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PubMed1979

[Cardiac output and central-hemodynamic parameter under bencyclan (author's transl)].

In 17 patients with peripheral arterial occlusive disease the influence of intra-veinously applicated Bencyclane (Fludilat) on cardiac output and central-hemodynamic parameter has been investigated. While 100 mg (n = 8) of Bencyclane almost do not influence cardiac output, 200 mg (n = 9) cause a significant decrease of minute-volume of the heart by-17.22% and of heartfrequency by-8.85%. With either dose there is also a significant increase of aortic pressure, pulmonary arterial pressure and pulmonary vessel resistance to be seen. These results correlate with the animal-experimental proof of a negative inotropy under Bencyclane, and they have to be considered in therapeutical use.

Arterial Occlusive Diseases↗
PubMed1987

The effect of beta 1-adrenoceptor blockade on cardiac output and organ blood flow in conscious rats.

The acute effects of the beta 1-adrenoceptor inhibition by atenolol were investigated on conscious rats. Cardiac output and organ blood flow were measured by 15-microns radiolabelled microspheres during control and 20 min after administration of atenolol (1 mg/kg body wt). Arterial blood pressure and heart rate were measured continuously. Arterial blood gases and pH were determined immediately after the two microsphere injections and arterial blood samplings. The mean arterial blood pressure fell significantly shortly after the injection of atenolol and was reduced by 9% (p less than 0.02) after 20 min. Heart rate fell by 17% (p less than 0.05). The total peripheral vascular resistance increased by 25% (p less than 0.05). At the same time the arterial acid-base chemistry remained unaltered from the control. The cardiac output fell by 24% (p less than 0.05). Blood flow fell to all organs and tissues (0-67%) except to the brain, adrenals, liver, ears and diaphragm. The greatest decrease was seen in perfusion of the adipose tissue (67%) and of the spleen (60%), indicating that the blood flow to these organs are normally highly influenced by beta 1-adrenoceptor stimulation. The estimated work load of the heart was reduced by 20% which correlated well to a reduction of myocardial blood flow to the same degree.

Animals↗
PubMedDate not supplied

High-output cardiac failure in a patient with prostate cancer.

The authors describe a case of high-output cardiac failure in a patient with rapidly progressing prostate cancer for which no previously described cause could be found. His new onset and increasingly worsening heart failure corresponded to the rapid spread of his prostate cancer. The authors hypothesize that a cytokine released from the neoplastic cells or the bone was responsible for the high-output cardiac failure observed in this patient. (c)2001 CHF, Inc.

Journal Article↗
PubMed1997

Effects of volume expansion on cardiac output in the preterm infant.

Clinical and echocardiographic haemodynamic evaluations of response to volume expansion are described in 12 preterm neonates aged < 7 days presenting without cardiac dysfunction and with a low cardiac output. They received 10% albumin solution (20 ml kg-1) for 3 h. Measurements were made before infusion, at volumes 5, 12.5 and 20 ml kg-1 and 1 h later. All infants increased significantly their cardiac output (CO) (from a median of 177 to 283 ml kg-1 min-1). The rise of CO decreased with the volume infused. The index of systemic vascular resistance (SVR = ratio of mean arterial pressure to the CO) decreased for the six patients without PDA (from 272 to 193 mmHg l-1 kg-1 min-1, p < 0.05) showing that the hypovolaemic preterm infant is able to shut down peripherally in response to hypovolaemia. The four hypotensive infants responded by increasing mean arterial blood pressure (from 29 to 44 mmHg). Cutaneous refilling time decreased during infusion (from 6.7 to 3.8 s. p < 0.01). One infant had an haemodynamically significant ductus arteriosus revealed by volume expansion, another one developed myocardial dysfunction.

Albumins↗
PubMed1986

Influence of vagal cooling on cardiac output in normal and beta-blocked exercising dogs.

To study the relative influence of parasympathetic and sympathetic innervation on the early adaptation of cardiac output (CO) to exercise, we determined the time constant and amplitude of the CO change in dogs following a stepwise increase in treadmill velocity. The animals were studied during control conditions, beta-blockade, vagal blockade and combined beta-blockade and vagal blockade. To measure CO, an electromagnetic flow probe was implanted around the ascending aorta. Vagal activity was blocked with coolers, implanted around the cervical vagosympathetic trunks. The time constant during beta-blockade (12.1 s) was not different from the control situation (11.4 s), but during vagal cooling it increased significantly (16.2 s), and with combined vagal cooling and beta-blockade it rose to 20.7 s. Thus the increase in cardiac output with exercise is accelerated most by the loss of vagal tone and to a lesser degree by sympathetic activation. The amplitude of the change in CO during control was 112%. Heart rate (HR) rose by 74% and stroke volume (SV) by 22%. Beta-blockade lowered the initial CO but did not alter the percentage increase. Vagal cooling, with or without beta-blockade, caused an increased initial HR but did not influence basal CO because of a concomitant reduction in SV. Exercise now increased HR less (21% and 30%, respectively) and SV more (52% and 52%) but the increase in CO did not change significantly (87% and 97%).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Pulmonary circulation in low cardiac output syndrome following open heart surgery.

The pulmonary circulation of 41 patients with low cardiac output syndrome (LOS) in the recovery period following open heart surgery was studied. Cardiac indices (CI) of these patients in LOS was 1.64 +/- 0.28 (Mean +/- SD) L/min X m2 and increased to 2.60 +/- 0.50 L/min X m2 after the stabilization of hemodynamic conditions. Mean pulmonary arterial pressure, pulmonary arteriolar resistance index (PARI) and total pulmonary resistance index (TPRI) in the condition of LOS were very high and significantly decreased after recovery from LOS, although the mean left atrial pressure showed no significant change. The correlation coefficient (r) between CI and PARI was found to be -0.574. High Pao2 with reductions of alveolar-arterial oxygen tension difference (A-aDo2) and physiological pulmonary shunt ratio (Qs/Qt) in LOS significantly decreased concomitant with significant increases in both A-aDo2 and Qs/Qt after the stabilization of the hemodynamic condition. Moderate correlations were obtained between CI and Pao2 (r = -0.478), and high correlations were established between CI and physiological pulmonary shunt flow (Qps) (r = 0.747). These studies showed that pulmonary vasoconstriction was playing a major role in the elevation of pulmonary vascular resistance in LOS, which eventually leads to the reduction of intrapulmonary shunting.

Aortic Valve↗
PubMed1998

Cardiac output and pulmonary gas exchange at maximal exercise after atrial redirection for complete transposition.

AIMS: To assess the determinants of exercise capacity and exercise oxygenation after atrial redirection for complete transposition. METHODS AND RESULTS: At graded bicycle ergometry, including respiratory and arterial blood gas analyses, intra-arterial blood pressure recording, and cardiac output determination (dye-dilution technique), we tested 17 post-Mustard/Senning patients, 8.9-22.0 years old (mean 14.5, SD 4.0). Reference data were obtained by similar methods. At maximal exercise, oxygen uptake (29.6 ml x kg(-1) x min(-1)) and heart rate (167 beats x min(-1)) were low (P<0.001). Right-to-left shunts were detected in five patients. Arterial oxygen partial pressure and saturation fell in all subjects (P<0.0001). In 15/16 (94%) the alveolar-arterial oxygen partial pressure difference was > +2 SD. In 13/15 (87%) stroke volumes fell during exercise. Cardiac output per oxygen uptake was low (P<0.0001), which implies a high arteriovenous oxygen difference and a low mixed venous oxygen content at peak exercise. CONCLUSION: The low exercise capacity was caused by a combination of low maximally attained heart rate and falling stroke volumes. The impaired arterial oxygenation may be caused by a combination of pulmonary ventilation/perfusion mismatch, a low mixed venous content and atrial shunting in some patients.

Adolescent↗
PubMed1987

The effects of negative pressure external high frequency oscillation on cerebral blood flow and cardiac output of the monkey.

The cerebral and systemic hemodynamic effects of negative pressure ventilation by external high frequency oscillation, utilizing a thoracoabdominal chamber, were investigated in six healthy adult monkeys. Cardiac output and cerebral blood flow were compared on external high frequency oscillation and conventional, positive pressure, mechanical ventilation in each animal. Cardiac output was measured by thermodilution and cerebral blood flow was measured by the intraarterial Xenon133 clearance technique. Oxygen delivery and consumption and systemic and pulmonary vascular resistances were calculated. There was no significant difference between the two ventilatory modes for any of these variables. Cardiac index on conventional mechanical ventilation was 2.87 +/- 0.39 1 X min-1 X m-2 (mean +/- SD) and on external high frequency oscillation was 2.96 +/- 0.87 1 X min-1 X min-2. Cerebral blood flow was 43.9 +/- 9.1 ml X 100 g-1 X min-1 on conventional and 39.0 +/- 9.0 ml X 100 g-1 X min-1 on external high frequency ventilation. External high frequency oscillation is not associated with any adverse cardiovascular or cerebrovascular effects and could be introduced for short-term human trials.

Animals↗
PubMedDate not supplied

On the relationship between cardiac output and peripheral arterial resistance.

The concept of 'whole body auto-regulation' is a somewhat unsatisfactory explanation of the increased peripheral arterial resistance which follows a rise in cardiac output in 'volume' forms of hypertension. This analysis suggests that the resistance change may be due to the sodium retention and increased cardiac output having a direct effect to alter haemodynamics of flow through the arterioles in such a way as to damage their walls, and so lead to the gradual development of structural arteriolar narrowing. Studies are presented in the DOCA/salt hypertensive rat consistent with this proposal.

Animals↗
PubMed1982

Increased cardiac output following occlusion of the descending thoracic aorta in dogs.

Occlusion of the thoracic aorta (AO) in dogs with a constant volume right ventricular extracorporeal bypass increased cardiac output (Q) by 43% and mean arterial pressure by 46%, while mean systemic pressure (MSP) was unchanged. We compared AO with occlusion of the brachiocephalic and left subclavian arteries (BSO) which decreased cardiac output by 5%, increased mean arterial pressure by 32%, and increased MSP by 11%. We feel these results confirm that AO elevates preload by transferring blood volume from the splanchnic veins to the vascular system drained by the superior vena cava. If the heart is competent to keep right arterial pressure at or near zero, this increase in preload will elevate Q above control levels. Comparing our data with results of other authors who have not controlled right atrial pressure, emphasizes the importance of a competent right ventricle in allowing venous return to determine Q.

Animals↗
PubMedDate not supplied

Stroke volume and cardiac output hypoxemic hypoxia produced by intravenous infusion of carbon dioxide.

Hypoxia produced by intravenous infusion of gaseous carbon dioxide was associated in conscious rabbits with decreases in cardiac output and stroke volume. At the same time the arterial blood pressure, oxygen uptake and blood pH decreased, whereas carbon dioxide pressure and lactate level in the arterial blood increased. Pulmonary ventilation increased too, due to the rise in the respiratory frequency and tidal volume. The fall in cardiac output and stroke volume explains a great fall of oxygen uptake in response to decrease of oxygen pressure in the blood.

Animals↗
PubMed2001

Cardiac output changes during hyperbaric hyperoxia.

OBJECTIVES: Increased ambient pressure and oxygen partial pressure (pO2) influence cardiovascular regulation during diving and caisson work. We measured the cardiac output (Q) in subjects who practiced moderate work at a usual diving depth of 30 m. METHODS: In 23 healthy male Navy divers who performed steady state bicycle exercises (100 W workload) in a hyperbaric chamber Q was measured by a CO2-rebreathing technique at normal pressure (100 kPa) and at raised ambient pressure (400 kPa), in a random order. During the rebreathing maneuver the subjects were exposed to pO2 values which theoretically may have reached a maximum value of 87 kPa (normobaric) and 388 kPa (hyperbaric). During the experiments the ambient temperature ranged between 22 and 25 degrees C. RESULTS: There was a significant decrease of the directly measured Q, heart rate (HR) and the calculated stroke volume at depth when compared with normoxic and normobaric exercise. The decrease of Q amounted to 64% of the normobaric value (8.9 l min-1 versus 13.9 l min-1). The mean HR decreased from 104.7 min-1 (100 kPa) to 94.0 min-1 (400 kPa). The calculated mean stroke volume decreased from 133 ml (100 kPa) to 96 ml (400 kPa). CONCLUSIONS: During hyperoxic hyperbaria the peripheral vascular tonus increases due to the consecutively increased arterial oxygen content. The cardiac output may correlate to the peripheral vasoconstriction and is therefore indirectly influenced by elevation of inspiratory pO2 i.e. during the rebreathing maneuver.

Adult↗
PubMed2005

Predictors of low cardiac output syndrome after isolated aortic valve surgery.

BACKGROUND: Low cardiac output syndrome (LCOS), defined as the need for postoperative intraaortic balloon pump or inotropic support for >30 minutes in the intensive care unit, remains a relatively common complication of aortic valve (AV) surgery. The aim of this study is to identify the preoperative predictors of LCOS in patients undergoing isolated AV surgery. METHODS AND RESULTS: We conducted a retrospective review of data prospectively entered into an institutional database. Between 1990 and 2003, 2255 patients underwent isolated AV surgery with no other concomitant cardiac surgery. The independent predictors of LCOS and operative mortality (OM) were determined by stepwise logistic regression analysis. The overall prevalence of LCOS was 3.9%. The independent predictors of LCOS were (odds ratio in parentheses) renal failure (5.0), earlier year of operation (4.4), left ventricular ejection fraction <40% (3.6), shock (3.2), female gender (2.8), and increasing age (1.02). Overall OM was 2.9%. The OM was higher in patients who experienced LCOS (38% versus 1.5%; P<0.001). The independent predictors of mortality were (odds ratio in parentheses) preoperative renal failure (8.3), urgency of surgery (3.4), previous stroke (2.9), congestive heart failure (2.6), previous cardiac surgery (2.3), hypertension (1.7), and small AV size (1.3). CONCLUSIONS: Low-output syndrome is associated with significantly increased morbidity and mortality. Novel strategies to preserve renal function, optimization of preexisting heart failure symptoms, and avoidance of prosthesis-patient mismatch may reduce the incidence of LCOS and lead to improved results after AV surgery.

Aged↗
PubMed1985

Continuous, on-line, real-time measurement of cardiac output and derived cardiorespiratory variables in the critically ill.

A previously reported monitoring system provided continuous direct measurements of oxygen consumption and intravascular pressures. These data were combined with interval measurements of cardiac output and blood oxygen saturations to derive various hemodynamic and oxygen transport variables. This system has now been modified so that cardiac output is measured continuously in real-time.

Blood Pressure↗
PubMed2000

Noninvasive measurement of pulmonary vascular resistances by assessment of cardiac output and pulmonary transit time.

RATIONALE AND OBJECTIVES: Pulmonary vascular resistance is of special interest in many diseases. Usually it is determined invasively by catheterization, but cardiac output and pulmonary transit time can be ascertained by several noninvasive methods. METHODS: Fourteen heart recipients (age 34-71 years) were examined by electron-beam CT of the heart. Cine and flow studies were performed using a total of 60 mL of contrast and a breath-hold of 20 seconds. RESULTS: A mathematical model for calculating pulmonary vascular resistances from noninvasively measured cardiac outputs and pulmonary transit times was developed. Right-sided heart catheterization served as the reference method. CONCLUSIONS: The formula created seems to allow a clinically valid estimate of pulmonary vascular resistance from noninvasively acquired data.

Algorithms↗
PubMed1992

[Changes in cardiac output in the initial phases of hypertension].

In what concerns to the early phases of arterial hypertension, the difficulty of definition, the usually found hemodynamic changes, especially of cardiac output, and its changes during evolution to established hypertension, are referred. The role of genetic determinants of predisposition to hypertension and of strain situations as factors of precipitation, with acute rise of blood pressure and cardiac output, is emphasized. It is also referred the importance of the early detection of true hypertensives by studying their reaction to strain situations, being particularly promising the mental stress tests and the dynamic exercise tests.

Animals↗
PubMed1980

Determination of cardiac output by thermodilution during hypothermia.

The thermodilution method for estimating cardiac output was compared with the electromagnetic flowmeter technique in 10 mongrel dogs at normothermia and during surface-induced deep hypothermia. Thermodilution curves obtained during cooling or rewarming must be corrected for the baseline drift caused by changing core temperature. At normothermia, the correlation coefficient between the two methods was 0.96 and the reproducibility of the thermodilution technique was 5 percent. Comparable correlation was present during hypothermia. Curves corrected for baseline drift resulted in significantly different output values from those derived from uncorrected curves (p < 0.05). The thermodilution method is valid at low body temperatures. Clinical confirmation of these results, particularly during open heart surgery in infants, is warranted.

Animals↗
PubMed1977

Effects of dibutyryl cyclic-AMP on cardiac output and myocardial contractility in dogs.

Dibutyryl cyclic-AMP was administered to a group of anesthetized dogs at the doses of 5, 10, 20 and 40 mg/kg, and changes in stroke volume, cardiac output and myocardial contractility were observed. Also, effects of this substance on contractile performance of isolated cardiac muscle were investigated in another group of dogs. Results were as follows: 1) Dibutyryl cyclic-AMP increased heart rate, stroke volume and cardiac output in a dose-related manner in the range from 5 to 40 mg/kg. 2) As indices of myocardial contractility, Vmax and maximum dF/dt were examined. These also showed a dose-dependent increase in response to dibutyryl cyclic-AMP. In isolated dog hearts, dibutyryl cyclic-AMP raised the maximum velocity of shortening (V'max) dose-dependently. 3) Total peripheral resistance declined in a dose-related way. On the other hand, mean arterial pressure and CVP dropped slightly without showing dose-dependence. These results show that dibutyryl cyclic-AMP produces positive inotropic and chronotropic effects and cause dilatation of the peripheral vessels in dose-dependent manners.

Animals↗