Significant Increase In Cardiac Output Research Articles

Effects of Hypocapnia and Hypercapnia on Splanchnic Circulation and Hepatic Function in the Beagle

The effects of mild hypocapnia (PaCO2 22 mm Hg) and hypercapnia (PaCO2 59 mm Hg) on the splanchnic circulation and hepatic function were studied in six pentobarbital anesthetized, laparotomized, mechanically ventilated beagles. Tidal volume and respiratory frequency were held constant throughout the measurements. Hepatic artery blood flow (HABF) and portal vein blood flow (PVBF) were measured by electromagnetic flowmeters. Hepatic function was assessed by indocyanine green (ICG) elimination kinetic analysis after intravenous injection of the dye. Hypocapnia caused a decrease in HABF without affecting the systemic circulation. Hypercapnia, on the other hand, caused a significant increase in cardiac output without changing mean arterial pressure. There was a significant increase in PVBF and total hepatic blood flow (THBF = PVBF + HABF). Despite the increases in PVBF and THBF, the half-life of ICG was significantly longer during hypercapnia (9.09 +/- 0.79 min) than during hypocapnia (7.16 +/- 0.37 min), and plasma ICG clearance was smaller during hypercapnia (4.79 +/- 0.44 ml.min-1) than during hypocapnia (5.44 +/- 0.33 ml.min-1) or normocapnia (5.27 +/- 0.50 ml.min-1), indicating the depressed hepatic function during hypercapnia. We conclude that mild hypocapnia decreases HABF without affecting hepatic function and that mild hypercapnia is associated with a depression of hepatic function in spite of the increases in PVBF and THBF.

Systemic, Pulmonary and Renal Haemodynamic and Renal Morphologic Effects of Intravenously Infused Iodixanol

The systemic, pulmonary and renal haemodynamic effects following an intravenous infusion (1 ml/s, 4 ml/kg) of a non-ionic iso-osmolar contrast medium (iodixanol) were investigated in 8 pigs. Histopathologic changes occurring after infusion of iodixanol were studied by repeated renal biopsies. Iodixanol caused a significant increase of cardiac output, mean right atrial pressure, mean pulmonary arterial pressure, mean pulmonary arterial occlusion pressure and mean arterial pressure. There was a decrease of the systemic and pulmonary vascular resistances. Most renal biopsies showed no pathologic findings after infusion of iodixanol but in 3 specimens proteinaceous content was observed 15 min after infusion.

Systemic, Pulmonary and Renal Haemodynamic and Renal Morphologic Effects of Intravenously Infused Iodixanol

The systemic, pulmonary and renal haemodynamic effects following an intravenous infusion (1 ml/s, 4 ml/kg) of a non-ionic iso-osmolar contrast medium (iodixanol) were investigated in 8 pigs. Histopathologic changes occurring after infusion of iodixanol were studied by repeated renal biopsies. Iodixanol caused a significant increase of cardiac output, mean right atrial pressure, mean pulmonary arterial pressure, mean pulmonary arterial occlusion pressure and mean arterial pressure. There was a decrease of the systemic and pulmonary vascular resistances. Most renal biopsies showed no pathologic findings after infusion of iodixanol but in 3 specimens proteinaceous content was observed 15 min after infusion.

Hemodynamics of conscious unrestrained baboons, including cardiac output

A method is described for comprehensive hemodynamic study of undisturbed baboons (Papio hamadryas) that incorporates cardiac output measurement by thermodilution. Instrumentation includes arterial, aortic, and central venous catheterization by a surgical technique that does not require entry to peritoneal or thoracic cavities. It provides a means for right atrial indicator delivery with aortic temperature recording of thermodilution curves. Accuracy was confirmed by comparison to measurement by Swan-Ganz catheters. Diurnal variations of systemic arterial pressure in long-term study of conscious baboons were shown to result from significant increases in cardiac output by day (P less than 0.001), despite concomitant falls in systemic vascular resistance. The cardiac output values obtained were 0.13 l.min-1.kg-1 at night and 0.16 l.min-1.kg-1 by day. Comparison of these results to previous reports of cardiac output in baboons highlights the inadequacies of methods that require physical restraint or anesthesia. This technique also leaves the baboons intact for subsequent breeding or experimental use after catheter removal without the need for further surgery.

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.

Fiberoptic Bronchoscopy in Ventilated Patients: Evaluation of Cardiopulmonary Risk under Midazolam Sedation

One hundred seven acutely ill ventilated patients were prospectively studied to ascertain the severity and frequency of alterations in gas exchange and hemodynamic parameters during brief bronchoscopy. Sedation was performed using midazolam (0.1 mg/kg IV) without topical anesthesia. An average decline in PaO2 of 26 percent was observed at the end of the procedure, compared to the baseline value, and this was associated with a mild increase in PaCO2 in spite of the use of a special adapter. Alterations in mean systolic blood pressure appeared to be modest, consisting of a 10 percent decrease from the control level, related to sedation, and a 10 percent rise from baseline during the procedure, associated with a concomitant mild tachycardia. At that time, central hemodynamic measurements performed in a subset of 31 patients showed a significant increase in cardiac output associated with higher pulmonary wedge pressure. Fourteen patients developed hypoxemia of less than 60 mm Hg on FIO2 adjusted to 0.8. Of the ten risk factors univariately associated with hypoxemia, only the presence of ARDS (p less than 0.001) and "fighting" the ventilator during the procedure (p less than 0.05) remained significant after stepwise logistic regression. Attempts to prevent hypoxemia in critically ill patients should focus on inducing complete sedation, with careful attention to hemodynamic status, or providing maximal levels of oxygen to the ventilator (or both).

Systemic, Pulmonary and Renal Haemodynamic and Renal Morphologic Effects of Intravenously Infused Iodixanol

The systemic, pulmonary and renal haemodynamic effects following an intravenous infusion (1 ml/s, 4 ml/kg) of a non-ionic isoosmolar contrast medium (iodixanol) were investigated in 8 pigs. Histopathologic changes occurring after infusion of iodixanol were studied by repeated renal biopsies. Iodixanol caused a significant increase of cardiac output, mean right atrial pressure, mean pulmonary arterial pressure, mean pulmonary arterial occlusion pressure and mean arterial pressure. There was a decrease of the systemic and pulmonary vascular resistances. Most renal biopsies showed no pathologic findings after infusion of iodixanol but in 3 specimens proteinaceous content was observed 15 min after infusion.

Effect of Intravenous Pimobendan (UDCG 115 BS) on Hemodynamics and Left Ventricular Volumes in Idiopathic Dilative Cardiomyopathy

Acute cardiovascular effects of 5 mg (group I, n = 6) and 10 mg (group II, n = 6) intravenous pimobendan (UDCG 115 BS) were studied by right and left heart catheterizations in patients suffering from idiopathic dilative cardiomyopathy (NYHA II and III). Before and 2.5 h after application of pimobendan, left ventricular volumes and left ventricular dP/dtmax were evaluated by left heart catheterization. Right atrial pressure (RAP), pulmonary capillary wedge pressure (PCP), cardiac output (CO), heart rate (HR), and sytemic blood pressure (BP) were assessed before and 2.5, 4, and 6 h after administration of pimobendan. PCP was reduced from 12.2 +/- 7.5 to 8.3 +/- 7.1 mm Hg (p less than 0.05) by 5 mg pimobendan, and from 18.3 +/- 6.2 to 6.2 +/- 3.4 mm Hg (p less than 0.005) by 10 mg pimobendan. Reduction of RAP was only significant in group II (6.2 +/- 3.2 to 1.2 +/- 0.9 mm Hg; p less than 0.05). In contrast to other hemodynamic parameters, the significant increase of CO exhibited no dose dependency. Only at 10 mg pimobendan induced a temporary reduction of mean arterial blood pressure (MAP). An increase in HR occurred only in group I and was merely transient. Left ventricular end-diastolic (EDVI) and end-systolic volume (ESVI) indices were clearly reduced by 5 mg, as well as by 10 mg pimobendan. However, a significant rise of left ventricular ejection fraction (EF) only occurred in group II. On the other hand, left ventricular dP/dtmax was increased significantly in both groups. No adverse effects were noted during acute administration of pimobendan.(ABSTRACT TRUNCATED AT 250 WORDS)

Nifedipine, but not propranolol, improves left ventricular systolic and diastolic function in patients with hypertension

The effects of nifedipine and propranolol on cardiac function both at rest and at peak exercise were compared in 22 hypertensive patients whose diastolic blood pressures remained in excess of 95 mm Hg despite diuretic therapy. In this double-blind, placebo-controlled study, left ventricular systolic and diastolic function at rest and at peak exercise during bicycle ergometry was assessed by first-pass radionuclide angiography using the Baird Scinticor before and after treatment with either nifedipine or propranolol. Both agents effectively reduced blood pressure in the supine and upright positions and at peak exercise. Nifedipine was associated with a significant increase in cardiac output and stroke volume at rest and at peak exercise, while propranolol decreased cardiac output at rest and at peak exercise. Systemic vascular resistance decreased with nifedipine treatment at rest and at peak exercise, but increased significantly with propranolol. Nifedipine increased ejection fraction in patients at rest and also increased maximal oxygen consumption at peak exercise, while propranolol decreased maximal oxygen consumption at peak exercise. At rest and at peak exercise, nifedipine increased peak filling rate, but time to peak filling rate was not affected by either drug. The fraction of total diastolik filling at the midpoint of diastole was significantly increased by nifedipine therapy at rest but was not affected by propranolol therapy. Nifedipine significantly decreased atrial filling volume white propranolol had no effect. Propranolol therapy did not result in any improvement in left ventricular function. In contrast, nifedipine improved left ventricular systolic and diastolic function at rest and peak exercise. Future selection of an antihypertensive agent should include consideration of the impact of therapy on left ventricular function.

Validation of continuous-wave Doppler measurements of mitral valve gradients during exercise--a simultaneous Doppler-catheter study.

In patients with mitral stenosis, continuous-wave Doppler measurements of the maximal transmitral inflow velocity can be converted into transvalvular pressure gradients using the modified Bernoulli equation. Because of close correlations between Doppler- and catheter-measured gradients this method has become a valuable tool in non-invasive evaluation of mitral stenosis at rest. However, in some patients, exercise studies are necessary to determine the haemodynamic significance of the valve stenosis. The accuracy of continuous-wave Doppler in this setting has not yet been validated. Thus, in 20 selected patients with pure or predominant mitral stenosis, continuous-wave Doppler echocardiography was performed during left- and right-heart catheterization. At rest and during submaximal bicycle exercise, Doppler and pressure measurements were simultaneously performed. The Doppler gradient was calculated according to the modified Bernoulli equation while the mean manometric gradient was determined from the simultaneous pulmonary wedge and left ventricular pressure curves. Exercise caused a significant increase of cardiac output (4.8 +/- 1.3 to 5.7 +/- 1.31 min-1) and heart rate (59.7 +/- 12.0 to 95.3 +/- 14.3 beats min-1). The mean Doppler gradient increased from 6.8 +/- 2.1 to 12.2 +/- 3.2 mmHg. The manometric gradient showed a comparable increase of 9.5 +/- 2.4 to 17.2 +/- 3.7 mmHg, respectively. Correlation between Doppler and manometric data was close (y = 0.79x-0.67,r = 0.90,SEE = 0.97 mmHg) at rest and still good during exercise (y = 0.71x-0.10,r = 0.82,SEE = 1.97 mmHg). Thus, in some patients with borderline resting gradients and valve areas, exercise Doppler might allow further identification of the haemodynamic severity of mitral stenosis.

Effects of Hypocapnia and Hypercapnia on Splanchnic Circulation and Hepatic Function in the Beagle

The effects of mild hypocapnia (Paco2 22 mm Hg) and hypercapnia (Paco2 59 mm Hg) on the splanchnic circulation and hepatic function were studied in six pentobarbital anesthetized, laparotomized, mechanically ventilated beagles. Tidal volume and respiratory frequency were held constant throughout the measurements. Hepatic artery blood flow (HABF) and portal vein blood flow (PVBF) were measured by electromagnetic flowmeters. Hepatic function was assessed by indocyanine green (ICG) elimination kinetic analysis after intravenous injection of the dye. Hypocapnia caused a decrease in HABF without affecting the systemic circulation. Hypercapnia, on the other hand, caused a significant increase in cardiac output without changing mean arterial pressure. There was a significant increase in PVBF and total hepatic blood flow (THBF = PVBF + HABF). Despite the increases in PVBF and THBF, the half-life of ICG was significantly longer during hypercapnia (9.09 ± 0.79 min) than during hypocapnia (7.16 ± 0.37 min), and plasma ICG clearance was smaller during hypercapnia (4.79 ± 0.44 ml·min−1) than during hypocapnia (5.44 ± 0.33 ml·min−1) or normocapnia (5.27 ± 0.50 ml·min−1), indicating the depressed hepatic function during hypercapnia. We conclude that mild hypocapnia decreases HABF without affecting hepatic function and that mild hypercapnia is associated with a depression of hepatic function in spite of the increases in PVBF and THBF.

The Role of Beta Receptors in the Peripheral Vasculature of Calves with a Total Artificial Heart

Drugs given to a total artificial heart (TAH) calf isolate their vascular effects independent of the myocardium. During experiments, the TAH maintains full ejection, constant heart rate, and percent systole, and uses no vacuum. Cardiac output (CO) varies solely and directly with preload. Six calves received an infusion of isoproterenol, a beta agonist, and three calves received propranolol, a beta antagonist. The isoproterenol was resumed after beta blockade. Isoproterenol alone caused a significant increase in CO, an effect that was attenuated but not eliminated with beta blockade. Both isoproterenol and propranolol decreased AoP, but only isoproterenol increased preload. Beta receptors play a significant role in decreasing venous capacitance with increased preload and CO, independent of the myocardium.

Central and regional hemodynamic effects of flosequinan for congestive heart failure

The central and regional hemodynamic effects of flosequinan, a new orally administered vasodilator, were examined in 10 patients with moderate to severe congestive heart failure. A single-blind design was used to compare a standard dose of flosequinan (100 mg) with placebo. Flosequinan produced a statistically significant increase in cardiac output, primarily through its augmentation of stroke volume. This response was accompanied by significant reductions in systemic vascular resistances and right and left ventricular filling pressures. A reduction in pulmonary artery pressure and total pulmonary vascular resistance also was observed. The vasodilatory actions of flosequinan improved overall left ventricular performance; the inotropic indexes measured were not altered. There were no significant changes in upper limb, renal or hepatic-splanchnic blood flow or in the vascular resistance of these regions after flosequinan administration. The upper limb venous capacitance increased significantly. First-dose flosequinan evokes favorable central hemodynamic changes and improves overall left ventricular performance in patients with congestive heart failure. The acute augmentation in cardiac output, however, is not accompanied by a preferential alternation of flow to any of the major vascular regions studied.

Intra-aortic balloon counterpulsation: a treatment for ischaemic stroke?

Intra-aortic balloon counterpulsation (IABC) augments cardiac output (CO) and pulse pressure (PP) allowing patients with low output heart failure to be supported for a period of time. Augmentation of CO and PP may also be beneficial to the patient with acute cerebral ischaemia. In this paper we investigated the possibility of using IABC to increase local cerebral blood flow (CBF) in ischaemic brain. In 12 anaesthetized mongrel dogs, a canine stroke model was produced by occluding the left internal carotid and middle cerebral arteries with aneurysm clips. Six dogs were then treated with IABC for 2 h, and 6 other dogs acted as controls (no IABC). Haemodynamic data were measured continuously and CBF (microsphere technique) and CO measurements were performed pre- and post-occlusion, and then twice during the treatment period. In the IABC-treated animals, PP increased from 32 +/- 5.9 to 39 +/- 7.8 mmHg (p less than 0.01) but CO and local CBF in the ischaemic brain did not change significantly during IABC. However, in 4 dogs with significant increases in CO due to IABC [1.7 +/- 0.3 to 2.8 +/- 0.7 l/min (p less than 0.05)], local CBF in ischaemic brain also increased significantly from 22 +/- 12 to 26 +/- 11 cc/100 g/min (p less than 0.05). In the control animals, CO and local CBF did not change significantly during the observation period. These data suggest that augmentation of CO and PP by IABC results in an increase in local CBF in ischaemic brain. IABC may be an effective treatment for ischaemic stroke in those patients with compromised cardiac performance whose cardiac output and pulse pressure can be augmented by IABC.

Relationship between oxygen transport and oxygen uptake in patients with cirrhosis: Effects of vasoactive drugs

To elucidate the relationship between oxygen transport and uptake in cirrhosis, we studied the effects of three vasoactive drugs that change O2 transport. Systemic hemodynamics, blood gases and lactate concentration were measured in patients with alcoholic cirrhosis before and after intravenous dobutamine, propranolol and nitroglycerin. Nine patients received successively dobutamine and then propranolol. Ten patients received nitroglycerin. Three other patients without cirrhosis (controls) received dobutamine. In patients with cirrhosis, dobutamine infusion was accompanied by a significant increase in cardiac output (+21%), systemic O2 transport (+21%) and O2 uptake (+12%), whereas O2 extraction ratio and arterial lactate concentration did not change significantly. Propranolol administration was followed by a significant decrease in cardiac output (-24%) and systemic O2 transport (-25%) and a significant increase in O2 extraction ratio (+19%), whereas O2 uptake and arterial lactate concentration did not change. Nitroglycerin infusion was accompanied by a significant decrease in cardiac output (-21%), systemic O2 transport (-26%) and O2 uptake (-10%), whereas O2 extraction ratio (+18%) and arterial lactate concentration (+31%) significantly increased. In control patients, dobutamine infusion was accompanied by an increase in cardiac output and in systemic O2 transport and by a decrease in O2 extraction ratio, whereas O2 uptake was not modified. These results suggest that O2 uptake may be abnormally dependent on O2 transport in patients with cirrhosis.

Cardiorespiratory effects of the intravenous administration of tiletamine-zolazepam to dogs.

The anesthetic, hemodynamic, and respiratory effects of an intravenously administered 1:1 combination of tiletamine and zolazepam were evaluated in dogs. Each dog received tiletamine-zolazepam (6.6, 13.2, 19.8 mg/kg) on two occasions, once when awake and a second time with residual isoflurane anesthesia while instrumented for the recording of hemodynamic data. Tiletamine-zolazepam administered to conscious dogs resulted in good, rapid induction of anesthesia. Time to sternal recumbency (recovery) was dose-dependent. Character of recovery tended to be better with the lower dose. Tiletamine-zolazepam caused significant increases in heart rate after all doses and significant increases in cardiac output after the two larger doses. All doses caused significant decreases in arterial blood pressure at 1 minute. Arterial blood pressures returned to baseline and then increased significantly above baseline values. The rate of development of left ventricular pressure was significantly decreased 1 minute after the two higher doses, returned to normal, and then was significantly increased above baseline for all doses. Peripheral vascular resistance increased transiently 1 minute after the 6.6 mg/kg dose. Peripheral vascular resistance decreased significantly after the 13.2 and 19.8 mg/kg doses. Minute ventilation was significantly decreased only after the 19.8 mg/kg dose.

Hemodynamic and Metabolic Changes in Hepatic Transplantation

In this study, we retrospectively analyzed the intraoperative hemodynamic, laboratory, and coagulation data on the first 83 patients who underwent an initial liver transplantation procedure at our institution. The major hemodynamic changes at the time of reperfusion of the donor liver were significant decreases in arterial blood pressure, systemic vascular resistance, and pulmonary artery temperature and significant increases in cardiac output and pulmonary capillary wedge pressure. The alterations in laboratory values reflected intraoperative therapeutic manipulations. Citrate toxicity is a concern, and the amount of calcium chloride administered reflected the volume of blood transfused. On reperfusion, the fibrinogen concentration decreased and both the prothrombin time and the activated partial thromboplastin time increased. This coagulopathy was also evident in the thromboelastographic values. Aggressive monitoring and prompt intervention are necessary to maintain hemodynamic and metabolic homeostasis in these patients.

Effects of Hemodilution on Peripheral Circulation

In 7 anesthetized dogs the authors produced anemia by exchanging isovo lemic blood with plasma substitute and thus reducing hemoglobin gradually from 17.9 ± 0.7 to 8.5 ± 0.7 gr/dL in three steps. Samples were taken from pe ripheral blood at the animals' normal hemoglobin and at different degrees of hemodilution for the determination of Hb, viscosity, fibrinogen, venous blood lactate and pyruvate, pH, pO2, and oxygen saturation, while cardiac output, heart rate, and aortic pressure were measured. Total peripheral resistance, oxy gen content, and oxygen transport were calculated. Progressive hemodilution resulted in a significant increase in cardiac output from 2.5±0.1 to 4.2±0.2 L/min (p < 0.001), while peripheral resistance decreased clearly parallel with the whole blood viscosity (from 2.2±0.1 to 1.2±0.1 mm Hg/mL/sec, p < 0.001). The value of arterial oxygen content was decreased from 22.6±1.1 to 10.1 ±0.7 mL/dL of blood (p < 0.001), but the systemic oxygen transport was completely compensated at hemodilution step A, and moderately at steps B and C, because of the increased cardiac output. Oxygen consumption was slightly decreased, while aortic pressure, pH, pO2, and oxygen saturation did not change. These data support the concept that moderate normovolemic hemodilution improves the peripheral circulation and does not jeopardize tissue oxygenation.

Pulmonary vascular and renal effects of cromakalim in anaesthetized dogs.

1) CROM reduced hypoxia-induced pulmonary vasoconstriction and maintained PaO2 with an increase in cardiac output. 2) Low doses of CROM infused into the kidney caused pronounced renal vasodilation, marked natriuresis and a significant increase in cardiac output with minor changes in blood pressure. In addition to its previously described systemic antihypertensive effects, CROM also reduces hypoxia-induced pulmonary hypertension and shows marked renal vasodilation with natriuresis in anaesthetized dogs.

Renal and hormonal effects of phosphodiesterase III inhibition in congestive heart failure

Evaluation of the impact of therapeutic interventions in congestive heart failure (CHF) with compounds such as the phosphodiesterase (PDE) III inhibitors must include the determination of regional blood flow and functional changes. Thus, whereas PDE III inhibitors produce a significant increase in cardiac output and reduction of systemic vascular resistance, it is necessary to understand their effects on the kidney and neurohormonal parameters. The evaluation of these effects must take into consideration both the baseline renal and neurohormonal abnormalities in CHF, and the cellular actions of PDE III inhibition, which include an increase in cyclic adenosine monophosphate and cytosolic calcium. In a group of 13 patients with CHF, milrinone therapy for 1 month did not increase renal blood flow or glomerular filtration rate, or favorably affect neurohormonal parameters. However, forearm blood flow increased proportionately with cardiac output. Therefore PDE III inhibition produces a preferential increase in skeletal muscle blood flow, which may be a relative shunting of blood from the kidney. Alternatively, PDE III inhibition may activate renal cellular mechanisms that offset the anticipated favorable response to the increase of cardiac output produced by milrinone.