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PubMed1988

[Uses and risks of hemodynamic monitoring by inflow catheter in acute myocardial infarct].

Using hemodynamic monitoring by flow-directed heart catheterization in acute myocardial infarction, left ventricular dysfunction can be analyzed and quantified. Differential therapy concerning substitution of volume and administration of drugs with influence on pre- and after-load is facilitated. Since the introduction of the Swan-Ganz flow-directed catheter the monitoring has been technically improved with the additional advantage of lower incidence of catheter-induced arrhythmias and the possibility to measure the pulmonary capillary wedge pressure. The Swan-Ganz thermodilution catheter further improved the technical assessment of cardiac output. Using hemodynamic monitoring during acute myocardial infarction different phases of cardiac failure can be discerned, e.g., backward failure with increased filling pressure, foreward failure with decreased cardiac output, and cardiogenic shock with the combination of both. In some cases a hyperkinetic hemodynamic status is observed. The differential diagnosis of pulmonary embolism, and cardiac and pulmonary shock can be clarified. Complications of myocardial infarction as acute mitral insufficiency due to papillary muscle rupture in inferior myocardial infarction, rupture of the septal myocardium in septal infarction, as well as myocardial rupture with pericardial tamponade show characteristic diagnostic findings. Drug therapy with influence on pre- and after-load and therapy with positive-inotropic agents can be adjusted to the individual hemodynamic status and to the monitored drug effects.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Catheterization↗
PubMed1988

The influence of prostacyclin on hemodynamic and coronary blood flow in dogs.

Continuous intravenous infusion of prostacyclin (PGI2) was carried out for 30 to 120 min at the rates 25, 50, 75, 100 ng/kg/min in 149 experiments in 30 anesthetized dogs. PGI2 caused significant dose-dependent rise in heart rate, cardiac output, stroke volume and mean coronary artery blood flow. At the same time arterial blood pressures, total peripheral resistance and coronary vascular resistance decreased significantly while pulmonary artery pressures, central venous pressure, mean femoral artery blood flow and pressure rise velocity in left ventricle remained practically unaltered. Stady state of hemodynamic parameters was reached in 10 to 12 min. after the beginning of infusion. After discontinuation of infusion of PGI2 the values of recorded hemodynamic parameters returned to pre-infusion level in 10 to 15 min. Hemodynamic changes were well reproducible during repetitive infusions of PGI2 The purpose of this study was to determine the effects of PGI2 on various hemodynamic parameters.

Animals↗
PubMed1988

Systemic and regional hemodynamic effects of cyclo-oxygenase and thromboxane synthetase inhibition in normal and hyperdynamic endotoxemic rabbits.

We tested the hypothesis that prostaglandins (PGs) and thromboxane (Tx) A2 are important mediators of the hemodynamic derangements occurring in a rabbit model of hyperdynamic endotoxicosis. Rabbits were injected with either normal saline (NS) or Escherichia coli lipopolysaccharide (LPS; 1-3 micrograms/kg) and studied 6 hr later. Cardiac index (CI) and regional blood flow were determined using thermodilution and radioactive microspheres, respectively. Systemic and regional hemodynamics were determined before and 40 min after administering indomethacin (cyclo-oxygenase inhibitor; 5 mg/kg), UK38485 (Tx synthetase inhibitor; 10 mg/kg), or NS. LPS increased CI (P = .0024) and decreased mean arterial pressure (P = .0031) and systemic vascular resistance index (P = .0001). LPS increased flow to the heart and small intestine and decreased flow to the hepatic artery and pancreas. The systemic and regional hemodynamic effects of indomethacin were similar in NS- and LPS-treated rabbits. UK38485 decreased perfusion of skeletal muscle and diaphragm in both endotoxemic and control animals. This agent increased splenic perfusion only in NS-treated rabbits. Plasma levels of 6-keto PGF1 alpha (PGI2 metabolite) were typically undetectable in both NS- and LPS-treated rabbits. These data do not support the hypothesis that PG's or TxA2 are major determinants of the hemodynamic perturbations that occur in this endotoxicosis model.

6-Ketoprostaglandin F1 alpha↗
PubMed1988

[Experimental hemodynamic study on carotid ligation combined with EC-IC bypass for giant aneurysm].

Although carotid ligation or balloon occlusion has been an accepted method for the inaccessible ICA aneurysm, there have been several reports of growth or rupture of the aneurysm, and cerebral embolism originating from the site of arterial occlusion or from the aneurysm. The hemodynamic changes after operation are suspected to play some role in these events. It is, therefore, very important to predict what will happen after operation in individual patients. However, it is usually difficult because multiple factors are related in a complex fashion in a living body. One of the effective means is to simulate these hemodynamic conditions by a hydraulic vascular model. We have already reported the hemodynamic changes resulting from EC-IC bypass for MCA stenosis. In this research, a glass-model aneurysm of 2.5 cm in diameter is placed at the ICA bifurcation of the model to evaluate hemodynamics after therapeutic carotid occlusion with or without EC-IC bypass. Dye was injected into the aneurysm and intensity change of the light transmitted there was measured by a photocell. Half-life of the dye was calculated from thus obtained clearance curve and was regarded as an index of intraaneurysmal stagnation, while embolus formation in an aneurysm is considered to be due to the stagnation there. The results obtained are: 1. Half-life of the dye increases significantly after carotid ligation even if collateral flow through the anterior communicating artery (A-com) or EC-IC bypass equals the ICA flow before ligation. 2. The higher collateral flow through A-com results in the more normograde flow in M1 portion, which shortens the half-life.(ABSTRACT TRUNCATED AT 250 WORDS)

Carotid Arteries↗
PubMed1988

[Age-related characteristics of hemodynamic adaptation to adipose tissue changes in men without arterial hypertension].

A combined clinical-instrumental study of hemodynamics and anthropometry of fatty and fatless body masses (FBM, FLBM) based on caliperometry of 8 skin fatty folds, were performed in 138 men aged 20 to 59 without arterial hypertension. An increase in age and excessive adipose deposits with the growth of relative FBM were accompanied by adaptive changes of the central and regional hemodynamics characterized by a decrease in cardiac output, an increase in peripheral vascular resistance, and a decrease in the volumetric crural blood flow. The influence of adiposity on hemodynamics, mostly expressed in a young age, particularly at the age of 30-39, made more rapid the appearance in young men with excessive adipose deposits of hemodynamic shifts typical of older age persons.

Adaptation, Physiological↗
PubMedDate not supplied

[Influence of kordaron, anaprilin, dimedrol and riboxin on the hemodynamic effects of strophanthin in experimental heart failure].

In experiments on 183 rats it was shown that cordarone, anapriline, dimedrol and riboxine increasing in experimental cardiac insufficiency tolerance to the cardiotoxic effect of strophanthin differ significantly by their influence on the hemodynamic effects of this cardiac glycoside. Cordarone increased intensity of the hemodynamic effects of strophanthin and accelerated their development. Under the action of anapriline and dimedrol the stimulating effect of strophanthin on hemodynamics decreased to a much lesser degree than its cardiotoxicity. Riboxine virtually abolished the hemodynamic effects of strophanthin.

Amiodarone↗
PubMed1987

Hemodynamic effects of infusions of the emulsion formulation of propofol during nitrous oxide anesthesia in humans.

The hemodynamic response to anesthesia with the aqueous emulsion formulation of propofol was studied in healthy patients (ASA I or II), aged 39-57 yr, premedicated with morphine, 0.15 mg/kg. Anesthesia was induced in all patients with propofol, 2 mg/kg. Subsequently, patients were randomly assigned to two groups and maintained by a continuous intravenous infusion (group 1 received 54 micrograms X kg-1 X min-1, group 2 received 108 micrograms X kg-1 X min-1) to supplement 67% nitrous oxide. Three minutes after induction, systolic arterial pressure (SAP) decreased 28% (P less than 0.01) and was associated with decreased (-12%) cardiac output (Q70) and decreased (-15%) systemic vascular resistance (SVR). The hemodynamic response to tracheal intubation was not obtunded, but peak values of arterial pressures and heart rate did not exceed those recorded awake. Thirty minutes elapsed before repeating measurements prior to the first surgical incision. In group 1, SAP and Q70 decreased to 65% and 68% of awake values and in group 2 to 55% and 74% (P less than 0.05). Mild ventilatory depression persisted for the duration of spontaneous ventilation and was not reduced by the stimulus of surgery, which caused no significant hemodynamic responses in either group. Decreasing arterial PCO2 to the awake value by controlled ventilation increased SVR (P less than 0.05), but the associated increased SAP and decreased Q70 did not reach statistical significance. No patient reported awareness. The infusion of the emulsion formulation of propofol was associated with satisfactory anesthesia and recovery and with hemodynamic effects similar to those recorded with other intravenous anesthetics.

Adult↗
PubMed1987

Low-dose enflurane as adjunct to high-dose fentanyl in patients undergoing coronary artery surgery: stable hemodynamics and maintained myocardial oxygen balance.

The effects of enflurane (end-tidal concentration 0.7%) on central and coronary hemodynamics and myocardial oxygenation were studied during steady state, high-dose fentanyl anesthesia in ten patients undergoing coronary artery bypass grafting operations. Compared with the response in ten patients receiving the same fentanyl anesthesia (100 micrograms/kg) without enflurane supplementation, enflurane caused a moderate reduction in mean arterial pressure, systemic vascular resistance, and left ventricular stroke work index. No patient showed signs of myocardial ischemia, and mean coronary sinus flow and calculated coronary resistance remained unchanged. Surgical stimulation induced no central or coronary hemodynamic responses in the enflurane-fentanyl group. No coronary hemodynamic changes occurred in the fentanyl group, but a marked increase in arterial pressure and systemic vascular resistance was seen. Myocardial oxygen extraction decreased in the enflurane supplemented group although it increased in the fentanyl group after surgical stimulation. Three fentanyl group patients and one enflurane-fentanyl group patient had a low myocardial lactate extraction as a sign of myocardial ischemia during surgery. We conclude that a 0.7% enflurane supplementation of 100 micrograms/kg fentanyl anesthesia does not endanger myocardial oxygenation and effectively prevents central and coronary hemodynamic responses to skin incision and sternotomy in patients undergoing coronary artery surgery.

Anesthesia, General↗
PubMed1986

Hemodynamic determinants of mortality in human septic shock.

To assess the relative importance of cardiac versus peripheral vascular failure in patients dying of septic shock, a series of 42 patients with documented septic shock was retrospectively evaluated. Patients were included in the study if serial hemodynamic and metabolic studies had been performed: the first one within 12 hours after onset of septic shock and the last one within 12 hours (median 2 hours; range 0.1 to 12 hours) before death in nonsurvivors. Nonsurvivors were included only if they died in shock. From the patient records the first, highest, and last measured cardiac indexes (CI) (t = 1, t = 2, and t = 3) with concomitant hemodynamic and metabolic variables were obtained. Group I (n = 21) consisted of survivors and group II (n = 21) of nonsurvivors. Group II was divided into three subgroups: group IIa (n = 4) consisted of nonsurvivors with liver cirrhosis, group IIb (n = 9) patients with final CI less than 4 1 X min-1 X m-2, and group IIc (n = 8) patients with final CI greater than 4 1 X min-1 X m-2. At t = 1 no significant differences in hemodynamic variables were found between groups I and II, and all patients, whether surviving or not, were able to increase CI to similar levels. At t = 3 group II showed a marked decrease in mean arterial pressure and systemic vascular resistance index compared with group I (p less than 0.001), whereas CI did not differ significantly. The nonsurvivors showed progressive lactic acidemia. Even group IIb patients showed persistent vasodilation despite a decrease in CI. Our data suggest that many patients in septic shock die as a result of peripheral vascular rather than cardiac failure, since persistent vasodilation, irrespective of CI, was a major hemodynamic determinant in nonsurvivors, of whom 57% maintained a high CI until shortly before death.

Adult↗
PubMed1987

[Metabolic responses to ergometry and their role in the development of physical work capacity in patients with ischemic heart disease and different types of hemodynamics].

Blood coagulation and fibrinolysis, lipid and lactate levels and some enzyme activities were measured in 283 coronary patients during bicycle ergometry. Hemodynamic type was established on the basis of the cardiac index. A negative correlation is demonstrated between the cardiac output and blood lipids. Fibrinolytic reserve was intact in 32.3% of patients with eu- and hyperkinetic hemodynamic types and in just 9.3% of patients with hypokinetic hemodynamics. The latter type was associated with the greatest disturbance of aerobic/anaerobic metabolism ratios. The extent of disturbance in lipid metabolism and blood coagulation is closely correlated with hemodynamic types that reflect the state of myocardial contractility.

Blood Coagulation↗
PubMed1987

Hemodynamic effects of portal triad clamping in humans.

The hemodynamic effects of portal triad clamping (PTC) were studied in 48 adult patients scheduled for elective liver resection. Prior to hepatic resection the effects of a short period of PTC (3-5 min) were evaluated in all 48 patients: mean arterial pressure increased 21%, whereas pulmonary capillary wedge pressure and cardiac index decreased 10 and 17%, respectively. Systemic vascular resistance increased 48%. In 34 patients a liver resection was performed during PTC and hemodynamic measurements were repeated throughout the duration of liver ischemia, which ranged from 14 to 68 min. Hemodynamic changes occurred in the first 3 min and persisted thereafter. After releasing the clamp, hemodynamic parameters returned to initial values in 3 min. These results confirm that PTC does not induce the cardiovascular collapse in humans that it does in common laboratory animals and demonstrate that humans tolerate PTC for periods up to 1 hr.

Adult↗
PubMed1987

[Changes in the hemodynamics and work capacity of patients following mitral commissurotomy].

A radiocardiographic study of the hemodynamic patterns in 256 patients at different times after mitral commissurotomy and their impact on postoperative working capacity demonstrated that the hemodynamic effect of mitral commissurotomy was more pronounced, earlier and more persistent in patients, operated on during the 3d stage of the disease. More advanced stages of circulatory insufficiency were associated with worse major hemodynamic parameters. The cardiac index can be used as an objective indicator of hemodynamic status and the extent of circulatory insufficiency, as well as a criterion for the assessment of working capacity after mitral commissurotomy.

Disability Evaluation↗
PubMed1979

[State of systemic and cerebral hemodynamics in patients with transient cerebral circulatory disorders].

In 50 patients with transient disorders of cerebral circulation due to hypertensive disease (27 cases), and combinations of hypertensive disease with atherosclerosis (23 cases) the authors by means of diluting Ewans blue stain (T-1824) studied the indices of general hemodynamics compared to that of REG data . For control purposes 10 patients with hypertensive disease in concomitance with atherosclerosis without transient disorders of cerebral circulation and 20 normals were studied. The study permitted to detect signs of disturbed general and cerebral hemodynamics which were most expressed in patients with severe cerebro-vascular crises, accompanied by a drop in the cardiac and pulse index, an increase of the general and specific peripheral resistance, a slowing of the blood flow rate on the segment hand-ear, an increase of the tone and drop of elasticity in the cerebral vessels, a decrease of cerebral blood repletion. Insufficiency of general hemodynamics leads to disorders of cerebral hemodynamics and unfavourably influences the development of the disease and the outcome of cerebrovascular crises.

Adult↗
PubMed1987

Specific bradycardic agents, a new therapeutic modality for anesthesiology: hemodynamic effects of UL-FS 49 and propranolol in conscious and isoflurane-anesthetized dogs.

A "specific bradycardic agent" has direct negative chronotropic actions without producing other systemic or coronary hemodynamic alterations. UL-FS 49, a recently synthesized structural analog of verapamil without classical slow channel calcium blocking activity, is proposed as such an agent. The purpose of this investigation was to characterize the hemodynamic and electrocardiographic actions of UL-FS 49 (0.25, 0.50, and 1.0 mg/kg) and compare its effects with those of propranolol (0.25, 0.50, and 1.0 mg/kg) in conscious or isoflurane-anesthetized (with and without neuromuscular blockade by pancuronium) chronically instrumented dogs. In six groups, comprising 52 experiments, UL-FS 49 was found to be more efficacious than propranolol in reducing heart rate, although this agent did not block the hemodynamic response to isoproterenol. UL-FS 49 produced 45-50% reductions in heart rate in dogs with isoflurane-induced tachycardia as compared to 15 and 30% reductions following propranolol. Furthermore, few other hemodynamic alterations were produced by UL-FS 49 indicating the remarkable specificity of this drug for reducing heart rate. A "specific bradycardic agent" such as UL-FS 49 may be useful clinically during the perioperative period. Such a drug may be especially advantageous for patients with documented or suspected ischemic heart disease, those who cannot tolerate the side effects of beta adrenergic blockade, as well as patients requiring a greater reduction in heart rate than can be obtained with beta adrenergic receptor antagonists.

Anesthesia, Inhalation↗
PubMed1987

Nicotine-induced release of vasopressin in the conscious rat: role of opioid peptides and hemodynamic effects.

Nicotine has been shown to stimulate the release of vasopressin and to cause significant hemodynamic changes. The mechanisms leading to enhanced vasopressin secretion and the vascular consequences of the high plasma vasopressin levels during nicotine infusion have not yet been determined. Therefore, the purposes of the present study were 1) to examine in normal conscious rats the role of opioid peptides in the nicotine-induced increase in plasma vasopressin levels and 2) to assess the role of vasopressin in the hemodynamic effects of nicotine (20 micrograms/min for 15 min) using a specific V1 antagonist of the vascular actions of vasopressin. Plasma vasopressin levels were significantly increased in the nicotine-treated animals (39.5 +/- 10 vs. 3.7 +/- 0.6 pg/ml in the controls, P less than .01). Pretreatment with naloxone, an antagonist of opioids at their receptors, did not reduce the vasopressin levels (47.7 +/- 9 pg/ml). Nicotine also increased mean blood pressure (122.5 +/- 2.5 to 145.2 +/- 3.3 mm Hg, P less than .01) and decreased heart rate (461 +/- 6 to 386 +/- 14.5 beats/min, P less than .05). Administration of the vasopressin V1 antagonist before the nicotine infusion did not affect the systemic hemodynamics or the regional blood flow distribution, as assessed by radiolabeled microspheres. Thus, these results suggest that the nicotine-induced secretion of vasopressin is not mediated by opioid receptors and that the high plasma vasopressin levels do not exert any significant hemodynamic effect on cardiac output or blood flow distribution.

Animals↗
PubMed1986

[Features of the hemodynamics of myocardial infarct patients undergoing the most widely used rehabilitation programs].

Integrated body rheography, radiocardiography and radionuclide ventriculography were used to investigate hemodynamic changes in 101 myocardial infarction patients during the hospital stage of the disease. Changes in major hemodynamic parameters were demonstrated by the end of the 1st week and when walking was resumed. At the resumed-walking stage, the mechanism of declining stroke and cardiac indices was shown to depend on physical activation rates. Hemodynamic response is mostly conditioned by myocardial insufficiency when walking is resumed rapidly during the 2nd week, and by smaller venous return due to hypovolemia where it is resumed slowly during the 4th week. Expanding motion regimens at slow rates results in persistent hemodynamic disturbances in myocardial infarction patients.

Adult↗
PubMed1986

[Modification of hemodynamics by intravenous administration of flecainide].

We investigated the influence of the new class-I antiarrhythmic drug flecainide on myocardial performance and hemodynamic parameters in Wistar rats (2 mg, 4 mg, 8 mg flecainide/kg). Left ventricular and aortic pressures, dp/dt max, cardiac output and additionally isovolumic left ventricular maxima curves were registered 5 min and 15 min after flecainide (n = 28) or saline (controls; n = 12) i.v. infusion (7 min). 2 mg and 4 mg flecainide/kg had no significant effect on isovolumic indices. 5 min after infusion of 8 mg flecainide/kg peak isovolumic left ventricular pressure was reduced by 84.9 +/- 2.6% vs. 95.6 +/- 1.1% (NaCl), mean +/- SEM (p less than 0.01) and peak isovolumic dp/dt max by 44.5 +/- 4.5% vs. 91.5 +/- 3.6% (NaCl), mean +/- SEM (p less than 0.01). Flecainide caused a significant reduction of heart rate (81.9 +/- 4.7%, 2 mg flecainide/kg vs. 95.4 + 2.5% (NaCl), an AV-block occurred only after administration of 8 mg/kg. Mean aortic pressure was decreased after 4 mg and 8 mg flecainide/kg. 8 mg flecainide/kg significantly reduced the cardiac output (73.1 +/- 7.7%, p less than 0.05). 15 min after 2 mg and 4 mg flecainide/kg infusion the determined parameters were normalized, only a dose of 8 mg/kg caused a prolonged hemodynamic depression. Our results demonstrate that in clinically used dosages no hemodynamic side-effects are detectable. A significant reduction of isovolumic indices of myocardial performance occurs only after infusion of 8 mg flecainide/kg. A transfer of laboratory experiments to the clinical situation is only possible with limitations, but our data might indicate that the myocardial and hemodynamic side-effects of flecainide are relatively small at therapeutic dosages.

Animals↗
PubMed1986

Evaluation of acute hemodynamic effects and pharmacokinetic behaviour of ibopamine in patients with severe heart failure.

The aim of the present investigation was to evaluate the acute hemodynamic effects of a single oral dose of 200 mg ibopamine (SB-7505), the 3,4-diisobutyryl ester of N-methyldopamine (epinine) in 11 patients with congestive heart failure (CHF) and to compare the influence of dopamine infusion and oral ibopamine on left ventricular function. Free and conjugated epinine plasma levels were also investigated in these patients and in a group of healthy volunteers to evaluate the correlation between epinine plasma levels and hemodynamic effects. The oral administration of 200 mg ibopamine to patients with CHF, increased cardiac index (+35%) and reduced peripheral and pulmonary vascular resistance (-29% and -26%) without modifying heart rate and systemic or pulmonary arterial pressure. The hemodynamic effect reached its maximum at about 90 min and was still present at 240 min. Ibopamine at a dose of 200 mg elicited similar effects to those observed with dopamine, 2-4 micrograms/kg/min. The pharmacokinetic behaviour of ibopamine in these patients was similar to that observed in a group of healthy volunteers. Free epinine plasma levels peaked at 30-60 min and decreased rapidly, thus showing a shorter time course than the hemodynamic effects.

Adult↗