Comparison of Dopamine and Dobutamine Following Coronary Artery Bypass Grafting

A prospective, randomized comparison of the hemodynamic effects of dopamine and dobutamine was performed in 20 patients following coronary artery bypass grafting. Approximately 6 hours postoperatively, when patients were hemodynamically stable, either dopamine or dobutamine was administered at 2.5, 5.0, and 7.5 μg per kilogram of body weight per minute. At 5.0 μg/kg, both drugs increased cardiac index without changing heart rate, mean arterial pressure, pulmonary capillary wedge pressure, or peripheral vascular resistance. At 7.5 μg/kg, dobutamine caused a further increase in cardiac index without changing the other variables. In contrast, increasing dopamine from 5.0 to 7.5 μg/kg/min caused significant increases in mean arterial pressure, pulmonary capillary wedge pressure, and pulmonary vascular resistance but no further increase in cardiac index. We conclude that dobutamine is preferable to dopamine in patients following coronary artery bypass grafting, since it produces consistent, dose-related increases in cardiac index without increases in heart rate, mean arterial pressure, pulmonary capillary wedge pressure, or pulmonary vascular resistance.     

The Hemodynamic Response to Dopamine and Nitroprusside Following Right Atrium–Pulmonary Artery Bypass (Fontan Procedure)

Cardiac output is critically dependent upon pulmonary vascular resistance after right atrium-pulmonary artery bypass (Fontan procedure), since there is no pulmonary ventricle in the circulation. Inotropic agents, including dopamine, may increase pulmonary vascular resistance and, therefore, might have an adverse effect on cardiac output.The present study determined the hemodynamic responses to dopamine and nitroprusside of 9 patients following right atrium–pulmonary artery bypass. Particular attention was given to effects on cardiac output (CI), pulmonary vascular resistance, and right atrial pressure (RAP). Baseline hemodynamic data were measured without drugs, with dopamine at 7.5 μg/kg/min, with sodium nitroprusside up to 5.0 μg/kg/min, and with a combination of dopamine, 7.5 μg/kg/min, and sodium nitroprusside, 1.0 7.5 μg/kg/min. Right and left atrial pressures (LAP), mean arterial blood pressure

, heart rate (HR), and CI were measured. Stroke volume index and pulmonary arteriolar resistance index were calculated. The increase in CI from baseline (1.98 ± 0.86 liters per minute) was significant for infusions of dopamine (2.75 ± 1.05, p < 0.001), sodium nitroprusside (2.57 ± 0.78, p < 0.001), and both drugs (2.74 ± 0.84, p < 0.001). The increased CI was achieved primarily by a significant increase in HR with dopamine and by an increase in stroke volume index with sodium nitroprusside. With a similar increment in CI, the RAP was significantly decreased from baseline (21 ± 4 torr) with sodium nitroprusside (15 ± 3, p < 0.001) but was unchanged with dopamine. Pulmonary arteriolar resistance index decreased significantly from baseline (375 ± 230 dynes sec cm^?5/m²) with sodium nitroprusside (169 ± 132, p < 0.001), and, interestingly, with dopamine as well (273 ± 165, p < 0.05). Both dopamine and sodium nitroprusside in these dosages have favorable effects on CI and pulmonary arteriolar resistance index in patients after right atrium-pulmonary artery bypass. Whenever feasible, sodium nitroprusside is preferred for increasing CI after such a bypass procedure, since lower RAP decreases the severity of fluid retention, ascites, and chest tube drainage.     

Enhanced cardiac efficiency with dobutamine after global ischemia

Dopamine and dobutamine are used in low output states following cardiopulmonary bypass but the consequences of increased inotropic activity on myocardium recovering from ischemia is unknown. Dogs on cardiopulmonary bypass were subjected to 20 min of normothermic global ischemia followed by 20 min of reperfusion. Dopamine or dobutamine (both at 10 μg/kg/min) or normal saline infusion was begun and 10 min later the dogs weaned from cardiopulmonary bypass while the infusions continued. Serial measurements were made of regional myocardial and systemic blood flow (15 μm radiolabeled spheres), myocardial oxygen consumption, creatine phosphate, and ATP levels. On bypass mean aortic pressure was decreased and heart rate, oxygen consumption, and left ventricular blood flow were increased by both catecholamine infusions (P < 0.01), but neither drug lowered ATP or creatine phosphate levels. Renal blood flow was decreased in dobutamine-treated dogs (P < 0.01). Off bypass, heart rate and mean aortic pressure were similar in all groups. While both drugs increased left ventricular blood flow to a similar extent (P < 0.01), dopamine treatment raised cardiac output by only 30% (P < 0.05) and dobutamine treatment increased cardiac output by 85% (P < 0.01). In addition, myocardial oxygen consumption was increased in dopamine-treated dogs (P < 0.05) while values in dobutamine animals were similar to controls. Therefore, dobutamine seems advantageous to dopamine following bypass because it increases cardiac output (by increasing stroke volume) but does not increase myocardial oxygen consumption. Both drugs are potentially detrimental on bypass because they greatly increase heart rate and oxygen consumption and, in addition, dobutamine causes an unexplained fall in renal blood flow.     

The hemodynamic effect of dopamine in children.

Although dopamine is a useful therapeutic agent to augment cardiac function in adults, there is little information about the hemodynamic effects of dopamine in children. To delineate the hemodynamic effects of dopamine in children, we infused two doses of dopamine (2 and 7.75 micrograms/kg/min) into 10 children during diagnostic cardiac catheterization. We measured heart rate, systemic arterial, pulmonary arterial, right atrial, and pulmonary capillary blood pressure, and cardiac output. During infusion of 7.75 micrograms/kg/min of dopamine, cardiac index increased from 3.9 to 5.4 L/min/m2, stroke volume increased from 43 to 57 ml/stroke and systemic vascular resistance declined from 1,697 to 1,165 dynes-cm-5-sec-m2. These indices also were changed significantly from control during infusion of 2 micrograms/kg/min of dopamine. The ratio of mean pulmonary arterial blood pressure to mean systemic arterial blood pressure in one patient with pulmonary vascular obstructive disease increased from 0.73 to 1.15, and ventricular bigeminy occurred during infusion of 7.75 micrograms/kg/min of dopamine. Dopamine is a potentially useful inotropic agent in children, but the use of dopamine may be contraindicated in patients with elevated and fixed vascular resistance.     

Renal and hemodynamic effects of dopamine in infants following cardiac surgery

The renal and hemodynamic effects of dopamine were measured during the immediate postoperative period in six infants following repair of congenital cardiac defects. Dopamine was infused at rates of 5, 10, and 15 micrograms/kg/min. Cardiac index (CI) increased significantly at a dopamine infusion rate of 15 micrograms/kg/min. The glomerular filtration rate (GFR) and urine output increased at dopamine infusion rates of 5 and 10 micrograms/kg/min and returned to baseline at 15 micrograms/kg/min. No significant changes occurred in right atrial pressure (RAP), left atrial pressure (LAP), systemic artery pressure, systemic vascular resistance (SVR), or pulmonary vascular resistance (PVR). Heart rate (HR) increased slightly at a dopamine infusion rate of 15 micrograms/kg/min. Pulmonary artery pressure (PAP) increased significantly in only one patient. These data demonstrate that infants require high doses of dopamine to produce the hemodynamic effects seen in adults and that these higher doses may be used without adverse renal effects.     

The effect of dopamine on glomerular filtration rate in normotensive,oliguric premature neonates

We examined the effect of dopamine on glomerular filtration rate (GFR) at infusion rates of 0.5, 2.5, and 7.5 micro g/kg per min in 15 premature neonates. Study infants (mean gestational age 34+/-2 weeks, mean birth weight 2.43+/-0.6 kg) had respiratory distress, were normotensive, and had a low urine output (0.9+/-0.1 ml/kg per hour). GFR was determined by the plasma clearance of inulin after a single bolus injection (200 mg/kg). Four hours after inulin administration, dopamine infusion was begun and continued over 6 h. GFR was estimated before and after beginning the dopamine infusions from the slope of the log of plasma inulin concentration versus time. Gestational age, weight, and baseline GFR were similar in all three groups. With a dopamine infusion rate of 0.5 micro g/kg per min there were no changes in GFR, urine output, heart rate, or blood pressure. At an infusion rate of 7.5 micro g/kg per min there was no change in GFR, although urine output, heart rate, and blood pressure all increased. At 2.5 micro g/kg per min there were significant increases in GFR and urine output, with no changes in blood pressure or heart rate. In oliguric, non-hypotensive neonates, GFR increased significantly at 2.5 micro g/kg per min of dopamine. This probably reflects the effects of afferent vasodilatation and may be important clinically when enhancement of GFR is the major treatment objective.     

Use of the Bovine with an Artificial Heart as an Experimental Pharmacologic Model Peripheral Vascular and Direct Cardiac Effects of a Large Dose of Dopamine

Peripheral vascular and direct cardiac effects of a single intravenous injection of a large dose of dopamine (50μg/Kg) were determined in ten unanesthetized calves before and after replacement of their natural hearts (NH) with pneumatically driven artificial hearts (AH). Data were recorded before and three minutes after injection of dopamine, when alpha adrenergic effects were maximal. Dopamine markedly increased systemic vascular resistance (from 919 to 1490 dyne ˙ sec/cm⁵ in NH calves and 896 to 1420 dyne ˙ sec/cm⁵ in AH calves), mean aortic pressure (from 105 to 144 torr in NH calves and 109 to 129 torr in AH calves), mean pulmonary artery pressure (from 20 to 25 torr in NH calves and 18 to 30 torr in AH calves), and mean right atrial pressure (from 5 to 8 torr in NH calves and 6 to 10 torr in AH calves). Dopamine significantly decreased stroke volume (from 100 to 90 ml in NH calves and 101 to 74 ml in AH calves) and cardiac output (from 8.7 to 7.3 L/min in NH calves and 9.2 to 6.7 L/min in AH calves). Heart rate was significantly reduced by dopamine in NH calves (from 87 to 81 beats/min) but was fixed (91 beats/min) in AH animals. Changes in stroke volume, cardiac output and mean pulmonary artery pressure were significantly greater in AH calves while mean aortic pressure was increased significantly more in NH calves. Increases in right atrial pressure and systemic vascular resistance after dopamine were similar in both groups of animals. Dopamine also produced marked changes in respiratory dynamics. The compound significantly decreased tidal volume (from 612 to 344 ml in NH calves and 582 to 236 ml in AH calves), minute volume (from 19.6 to 10.3 L/min in NH calves and 20.4 to 6.6 L/min in AH calves) and minute oxygen uptake (from 488 to 430 ml in NH calves and 507 to 355 ml in AH calves). Dopamine also reduced respiratory rate, but only in AH calves (from 35 to 28 breaths/min). Changes in respiratory rate, minute ventilation and oxygen uptake were significantly greater in AH than NH animals. These data demonstrate that large bolus injections of dopamine can produce significant decreases in cardiac output and respiratory dynamics. They also indicate that an animal with an artificial heart, or at least an artificial heart which is unable to respond to the positive inotropic effect of dopamine, will experience a more marked reduction in cardiac output and minute ventilation than an animal with its natural heart.     

The basics of catecholamine therapy. 2. A guide to clinical use

Myocardial function is determined by preload, afterload, contractility and heart rate. Pathologic changes of these variables may result in decrease of blood pressure, acute heart failure or cardiogenic shock. Hyperdynamic septic shock is associated with systemic hypotension despite increased cardiac output. Mediators of sepsis induce both myocardial depression and pulmonary arterial hypertension. Moreover, sepsis is characterized by microcirculatory disturbances and dysbalance in regional oxygen delivery and consumption. Severe systemic hypotension is a symptom often requiring catecholamine therapy to restore systemic circulation and to avoid organ damage. As the use of catecholamines is not a causal therapy administration should be limited to an initial measure until correction of the underlying abnormalities can be achieved. Different etiologies of shock as well as diseases requiring specific interventions as pulmonary embolectomy, systemic lysis or coronary angioplasty have to be considered. First line intervention consists of optimizing preload by fluid resuscitation as appropriate and use of dopamine (4-12 micrograms/kg.min) as primary catecholamine to increase contractility and blood pressure. In acute left heart failure inotropic support with dobutamine (4-12 micrograms/kg.min) or epinephrine (0.05-1 microgram/kg.min) may be necessary, frequently combined with a vasodilator (sodium nitroprusside 0.2-5 micrograms/kg.min or nitroglycerine 0.5-2.5 micrograms/kg.min) or phosphodiesterase-III-inhibitor (milrinone 0.3-0.8 microgram/kg.min). In right heart failure norepinephrine is preferred to increase coronary perfusion pressure. Hyperdynamic septic shock with decreased vascular resistance is treated with norepinephrine to restore mean arterial pressure and to improve right ventricular dysfunction induced by pulmonary hypertension.     

Pharmacologic antagonism of beta adrenergic blockade in dogs. II. Hemodynamic effects of simultaneous intravenous infusion of isoproterenol and dopamine during chronic propranolol administration

Chronic beta adrenergic blockade was induced in eight dogs with 240 to 360 mg of oral propranolol dailty for 2 to 6 weeks. Beta blockade was confirmed by a minimal heart rate response to isoproterenol, 0.06 micrograms/kg/min, in a pentobarbital-anesthetized, open-chest preparation. Subsequent to confirmation of beta blockade, hemodynamic effects of isoproterenol and dopamine were examined individually and in combination. A desirable balance of arterial pressure and cardiac output was achieved by combining isoproterenol, 0.2 to 2.0 micrograms/kg/min, with dopamine, 5 to 20 micrograms/kg/min. This combination increased mean arterial pressure (109 +/- 9 versus 81 +/- 7), cardiac output (4.3 +/- .5 versus 2.8 +/- .3 L/min) and heart rate 156 +/- 4 versus 120 +/- 7) (p less than 0.05). The hemodynamic effects of combined isoproterenol-dopamine were superior to the effects of either drug alone and suggest a method for effective circulatory support of man during chronic beta adrenergic blockade.     

The effect of dopamine,atropine, phenylephrine and cardiac pacing on oxygen consumption during fentanyl-nitrous oxide anaesthesia in the dog

In animals deeply anaesthetized with fentanyl and nitrous oxide the artierial blood pressure and heart rate were increased using dopamine, atropine, electrical pacing and phenylephrine in order to study the accompanying change in whole body oxygen consumption. Seven dogs (16–24 kg) were anaesthetized with fentanyl 1 μg · kg^-1 · min^-1. After completing instrumentation a dopamine infusion was started at a rate of 39 μg · kg^-1 · min^-1. After the mean blood pressure reached 18.6 kPa the infusion was reduced to 10 μg · kg^-1 · min^-1 and maintained for 10 minutes. After waiting 45 minutes an infusion of atropine 20 μg · kg^-1 · min^-1 was started and when the heart rate reached 120 b/min the infusion was slowed to 1.25 μg · kg^-1 ’ · min^-1 and maintained for 10 minutes. Twenty-five minutes later the heart rate was increased to 150 beats/min and maintained at that level for 10 minutes using electrical pacing. The pacing was removed and an infusion of phenylephrine 5 μg·kg^-1·min^-1 was started. When the blood pressure reached 21.3 kPa the infusion was reduced to 2.5 μg · kg^-1· min^-1 and maintained for 10 minutes. The results show increases in oxygen consumption of 14 per cent with dopamine, 19 per cent with atropine, 16 per cent with pacing, and 14 per cent with phenylephrine. All changes were significantly different from the control values. The magnitude of change in whole body oxygen consumption was best predicted by either the cardiac output x blood pressure product or by the cardiac output alone.     

The haemodynamic effects of dobutamine and dopamine in patients with coronary artery disease. A study performed under general anaesthesia (author's transl)]

The haemodynamic effects of dobutamine (2 microgram/kg . min and 4 microgram/kg . min) and dopamine (4 microgram/kg . min and 8 microgram/kg . min) were studied in 17 patients with coronary artery disease prior to coronary bypass surgery. The study was performed under general anaesthesia (modified neurolept analgesia) and controlled ventilation. Dopamine improved cardiac index significantly, increased mean aortic pressure slightly while heart rate and total peripheral resistance remained unchanged. Dobutamine failed to increase cardiac and stroke index significantly, but increased mean aortic pressure distinctly due to an elevated total peripheral resistance. Both catecholamines increased left ventricular filling and mean pulmonary artery pressure. The HR x ASP-product which is closely related to left ventricular oxygen consumption was found to be augmented to a greater extent during dobutamine. For the above reasons dopamine should be favoured for increasing cardiac output in patients undergoing aortocoronary bypass surgery. Our study does not confirm earlier results which have shown dobutamine to be the preferable catecholamine. The possible reasons for this discrepancy are discussed.     

The effects of vasoactive drugs on hepatic blood flow changes induced by CO2 laparoscopy: an animal study.

Laparoscopic surgery is associated with systemic and splanchnic hemodynamic alterations. Recent data suggest that small-dose dobutamine may attenuate the reduction in splanchnic blood flow associated with increments in intraabdominal pressure. We conducted this study to analyze the effects of dopamine and dobutamine on the hepatic circulation in this setting. Twenty-one pigs were anesthetized and mechanically ventilated. A flow-directed pulmonary artery and carotid artery catheters were inserted. Perivascular flow probes were placed around the main hepatic artery and the portal vein. CO2 was insufflated into the peritoneal cavity to reach an intraabdominal pressure of 15 mm Hg. After 60 min, animals received dopamine (5 microg x kg(-1) x min(-1); n = 8), dobutamine (5 microg x kg(-1) x min(-1); n = 8), or saline (n = 5) for 30 min. Pneumoperitoneum induced significant increases in heart rate, mean arterial pressure, and systemic vascular resistance, with decreases in cardiac output and hepatic artery and portal vein blood flows. Dobutamine infusion, in contrast to dopamine, corrected, at least in part, cardiac output, systemic vascular resistance, and hepatic artery blood flow alterations, but neither drug restored total hepatic blood flow. IMPLICATIONS: Hepatic blood flow decreases during laparoscopic surgery. A small-dose infusion of neither dobutamine nor dopamine corrects the total hepatic blood flow impairment, but the former is able to restore the hepatic arterial blood supply in an animal model mimicking this condition.     

Effects of four anticholinesterase-anticholinergic combinations and tracheal extubation on QTc interval of the ECG, heart rate and arterial pressure

Background : Imbalance in cardiac sympathetic tone causes prolongation of the QTc interval of the ECG. On the other hand, impairment of the parasympathetic control of the heart rate caused by anticholinesterase-anticholinergic combinations might also affect the cardiac sympathetic tone and hence the QTc interval of the ECG. The main purpose of the present study was to compare the effects of four anticholinesterase-anticholinergic combinations used for the antagonism of the neuromuscular block on the QTc interval of the ECG, heart rate and arterial pressure. Methods : Eighty-four ASA class I-II patients with a mean age of 32 to 37 yr undergoing otolaryngological surgery were randomly allocated to one of the following groups: neostigmine 40 μg/kg+glycopyrronium 8 μg/kg (Ne-Glyc), neostigmine 40 μg/kg+atropine 20 μg/kg (Ne-Atr), edrophonium 200 μg/ kg+atropine 300 μg (Edr-Atr (1)), edrophonium 500 μg/ kg+atropine 7 μg/kg (Edr-Atr (2)). QTc interval and heart rate were measured by a signal processing method based on an IBM/PC/xT-compatible microcomputer and arterial pressure with a sphygmomanometer at 1-min intervals up to 10 min after the injection of the drugs and immediately and 2 min after extubation. The ECG, lead II, was continuously recorded. Neuro-muscular block was measured by a Datex relaxograph. Results : In all groups, the most pronounced increase in both QTc interval, heart rate and arterial pressure occurred 1 min after the study drugs and immediately after extubation. In all groups, the mean QTc intervals at 1 and 2 min after the study drugs and after extubation were longer than the upper limit of the normal range (440 ms). Junctional rhythm occurred in 1 to 3 patients in all other groups with the exception of the Edr-Atr(1) group in which no cardiac arrhythmias occurred. At 1 min, the heart rate in the Ne-Atr group was at a significantly higher level than that in the Ne-Glyc group. From 3 to 6 min, the heart rate in the Edr-Atr(2) group and at 3 min in the Edr-Atr(1) group was at a lower level than the heart rate in the Ne-Glyc group. Conclusions : On the basis of the present results, anticholinesterase-anticholinergic combinations should be avoided in patients having a long QT interval syndrome or a prolonged QT interval from other causes. In addition, the cardiovascular stimulation caused by tracheal extubation should also be avoided in these patients.     

Hemodynamic function in acute pancreatitis

Acute pancreatitis is often associated with impaired cardiovascular function. This study examined the systemic cardiovascular effect of acute pancreatitis induced by injection of autologous bile (0.5 ml/kg) into the canine pancreatic duct. After acute pancreatitis was induced, eight dogs were given no resuscitation (group 1, untreated pancreatitis), and lactated Ringer's solution was infused in 11 dogs (group II, treated pancreatitis) to maintain mean arterial pressure and pulmonary wedge pressure at control values. In the untreated pancreatitis group, mean arterial pressure, cardiac output, stroke volume, and stroke work values decreased (mean arterial pressure from 101 +/- 4 to 74 +/- 12 mm Hg, cardiac output from 118 +/- 7 to 56.2 +/- 1.1 ml/min/kg; stroke volume from 0.93 +/- 0.08 to 0.22 +/- 0.07 ml/beat/kg; p less than 0.05), whereas heart rate and peripheral resistance increased (heart rate from 125 +/- 7 to 185 +/- 10 beats/min, peripheral vascular resistance from 3130 +/- 410 to 4436 +/- 610 dynes/sec/cm5; p less than 0.05). Although coronary blood flow, endocardial-epicardial flow ratio, and myocardial oxygen delivery values decreased progressively in group I after induction of pancreatitis, these changes did not achieve statistical significance. All indices of cardiovascular function and coronary blood flow remained unchanged in group II. Neither dP/dt max, the maximal rate of left ventricular pressure increase, nor dP/dt at a developed pressure of 40 mm Hg (an index of myocardial contractility minimally affected by changes in preload and afterload) were depressed by bile-induced acute canine pancreatitis in either group. Our data indicate that the detrimental effects of acute pancreatitis on cardiovascular function are related solely to hypovolemia and reduced cardiac filling and not to humoral or reflex effects induced by the disease.     

Dopamine versus Dobutamine after Open-Heart Surgery

The haemodynamic effects of dopamine and dobutamine were compared in a cross-over study of 12 patients in the early postoperative phase after open-heart surgery. The drug infusion rates (dopamine (μg/kg/min) mean 6.5, range 2.8–12, dobutamine (μg/kg/min) mean 7.9, range 4.3–12.3) were adjusted so that the cardiac output increased by 50%. With both drugs this was achieved through simultaneous increases in stroke volume (dopamine + 16%, dobutamine + 9%) and heart rate (dopamine + 31 %, dobutamine + 38%). The systemic vascular resistance did not change with dopamine but decreased significantly (—18%) with dobutamine. Therefore, the systolic and diastolic arterial blood pressures rose significantly more with dopamine than with dobutamine. The left atrial pressure increased with dopamine but was unchanged with dobutamine. The urine output was significantly higher with dopamine than with dobutamine.     

The hemodynamic effects of a treatment with beta-receptor blockers during coronary surgery. A comparison between acebutolol and esmolol

Patients undergoing coronary artery bypass grafting are at risk for perioperative myocardial ischemia. Most such ischemic episodes occur without obvious hemodynamic changes. Tachycardia as a predictor for increased myocardial oxygen consumption doubles the incidence of myocardial ischemia when heart rate increases to over 110 beats/min. During the operative procedure for coronary revascularization, some maneuvers, e.g. intubation, sternotomy and mediastinal preparation, may be associated with tachycardia and increases in blood pressure despite an adequate level of anesthesia, so that the administration of beta-receptor blocking agents seems to be indicated. METHODS. The study included 20 patients undergoing elective aortocoronary bypass grafting. All patients developed tachycardia (heart rate greater than 100 beats/min) before the start of extracorporeal circulation. The hemodynamic effects of 0.1 mg/kg acebutolol given i.v. as a bolus over 30 s and hemodynamic effects of the ultrashort-acting esmolol by continuous infusion (loading dose 500 micrograms/kg over 1 min followed by a dose of 100 micrograms/kg per min) were randomly investigated. Anesthesia was maintained with fentanyl, midazolam and pancuronium bromide. All patients were invasively monitored by means of a pulmonary artery catheter. In addition, left ventricular pressure (LVP), left ventricular end diastolic pressure (LVEDP) and dp/dtmax were measured. RESULTS. Both acebutolol and esmolol, decreased the heart rate significantly (-24%, -27.5%), while the mean arterial pressure remained nearly unchanged. The cardiac index was diminished following acebutolol (-15.4%) and esmolol (-27.4%), while no significant change in stroke volume index was observed; systemic vascular resistance rose in all patients. Pulmonary artery pressure, PCP, PRA, LVP and LVEDP were unchanged, whereas dp/dtmax decreased both with acebutolol (-23.5%) and with esmolol (-36.5%). CONCLUSION. Both beta-receptor blockers--acebutolol and the ultrashort-acting esmolol--diminish heart rate sufficiently when tachycardia occurs during coronary artery bypass grafting. Reduction of heart rate is associated with a decrease of cardiac output and an impairment of myocardial contractility. From the hemodynamic point of view there is no major difference between the two beta-receptor blockers investigated, but esmolol may have an advantage over acebutolol because of its short elimination half-life.     

Effects of pentoxifylline on central hemodynamics in patients with congestive heart failure

Pentoxifylline, a xanthine derivative with vasoactive and hemorheologic properties, was studied in regard to effect on central hemodynamics in ten patients with congestive heart failure due to aortic or mitral valve disease, mainly in NYHA group III or IV. The drug was infused intravenously in a dose of 4 mg/kg b.w. during a stable hemodynamic situation after valve replacement. The heart rate, systemic blood pressure, central venous and pulmonary artery pressures and cardiac output were recorded, and the stroke volume, cardiac index and systemic vascular resistance were calculated. Significant increase in cardiac output from the baseline value of 4.92 l/min was found 5-10 min (+22.6%) and 25-30 min (+19.5%) after pentoxifylline infusion. Cardiac index similarly increased from baseline, 2.73 dsc-5 (+22.3 and +18.3, respectively). The systemic vascular resistance showed significant decrease at the same intervals (-20.6 and -15.5%). The heart rate and stroke volume were significantly increased after 5-10 min. The systemic mean blood pressure and the pulmonary artery and central venous pressures showed no significant changes. There were no adverse effects of pentoxifylline.     

Dopamine stabilizes milrinone-induced changes in heart rate and arterial pressure during anaesthesia with isoflurane

BACKGROUND AND OBJECTIVE: Phosphodiesterase-III inhibitors and dobutamine effectively improve cardiac function in patients with cardiac failure, but they are limited by possible hypotensive effects. We tested the hypothesis that dopamine contributes to stabilizing milrinone-induced haemodynamic changes. METHODS: Nine patients undergoing major surgery were anaesthetized using nitrous oxide and oxygen supplemented with isoflurane 1-2%. After baseline haemodynamics were recorded, milrinone (25 or 50 microg kg(-1)) was administered over 10min, followed by a continuous infusion (0.5 microg kg(-1) min(-1). The second set of haemodynamic values was measured 50 min after beginning the continuous infusion of milrinone. Dopamine (4 microg kg(-1) min(-1)) was then administered with milrinone. RESULTS: Milrinone significantly increased the heart rate from 81 +/- 8 to 102 +/- 16beats min(-1), but it decreased the mean arterial pressure from 83 +/- 10 to 66 +/- 10 mmHg and systemic vascular resistance (P < 0.05 for each). The pulmonary capillary wedge pressure, cardiac index and pulmonary vascular resistance did not change significantly. The addition of dopamine to the milrinone infusion significantly decreased the heart rate (94 +/- 12 beats min(-1)) and increased the mean arterial pressure (82 +/- 11 mmHg). Dopamine and milrinone, but not milrinone alone, significantly increased the cardiac index and the rate-pressure product. CONCLUSIONS: The combination regimen of milrinone and dopamine improved cardiac function, and changes in heart rate and mean arterial pressure induced by milrinone were attenuated by dopamine. The results suggest that a combination regimen of milrinone and dopamine rather than milrinone alone should be used to maintain arterial pressure.     

Effects of dantrolene and verapamil on atrioventricular conduction and cardiovascular performance in dogs

The effects of intravenous dantrolene sodium, alone and in combination with verapamil, upon atrioventricular conduction, cardiovascular function, and neuromuscular function were studied in chloralose-urethane anesthetized dogs. Hemodynamic variables (systemic arterial, central venous, and pulmonary arterial pressures and cardiac output) and His-bundle electrograms were monitored, and measurements were made during atrial pacing at 175 beats/min, as well as at the spontaneous heart rate. In one part of the study animals received dantrolene sodium incrementally at 30-min intervals to cumulative doses of 1, 2.5, 5, and 10 mg/kg. Subsequently, verapamil was administered incrementally at 30-min intervals to cumulative doses of 0.1, 0.2, 0.4, and 0.6 mg/kg. In the second part of the study, dogs received identical dosage sequences, but verapamil preceded dantrolene administration. Dantrolene caused no significant depression of atrioventricular conduction or cardiac performance but did increase systemic vascular resistance at doses above 2.5 mg/kg. Verapamil alone (greater than or equal to 0.2 mg/kg) or with dantrolene (greater than or equal to 0.1 mg/kg) increased the atrial-His-bundle conduction interval. In the presence of verapamil, dantrolene (greater than or equal to 2.5 mg/kg) decreased cardiac index and increased pulmonary artery occlusion pressure. Although 0.6 mg/kg verapamil depressed cardiac index and increased pulmonary artery occlusion pressure, this effect was observed at 0.4 mg/kg after prior treatment with dantrolene. Verapamil did not augment the dose-dependent twitch depression observed with dantrolene. Dantrolene alone had no apparent effect on atrioventricular conduction and caused little enhancement of the effects of verapamil. However, each drug appeared to enhance the myocardial depressant effects of the other.     

Systemic and renal effects of dopamine in the infant pig

Dopamine is commonly employed in the management of hypotensive patients. Although this medication increases cardiac index (CI) and renal artery (RA) flow in adults, its effect in infants has not been adequately studied. In 13 infant pigs (mean wt 3.05 ± 0.75 kg; age 3–4 weeks) CI, RA flow and systemic blood pressure (BP) were measured at varying renal artery perfusion pressures before and after the administration of dopamine. Pigs were anesthetized with ketamine, intubated, and maintained on a ventilator with succinylcholine. Jugular vein, pulmonary (Swan-Ganz), carotid, and femoral artery catheters were placed. Laparotomy was performed and RA flow was measured with an electromagnetic flow probe. A Blalock clamp was placed around the suprarenal aorta to obtain graded aortic occlusions to pressures of 80 and 50 mm Hg. Dopamine had no significant effect on the CI vs control at 5, 10, 15, 20, 25, or 50 μg/kg/min. BP increased 25 mm Hg on Dopamine (10 μg/kg/min) P > 0.05). RA flow remained stable (318 ± 74 vs 300 ± 68 ml/min) despite reduction in perfusion pressure to 80 mm Hg, suggesting an autoregulatory flow mechanism. At 50 mm Hg perfusion pressure however, RA flow decreased significantly to 220 ± 54 ml/min (P < 0.05) indicating a loss of autoregulation at lower perfusion pressures.Dopamine (10 μg/kg/min) did not change RA flow at control BP (335 ± 76 vs 318 ± 74 ml/min). At 80 mm Hg perfusion pressure however, RA flow fell from 335 ± 74 to 175 ± 50 ml/min (P < 0.001) demonstrating a suppression of renal autoregulation by dopamine. At 50 mm Hg, RA flow was markedly reduced to 22 ± 31 ml/min (P < 0.001). These data suggest: (1) dopamine has no significant effect on CI in infant pigs, (2) an RA flow mechanism is present in infant pigs which protects the kidney at reduced perfusion pressures, and (3) dopamine interferes with autoregulation and may be harmful to the infant kidney in hypotensive states.