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Biomedical subjects

P A Casthely

Publications and source records attributed to P A Casthely.

17 recordsLinked to original sources
PubMed1990

Phlebotomy via the pulmonary artery catheter introducer for intraoperative autotransfusion.

Fear of the acquired immune deficiency syndrome and other blood-transmitted diseases has created a revival of autologous transfusion during cardiac surgery. The present report is of 200 patients undergoing cardiopulmonary bypass during cardiac surgery in whom phlebotomy was performed via the sideport of the introducer for the pulmonary artery catheter for later reinfusion. Each unit of phlebotomized blood was replaced with 500 mL of normal saline. Cardiac output and mean arterial blood pressure decreased significantly after phlebotomy (P less than 0.05) and returned toward control values after administration of the sodium chloride. The autologous blood was replaced after cardiopulmonary bypass. Fresh frozen plasma and platelets were not administered to the patients in the operating room. Eleven patients undergoing coronary artery bypass grafting received fresh frozen plasma in the recovery room because they were receiving aspirin and dipyridamole up to the day of surgery. Prolonged duration of cardiopulmonary bypass in two double-valve replacements, and one coronary artery bypass graft patient who required insertion of an intra-aortic balloon, accounted for the administration of fresh frozen plasma and platelets in three patients. The average volume of phlebotomized blood was 875 mL, which resulted in a decrease of the hematocrit from 40.5% +/- 0.5% (P less than 0.05) to 29.75% +/- 0.5% and 30.5% +/- 0.5% at the end of surgery and at discharge from the hospital, respectively. Phlebotomy via the Y port of the introducer of the pulmonary artery catheter is an easy, simple, and cost-effective way to remove autologous blood in patients undergoing cardiac surgery.

Adult↗
PubMed1990

Histamine blockade and cardiovascular changes following heparin administration during cardiac surgery.

Large doses of heparin given as a bolus may produce hypotension; however, conflicting reports exist about the mechanisms involved. This study was undertaken to determine the role of histamine in beef lung heparin-induced hypotension and the efficacy of histamine-receptor blockade in attenuating this undesirable side effect in patients undergoing cardiac surgery. Two hundred patients with good ventricular function were studied after they were randomized into four equal groups. Group I (control) received no histamine-receptor blockade, group II received 1 mg/kg of diphenhydramine 30 minutes prior to heparin administration, group III received 5 mg/kg of cimetidine 4 hours and again 30 minutes before heparin administration, and group IV received 1 mg/kg of diphenhydramine 30 minutes prior to heparin administration and 5 mg/kg of cimetidine 4 hours and 30 minutes before heparin administration. Hemodynamic variables, plasma histamine, and ionized calcium levels were measured before and after heparin administration. Significant hypotension occurred in group I patients after heparin administration. Mean arterial pressure decreased from 95 +/- 5 to 67 +/- 1.5 mm Hg (P less than 0.005) after 1 minute and to 85 +/- 2 mm Hg (P less than 0.05) at 4 minutes. Those changes were significantly greater than in group II (P less than 0.025) and Group IV (P less than 0.005) patients, in whom no significant hypotension was found. In group III, mean arterial pressure decreased from 92 +/- 3 to 75 +/- 1 mm Hg (P less than 0.05) after 1 minute and returned toward baseline values after 4 minutes. Histamine levels increased significantly in all groups of patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗
PubMed1989

Hemodynamic changes after nafcillin administration during coronary artery bypass surgery.

The hemodynamic response to nafcillin administration was studied in 45 patients with good left ventricular function and no known history of hypersensitivity to penicillin during coronary artery bypass grafting (CABG). Group I (15 patients) received 1 gram of nafcillin in 10 mL of saline as an intravenous (IV) bolus, group II (15 patients) received 1 gram of nafcillin in 50 mL of saline as a slow IV infusion over 15 minutes, and group III (15 patients) did not receive nafcillin. Hemodynamic variables and plasma histamine and catecholamine levels were measured before and after nafcillin administration, after 500 mg of CaCl2, and after 0.1 mg of phenylephrine. Bolus nafcillin administration produced profound hypotension secondary to vasodilatation with significant increases in cardiac index and decreases in systemic and pulmonary vascular resistances. Cardiac index increased from 3.15 +/- 0.3 L/min/m2 to 5.75 +/- 0.25 L/min/m2 (P less than 0.005) one minute after nafcillin administration, and remained at 5.1 +/- 0.35 L/min/m2 after administration of CaCl2 (P less than 0.005). All hemodynamic parameters returned toward control values after administration of 0.1 mg of phenylephrine, IV. Plasma epinephrine, norepinephrine, and histamine levels increased more than 100%. In group II, cardiac index increased, while systemic and pulmonary vascular resistances and mean arterial pressure decreased. However, these changes were less significant than those found in group I.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗
PubMed1988

Pharmacokinetics of sufentanil in patients undergoing renal transplantation.

Renal failure and chronic haemodialysis are often associated with alterations in fluid status and plasma proteins. These changes, in turn, may result in pharmacokinetic alterations in affected patients. The purpose of this study was to investigate the pharmacokinetics of sufentanil in chronic renal failure patients undergoing kidney transplantation. Ten male patients were studied. Following induction of anaesthesia each patient received sufentanil 2.0 micrograms.kg-1 IV with subsequent serial plasma sampling for drug measurement from one to 360 minutes. A biexponential equation provided the best fit of the sufentanil concentration data with mean +/- SEM distribution (alpha) and elimination (beta) half-lives of 2.9 +/- 1.3 and 176 +/- 87 minutes, respectively. The mean Vc and Vd beta values were 0.15 +/- 0.05 L.kg-1 and 0.85 +/- 0.16 L.kg-1, respectively; plasma drug clearance was 11.5 +/- 3.7 ml.kg-1.min-1. Mean values for K10, K12 and K21 were 0.15 +/- 0.06.min-1, 0.4 +/- 0.14.min-1 and 0.1 +/- 0.04.min-1, respectively. With the exception of Vd beta, these pharmacokinetic values are similar to those reported in previous studies in general surgical, elderly and burn patients. The Vd beta values observed in this study may have resulted from alterations in drug distribution or elimination following revascularization of the implanted kidneys. Nevertheless, it appears that modification of sufentanil doses is unnecessary in chronic renal failure patients undergoing renal transplantation.

Adult↗
PubMed1986

Ventricular fibrillation during general anaesthesia in a seven-year-old patient with mitral valve prolapse.

A case report is presented of a seven-year-old boy who developed ventricular fibrillation during general anaesthesia with atracurium, O2, N2O and halothane, following tracheal intubation for hypospadias revision. He spontaneously defibrillated and the surgery was cancelled. Echocardiography done two days later was normal. The patient returned two weeks later for the same procedure. He developed nodal tachycardia, and premature ventricular contractions, which responded to lidocaine. A second echocardiographic examination done postoperatively while the child was crying showed mitral valve prolapse.

Anesthesia, General↗
PubMed1986

Hemodynamic effects of metocurine during isoflurane anesthesia.

Anesthesia was induced in 42 adults with thiopentone 3-7 mg/kg i.v. and maintained with isoflurane at a constant inspired concentration of 1-2%. After 30 min of hemodynamic stabilization with continuous muscle relaxation and an absence of surgical stimulation, each patient was randomly assigned to one of four metocurine dosage groups: I - control (n = 11); II - 0.2 mg/kg (n = 10); III - 0.3 mg/kg (n = 10); and IV - 0.4 mg/kg (n = 11). There were no significant hemodynamic changes in Groups I or II. In Groups III and IV mean arterial pressure (MAP) decreased 32% and 26% respectively, and systemic vascular resistance (SVR) decreased 42% and 36%, respectively (P less than 0.01). In Group IV, an increase of 24% in cardiac output was also significant (P less than 0.05). These results, especially in Group IV patients, stand in marked contrast to the lack of hemodynamic effects produced by metocurine during balanced anesthesia.

Adult↗
PubMed1986

Hemodynamic changes after the administration of protamine.

Hemodynamic changes associated with the administration of protamine were studied in 30 dogs divided into three equal groups. Protamine (1 mg X kg-1 X min-1 for 4 min) was administered 10 min after 4 mg X hg-1 heparin was given via a left atrial (LA) line in group A, via a central vein in group B, and via a peripheral vein in group C. Protamine given through the central venous pressure (CVP) line resulted in an immediate and significant decrease in mean arterial pressure (MAP) to 60 +/- 4.5 mm Hg (P less than 0.025) from 72 +/- 7 mm Hg immediately after the protamine and to 58 +/- 5 mm Hg (P less than 0.025) 5 min later and with an increase in cardiac index (CI) to 3.7 +/- 0.3 L X min-1 X m-2 from 2.8 +/- .25 L X min-1 X m-2 immediately after the protamine (P less than 0.005), followed by a decrease back to 2.7 +/- 0.3 L X min-1 X m-2 5 min later. Mean arterial pressure and CI remained unchanged after administration of protamine via the peripheral vein or the left atrium. Systemic vascular resistance (SVR) decreased significantly only after administration of protamine via the CVP and was statistically unchanged when administered via the peripheral and LA line. Plasma histamine levels increased significantly after administration of protamine through the central line but remained unchanged after administration via a peripheral vein or the left atrium.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Anaesthesia for aortic arch aneurysm repair: experience with 17 patients.

Mortality and morbidity during aortic arch aneurysm repair is high despite improvements in surgical technique which attempt to assure brain protection during surgery. We successfully managed 17 patients using deep hypothermia and circulatory arrest. Anaesthesia consisted of pancuronium, fentanyl, plus isoflurane or halothane if needed. Pulmonary artery and arterial catheters were inserted. Surface cooling was performed followed by core cooling on cardiopulmonary bypass, using a heat exchanger. Total circulatory arrest was performed when esophageal temperature reached 12-14 degrees C after previous administration of thiopentone 30 mg X kg-1, methylprednisolone 2 gm, furosemide 40 mg and mannitol 25 gm. At that time the head was packed in ice and surgical correction performed. Mean arrest time was 36.5 +/- 13 minutes at a mean oesophageal temperature of 12.5 +/- 0.75 degrees C. No serious, permanent neurological deficit was found. Tracheostomy was required in five patients of whom two had chronic obstructive pulmonary disease (COPD). Two of these patients died of adult respiratory distress syndrome (ARDS) and renal failure. The reported technique is safe and can be easily used in patients undergoing aortic arch aneurysm repair.

Adjuvants, Anesthesia↗
PubMed1985

Comparison of metaproterenol, isoetharine and salbutamol in the relief of methacholine-induced bronchospasm in dogs.

We evaluated cardiovascular effects and effectiveness of isoetharine, metaproterenol and salbutamol, when administered intratracheally to relieve methacholine-induced bronchospasm in dogs anaesthetized with 50 per cent nitrous oxide, oxygen, halothane and mechanically ventilated. Methacholine 2 micrograms X kg-1 X hour-1 was administrated first followed by halothane (1 MAC) for 30 minutes (control), then metaproterenol, isoetharine or salbutamol. Metaproterenol (15 mg) significantly decreased transpulmonary pressure to 20.1 +/- 0.5 (SE) from 22.5 +/- 1.15 cmH2O (p less than 0.025) after three min and to 15 +/- 0.5 cmH2O (p less than 0.005) after 90 min. Isoetharine (2.5 mg) decreased transpulmonary pressure after five min to 22.1 +/- 1 from 24.5 +/- 1.5 cmH2O (p less than 0.05), and to 21.75 +/- 0.55 mmH2O after 90 min. Salbutamol 25 micrograms X kg-1 decreased transpulmonary pressure to 20.7 +/- 0.75 from 24.25 +/- 1.28 after three min and to 16 +/- .5 after 90 min. The peak effects on airway pressure occurred at 15 min for metaproterenol, 25 min for salbutamol and 20 min for isoetharine. Pulmonary vascular resistance was not significantly changed during halothane anaesthesia alone but decreased significantly after metaproterenol and isoetharine infusion. Heart rate increased ten per cent after metaproterenol, three per cent after isoetharine, and five per cent after salbutamol. No arrhythmias occurred in any group. Cardiac output increased significantly to 3.25 +/- 0.2 from 1.5 +/- 0.17 L X min-1 (p less than 0.025) after metaproterenol to 3.2 +/- .025 from 1.45 +/- .009 after salbutamol and was unchanged after isoetharine. Metaproterenol and salbutamol in the presence of 1 MAC halothane anaesthesia relieved methacholine-induced bronchospasm more rapidly than did isoetharine. The onset of effect was 3 +/- 0.05 min for metaproterenol and salbutamol and 5 +/- 0.01 min for isoetharine. The effect lasted 210 +/- 10.5 min for metaproterenol, 170 +/- 12.5 min for salbutamol and 90 +/- 4.75 min for isoetharine.

Airway Resistance↗
PubMed1985

Intrapulmonary shunting during deliberate hypotension with nifedipine, diltiazem and labetalol in dogs.

Pulmonary shunt (Qs/Qt) was calculated in 49 mongrel dogs weighing 18-20 kg during mechanical ventilation, before and during deliberate hypotension with either nifedipine (group N), diltiazem (group D), labetalol (group L), or ethyl alcohol and polyethylene glycol (group E). A 30 per cent decrease in mean arterial blood pressure occurred after two minutes of nifedipine infusion, two minutes after diltiazem, and three minutes after labetalol; these effects lasted two hours after nifedipine administration, 90 minutes after diltiazem and three hours after labetalol. There was an accompanying significant decrease in systemic and pulmonary vascular resistance. Qs/Qt and cardiac output increased significantly after nifedipine infusion. Shunt increased (mean +/- S.E.) from 9.7 +/- 0.8 to 18.25 +/- 1.05 per cent at two minutes (p less than 0.0005); 19.05 +/- 1.2 per cent at 30 minutes (p less than 0.005); 17.5 +/- 1.6 per cent at two hours (p less than 0.01); and 12 +/- 1.1 per cent at three hours (p less than 0.025). No increase in shunt occurred after the administration of diltiazem, labetalol or polyethylene glycol and ethyl alcohol. Arterial oxygen tension (PaO2) decreased significantly after nifedipine infusion from 146 +/- 11.5 to 105 +/- 3.5 mmHg two minutes after infusion; to 89.5 +/- 3 mmHg 30 minutes after; 115 +/- 4.75 mmHg two hours after; and 130 +/- 10.75 mmHg three hours later. PaO2 was not significantly different after diltiazem, labetalol, or polyethylene glycol and ethyl alcohol administration. With nifedipine cardiac output increased from 2.25 +/- 0.3 to 3.95 +/- 0.25 after two minutes (p less than 0.005) to 3.85 +/- 0.35 after 30 minutes (p less than 0.005), 3.7 +/- 3 after two hours (p less than 0.01) to 2.9 +/- 1.1 after three hours. No significant increase in cardiac output occurred in groups D or L. These results suggest that only nifedipine infusion significantly alters oxygenation in dogs and therefore its use warrants caution in the presence of a preexisting abnormal Qs/Qt.

Anesthesia↗