ECC and their treatment].

Etiologic circumtances of low cardiac outputs are studied according as they concern a diminution of the precharge (hypovolemy of different reasons), an augmentation of the postcharge (by augmentation of aortic impedance or resistance to blood flow) or a cardiac deficiency. The latter can be of non-ischemic origin (effects of beta-blocking drugs, cardiac arrhytmias tamponade, deficience of myocardiac fiber, metabolic disease) or ischemic:--during E.C.C.: diminution of available oxygen (hypothermial), arterial pressure and output too low, clamping time or ventricular fibrillation too long;--after E.C.C.: insufficient surgical correction, coronary embolism lack of balance between apport and expense of oxygen. Therapeutics ways are discussed regarding the different etiologies. The central rule is that it is better to relieve an ischemic myocardia than lash it. But treatment of low cardiac outputs is most often an average solution which must be choose in regard to a well understood physiopathology.

Adrenergic beta-Antagonists↗
PubMed2000

Relationships between steady state blood concentrations and cardiac output during intravenous infusions.

The blood concentration of a drug at steady state can be calculated from the ratio of infusion rate over the total body drug clearance. When the blood is assumed to be a homogenous pool, the clearance is not usually referenced to any particular site within the circulation. In contrast, in recirculating systems, the relative sites of an infusion, the lungs and organs of elimination, and dilution in the cardiac output, produce concentration gradients in the blood. Equations that describe the relationship between the steady state concentrations of a drug in arterial, pulmonary artery, mixed venous and eliminating organ (e.g. liver or kidney) blood and the intrinsic clearance of the drug in the lungs and the eliminating organ were derived analytically. The concentrations at all sites were shown to be cardiac output dependent with the following exceptions: (1) in arterial blood, when the drug is highly extracted by the lungs, and (2) in eliminating organ blood when there is no lung clearance of the drug. The arterial and pulmonary artery concentrations will be least affected by cardiac output in the absence of lung clearance, and if the intrinsic clearance in the eliminating organ is substantially less than cardiac output.

Blood Circulation↗
PubMed2000

The initial distribution volume of glucose rather than indocyanine green derived plasma volume is correlated with cardiac output following major surgery.

OBJECTIVES: To determine whether the initial distribution volume of glucose (IDVG) rather than plasma volume or blood volume is correlated better with cardiac output during the 4 days following major surgery. DESIGN AND SETTING: Prospective clinical investigation in the general intensive care unit of a university hospital. PATIENTS AND METHODS: 31 consecutive patients who underwent radical surgery for esophageal carcinoma were enrolled. Continuous thermodilution cardiac output monitor was placed in the operating room. Indocyanine green (ICG; 25 mg) and glucose (5 g) were administered simultaneously to calculate IDVG and plasma volume determined using the ICG dilution method. Blood volume was also calculated from plasma volume ICG and hematocrit. Those volumes were measured on admission to the ICU and daily on the first 3 postoperative days. The relationships between each volume and cardiac index (CI), and between routine clinical variables and CI were evaluated. RESULTS: IDVG had a linear correlation with CI in the early postoperative days (r = 0.71, n = 124, p < 0.000001). Measurements of neither the plasma volume nor the blood volume yielded a better correlation with CI than did IDVG (r = 0.45, n = 124, p < 0.000001, and r = 0.23, n = 124, p < 0.01, respectively). No correlation was found between pulmonary artery wedge pressure and CI or between central venous pressure and CI. CONCLUSIONS: Our results indicate that IDVG rather than intravascular volume is correlated with cardiac output. We suggest that IDVG has potential as an alternative indicator of cardiac preload following major surgery.

Adult↗
PubMed1994

[Treatment of acute low cardiac output syndrome after surgery of congenital heart defects: value of enoximone].

Children undergoing cardiac surgery are at additional risk for postoperative low cardiac output syndrome (LCOS). Anticipation of the syndrome from preoperative hemodynamic condition, surgical procedure, and adverse intraoperative events is a key to successful postoperative management. Inotropic support is primarily based on catecholamines. However, uncoupling of human cardiac beta-adrenoceptors during cardiopulmonary bypass with cardioplegic cardiac arrest may be the reason why many patients respond only weakly to beta-adrenoceptor agonists. Phosphodiesterase (PDE) inhibitors act by reducing intracellular breakdown of cAMP, which is elevated independently from beta-receptors. The use of PDE-inhibitors might be advantageous in patients with uncoupled beta-adrenoceptors, as occurs after cardiopulmonary bypass. In addition, PDE-inhibitors can prevent further downregulation of the adrenoceptors due to avoiding prolonged therapy by beta-agonists. In this context, the addition of enoximone, a PDE-inhibitor, to adrenergic agents has been found useful in increasing cardiac output in children with catecholamine-resistant LCO, as well as in children with compensated hemodynamics during catecholamine therapy.

Cardiac Output, Low↗
PubMed1993

[Cardiac output measurement with transtracheal Doppler in children].

Cardiac output (CO) measurement with transtracheal Doppler (TTD) was compared with that measured by transthoracic electrical bioimpedance (TEB) in normal children, and with that by thermodilution (TD) in children with heart disease. In CO measurement, TTD correlated significantly with TD (r = 0.65, P < 0.05), but not with TEB. Although aortic diameters, which were necessary for CO measurement with TTD, were far from the values in Woezik's nomogram of normal children, they correlated significantly with those measured from angiographies in children with heart disease (r = 0.92, P < 0.05). However, it is assumed that the significant correlation of diameters in children with heart disease might be produced by the offset of measurement errors in position and angle of the Doppler probe.

Cardiac Output↗
PubMed1996

Methods of estimating cardiac output in the field.

Simultaneous estimation of cardiac output (CO) by thoracic electrical bioimpedance (TEB) and thermodilution (TD) confirmed the results of a previous study which showed good agreement between these methods in selected, principally non-septic, patients. Poor agreement was found between simultaneous TEB and oesophageal Doppler monitoring (ODM) estimates of baseline and acute changes in CO. Taken with the results of previous studies, this implies that although isolated ODM estimates of CO, which tend to underestimate, are less reliable, ODM is the preferred method to monitor acute changes in CO. For many reasons, not least the speed with which a large number of seriously injured soldiers could be assessed, ODM is probably the better method if a non-invasive estimate of CO is required in field hospitals.

Adult↗