Hemodynamic effects of mexiletine]

The haemodynamic changes caused by intravenous mexiletine were studied in 12 patients. Initially the drug was given rapidly at the rate of 3 mg/kg/min for 10 minutes and then slowly at a rate of 0,06 mg/kg/min for 30 minutes. The plasma Mexiletine level measured after 20 minutes was used to divide the series of patients into two groups: in Group A the level was over 0,7 g/ml (0,961 +/- 0,109 microgram/ml) whilst in Group B the level was only 0,547 +/- 0,101 microgram/ml. The mean aortic pressure, heart rate and left ventricular end diastolic volume did not vary significantly in the two groups. The left ventricular end diastolic pressure rose, and the cardiac index and the ejection fraction fell in Group A. The indices of left ventricular contractility fell in all patients of the start of the injection. This depression only persisted to the end of the injection in Group A. Mexiteline did not cause significant changes in post extrasystolic potentialisation in the 5 cases in which this phenomenon was studied.     

Hemodynamic effects of anti-arrhythmia substances]

Medical treatment of cardiac arrhythmias is limited by several side effects. Haemodynamic and proarrhythmic effects are the most important limitations of antiarrhythmic drug therapy. In this paper we present data from several studies on the haemodynamic side effects of antiarrhythmic drugs of Class I and III according to Vaughan-Williams. The results were discussed with special regard to the influence of these drugs on myocardial contractility. From the results presented it is concluded that there are no important differences in the negative inotropic effects among the Class I drugs. The clinically observed more marked cardiodepressant action of some of these drugs is probably due to their unfavourable effects on pre- and afterload of the left ventricle. From a theoretical point of view, Class III drugs should have a more favourable haemodynamic profile. However, after acute administration the commercially available Class III drugs also had a cardiodepressant action. A possible explanation for this finding might be other side effects of the Class III drugs currently available, since a pure Class III drug does not exist at present. Therefore, the special haemodynamic profile of each drug should be taken into consideration for antiarrhythmic treatment.     

Hemodynamic effects of intravenous amiodarone in humans]

The haemodynamic action of I-V Cordarone have been studied in 20 subjects over a 15 minute period. Over the 15 minute period we studied variations in left pulmonary and ventricular pressures, in cardiac output, and in the paramaters of contraction VEC max, V max and Taylor's index. At a dose of 5 mg/kg there is a fall in peripheral resistance (1274 +/- 232 to 915 dynes/s/cm-5), and the measurements of contraction hardly vary. At a dose of 10 mg/kg, after an initial increase in output and a fall in peripheral resistance there occurs, after 4 minutes, an increase in left ventricular end-diastolic pressure (from 6 +/- 2 to 13 +/- 4 mmHg, P less than 0.01), and a lowering of contractility (VEC max reduced from 49.7 +/- 12.4 to 27.1 +/- 3.8, P less than 0.001). We have shown that the first phase of this response is due to the solvent (Tween 80), while the fall in contractility is due to the amiodarone. Doses above 10 mg/kg must be used with care, and only if there is no evidence of impaired cardiac function.     

Hemodynamic effects of alcohol ingestion on anaerobic threshold]

Hemodynamic influence of alcohol ingestion was evaluated using expiratory gas analysis in 10 healthy men whose mean age was 26.1 +/- 2.2 years. Protocol of the control study (C) was as follows: Oxygen uptake (VO2) at rest and during warm-up, anaerobic threshold (AT) and peak VO2 were measured with ramp protocol using a bicycle ergometer. AT was determined by the V-slope method. Protocol of the alcohol study (A) was as follows: On a different day, the same parameters as C were measured after the ingestion of 0.7 g ethanol per kg body weight. The following results were obtained: 1) The serum ethanol concentration was 79.1 +/- 13.5 mg/dl. 2) VO2 in the resting state was higher in A than in C (4.51 +/- 0.74 vs 3.61 +/- 0.62 ml/min/kg), (p < 0.05). 3) AT and peak VO2 in C and A were 17.15 +/- 2.76, 32.09 +/- 6.77 ml/min/kg and 15.43 +/- 2.86, 29.60 +/- 5.35 ml/min/kg, respectively. 4) Exercise time to the AT in C and A was 222.90 +/- 37.32 and 172.0 +/- 33.1 sec, respectively. 5) The heart rate was higher in A than in C. It was concluded that peak VO2 and AT decreased by alcohol ingestion.     

Hemodynamic effects of intravenous allapinine in patients with myocardial infarction]

Single intravenous allapinine, 30 mg, given to patients with acute myocardial infarction, including those with moderate circulatory insufficiency, fails to affect central hemodynamic parameters or has a favourable action: normalizes pulmonary diastolic pressure, cardiac index, diminishes total peripheral vascular resistance. The agent also produces a weak antihypertensive effect and increases heart rate.     

Hemodynamic effects of purine nucleosides in regional ischemia and reperfusion]

The rat hearts were subjected to 60-min ischemia by left coronary artery ligation followed by 60-min reperfusion, involving intravenous adenosine inosine or guanosine given in a dose of 1 mg/kg.min-1 in the first 30 minutes of reperfusion. Ischemia and subsequent reperfusion caused a progressive decrease in cardiac output and coronary blood flow. Adenosine was found to enhance coronary blood flow and increase cardiac and stroke outputs. Inosine produced nearly the same, but less pronounced effect. Guanosine increased cardiac output without changing coronary blood flow.     

Hemodynamic effects of hydralazine in the cardiac insufficiency of non-obstructive myocardiopathy]

The haemodynamic effects of a single dose of between 0.15 and 0.25 mg/kg hydralazine were studied during cardiac catheterisation of 9 patients with primary congestive cardiomyopathy and heart failure. The systemic arterial resistances decreased (--1 370 +/- 400 dynes/s.cm-5/m2, p less than 0.05); the reduction of pulmonary arterial resistances was less marked (--420 +/- 400 dynes/s.cm-5/m2, p less than 0.05). Intraaortic pressure was reduced (--16 +/- 12 mmHg, p less than 0.02) as was average pulmonary arterial (--4.2 +/- 4,2 mmHg, p less than 0.05) and left ventricular end diastolic pressures (--4.2 +/- 3.0 mmHg, p less than 0,02). Systolic index increased in all cases (+13 +/- 5 ml/syst/m2, p less than 0.001). Heart rate was unchanged. This was due to the improvement of left ventricular function by the reduced impedence. These results confirm the place of hydralazine in the treatment of certain forms of heart failure.     

Hemodynamic effects of enalapril in patients with non-complicated acute myocardial infarct]

To evaluate the hemodynamic effects of the first oral administration of enalapril maleate, a long-acting ACE-inhibitor, in the early phase of an acute uncomplicated myocardial infarction, we studied 15 patients, in Killip class I or II, within 72 hours from the onset of symptoms. Hemodynamic measurements were obtained by a triple lumen 7 F Swan-Ganz catheter, inserted into the pulmonary artery, under control conditions and 2, 4, 6, 8 and 12 hours after 10 mg (15 patients) and 20 mg (11 patients) of the drug. Ten milligrams of enalapril reduced systolic and mean arterial blood pressure (from 118 +/- 17 to 111 +/- 18 mmHg, p < .05, and from 92 +/- 12 to 83 +/- 12 mmHg, p < .01, respectively), with a maximum effect after 4 hours from administration. Heart rate and vascular resistances showed an insignificant trend toward reduction, and no changes were observed in left ventricular systolic work index, right and left ventricular filling pressures or cardiac index. Hemodynamic changes induced by 20 mg of the drug, in a smaller group of patients, had a similar trend, which did not reach a statistical significance. In conclusion, in patients with acute uncomplicated myocardial infarction, a single oral dose of enalapril maleate is safe and well tolerated, does not induce severe hypotension, and produces potentially beneficial changes in hemodynamics.     

Hemodynamic effects of antiarrhythmic drugs

In order to use antiarrhythmic drugs safely, one must understand their hemodynamic effects. Quinidine and the calcium antagonists have direct cardiac effects and frequently opposing autonomically mediated or indirect cardiac effects. Lidocaine is exceptionally well tolerated, even by patients with severe left ventricular dysfunction. Phenytoin and procainamide have the potential for serious adverse effects, but are generally well tolerated at usual doses. Disopyramide causes serious depression of left ventricular function in many patients because of its direct myocardial depressant and peripheral vasoconstricting actions. Although bretylium causes an immediate increase in contractility, it can ultimately result in important hypotension. In this review the in vitro and in vivo hemodynamic effects of these and other antiarrhythmic drugs are discussed to provide information that will assist the clinician in using these drugs properly.     

Hemodynamic effects of intravenous amiodarone

Amiodarone is a potent antiarrhythmic agent that is effective in controlling both atrial and ventricular arrhythmias. Recently, intravenous administration was demonstrated to be effective in the acute management of rhythm disorders and, in addition, appeared to shorten the loading period normally required for oral drug administration. This investigation examined the hemodynamic effects of amiodarone after both acute intravenous bolus and continuous intravenous administration. Patients with a left ventricular ejection fraction greater than 0.35 experienced improved cardiac performance due to both acute and chronic peripheral vasodilation. However, patients with a lower ejection fraction developed a 20% decrease in cardiac index and clinically significant elevation of right heart pressures after acute bolus administration; these changes were variably compensated for by peripheral vasodilation when the drug was administered intravenously over 3 to 5 days continuously. Therefore, intravenous amiodarone can result in significant impairment of left ventricular performance in patients with preexisting left ventricular dysfunction.     

Hemodynamic effects of stimulation of alpha 1-adrenoreceptors in healthy elderly and aged persons]

The effect of intramuscular administration of alpha 1-adreno-stimulator phenylephrine (standard dose of 0.15 mg/kg body wt.) on the chronotropic, pump, systolic, and diastolic heart function, renal blood circulation and microcirculation in different vessel regions was studied in 60 healthy human subjects of different ages (20-34, 60-74, and 75-89 years). In aging, the overall effect of standard phenylephrine dosage has been found to decrease. Parallel to this, there was a change in the structure of the response of cardiovascular system to alpha 1-adreno-stimulaor administration. In older population groups, the positive effect of phenylephrine upon the pump and systolic heart function decreased, while its negative effect on the renal blood circulation and microcirculation in different vascular regions increased.     

Hemodynamic effects of intravenous metoprolol.

The hemodynamic effects of the cardioselective beta adrenergic blocking agent metoprolol, at a dose of 0.1 mg/kg body weight administered intravenously, were studied in 10 patients undergoing routine cardiac catheterization. The beta adrenergic blocking effect of the drug was confirmed by a highly significant reduction (53 percent, P less than 0.001) in the mean heart rate response to a challenge with isoproterenol, and by a mean heart rate rssponse to a challenge with isoproterenol, and by a highly significant reduction (73 percent, P less than 0.001) in the isoproterenol-induced increase in the first derivative of left ventricular pressure (dP/dt). An intrinsic negative inotropic effect was shown by a 43 percent reduction (P less than 0.05) in the response of mean left ventricular dP/dt when the heart rate was fixed by atrial pacing alone. With the combination of atrial pacing and isoproterenol, metoprolol produced a 48 percent reduction (P less than 0.01) in the response of mean left ventricular dP/dt, resulting from both the intrinsic depressor effect and the beta adrenergic blocking effect on the rate-independent beta agonist activity of isoproterenol. There was no significant change in right atrial, femoral arterial or left ventricular end-diastolic pressure; analysis of left ventricular angiograms performed during atrial pacing before and after metoprolol revealed no significant effect on angiographic ejection fraction, pressure-volume loops or diastolic compliance. In two patients improvement in segmental wall motion was noted, and no deterioration was seen in any patient. Metoprolol is an effective cardioselective beta adrenergic blocking agent that, under these conditions, reduces catecholamine-induced increases in heart rate and left ventricular dP/dt without significant alteration in ejection fraction, preload or afterload.