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PubMed2001

Changes in cardiac output and intrathoracic blood volume: a mathematical coupling of data?

BACKGROUND: Measurements of intrathoracic blood volume (ITBV) provide volumetric information about cardiac preload and are used to investigate the cause of alterations in cardiac output (CO). On the other hand, CO is required to calculate ITBV. Thus, concerns have been raised with respect to a mathematical coupling of data. The aim of this prospective, clinical study was to investigate whether a variation in CO induced by high-dose beta-blockade influences thermodilution measurements of ITBV in the absence of changes in intravascular volume in patients undergoing minimally invasive coronary artery bypass grafting. METHODS: Sixteen patients undergoing elective minimally invasive direct coronay artery bypass (MIDCAB) surgery were studied. Transpulmonary thermodilution measurements of ITBV and CO were simultaneously performed before bypass grafting, during beta-blockade induced by high-dose esmolol and at the end of surgery. RESULTS: During esmolol administration, CO significantly decreased by 33%, whereas ITBV remained unchanged compared to control values (876+/-46 ml m-2 during control versus 860+/-61 ml m-2 during esmolol administration). After the end of esmolol administration, CO significantly increased by 79%. Again, ITBV remained virtually unchanged (860+/-61 ml m-2 during esmolol administration versus 911+/-38 ml m-2 after esmolol administration). CONCLUSIONS: The results of the present study demonstrate that substantial alterations in CO as a consequence of high-dose esmolol infusion are not associated with changes in ITBV. Because haemodynamic changes were induced by factors other than variation of preload, these findings suggest that changes in cardiac output do not influence thermodilution measurements of ITBV in this setting.

Adrenergic beta-Antagonists↗
PubMed1984

[Hemodynamic effects of DBcAMP in patients with low cardiac output syndrome following open-heart surgery].

Hemodynamic effects of DBcAMP given at 0.05 to 0.3 mg/kg/min for 30 minutes to patients with low cardiac output less than 2.21/min/m2, to patients on IABP and on dopamine or dobutamine were investigated after open-heart surgery. Hemodynamic improvements were observed in cardiac index from 1.81 +/- 0.3 (mean +/- SD) to 2.56 +/- 0.401/min/m2 (p less than 0.001), stroke index from 20.5 +/- 5.2 to 26.4 +/- 5.2 ml/best/m2 (p less than 0.001). TRP decreased from 1963.8 +/- 682.8 to 1153.9 +/- 449.0 (p less than 0.001). These changes were similar to those of Groups II (3.0 greater than or equal to C1 greater than or equal to 2.21/min/m2) and of Group III (C1 greater than 3.01/min/m2). Increases were also observed in CI from 2.28 +/- 0.67 to 2.96 +/- 0.671/min/m2 (p less than 0.001) and in stroke index from 24.4 +/- 7.2 to 29.5 +/- 6.4 ml/best/m2 (p less than 0.001) and significant decreases were observed in TPR and PVR in patients receiving dopamine or dobutamine. These results strongly suggest the inotropic action of DBcAMP was independent on the beta receptor activity and could be a powerful adjunct in the treatment of low cardiac output patients on whom the dopamine or dobutamine was ineffective.

Adult↗
PubMed1990

Stroke volume and the three phase cardiac output rate relationship with ventricular pacing.

Knowledge of how stroke volume (SV), and hence cardiac output (CO), changes with ventricular pacing rate (R) constitutes a key aspect of sensor driven, variable rate pacemakers. It has been established that the relationship between CO and pacing rate exhibits three phases for rest and constant exercise. At low rates (phase 1), CO increases with increasing R; with additional rate increase (phase 2), CO either remains constant or increases slightly; and above some critical rate, CO decreases (phase 3). However, the nature of the relationship between SV and pacing rate has not been as clearly described. Therefore, the objectives of this study were (1) to describe and document the relationship between SV and R, and (2) to demonstrate the consequence of this relationship in terms of the three phase CO versus R relationship. In six anesthetized dogs, right ventricular SV was determined from pulmonary artery blood flow measured using an electromagnetic flow meter, and the right ventricle was paced over a range of rates. In general, SV decreased with increasing R, although the exact nature of the relationship varied from animal to animal. The results demonstrate that it is the manner in which SV decreases with increasing R that determines the three phase relationship between CO and R. The relationships described in this study have important implications for choosing pacing rates for patients receiving sensor driven, variable rate pacemakers.

Animals↗
PubMed1999

The role of heart rate in the modulation of the decreased cardiac output induced by acute nitric oxide synthesis inhibition in anaesthetized dogs.

1. The role of the heart rate modulating the decrease in cardiac output induced by the nitric oxide synthesis inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME) was investigated in anaesthetized dogs. This was achieved in dogs in which a positive pacemaker (PM) cable was located at the right ventricle. 2. The haemodynamic events were evaluated: mean arterial blood pressure (MABP), systemic vascular resistance index (SVRI), stroke volume index (SVI), heart rate (HR) and cardiac index (CI). 3. The infusion of L-NAME (0.01-10 mg kg(-1)) in the animals with the PM off caused a dose-dependent rise in MABP and SVRI, accompanied by significant decreases of HR and SVI. A resulting decrease in CI was observed at all doses of L-NAME used. 4. In the animals with the PM on, HR was maintained stable. Under this condition, the increase in MABP and SVRI as well as the decrease in SVI induced by the L-NAME infusion did not significantly differ from the PM-off animals. However, the resulting decreased CI was markedly attenuated compared to PM-off animals but significant decreases in CI were still observed at higher doses of L-NAME. 5. The results suggest that HR plays an important role in the L-NAME-mediated decreased cardiac output but other factors might also be involved.

Analysis of Variance↗
PubMed1981

Experimental study of afterload-reducing therapy: the effects of the reduction of systemic vascular resistance on cardiac output, aortic pressure and coronary circulation in isolated, ejecting canine hearts.

The relationship between cardiac output (CO) and peripheral resistance (Rp) was examined under the following conditions for coronary perfusion: constant coronary flow perfusion; perfusion with a pressure equal to mean aortic pressure (AoP perfusion); and perfusion with a pressure equal to the mean AoP - 30 mm Hg (AoP - 30 mm Hg perfusion). We also examined the coronary pressure-flow relationship. For these studies, we used paced, isolated, ejecting canine hearts, which were loaded by a hydraulic system that simulated the input impedance of a dog's systemic arterial tree. The CO in the constant coronary flow perfusion continued to increase with the reduction of Rp. The CO in the AoP perfusion became maximal at a slightly subphysiologic Rp, or at an average mean AoP of 65 mm Hg. This mean AoP was closely associated with the lower limit of the autoregulation of coronary blood flow. In the AoP - 30 mm Hg perfusion, the mean AoP at which CO became maximal was 72 mm Hg and the corresponding coronary perfusion pressure appeared to be lower than the lower limit of the perfusion pressure range for coronary flow autoregulation. The Rp value at that point was slightly higher than the physiologic range. We conclude that when coronary perfusion pressure changes with mean AoP, and when left ventricular end-diastolic pressure is fixed, there is a clear optimal Rp at which CO becomes maximal, and this optimal Rp is higher if coronary perfusion pressure is biased from mean AoP to a significant degree.

Animals↗
PubMed1988

Peripheral distribution of the increased cardiac output by secretin during acute ischemic left ventricular failure.

Secretin, a 27-amino acid peptide with both vasodilating and inotropic properties, was investigated according to its effects on peripheral flow distribution in acute ischemic left ventricular failure accomplished by embolization of the left coronary artery in anesthetized dogs. Electromagnetic monitoring of renal, carotid, femoral and superior mesenteric artery flow was used. During the induction of heart failure a general reduction of flow with preponderance of that of the carotid and femoral arteries occurred. The secretin infusion caused increases in renal flow by 58%, carotid flow by 63%, femoral flow by 50% and superior mesenteric flow by 34%. The corresponding reductions in arterial resistances were 33, 35, 31 and 24%, respectively. Compared to levels before induction of failure, restoration of flow in all arteries as well as cardiac output was achieved, with exception of renal flow that was 25% higher. The arterial pressure was not altered and a modest inotropic effect of secretin was confirmed. It was concluded that in acute left ventricular failure secretin caused a general distribution of the increased cardiac output in the arteries investigated with a preponderance of renal artery flow.

Acute Disease↗
PubMedDate not supplied

The effect of graded exercise on cardiac output of the Jarvik-7-70 total artificial heart in humans.

Animal exercise studies have shown a self-regulated change in cardiac output (CO) with the J-7 total artificial heart (TAH). A 49-year-old, 75 kg patient received a J-7-70 TAH as a bridge to transplant. During bicycle exercise, the TAH heart rate, drive pressures, percent systole, and vacuum were unchanged. Cardiac output was measured by analysis of diastolic air exhaust. Mean arterial pressure (MAP) was measured via a radial artery catheter. Daily recordings of hemodynamics were made from TAH day 35 to 56 at rest, cycling with zero resistance, 18 watts resistance, return to zero resistance, and at rest. Values were as follows: baseline MAP, 75.7 +/- 9.7; LCO, 6.4 +/- 0.2; RCO, 6.8 +/- 0.2. For zero watts resistance MAP was 92.2 +/- 7.2*; LCO, 7.1 +/- 0.2*; RCO, 7.8 +/- 0.3*. For eighteen watts resistance MAP was 101.3 +/- 6.2*; LCO, 7.6 +/- 0.3*; RCO, 8.4 +/- 0.4*. For zero watts resistance MAP was 98.5 +/- 4.9*; LCO, 7.2 +/- 0.4*; RCO, 8.0 +/- 0.4*. The postexercise MAP was 86.4 +/- 4.1*; LCO, 6.2 +/- 0.2; RCO, 6.9 +/- 0.2. For all but baseline and postexercise MAPs, the average response was over a 4 minute interval. The starred values were significant compared to baseline p less than 0.05. Exercise resulted in an autoregulated change in TAH CO in man. Increasing the work of exercise produced an increased CO, reflecting changes in venous return. A TAH patient can exercise for more than 30 minutes with an autoregulated CO and no deleterious effects.

Blood Pressure↗
PubMed1983

Maternal blood volume and cardiac output during pregnancy: a hypothesis of endocrinologic control.

During the course of gestation the increase of maternal total blood volume and cardiac output may result from two mechanisms acting in concert: 1) the production of several hormones by the fetus and the placenta, and 2) the uteroplacental circulation acting as an arteriovenous shunt. Plasma volume appears to increase as a consequence of renal Na+ reabsorption and water retention, which result from increased aldosterone production via the renin-angiotensin system, as a consequence of placental estrogen production. This estrogen production in turn results from increasing availability of the estrogen substrate dehydroepiandrosterone (chiefly from the fetal adrenal gland). Erythrocyte volume increases as a consequence of the erythropoietic effect of placental chorionic somatomammotropin, progesterone, and perhaps prolactin. In addition, maternal blood volume increases in response to the uteroplacental circulation functioning as a low-resistance circuit. In turn, this increases cardiac output and nutrient delivery for further growth of the products of gestation. Thus there may exist a feedback mechanism whereby fetal growth and, in particular, increasing steroidogenesis by the developing fetal adrenal gland result in the maternal cardiovascular adaptations to pregnancy that optimize further fetal development. In certain complications of pregnancy the less-than-normal maternal blood volume increase may result from failure of these mechanisms, while in turn contributing to the further genesis of these disorders.

Animals↗
PubMed1978

A new noninvasive method for the simultaneous determination of cardiac output, VA/QC disparity, and the magnitude of peripheral perfusion, suitable for use in the critically ill patient.

A noninvasive technique for determining cardiac output, lung blood-tissue volume, and the volume of perfused body tissue in shock states has been developed from analysis of the pulmonary washout of several physiologically inert tracer gases. Canine preparations and a computer-based simulation were used to evaluate the accuracy and feasibility of the technique. The dogs were ventilated with 10% helium, 10% N2O, 0.45% C2H2, 39.5% N2, and 40% O2 mixture, and washed out with 60% N2 and 40% O2. End-tidal volume excretion differences between the three inert gases helium, N2O, and C2H2 resulted from differences in the blood/gas partition constants (lambda) of the test gases. Helium, which has a very low lambda, is contained in lung air space, whereas N2O and C2H2, with moderate lambda's, are distributed to lung air space, blood, and perfused tissues. Computer modeling of the cardiopulmonary and body perfusion gas transport permitted calculation of alveolar ventilation, VA/VA disparity, pulmonary blood-tissue volume, pulmonary blood flow, VAQć, and perfused body volume in the canine experiments. In experimental shock settings and in a variety of control situations over an eightfold range of flows the pulmonary blood flow calculated from the N2O and C2H2 washout was generally within +/- 15% of the cardiac output determined by the cardiogreen technique.

Animals↗
PubMed1979

[Plasma renin activity, plasma volume extracellular fluid volume and cardiac output in essential hypertension (author's transl)].

The plasma renin activity (PRA), the plasma volume (PV), the extracellular fluid volume (ECV), the cardiac output and the peripheral vascular resistance (TPR) were determined in 51 patients (14 women, 37 men) with essential hypertension of varying severity. The following findings were achieved: 1. In 9 of the 51 patients with essential hypertension (approximately 18%) a low and non-sensitive PRA was detected. 2. PV, ECV, cardiac output and the calculated peripheral vascular resistance of the essential hypertensive patients with low and non-sensitive PRA did not differ significantly from those of the essential hypertensive patients with normal or elevated PRA. 3. The hypertensive patients with low and nonsensitive PRA had the highest average arterial pressure. From these findings it can be concluded that the essential hypertensive patients with low PRA are not an homogeneous group. It is assumed that in a subgroup the elevated blood pressure may be the cause of the renin suppression.

Adult↗
PubMed1998

Use of assumed versus measured oxygen consumption for the determination of cardiac output using the Fick principle.

Assumed oxygen consumption (VO2) is increasingly used as a convenient surrogate for measured VO2 for calculation of cardiac output. This substitution is often based on empirical formulae, previously validated only in relatively young patients. To assess the inaccuracy introduced by extrapolating these formulae to older patients, we compared measured VO2 with assumed VO2 in 57 patients. VO2 was measured using an open circuit analyzer. Assumed VO2 was calculated according to the LaFarge or Bergstra formulae. Agreement between both methods was assessed according to the method of Bland and Altman. The mean difference of measured VO2 minus assumed VO2 was 7.9 ml/min/m2 (P < 0.02) using the LaFarge formula, and -15.6 ml/min/m2 (P < 0.0002) using the Bergstra formula across a range of measured VO2 from 70 to 176 ml/min/m2. A systematic error was introduced by assumed VO2 from both formulae of underestimating higher and overestimating lower values of VO2, resulting in poor overall agreement with measured VO2. The same error and poor agreement was found when analyzing subgroups of patients > or =60 or <70 years of age. In summary, use of assumed VO2 introduces large, unpredictable errors in adult patients, suggesting requirement for measurement of VO2 when calculating cardiac output.

Adolescent↗
PubMed1990

Acute respiratory acidosis decreases left ventricular contractility but increases cardiac output in dogs.

To understand the cardiovascular response to respiratory acidosis, we measured hemodynamics, left ventricular pressure, and left ventricular volume (three ultrasonic crystal pairs) during eucapnia and respiratory acidosis in 10 fentanyl-anesthetized open-chest dogs. Left ventricular contractility was assessed primarily by measuring the slope (Emax) and intercept (V0) of the left ventricular end-systolic pressure-volume relation determined by combining end-systolic points from a vena caval occlusion and from brief aortic cross-clamping. Respiratory acidosis (pH 7.09, Pco2 92 mm Hg) reduced contractility by a decrease in Emax (11.4 to 9.2 mm Hg/ml, p less than 0.01) with no change in V0. Despite this, cardiac output increased (1.7 to 2.1 l/min, p less than 0.01), and heart rate increased (96 to 121 beats/min, p less than 0.05), with no change in blood pressure. Systemic vascular resistance fell by 26% (p less than 0.01). During eucapnia, propranolol reduced Emax (11.4 to 4.6 mm Hg/ml, p less than 0.01) with no change in V0. After propranolol treatment, respiratory acidosis further reduced Emax (4.6 to 3.6 mm Hg/ml, p less than 0.05) and increased end-systolic volume more than before propranolol (p less than 0.001). Now cardiac output did not increase even though heart rate increased (81 to 106 beats/min, p less than 0.001) and systemic vascular resistance fell by 20% (p less than 0.01). We conclude that the effect of respiratory acidosis on the circulation is to increase venous return (equals cardiac output) in the face of decreased left ventricular contractility. The beta-adrenergic response to respiratory acidosis substantially ameliorated the increase in end-systolic volume and supported the increase in venous return but did not alter the associated tachycardia or vasodilation. Respiratory acidosis, like propranolol treatment, decreases contractility by decreasing Emax.

Acidosis, Respiratory↗
PubMed2005

Cerebral distribution of cardiac output in newborn infants.

Cerebral blood flow and output of the left ventricle were simultaneously investigated in 17 infants using multichannel near infrared spectroscopy and pulse dye densitometry with indocyanine green. Cardiac output and cerebral blood flow were positively related. The control of cardiac output is important in the regulation of cerebral blood flow in infants.

Cardiac Output↗
PubMed1991

Cardiac output distribution and intrarenal haemodynamics: role of thromboxanes.

The effects of imidazole, an inhibitor of thromboxane synthesis, were studied on the distribution of cardiac output and on the intrarenal haemodynamics in anaesthetized, furthermore on the salt and water excretion in conscious rats. Imidazole treatment (10 mg/100 g b.m., intraperitoneally, twice a day for two days) failed to influence the arterial blood pressure, the cardiac output and its distribution in organs investigated (heart, muscle, lung [bronchial fraction], skin, liver, spleen, small intestine, adrenal gland and kidneys). The medullary blood flow increased, while cortical blood flow remained unchanged, but the intrarenal percentile blood flow shifted towards the medulla. Imidazole elevated the water turnover in the animals, but no change in sodium and potassium excretion occurred. It is supposed that thromboxanes may affect the renal medullary vascular tone without altering the vascular smooth muscle activity in other organs.

Animals↗
PubMed2006

Monitoring cardiac output using the femoral and radial arterial pressure waveform.

This study was performed to determine the interchangeability of femoral artery pressure and radial artery pressure measurements as the input for the PiCCO system (Pulsion Medical Systems, Munich, Germany). We studied 15 intensive care patients following cardiac surgery. Five-second averages of the cardiac output derived from the femoral artery pressure (COfem) were compared to 5-s averages derived from the radial artery pressure (COrad). One patient was excluded due to problems in the pattern recognition of the arterial pressure signal. In the remaining 14 patients, 14 734 comparative cardiac output values were analysed. The mean sample time was 88 min, range [30-119 min]. Mean (SD) COfem was 6.24 (1.1) l.min(-1) and mean COrad 6.23 (1.1) l.min(-1). Bland-Altman analysis showed an excellent agreement with a bias of - 0.01 l.min(-1), and limits of agreement from 0.60 to - 0.62 l.min(-1). If changes in CO were > 0.5 l.min(-1), the direction of changes in COfem and COrad were equal in 97% of instances. We conclude that femoral artery pressure and radial artery pressure are interchangeable as inputs for the PiCCO device.

Aged↗
PubMed2006

Second trimester cardiac output and its predictive value for preeclampsia.

OBJECTIVE: To predict women at risk of preeclampsia in the second trimester by the assessment of maternal cardiac output (CO). METHODS: Between October 2001 to November 2003, we carried out a cross-sectional, prospective, hospital-base study in Shiraz University of Medical Sciences, Shiraz, Iran. Cardiac output was measured in 102 normotensive women at gestational age 19-25 weeks by Doppler echocardiography. Patients with CO >7.4 L/min were considered high risk group (Group 1) and those with CO < or =7.4 L/min were in Group II. They were followed-up until delivery and the incidence of preeclampsia was determined in both groups. RESULTS: Twenty percent (6/30) of patient in Group 1, and 1.4% of patients in group II developed preeclampsia (p < 0.003). A cut off point of 7.34% L/min was chosen for prediction of preeclampsia that showed 85.7% sensitivity, 74.2% specificity with a negative predictive value of 98% and positive predictive value of 20%. CONCLUSION: Cardiac out put is significantly elevated in preclinical state of preeclampsia. Echocardiography is a non-invasive method to evaluate the maternal homodynamic during the second trimester and can help to identify high-risk patient before the development of preeclampsia, thereby it may improve the outcome of pregnancy.

Adult↗
PubMed1988

Application of noninvasive techniques for measuring cardiac output in hypertensive patients.

The hemodynamic hallmark of hypertension is increased systemic vascular resistance, although this variable is usually not determined in hypertensive patients because it has generally required invasive procedures to measure cardiac output. Reliable, totally noninvasive methods are now available that measure cardiac output accurately enough under a variety of conditions, including rest, exercise, and pharmacologic interventions. These methods include echocardiography, Doppler echocardiography, CO2 rebreathing, and impedance cardiography. Their serial application to large numbers of patients offers the opportunity to significantly broaden our understanding of the spectrum and course of hemodynamic alterations associated with hypertension. A more complete knowledge of underlying hemodynamics could improve our diagnostic and prognostic accuracy in hypertensive patients and enhance our understanding of the pathophysiology of hypertension and the mechanism of action of antihypertensive interventions.

Cardiac Output↗
PubMed1986

Persistent low cardiac output after the Fontan operation. Should takedown be considered?

Four of 44 patients who had undergone the Fontan operation had persistent low cardiac output necessitating takedown of the shunt 6 to 65 hours (average 23 hours) postoperatively. All four were in a group of 22 patients with complex lesions other than tricuspid atresia with ventriculoarterial concordance. The development of postoperative right atrial hypertension (average 24 torr), hepatomegaly, marked ascites, and decreasing lung compliance led to severe systemic hypotension with systolic arterial pressure ranging from 55 to 82 torr (average 68 torr), persistent metabolic acidosis, and oliguria despite massive colloid and crystalloid infusions (11,000 ml/m2/24 hr) and inotropic support. At reoperation the atriopulmonary anastomosis, which was found to be wide open, was taken down and an atrial septal defect was created in all patients. Three patients were left with a Glenn shunt and an aortopulmonary shunt to the left lung. One patient had bilateral aortopulmonary shunts. Two patients who survived reoperation had immediate postoperative improvement in systolic arterial and mean right atrial pressure (average 100 torr and 11.5 torr, respectively). Both are well 5 months and 4 years later. Repeat Fontan operation remains a possibility with acceptable risks because of the presence of the Glenn shunt in both patients. We believe that takedown should be considered in patients with persistent low cardiac output after the Fontan operation.

Cardiac Output, Low↗