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Biomedical subjects

H J Khambatta

Publications and source records attributed to H J Khambatta.

At least 19 recordsLinked to original sources

Cardiac performance preserved despite thiopental loading.

BACKGROUND: Some cerebral artery aneurysms require cardiopulmonary bypass and deep hypothermic circulatory arrest to be clipped safely. During bypass these neurosurgical patients often are given large doses of thiopental in the hope that additional cerebral protection will be provided. However, thiopental loading during bypass has been associated with subsequent cardiac dysfunction in patients with heart disease. This study was undertaken to determine how patients without concomitant heart disease would respond to thiopental loading. METHODS: Twenty-four neurosurgical patients with giant cerebral aneurysms and little or no cardiac disease were anesthetized with fentanyl, nitrous oxide, and isoflurane. Thiopental was titrated to achieve electroencephalographic burst-suppression before bypass, and the infusion was continued until after separation. Prebypass hemodynamic and echocardiographic measurements were obtained during a stable baseline and 15 min after thiopental loading began. They were repeated after bypass. RESULTS: Prebypass thiopental loading increased heart rate from 61 +/- 11 to 72 +/- 13 beats/min and decreased stroke volume from 43 +/- 10 to 38 +/- 8 ml.beat-1.m-2, but arterial and filling pressures, vascular resistance, cardiac index, and ejection fraction remained the same. Before bypass, thiopental plasma concentration measured 28 +/- 8 micrograms/ml. Loading continued for 2-3 h until after bypass was terminated, and the overall infusion rate was 18 +/- 5 mg.kg-1.h-1. All patients were easily separated from bypass without inotropic support. Following bypass, vascular resistance was decreased; heart rate, filling pressures, and cardiac index were increased; stroke volume had returned to its baseline; and ejection fraction was unchanged. CONCLUSIONS: It was concluded that if preoperative ventricular function is good, thiopental loading to electroencephalographic burst-suppression causes negligible cardiac impairment and does not impede separation from cardiopulmonary bypass.

Adult

Risk of myocardial ischaemia during anaesthesia in treated and untreated hypertensive patients.

Hypertensive patients were monitored for myocardial ischaemia during anaesthesia and surgery with the V5 lead of a standard electrocardiograph. Myocardial ischaemia was detected in 11 of 39 untreated hypertensive patients and in four of seven receiving therapy with a diuretic, but in none of 44 receiving atenolol. Fourteen of the atenolol-treated patients were receiving the drug on a long-term basis and the remaining 30 were treated acutely only on the morning of surgery. When myocardial ischaemia was observed, it was always associated with noxious stimulation and tachycardia, but a conspicuous increase in arterial pressure was not usually present. We conclude that myocardial ischaemia is prevalent during anaesthesia in untreated hypertensive patients, and that pretreatment with atenolol, but not diuretics, provides prophylaxis.

Anesthesia

Myocardial ischemia in untreated hypertensive patients: effect of a single small oral dose of a beta-adrenergic blocking agent.

In a non-double-blind, prospective, randomized study, the intra-operative electrocardiograms of 128 mildly hypertensive surgical patients were examined in order to determine the incidence of myocardial ischemia during anesthesia. No patient had been receiving chronic antihypertensive therapy prior to the study, but a single small oral dose of a beta-adrenergic blocking agent (labetalol, atenolol, or oxprenolol) was given to 89 of them along with premedication. Forty-four per cent of the untreated control patients and 61% of the patients pretreated with a beta-adrenergic blocking agent had normal preoperative electrocardiograms and no risk factors for coronary artery disease other than hypertension (this difference between groups was not statistically significant). During tracheal intubation and/or emergence from anesthesia, a brief, self-limited episode of myocardial ischemia was detected in 11 of 39 untreated control patients, and in two of 89 patients pretreated with a beta-adrenergic blocking agent (P less than 0.001). Tachycardia always accompanied the ischemic events, but a conspicuous increase in blood pressure did not. The authors conclude that mild hypertension, when untreated prior to the induction of anesthesia, is associated with a high incidence of myocardial ischemia; and that a single small oral dose of a beta-adrenergic blocking agent, given with pre-medication, can significantly reduce that risk.

Administration, Oral

Global and regional myocardial blood flow and metabolism during equipotent halothane and isoflurane anesthesia in patients with coronary artery disease.

Global and regional myocardial blood flow and metabolism were examined in 20 patients with coronary artery disease before surgical stimulation. Half were anesthetized with halothane (0.8%) and half with isoflurane (1.2%). Coronary perfusion pressure decreased similarly in both groups. During halothane anesthesia coronary sinus blood flow, an index of global perfusion, decreased from an awake value of 129 +/- 7 to 97 +/- 7 ml/min (P less than 0.05), and great cardiac vein blood flow, an index of regional perfusion, decreased from 60 +/- 8 to 44 +/- 5 ml/min (P less than 0.05). In contrast, during isoflurane anesthesia global coronary blood flow increased from 131 +/- 13 to 153 +/- 16 ml/min (P less than 0.05), while regional blood flow decreased from 68 +/- 7 to 56 +/- 6 ml/min (P less than 0.05). Thus, the ratio of great cardiac vein blood flow to coronary sinus blood flow was unchanged during halothane anesthesia but decreased significantly during isoflurane. Neither global nor regional coronary vascular resistance was altered by halothane, whereas isoflurane decreased global coronary vascular resistance without affecting regional coronary vascular resistance. All patients receiving halothane had net myocardial lactate extraction. In the isoflurane group, four patients showed global lactate production and three regional lactate production. All patients demonstrating lactate production also developed electrocardiographic evidence of myocardial ischemia, which was not present before induction. The authors conclude that halothane is a preferable anesthetic to isoflurane in patients with coronary artery disease because the latter has the propensity to induce maldistribution of the coronary circulation and myocardial ischemia.

Adult

Propranolol increases oxygen utilization during hypoxia.

The effects of propranolol on whole body oxygen consumption and blood oxygen content were measured in the dog during extreme hypoxic conditions. At 9% inspired oxygen four of eight control animals died within 40 min. An identical second group was pretreated with propranolol and none died during the same hypoxic stress. Hypoxia decreased oxygen consumption in both groups, but the decrease was less in the propranolol-pretreated dogs. A second set of 16 dogs was ventilated with 10% oxygen and all animals survived. A similar, although less pronounced, effect on oxygen consumption was noted and propranolol once again lessened the hypoxia-induced decrease in oxygen consumption. With hypoxaemia, metabolic acidosis developed in all animals and the arterio-venous oxygen content difference decreased; however, propranolol lessened the acidosis and the decrease in arterio-venous oxygen content difference. We conclude that, during hypoxia, propranolol increases oxygen utilization by the tissues and this might account for better survival.

Animals

Effects of propofol on cardiovascular dynamics, myocardial blood flow and myocardial metabolism in patients with coronary artery disease.

The effects of propofol (emulsion formulation) on cardiovascular dynamics, myocardial blood flow and myocardial metabolism were studied in 12 patients scheduled for elective coronary artery bypass surgery. Measurements were performed with the patient awake, during steady-state maintenance anaesthesia with propofol 200 micrograms kg-1 min-1 at rest, and during sternotomy when the propofol was supplemented with fentanyl 10 micrograms kg-1. Propofol alone decreased mean arterial pressure and cardiac index; heart rate was increased. Myocardial blood flow and myocardial oxygen consumption were decreased by 26% and 31%, respectively. Myocardial lactate production was seen in one patient during this period. Surgical stimulation, under propofol-fentanyl anaesthesia, led to the return of arterial pressure and heart rate towards baseline; cardiac index decreased further. Myocardial blood flow and oxygen consumption increased such that they almost achieved their baseline values. Myocardial lactate production was seen in one patient. These results suggest that propofol may on occasions, lead to myocardial ischaemia in patients with coronary artery disease, but that it is able to block the sympathetic responses to surgical stimulation when combined with a suitable analgesic.

Adult

Propranolol premedication blunts stress response to nitroprusside hypotension.

Hypotension was induced in sixteen patients with nitroprusside during anesthesia for surgical correction of cerebral aneurysms. Eight patients were premedicated with propranolol (180 mg orally) for one day and the other eight were not. Before the start of anesthesia, the untreated patients had a mean arterial pressure of 102 +/- 3 mm Hg, a heart rate of 76 +/- 2 beats/min, and plasma epinephrine and norepinephrine concentrations of 114 +/- 21 and 258 +/- 34 pg/ml, respectively. The propranolol-premedicated patients came to the operating room in a significantly different clinical state with a mean arterial pressure of 92 +/- 3 mm Hg, a heart rate of 71 +/- 2 beats/min, and plasma epinephrine and norepinephrine concentrations of 76 +/- 28 and 144 +/- 28 pg/ml. During induced hypotension, plasma epinephrine and norepinephrine concentrations increased significantly in both groups (454 +/- 42 and 730 +/- 58 pg/ml in the untreated patients, 160 +/- 48 and 419 +/- 67 pg/ml in the propranolol premedicated patients), but the increase in catecholamines was significantly greater in the untreated patients. Thirty minutes after nitroprusside was discontinued, epinephrine and norepinephrine concentrations were higher than in the awake state in untreated patients and were associated with rebound hypertension and tachycardia. In contrast, in propranolol-premedicated patients, plasma epinephrine and norepinephrine concentrations decreased towards the preanesthesia values, mean arterial pressure gradually returned to the prehypotension level, and heart rate remained unchanged. This study thus demonstrates that propranolol premedication attenuates the release of catecholamines in response to nitroprusside-induced hypotension.

Adult

Influence of volume loading on intraoperative hemodynamics and perioperative fluid retention in patients with valvular regurgitation undergoing prosthetic replacement.

Preload and afterload were controlled intraoperatively in 2 groups of patients with valvular regurgitation and congestive heart failure in order to determine the effect of fluid loading on weight gain and subsequent recovery. As a part of their anesthetic management before cardiopulmonary bypass, 16 patients were given 1 liter of crystalloid with nitroprusside infused at 1 microgram/kg/min and 16 received 4 liters of crystalloid with nitroprusside at 4 micrograms/kg/min. Arterial and filling pressures were kept the same in both groups. Heart rate and vascular resistance became significantly lower and cardiac index and stroke volume significantly higher in the fluid-augmented group. The transition to cardiopulmonary bypass was smoother for the fluid-augmented patients. All patients survived, and 2 in each group were ventilated beyond 24 hours. The mean weight gain at surgery was the same in the 2 groups (3 kg). For the first 2 postoperative days, body weight remained unchanged and thereafter, both groups lost weight at 0.6 kg/day. Preoperative weight was reached on day 7 and discharge occurred on day 15, 2 kg below control. Thus, a modest operative weight gain in these patients is inevitable, benign, and independent of the volume of fluid infused before bypass.

Aortic Valve

Catheter-induced pulmonary arterial trauma: can it always be averted?

Catheter-induced pulmonary arterial hemorrhage is a serious and still recurring complication. This report describes our experience with 200 cases managed successfully by a prophylactic approach to the problem. The technique involves partial withdrawal of the pulmonary arterial catheter into a sterile protective sleeve during cardiopulmonary bypass and subsequent reinsertion when the normal circulation is restored.

Adult

Propranolol alters renin release during nitroprusside-induced hypotension and prevents hypertension on discontinuation of nitroprusside.

Ten patients who received hypotensive anesthesia for surgical correction of a cerebral aneurysm were pretreated for 1 day with propranolol. In the awake state, before start of anesthesia, mean arterial pressure was 91 +/- 3 torr and plasma renin activity 3.0 +/- 0.1 ng/ml/hr. Thirty minutes after the induction of anesthesia mean arterial pressure decreased to 79 +/- 2 torr and plasma renin activity increased to 3.5 +/- 0.1 ng/ml/hr. There was no further significant change in either measurement with surgical stimulation. During sodium nitroprusside-induced hypotension (the dose used was 0.35 +/- 0.02 mg/kg) mean arterial pressure was reduced to 53 +/- 2 torr, and plasma renin activity increased to 8.8 +/- 0.9 ng/ml/hr. Heart rate did not change. Discontinuation of sodium nitroprusside resulted in a gradual reduction of plasma renin activity to the awake level and concurrent gradual increase in mean arterial pressure to its basal anesthetic value. When compared with previous work, these results indicate that propranolol attenuates nitroprusside-induced renin release, reduces the dosage of nitroprusside required to induce hypotension, suppresses reflex tachycardia, and prevents overshoot hypertension on discontinuation of nitroprusside.

Adult

Catheter-induced pulmonary artery hemorrhage. Diagnosis and management in cardiac operations.

Three case reports describing catheter-induced pulmonary artery hemorrhage in patients having cardiac operations are presented--a 0.2% incidence of this complication. One patient exsanguinated and died, another survived after undergoing an emergency lobectomy, and the third escaped without surgical intervention. As a result of this experience and the recommendations in the literature, we have developed and describe herein a rational therapy for this highly lethal complication.

Aged

Nitroprusside and mitral stenosis.

The cardiovascular effects of an intravenous nitroprusside infusion were evaluated intraoperatively in seven patients with pure mitral stenosis and seven patients with predominant mitral stenosis. Prior to therapy the adverse hemodynamic consequences of light anesthesia and surgical stimulation were evident in all patients: systemic and/or pulmonary hypertension were present, systemic vascular resistance was twice normal, and cardiac function was depressed. Nitroprusside consistently reduced systemic vascular resistance and systemic arterial as well as pulmonary arterial and wedge pressures, but cardiac index increased only when severe pulmonary hypertension and/or some mitral regurgitation coexisted with mitral stenosis. In the group with predominant mitral stenosis, cardiac index increased from 1.8 to 2.1 L/min/m2 with nitroprusside (p < 0.05). In three individuals who demonstrated severe pulmonary hypertension (one with pure mitral stenosis and two with predominant mitral stenosis), nitroprusside induced an increase of almost 50% in cardiac index and stroke volume. In contrast, patients with pure mitral stenosis and mild pulmonary hypertension showed little change in cardiac index or stroke volume. It is concluded that nitroprusside can safely be used to control systemic or pulmonary hypertension during anesthesia and surgery in patients with mitral stenosis and that if severe pulmonary hypertension and/or mitral regurgitation coexist with mitral stenosis, cardiac function will also improve.

Ferricyanides