Improvement In Cardiac Performance Research Articles

A haemodynamic study of the effects of combined slow-calcium channel blockade (nisoldipine) and beta-blockade (metoprolol) in coronary heart disease

The interaction of a new slow-calcium blocker (nisoldipine) and the beta-blocker metoprolol was evaluated in 16 patients with stable angina. Haemodynamic parameters were determined in a control rest and exercise period. Patients were then randomised equally to nisoldipine (4–8 μg/kg) or metoprolol (10 mg) and the haemodynamics of monotherapy assessed; finally the second drug was administered and the effects of combination determined. At rest nisoldipine reduced systemic blood pressure and vascular resistance ( P < 0.01); heart rate, cardiac and stroke volume indices increased ( P < 0.01) at an unchanged pulmonary artery occluded pressure. Metoprolol alone reduced heart rate ( P < 0.05) and increased the pulmonary artery occluded pressure ( P < 0.05). Combination therapy reduced systemic blood pressure and vascular resistance ( P < 0.01); cardiac index and pulmonary artery occluded pressure increased ( P < 0.01) at an unchanged heart rate. The effect of combination was influenced by the order of administration; an improvement in cardiac performance was particularly evident when nisoldipine was added to metoprolol. The interaction during dynamic exercise was similar to that at rest. Thus these data indicated the haemodynamic safety of concurrent nisoldipine/metoprolol therapy; the addition of nisoldipine to metoprolol appeared to offset in part the cardiodepressant properties of beta-blockade.

Intrinsic mechanical properties of the perfused rainbow trout heart and the effects of catecholamines and extracellular calcium under control and acidotic conditions.

A perfused rainbow trout heart was developed which generated its own intrinsic heart rate and a physiological power output. This preparation was used to examine the intrinsic mechanical properties of the trout heart, the dose-response effects of catecholamines and extracellular calcium on these properties, and the effects of catecholamines and extracellular calcium during exposure to acidotic conditions. The trout heart was relatively pressure-insensitive to a physiological range of ventral aortic pressures. Preload exerted an important control over cardiac output through the Starling response. Heart rate was independent of both these intrinsic mechanisms. The intrinsic mechanical capabilities of the trout heart were greater than those observed previously in less active, benthic teleosts. Physiological concentrations of catecholamines significantly improved cardiac contractility through positive inotropy and chronotropy. Adrenaline was more potent than noradrenaline, indicating that these effects were mediated by beta 2-adrenoceptors. Elevated extracellular calcium produced only a modest improvement of cardiac contractility compared to that produced by adrenaline. Positive inotropy and negative chronotropy were observed with elevated extracellular calcium. Extracellular acidosis always reduced cardiac contractility through negative chronotropy and inotropy. Extracellular calcium improved the inotropic state of the acidotic heart and restored contractility, but the overall improvement of cardiac performance was compromised by an accompanying negative chronotropy. Physiological levels of adrenaline improved cardiac performance during extracellular acidosis. The roles of catecholamines and extracellular calcium are discussed with respect to post-exercise cardiac performance in trout.

Combined Digoxin-Molsidomine Therapy in Congestive Heart Failure Following Acute Myocardial Infarction

The acute hemodynamic effects of combining administration of digoxin (DIG)(0.01 mg/kg intravenously) with molsidomine (MLS)(4 mg sublingually) were compared with those of DIG and MLS considered alone in 12 patients with congestive heart failure following acute myocardial infarction. The patients were classified into two subgroups, A (cardiac index [CI] less than or equal to 2.2 L/min/m2 and B (CI greater than 2.2 L/min/m2), to verify differences between the responses to the three drug regimens. MLS significantly reduced systolic blood pressure from 121.2 +/- 12.3 (mean +/- SD) to 111.7 +/- 10.9 mm Hg (p less than 0.01) after 60 min, mean right atrial pressure (RAP) from 6.2 +/- 3.6 to 2.4 +/- 2.1 mm Hg (p less than 0.0001), mean pulmonary arterial pressure (PAP), left ventricular filling pressure (LVFP) from 20.6 +/- 2.1 to 12.2 +/- 2.8 mm Hg (p less than 0.0001), and pulmonary vascular resistance (PVR). Left ventricular stroke work index (LVSWI) significantly increased after 60 min. DIG induced a significant reduction in heart rate, RAP, PAP, and LVFP from 20.1 +/- 2 to 14.3 +/- 2.7 mm Hg (p less than 0.0001) after 90 min. Stroke volume index (SVI) increased from 24.7 +/- 4.2 to 27.7 +/- 3.1 ml/beat/m2 (p less than 0.001) and LVSWI from 25.9 +/- 7.2 to 31.9 +/- 5.4 g X m/m2 (p less than 0.0001). The combination of DIG and MLS produced a reduction in RAP, PAP, and LVFP greater than that achieved with either agent alone, with a further shift of the ventricular function curve to the left, thereby leading to an improvement in cardiac performance.(ABSTRACT TRUNCATED AT 250 WORDS)

Haemodynamic effects of insulin and beta receptor blockade during acute left ventricular failure in dogs.

Acute ischaemic heart failure was induced in 13 dogs by coronary embolisation. Severe dysfunction of the left ventricular (LV) performance was shown by a significant increase in LV end-diastolic pressure and significant decreases in maximum rate of LV pressure rise (LVdP/dtmax), stroke volume and cardiac output. 300 IU of fast-acting insulin was injected as a bolus dose in 7 dogs 90 min after the embolisation procedure. This was followed by infusion of glucose and potassium to maintain normal blood levels. After 15 min, insulin had significantly improved the performance of the failing left ventricle. Total peripheral resistance was decreased. Myocardial blood flow was significantly increased while myocardial oxygen consumption was unchanged. After beta receptor blockade with propranolol 0.5 mg kg-1 given intravenously, the improvement in cardiac performance was reduced, heart rate decreased, and a concomitant decrease in myocardial blood flow and oxygen consumption was recorded. Compared with values before treatment, the net effect of combined insulin and beta receptor blockade was unchanged LVdP/dtmax, LV end-diastolic pressure and cardiac output, significantly increased stroke volume and decreased heart rate, and moderately reduced total peripheral resistance and mean aortic blood pressure. Myocardial blood flow was unaltered, while myocardial oxygen consumption was significantly reduced. In the control group of 6 dogs propranolol was given before insulin, and similar haemodynamic alterations were found.

Hemodynamic and Metabolic Effects of Dopamine and Insulin During Acute Left Ventricular Failure in Dogs

Acute ischemic heart failure was induced in eight dogs by coronary embolization. Severe depression of the left ventricular (LV) performance was evidenced. At 15 min after the embolization procedure, dopamine was infused at a dosage sufficient to increase the maximum rate of LV pressure rise (LVdP/dtmax) by approximately 50%. The significant improvement in cardiac performance was obtained at unaltered myocardial oxygen consumption (MVo2). Dopamine infusion was concluded, and after a stabilization period 300 IU of insulin was injected. This was followed by the infusion of glucose and potassium to maintain levels. Insulin significantly improved the performance of the failing left ventricle at unaltered MVo2, but to a lesser extent than did dopamine. Additional dopamine infusion further significantly improved cardiac performance. The net effect of insulin and dopamine in combination as compared with dopamine alone was a significantly greater increase in stroke volume and cardiac output due to a more pronounced decrease in total peripheral resistance. Dopamine increased arterial concentrations and myocardial uptake of free fatty acids (FFA). The net metabolic effect of insulin and dopamine in combination as compared with dopamine alone was a shift in myocardial substrate uptake from FFA to carbohydrates.

Haemodynamic Dose–Response Effects of Intravenous Indoramin in Acute Heart Failure Complicating Myocardial Infarction

The haemodynamic dose-response effects of intravenous indoramin were evaluated in 12 patients with acute heart failure (pulmonary artery occluded pressure of greater than 20 mm Hg) complicating a recent myocardial infarction. Following a 1-h control period with confirmed stable haemodynamics, the effects of three intravenous bolus doses of indoramin (0.125, 0.125, and 0.25 mg/kg at 15-min intervals) were determined in the 10- to 15-min period following each intravenous injection. Plasma drug concentrations rose with the administered dose and were in the previously established therapeutic range. Ten patients tolerated all three doses of the drug; two patients were withdrawn following the second dose owing to clinically evident hypotension (systolic blood pressure of less than 100 mm Hg). Indoramin resulted in progressive falls in systolic, diastolic, and mean systemic arterial pressures (p less than 0.01) without change in cardiac index. There was a dose-related reduction in the heart rate (0.5 mg/kg; -7 beats/min; p less than 0.01). The left ventricular filling pressure showed a significant and quadratic reduction over the dose range (0.5 mg/kg, -5 mm Hg; p less than 0.01). The systemic vascular resistance index was reduced (-333 dynes X s X cm-5 X m2; p less than 0.001) and the stroke volume index increased (+3 ml/m2; p less than 0.05) following the maximum cumulative dosage. These data established the therapeutic safety of indoramin (0.125-0.5 mg/kg) in acute heart failure following myocardial infarction. An improvement in cardiac performance in these patients was compatible with circulatory actions on both cardiac preload and afterload.

Excessive reduction in peripheral resistance during exercise and risk of orthostatic symptoms with sustained-release nitroglycerin and diltiazem treatment of angina

Acute effects of placebo, sustained-release nitroglycerin, diltiazem capsules, and the combination of both drugs were monitored in nine stable angina patients. They were randomized to receive either placebo or 13 mg of slow-release nitroglycerin orally (double-blind). This was followed in 1 hour by 120 mg of diltiazem orally, given to all patients (unblinded). Invasive hemodynamic measurements were made before and after each treatment at supine and sitting rest, two levels of submaximal, and at maximal exercise and twice in recovery. Compared to the control test at maximal exercise, sustained-release nitroglycerin increased aerobic capacity 24%, lowered peripheral resistance −32%, and lowered systemic pressure −23%, while the respective changes with placebo were −3%, 5%, and 2%. When diltiazem was added to placebo compared to the control test, there was a 4% increase in oxygen consumption and −9% and −4% reduction in systemic resistance and systemic pressure, respectively. The addition of diltiazem to nitroglycerin was associated with a 20% increase in oxygen consumption a −42% reduction in systemic resistance and a −32% reduction in systemic pressure. Two patients who received introglycerin plus diltiazem experienced symptomatic hypotension, while one patient who received placebo plus diltiazem experienced hypotension. These side effects caused the study to be terminated prematurely. Thus, although the combination of nitroglycerin and diltiazem had a greater effect on afterload than either drug alone, the combination did not provide greater improvement in cardiac performance.

197 NALOXONE INDUCED GUT ISCHEMIA DURING RESUSCITATION OF EXPERIMENTAL NEONATAL SEPTIC SHOCK

Naloxone has been recommended for use in neonatal septic shock. To evaluate its effectiveness in peritonitis-induced septic shock, anesthetized newborn pigs were monitored and peritonitis was induced by intraperitoneal injection of E.coli and sterile pig feces. All pigs received fluid resuscitation, gentamicin, and bicarbonate to correct acidemia. When shock was evident, the pigs either received an initial IV bolus of naloxone (2 mg/kg) followed by a 2 mg/kg.hr infusion (Group I, n=9), or received no additional pharmacological intervention (Group II, n=7). Hemodynamic parameters assessed included mean arterial, pulmonary arterial, and central venous pressures; cardiac, stroke volume, and left ventricular stroke work indices; and systemic and pulmonary vascular resistance indices. There were no significant differences in any of the parameters measured between Groups I and II, although peripheral vascular resistance in Group I was transiently elevated acutely after naloxone infusion began. Mean survival times in the two groups were similar. Five of 9 Group I animals (56%), demonstrated gross and histologically proved intestinal ischemia (p<.02) while none of the animals in Group II demonstrated any notable sequelae. The data demonstrate that naloxone resuscitation results in an increase in vascular resistance without concomitant improvement in cardiac performance. These changes are associated with significant intestinal ischemia in this model.

P2H0211) - Improvement of cardiac performance by MDL 17043 and MDL 19205 in the experimental failing dog heart

P2H0211) - Improvement of cardiac performance by MDL 17043 and MDL 19205 in the experimental failing dog heart

Negative inotropic effects of aldosterone antagonists in isolated human and guinea-pig ventricular heart muscle

The effects of K+-canrenoate (Aldactone pro inj.) and its metabolite canrenone on isometric force of contraction were measured in isolated guinea-pig and human papillary muscle preparations driven electrically at a frequency of 1 Hz. In guinea-pig hearts both substances exerted a concentration-dependent negative inotropic effect; the IC50 of K+-canrenoate and canrenone were 129 +/- 22 mumol l-1 (n = 5) and 85 +/- 11 mumol l-1 (n = 12), respectively. At the maximally tested concentration canrenone (250 mumol l-1) and K+-canrenoate (1,000 mumol l-1) reduced force of contraction by 68 +/- 4% (n = 12) and 83 +/- 3% (n = 5), respectively. The negative inotropic effects of canrenone and K+-canrenoate were not affected by 10 mumol l-1 atropine. The negative inotropic effect of canrenone was also not affected by 14 mumol l-1 aldosterone, but canrenone (10 mumol l-1 diminished the maximal positive inotropic effect of dihydro-ouabain from 554 +/- 75% (n = 4) to 269 +/- 39% (n = 4) of the predrug value. In human heart muscles K+-canrenoate and canrenone also exerted a concentration-dependent negative inotropic effect. K+-canrenoate (1,000 mumol l-1) and canrenone (250 mumol l-1) reduced force of contraction by 57 +/- 7% (n = 8) and 67 +/- 2% (n = 6), respectively. A positive inotropic effect of both substances was never observed. It is concluded that the improvement of cardiac performance after application of aldosterone antagonists observed in patients cannot be explained by a direct effect on the heart. K+-canrenoate and canrenone are devoid of any direct cardiotonic action. Instead, K+-canrenoate and canrenone have direct negative inotropic effects at high concentrations.

Sustained beneficial hemodynamic responses to large doses of transdermal nitroglycerin in congestive heart failure and comparison with intravenous nitroglycerin

The hemodynamic effects of a new transdermal preparation of nitroglycerin were evaluated in 9 patients with chronic congestive heart failure (CHF). A graded infusion of nitroglycerin was administered initially to establish the dose-response relation for nitroglycerin and estimate the dose of topical nitroglycerin to be applied. Significant hemodynamic improvement was observed 0.5 to 1.0 hour after the cutaneous application of the nitroglycerin-impregnated polymer. The peak effect occurred at 6 hours, with the left ventricular filling pressure decreasing from 24 ± 2 to 18 ± 1 mm Hg (mean ± standard error of the mean) (p < 0.01) and the cardiac index increasing from 2.0 ± 0.2 to 2.6 ± 0.2 liters/min/m 2 (p < 0.01). The systemic vascular resistance decreased from 1,860 ± 198 to 1,531 ± 162 dynes s cm −5 (p < 0.01). Heart rate and mean arterial pressure were unchanged. Significant hemodynamic benefit was observed for 24 hours, and no rebound deterioration occurred upon withdrawal of the drug. The average dose of transdermal nitroglycerin applied was 51 ± 6 cm 2 (1.7 ± 0.2 mg/kg; 6 of the 9 patients received 64 cm 2). Thus, topical application of a new nitroglycerin-impregnated polymer induces an improvement in cardiac performance that is sustained for 24 hours in patients with chronic CHF. However, substantial doses of the drug may be required to produce a satisfactory hemodynamic response in most patients with CHF.

Cardiovascular effects of sulmazol administered intravenously to patients with severe heart failure.

Ten patients with severe heart failure (NYHA class IV) received sulmazol intravenously under haemodynamic and electrocardiographic surveillance. All patients were on maintenance doses of digitalis and diuretics. At 30 min intervals we increased the infusion rate of sulmazol from 1 to 2, 4, 6, and 8 mg min-1, to a total of 630 mg of sulmazol administered over 150 min. Statistically significant changes (P less than 0.001) were found for heart rate (from 97 to 103 min-1); right atrial pressure (from 9.5 to 1.5 mmHg); pulmonary artery diastolic pressure (from 25.0 to 9.0 mmHg); pulmonary capillary wedge pressure (from 22.0 to 9.0 mmHg); aortic diastolic pressure (from 62.5 to 52.5 mmHg); pulmonary artery oxygen saturation (from 53.0 to 68.5%); cardiac output (from 2.83 to 4.38 l min-1), and for indices derived from these measurements. No correlation was found between the improvement in cardiac performance and sulmazol plasma concentrations. Haemodynamic improvement persisted for more than 7.5 h after cessation of sulmazol administration. Renal function was measured before and after sulmazol administration; creatinine clearance (from 47.5 to 52.0 ml min-1) and p-amino hippuric acid clearance (from 146 to 125 ml min-1) were unchanged. Side-effects included yellow-colored vision, ventricular extrasystoles, and possibly sulmazol-induced liver function disturbances. Even in severe heart failure sulmazol improved cardiac performance in patients who were treated with the maximum tolerated dose of digoxin.

Hemodynamic and metabolic effects of vasodilator therapy for heart failure in acute myocardial infarction.

Hemodynamic effects of vasodilator agents (molsidomine, nitroglycerin, isosorbide dinitrate or prostaglandin I2) were studied in 53 patients with acute myocardial infarction. In 20 of these patients, effect on cardiac metabolism were also studied. Patients were divided into four groups according to the Forrester subset and hemodynamic effects of these agents were evaluated by the cardiac index (CI)-preload (PAEDP) relationship. In patients of Forrester subset II and IV, vasodilators were capable of producing a considerable reduction in preload without a significant decrease in cardiac output. However, in patients of Forrester subset IV, five of six patients had only a minimal improvement in cardiac performance with vasodilator therapy because of a severe pump failure. In these patients, a combination therapy with dopamine was necessary to maintain the cardiac output. In patients with Forrester subset III, vasodilator therapy decreased cardiac index and preload was also reduced. Thus, for these patients vasodilators could not be indicated but volume infusion may be indicated. In patients with Forrester subset I, although vasodilator therapy decreased cardiac output, coronary sinus flow and myocardial oxygen consumption were also decreased, indicating that the vasodilator therapy is also beneficial for patients even without heart failure because of the protective effect of unloading on ischemic myocardium. Three nitrate agents, i.e., molsidomine, nitroglycerin and isosorbide dinitrate, demonstrated the similar effect on hemodynamics; mean blood pressure and PAEDP decreased by 7-10% and 20-29%, respectively, while systemic vascular resistance was not significantly decreased. In contrast to nitrates, PGI2 decreased mean blood pressure and systemic vascular resistance significantly, whereas a decrease in PAEDP was minimal.(ABSTRACT TRUNCATED AT 250 WORDS)

Improvement of cardiac performance by AR-L 115 BS, a new cardiotonic drug, in the experimental failing dog heart.

The cardiotonic effect of AR-L 115 BS was assessed in 5 dog heart-lung preparations in which cardiac function had been severely depressed by pentobarbital. AR-L 115 BS in doses of 1-60 mg improved cardiac function in a dose-dependent manner and at 30 and 60 mg improved it beyond control values. These doses of AR-L 115 BS, however, produced neither a significant increase in heart rate nor arrhythmias. The results indicate that the drug would be of use in the treatment of heart failure.

Acute hemodynamic effects of combined therapy with digoxin and nifedipine in patients with chronic heart failure

The acute hemodynamic effects of combining administration of digoxin (DIG) (0.01 mg/kg intravenously) with nifedipine (NFP) (10 mg sublingually) were compared with those of DIG and NFP considered alone in 12 patients with chronic congestive heart failure due to coronary artery disease (CAD, seven patients) or primary congestive cardiomyopathy (CCM, five patients); four patients also had mitral regurgitation (MR). NFP significantly reduced systolic and diastolic blood pressure (BP), systemic vascular resistance (SVR) from 1925 ± 400 (mean ± SD) to 1333 ± 256 dyne · sec · cm −5 after 30 minutes ( p < 0.00001), and left ventricular filling pressure (LVFP) from 19 ± 7.5 to 15.6 ± 4.2 mm Hg ( p < 0.005). The cardiac index (CI) increased from 2.16 ± 0.47 to 2.81 ± 0.63 L/min/m 2 ( p < 0.00001). DIG induced a significant reduction in LVFP from 18.1 ± 7.7 to 14.3 ± 5.4 mm Hg after 90 minutes ( p < 0.005) and a slight increase in stroke volume index; no significant change in BP, Cl, and SVR was seen. The combination of DIG and NFP produced a significant increase in Cl from control value of 2.2 ± 0.48 to 2.95 ± 0.44 L/min/m 2 ( p < 0.00001), and a significant reduction in LVFP from 18.1 ± 7.7 to 13 ± 4.7 mm Hg ( p < 0.00001), and in SVR. Simultaneous administration of DIG and NFP resulted in an augmentation in cardiac performance greater than that achieved with either agent considered alone. The combination produced a greater output increase and a greater LVFP reduction, indicating a shift upwards and to the left to a more improved left ventricular function curve. No significant difference was seen between the hemodynamic response to the three drug regimens in patients with CAD versus patients with CCM. NFP produced a greater improvement in cardiac performance in patients with MR when compared with those without MR.

Long-term therapy with a new cardiotonic agent, WIN 47203: Drug-dependent improvement in cardiac performance and progression of the underlying disease

Seven patients with severe chronic congestive heart failure were treated with a new cardiotonic agent, WIN 47203 (an analog of amrinone), for an average of 7.4 weeks (range 2 to 15). At the initiation of therapy, hemodynamic improvement occurred in all patients as the cardiac index increased from 1.79 +/- 0.39 to 2.30 +/- 0.44 liters/min per m2 (probability [p] less than 0.05) and pulmonary capillary wedge pressure decreased from 24.1 +/- 6.7 to 16.1 +/- 7.8 mm Hg (p less than 0.05). Long-term therapy produced a substantial symptomatic improvement in five of the seven patients. This improvement was fully sustained in two patients and the remaining three experienced a partial return of their symptoms even though the initial hemodynamic improvements at rest remained evident in all seven patients. Withdrawal of WIN 47203 precipitated hemodynamic deterioration in all patients. The cardiac index decreased from 2.25 +/- 0.40 to 1.64 +/- 0.46 liters/min per m2 (p less than 0.05) while the pulmonary capillary wedge pressure increased from 17.1 +/- 7.8 to 23.2 +/- 12.0 mm Hg (p less than 0.05). Stroke volume index after withdrawal was lower than the control level before therapy (17.0 +/- 6.6 versus 20.3 +/- 4.7 ml/m2; p less than 0.05) and pulmonary capillary wedge pressure was similar. During long-term therapy, no undesirable side effects or hematologic changes were observed. Thus, drug-dependent hemodynamic benefits and apparent progression of the underlying cardiac disease were demonstrated during long-term therapy with WIN 47203.

Improvement in cardiac performance by oral long-acting theophylline in chronic obstructive pulmonary disease

Although oral theophylline is a widely used bronchodilator in chronic obstructive pulmonary disease (COPD), its effects upon cardiac performance have not been fully established. The effect of slow release oral theophylline upon right ventricular and left ventricular ejection fraction was evaluated using first-pass quantitative radionuclide angiocardiography in 15 patients with COPD. After 72 hours of therapy, oral theophylline significantly increased right ventricular ejection fraction (42% to 48%, p < 0.005). In 7 of 10 patients with depressed baseline right ventricular performance, including two with cor pulmonale, right ventricular ejection fraction normalized (≥ 45%). After long-term therapy, an average of 16 weeks, right ventricular fraction also increased (43% to 48%, p < 0.005). Left ventricular ejection fraction improved significantly from 64% to 68% ( p < 0.05) at 72 hours and from 61% to 65% ( p < 0.025) after long-term therapy. These data indicate that oral theophylline produces a sustained modest enhancement of resting biventricular performance in COPD.

The improvement of cardiac performance by amrinone, a new cardiotonic drug, in an experimental failing heart preparation of the dog.

The cardiac effects of amrinone were studied in 5 heart-lung preparations of the dog. Amrinone improved the cardiac performance during pentobarbital-induced heart failure.

Antihypertensive Therapy with Prazosin in Patients with Left Ventricular Dysfunction: Improvement in Cardiac Performance and Exercise Tolerance

Although the relationship between blood pressure and cardiac performance has been widely recognized, there are few published clinical observations concerning the effect of blood pressure control on cardiac function. We evaluated the effect of prazosin, an antihypertensive agent which also improves hemodynamic measurements in normotensive patients with heart failure, in 16 patients with moderate hypertension and reduced ejection fractions. Therapy with digoxin and diuretics was continued throughout the study, but other antihypertensive agents were withdrawn at least one week prior to the initiation of the study. Measurements of ejection fraction, cardiothoracic ratio and the duration of maximal treadmill exercise were made before and after two months of antihypertensive therapy with prazosin. On prazosin, blood pressure fell from a mean of 169/103 to 141/84. Excellent control was achieved in 13/16 patients and significant reductions were noted in the remaining three. Concomitantly, ejection fraction rose from .38 +/- .02 (SEM) to .43 +/- .03 (P less than .02), cardiothoracic ratio decreased from .55 +/- .02 to .53 +/- .02 (P less than .05) and exercise capacity increased from 9.2 +/- 0.9 to 11.9 +/- 1.1 minutes (P less than .005). Prazosin was well tolerated except in one patient who experienced worsening angina. These findings emphasize the importance of rigorous blood pressure control in hypertensive patients with left ventricular dysfunction and indicate that prazosin is effective in this setting.

A Proposed Method for Weaning from IABP Assist Following Sequential Hemodynamic Assessment Utilizing a Microcomputer

Before consideration is given for discontinuing an assist device (IABP) a set protocol should be developed by the cardiac assist team through which the necessary steps can be taken for proper manage ment and control of the patient’s status. Such a protocol is described in this preliminary report. At our institution the feasibility of weaning is established via sequential clinical and hemodynamic assessments which are made prior to the initiation of the assist device and continue throughout the assist and weaning period. In the patient who is a candidate for cardiac surgery, an initial hemodynamic assessment is accomplished prior to surgery which serves as a baseline for future cardiopulmonary profiles and aids in the initial evaluation of the patent. The profile consists of various hemodynamic variables that are entered into the TRS-80 system which provides a printout of cardiac parameters used during trend analysis of the patient status. Counterpulsation is initiated as indicated by a compromised post-bypass profile or obvious left ventricular failure. Sequential hemodynamic and clinical reassessments are performed every 2 to 4 hours to aid the operator in making decisions as to the effectiveness of the assist as well as inotropic and/or vasopressor therapy. Typically 12-24 hours of assist are carried out prior to reassessment for discontinuation. Once optimal hemodynamic status is obtained the process of weaning begins consisting of 4 hours for each 24 hours of assist. The first phase of our weaning technique consists of Sec reductions to 50% of total balloon volume. In this way diastolic augmentation and afterload reduction are gradually tapered, thus minimizing significant increases in cardiac workload and acute strain. The second phase consists of an assist ratio reduction from every beat to every fourth beat which accounts for one-fourth the total wean time. Hemodynamic assessments of the patient’s condition are made before and shortly after each change in wean condition. Complete weaning and balloon catheter removal occurs only after sequential clinical and hemodynamic assessments have indicated maximum possible improvement in cardiac performance and its persistance after a period of trial with minimal assist.