Pierre A. Casthely

Prevention of Nitroprusside-Induced Cyanide Toxicity with Hydroxocobalamin

To investigate hydroxocobalamins role in preventing cyanide intoxication from sodium nitroprusside, we studied two groups of patients. One group received nitroprusside alone, and the other received nitroprusside and hydroxocobalamin. Red-cell and plasma cyanide levels were 83.44 +/- 23.12 and 3.51 +/- 1.01 microgram per 100 ml after nitroprusside alone and were 33.18 +/- 17.29 and 2.18 +/- 0.65 microgram per 100 ml after nitroprusside plus hydroxocobalamin. Acidosis developed in patients with red-cell cyanide levels higher than 75 microgram per 100 ml. When hydroxocobalamin infusion was stopped before sodium nitroprusside infusion was discontinued, blood cyanide levels and base deficit increased in a manner similar to that in the untreated group. The dose of nitroprusside used in each group did not differ statistically. These data show that hydroxocobalamin prevents cyanide transfer from red cells and plasma to tissue after nitroprusside metabolism, and thereby prevents cyanide toxicity from large intravenous doses of the drug.

Intrapulmonary shunting during induced hypotension.

The effect of sodium nitroprusside (SNP) and nitroglycerin (TNG) on pulmonary shunting (&OV0422;s/&OV0422;t) in 14 consenting adults [nine with normal lung function and five with chronic obstructive pulmonary disease (COPD)] was studied under general anesthesia. &OV0422;s/&OV0422;t significantly increased (p > 0.005) from 5.19% to 8.81%, whereas pulmonary arterial pressure (PAP) decreased from 18.5 to 8 torr (p > 0.005) and pulmonary vascular resistance (PVR) decreased from 235 to 147.75 dynes sec/cm5 (p > 0.025) when SNP was administered to patients with normal lung function. Nitroglycerin increased &OV0422;s/&OV0422;t from 5.13% to 6.19% (p > 0.005), whereas PAP decreased from 18 to 10 torr (p > 0.005) and PVR decreased from 237 to 162.6 dynes sec/cm5 (p > 0.025) in these patients. In patients with COPD, SNP and TNG produced no significant changes in &OV0422;s/&OV0422;t, PAP, or PVR. Cardiac output remained unchanged in both groups of patients. Various mechanisms to explain these results can be postulated. When hypotension is induced in patients with normal pulmonary function, PAP decreases and the effect of gravity puts more blood through dependent areas where most of the shunt units are. In patients with COPD, destructive vascular changes increase PAP, preventing vasodilators from decreasing PVR. In addition, dilation of hypoxic pulmonary vasoconstriction (if present) by SNP and TNG will occur independent of the two previously mentioned mechanisms. These results provide evidence that SNP-and TNG-induced hypotension may cause significant impairment in pulmonary gas exchange in patients with normal lung function. In patients with COPD pulmonary gas exchange is not affected after deliberate hypotension with SNP or TNG.

Left ventricular diastolic function after coronary artery bypass grafting: A correlative study with three different myocardial protection techniques

BACKGROUND This study was designed to examine the effect of myocardial protection on diastolic function after cardiac operations. METHODS Subjects were patients with normal preoperative diastolic function who were scheduled for coronary artery bypass grafting. Group I received anterograde cardioplegia; group II received anterograde and retrograde cardioplegia; and group III was protected with ventricular fibrillation and intermittent aortic crossclamping. Operations were performed with mild hypothermia and ventricular venting through the left superior pulmonary vein in all cases. Left ventricular diastolic function was evaluated with pulsed-wave Doppler transesophageal echocardiography (samples at the mitral valve leaflet: four-chamber view) and left superior pulmonary vein flow velocity. The flow patterns were stored on videotape and sent to an independent investigator for analysis. Left ventricular ejection fraction was calculated with transesophageal echocardiography (short-axis view, two-dimensional and M-mode). RESULTS Left ventricular diastolic function, as measured by the ratio between the peak velocities during early filling and atrial contraction and by systolic diastolic superior pulmonary venous flow ratio, was significantly impaired in all three groups 5 minutes after discontinuation of cardiopulmonary bypass. At 1 hour after operation, these values had returned to control levels only in group III. There was an increased incidence of supraventricular arrhythmias in group III. There were no significant hemodynamic differences among the three groups. CONCLUSIONS Left ventricular diastolic function was severely impaired after cardiopulmonary bypass. The degree of impairment depended on the myocardial protection used. The impairment in diastolic function was less when ventricular fibrillation and intermittent aortic crossclamping were used, and greater when anterograde and retrograde cardioplegia were used.

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·kg−1 ·min1 for 4 min) was administered 10 min after 4 mg·hg1 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 < 0.025) from 72 ± 7 mm Hg immediately after the protamine and to 58 ± 5 mm Hg (P < 0.025) 5 min later and with an increase in cardiac index (CI) to 3.7 ± 0.3 L·min1·m−2 from 2.8 ± .25 L·min−1·m−2 immediately after the protamine (P < 0.005), followed by a decrease back to 2.7 ± 0.3L·min−1·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. We conclude that hemodynamic changes after protamine administration may be related to protamine-induced histamine release from the lung and are greatly influenced by the site of administration. The greatest hemodynamic effect occurred when protamine was administered via the right atrium and the least when administrated via the peripheral vein. This is probably due to the fact that protamine, when injected into the right atrium, forms protamine heparin complex, which goes to the lung to release histamine, whereas it becomes diluted before reaching the lung when injected into a peripheral vein or left atrium.

Retrograde intubation in patients undergoing open heart surgery

Cardiovascular changes during difficult intubation were studied in 25 patients undergoing open heart surgery. The study was divided into two phases. Phase A from the first laryngoscopy to the fourth unsuccessful one; Phase B from a stabilization period until after retrograde intubation was performed. During phase A, heart rate (HR) increased significantly from 75 ± 6.5 beatslmin before laryngoscopy to 95 ± 8.5 (p < 0.05) after the last laryn-goscopy. Mean arterial pressure (MAP) also increased from 82.5 ± 4.75 mmHgto 105 ± 5.15 (p<0.005) after the last laryngoscopy. Cardiac index (CI) decreased from 2.9 ± 0.3 L·min-1m-2 before to 2.55 ± 0.2 after the last laryngoscopy. Pulmonary capillary wedge pressure (PCWP) increased from 10.5 ± 1 mmHg before to 19.25 ± 1.5 (p< 0.01) after the last laryngoscopy. No statistically significant changes in HR, MAP, CI, and PCWP occurred before and after intubation during Phase B. Three patients had elevated ST segments during Phase A which responded to IV nitroglycerin and propranolol. None was detected during Phase B. There were more lacerated lips and teeth damaged during Phase A. One patient developed a small peritracheal haematoma after the retrograde intubation, for which no treatment was required. This technique is safe and produces minimal cardiovascular changes for difficult intubation in patients undergoing open heart surgery.RésuméLes effets hémodynamiques lors d’une intubation difficile ont été étudiés sur 25 patients subissants une chirurgie à cœur ouvert. Cette étude a été divisé en deux phases. La phase A comprend la période à partir de la première tentative de laryngoscopie jusqu’au quatrième échec de cette dernière; la phase B débute après une période de stabilisation jusqu’à l’accomplissement d’une intubation rétrograde. Pendant la phase A la fréquence cardiaque (HR) augmenta significativement de 75 ± 6.5 batte-mentslmin. avant laryngoscopie à 95 ± 8.5 (p < 0.05) après la dernière laryngoscopie. La pression artérielle moyenne (MAP) augmenta de 82.5 ± 4.75 mmHg à 105 ± 5.15(p < 0.005) après la dernière laryngoscopie. L’index cardiaque (CI) diminua de 2.9 ± OJL·min-1 m-2 avant la laryngoscopie à 2.55 ± 0.15 après la dernière tentative de laryngoscopie. La pression capillaire pulmonaire bloquié (PCWP) augmenta de 10.5 ± L mmHg avant laryngoscopie à 19.15 ± 1.5 (p<0.01) après la dernière laryngoscopie tentative de laryngoscopie. Aucun changement statistiquement significatif n’a été observé dans la fréquence cardiaque, tension artérielle moyenne, index cardiaque et pression capillaire pulmonaire bloquée avant et après intubation durant la phase B. Trois patients ont démontré une élévation du segment ST durant la phase A repondant à l’administration intraveineuse de nitroglycérine et depropranolol. Aucun changement du segment ST n’a été détecté durant la phase B. On observa des lacérations des lèvres et des bris de dents lors de la phase A. Un patient a développé un petit hématome péritrachéal après l’intubation rétrograde pour lequel aucun traitement ne fut requis. Cette technique est sécure et produit des altérations hémodynamiques minimes lors d’une intubation difficile chez les patients subissants une chirurgie à coeur ouvert.

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)

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 al two minutes (p < 0.005);19.05 ± 1.2 per cent at 30 minutes (p < 0.005); 17.5 ± 1.6 per cent at two hours (p < 0.01); and 12 ± 1.1 per cent at three hours (p < 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 < 0.005) to 3.85 ± 0.35 after 30 minutes (p < 0.005), 3.7 ± 3 after two hours (p < 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 QslQt.RésuméLe shunt pulmonaire (Qs/Qt) a été calculé chez 90 chiens bâtards pesant 18 à 20kg lors d’une ventilation mécanique avant et après hypotension provoquée par la nifédipine (groupe N), le diltiazem (groupe D) et labétalol (groupe L), polyéthylène glycol et éthyl alcool (groupe E). Une diminution de 30 pour cent de la tension artérielle moyenne survint après deux minutes de perfusion de nifédipine, deux minutes après diltiazem et trois minutes après labétalol. Ces effets ont duré Jeux heures après nifédipine, 90 minutes après diltiazem et trois heures après labétalol. Ils étaient accompagnés d’une diminution significative des résistances vasculaires pulmonaire et systémique.Le shunt imrapulmonaire et le débit cardiaque ont augmenté significativement après la perfusion de nifédipine. Le shunt a augmenté de 9.7 ± 0.8 à 18.25 ± 1.05 pour cent à deux minutes (p < 0.005); 19.05 ± 1.2 pour cent à 30 minutes (p < 0.005); 17.5 ± 1.6 pour cent à deux heures (p < 0.01); et 12 ± 1.1 pour cent à trois heures (p < 0.025). Aucune augmentation du shunt n’est survenue après administration de diltiazem, labétalol, polyéthylène glycol et éthyl alcool. La PO2 artérielle a diminué significativement après perfusion de nifédipine de 146 ± 11.5 à 105 ± 3.5 mmHg deux minutes après la perfusion; à 89.5 ± 3 mmHg 30 minutes après; 115 ± 4.75mmHg deux heures après; et 130 ± 10.75mmHg trois heures plus lard. La PO2 artérielle n’était pas significativement différente après diltiazem, labétalol, polyethylene glycol et éthyl alcool. Le débit cardiaque augmenta de 2.25 ± 0.3 à 3.95 ± 0.25 après deux minutes (p < 0.005) à 3.85 ± 0.35 après 30 minutes (p < 0.005) 3.7 ± 3 après deux heures (p < 0.01) à2.9 ± l.l après trois heures. Aucune augmentation significative dans le débit cardiaque n’est survenue dans le groupe D etL.Ces résultats suggèrent que seule la perfusion de nifédipine altère significativement l’oxygénation chez les chiens et ainsi suscite la prudence en présence d’une anomalie du Qs/Qt pré-existante.

Anesthetic management of patients undergoing Fontan procedure.

Major advances in surgical and anesthetic techniques have permitted critically ill patients to undergo surgical correction of complex congenital cardiac defects that were previously inoperable. Rodband and Wagner (1) performed the first experimental right ventricular bypass. Later, Glenn demonstrated that a right heart bypass could be successfully performed in humans by anastomosing the superior vena cava to the right pulmonary artery (2). This demonstrated for the first time that satisfactory pulmonary perfusion could be obtained with venous blood pressure. In 1971 the first successful case of total venous diversion was reported by Fontan and Baudet (3). The superior vena cava was anastomosed to the distal right pulmonary artery, and an aortic homograft was used to anastomose the right atrial appendage to the proximal right pulmonary artery. The Fontan procedure was initially developed for patients with tricuspid atresia. Because of the favorable outcome, indications for this procedure were expanded to include more complex cardiac lesions. Among these are transposition of the great vessels with a univentricular heart, pulmonary artery atresia or both. Although the surgical techniques for the Fontan procedure have been described in detail (3-8), there are no reports describing anesthetic management. Safe and effective management of these patients during the perioperative period requires appreciation of the pathological changes that occur before and after surgical repair. In this report, we review our anesthetic management of eight patients with various cardiac deformities who underwent the Fontan procedure.

Ketanserin in the preoperative and intraoperative management of a patient with carcinoid tumor undergoing tricuspid valve replacement

Carcinoid tumors originating from enterochromaffin cells in intestines, bronchus, and stomach have been associated with fatal cardiovascular and respiratory complications mainly caused by the release of serotonin (5-hydroxytryptamine), vasoactive substances, histamine, and bradykinin (1). Fibrous tissue deposition in the tricuspid and pulmonary valve may also occur. Preoperative preparation of these patients usually includes the use of antiserotonin medication (2-5). Ketanserin is a competitive serotonin receptor blocker that has been previously used to treat hypertension after coronary artery bypass surgery (6). We describe treatment with ketanserin of a case of severe hypertension during cardiopulmonary bypass in a patient with metastatic carcinoid undergoing tricuspid valve replacement.

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 ° C after previous administration of thiopenlone 30 mg*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 al a mean oesophageal temperature of 12.5 ± 0.75° 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.RésuméLe taux de mortalité et de morbidité durant la correction chirurgicale de t’aneurysme de l’arche de l’aorte est encore élevé malgré l’amélioration de la technique chirurgicale visant à assurer la protection du cerveau. Nous avons utilisé avec beaucoup de succès un système combinant l’hypothermie profonde et l’arrêt complet de la circulation. L’anesthésie administrée consistait en du pavulon, dufentanyl, de l’isoflurane ou de l’halothane si nécessaire. Le refroidissement de surface a précédé le refroidissement central pratiqué avec la machine cαurpoumon. L’arrêt complet de la circulation s’est produit quand la température de l’αsophage était de 12-14° C après l’administration de thiopentone de sodium (30 mgs.kg-1), de méthylprednisolone 2 g, de furosemide 40 mgs et de mannitol 25 gs. A ce moment la tête a été complètement recouverte de sacs de glace et la correction chirurgicale pratiquée. Le temps moyen d’arrêt circulatoire était de 36.5 ± 13 minutes et la température de l’αsophage 12.5 ± 0.75° C. Nous ne rapportons aucune fatalité durant l’intervention chirurgicale. Nous n’avons constaté aucun déficit neurologique permanent chez nos patients.La trachéotomie a été pratiquée chez cinq patients souffrant d’insuffisance respiratoire. Deux décès ont été rapportés des suites d’insuffisance rénale et respiratoire.Cette technique est sûre et pratique et diminue la chance de complications durant la résection de l’aneurysme de l’arche de l’aorte.