Phaeochromocytoma crisis in Sipple's syndrome with intrauterine death and disseminated intravascular coagulation.

Unrecognized phaeochromocytoma during pregnancy is dangerous for both fetus and mother. We report here a case of phaeochromocytoma crisis in Sipple's syndrome associated with disseminated intravascular coagulation that developed following intrauterine death. Early evacuation of the uterus seems advisable, to rid the patient with phaeochromocytoma of further complications associated with fetal death.

[Anesthetic management of cesarean section in a patient with pulmonary embolism due to deep venous thrombosis].

A 28-year-old primipara with pulmonary embolism due to deep venous thrombosis was scheduled for cesarean section under general anesthesia. Her Swan-Ganz catheter and blood gas data revealed pulmonary hypertension and hypoxemia, respectively. Heparin was discontinued 6 hours before operation. A transesophageal echocardiogram (TEE) probe and an inferior vena cava filter were inserted before surgery. Anesthesia was maintained with nitrous oxide and isoflurane in oxygen before delivery, and after delivery with nitrous oxide in oxygen, fentanyl and midazolam. Nitroglycerin and prostaglandin E1 were administered before and after delivery, respectively, to control pulmonary artery pressure, although they were not effective. The anesthetic course was uneventful and her baby's Apgar scores were satisfactory. Mean pulmonary artery pressure (MPAP) gradually decreased after surgery. The inferior vena cava filter may be effective in preventing new pulmonary embolism, and MPAP and TEE monitoring are useful for early detection of pulmonary emboli.

[Comparison of effects of intravenous versus intramuscular famotidine on pH and volume of gastric juice].

Famotidine, an H2-antagonist, is frequently used for prevention of acid aspiration in surgical patients. Intravenous as well as intramuscular administration of famotidine has proved effective to reduce gastric acid secretion during anesthesia. However, the onset and duration of action of famotidine following intravenous administration has not been extensively investigated. In the present study on 89 patients undergoing elective surgery, the effects of famotidine 20 mg administered intravenously 5-30 min before endotracheal intubation on pH and volume of gastric contents aspirated 0, 1, 2, and 4 hrs after tracheal intubation and immediately after extubation through nasogastric tube were compared with the effects of the drug administered intramuscularly one hour before endotracheal intubation. Famotidine administered intramuscularly 5-14 min before endotracheal intubation produced inadequate suppression of gastric secretion after tracheal intubation. In contrast, intravenous famotidine given 15-30 min before tracheal intubation, as well as the intramuscular administration of famotidine as premedication, effectively decreased gastric fluid volume and increased gastric pH. Suppression of gastric secretion by intravenous and intramuscular famotidine continued for over 4 hours. Intravenous famotidine has a rapid onset and a long duration of depressant action on gastric secretion, thus reducing the risk of aspiration pneumonitis during and after general anesthesia.

Effects of lidocaine on pulmonary circulation during hyperoxia and hypoxia in the dog.

BACKGROUND AND OBJECTIVES: High concentrations of lidocaine have been found to cause pulmonary vasoconstriction and low concentrations (0.5-0.9 microgram/mL) to cause reversal of nitrous oxide-induced depression of hypoxic pulmonary vasoconstriction. This study was undertaken to examine the effects of high concentrations of lidocaine on pulmonary circulation during hyperoxic and hypoxic ventilation. METHODS: With use of cross-circulation consisting of ventilation and constant-flow perfusion of the left lower lobe (LLL) independently of all other lobes of the dog lung under nitrous oxide and halothane anesthesia, lidocaine was infused into the inflow system, so that plasma lidocaine concentrations in the inflow blood were maintained at either 5, 10, 20, 40, 70, or 140 micrograms/mL during ventilation with 50% oxygen or 3% oxygen. Mean arterial and venous pressures in the LLL (PAPLLL and PVPLLL), airway pressure of the LLL, and blood gas in LLL inflow and outflow were measured. RESULTS: High plasma concentration of lidocaine (140 micrograms/mL) in the LLL inflow produced a significant increase in PAPLLL during hyperoxia, while PAPLLL did not change significantly at the 5-70-micrograms/mL lidocaine concentration. In LLL outflow blood, PO2 increased significantly following a 140 micrograms/mL lidocaine infusion during hyperoxia, while in LLL inflow blood, PO2 did not change. The airway pressure of LLL also did not change. During hypoxia, hypoxic pulmonary vasoconstriction did not occur, and lower plasma concentrations of lidocaine (40-70 micrograms/mL) significantly constricted the lobar vessels. In addition, lidocaine at the 140-micrograms/mL concentration constricted the upstream vessels (presumably the lobar arteries) more strongly than the lobar veins during hypoxia. CONCLUSIONS: Extremely high concentrations (140 micrograms/mL) but not low concentrations (5-70 micrograms/mL) of lidocaine produced pulmonary vasoconstriction and reduced shunt. Lower concentrations of lidocaine constricted the hypoxic lobar vessels.

Influence of alpha- and beta-adrenergic blockade on systemic and pulmonary hemodynamics during intravenous administration of local anesthetics.

The effects of alpha- and beta-adrenergic blockade on the systemic and pulmonary circulation during i.v. bolus injection of sub-seizure doses of lidocaine and bupivacaine were studied in dogs anesthetized with nitrous oxide. Pretreatment with hexamethonium or propranolol produced a marked decrease in cardiac output (CO), although pretreatment with phenoxybenzamine inhibited the decrease in CO during i.v. administration of lidocaine. Pretreatment with hexamethonium or phenoxybenzamine attenuated the increase in total peripheral resistance (TPR) following lidocaine 10 mg/kg i.v. In contrast, the propranolol-treated dogs developed a marked increase in TPR. The increases in mean pulmonary arterial pressure and pulmonary vascular resistance (PVR) following lidocaine 10 mg/kg i.v. were blocked by pretreatment with hexamethonium. Furthermore, PVR increased markedly with pretreatment with propranolol, although pretreatment with phenoxybenzamine prevented the large increase in PVR. These findings indicate that lidocaine has both a direct depressant effect and an indirect beta adrenergic stimulant effect on the heart. Systemic or pulmonary vasoconstriction following intravenous administration of lidocaine 10 mg/kg is associated primarily with an indirect stimulant effect mediated by alpha-adrenergic mechanisms. Bupivacaine, as well as lidocaine, has an indirect stimulant effect mediated by the autonomic nervous system.

Lung uptake of lidocaine during hyperoxia and hypoxia in the dog.

BACKGROUND: Lidocaine has been shown to accumulate in the lung following its administration. This study was undertaken to determine effects of dose of lidocaine on lung uptake during hyperoxic and hypoxic ventilation. METHODS: Using cross-circulation of ventilation and constant-flow perfusion of the left lower lobe independently from all other lobes of the dog lung under nitrous oxide and halothane anesthesia, lidocaine was infused into the inflow system, so that plasma lidocaine concentrations in the inflow blood were maintained at 5, 10, 20, 40 and 70 micrograms/ml respectively during ventilation with 50% O2 or 3% O2. During 20 micrograms/ml lidocaine infusion, indocyanine green (ICG), an intravascular marker, was mixed with the lidocaine solution, in such a fashion that plasma ICG concentration in the inflow blood was maintained at 20 micrograms/ml. Actual plasma lidocaine and ICG concentrations in blood drawn from the inflow ([Lid]pa,[ICG]pa) and the outflow ([Lid]pv,[ICG]pv)systems were measured, 1, 3, 5, 7 and 10 minutes after the beginning of lidocaine infusion. Percent lung uptake of perfused lidocaine was calculated as ¿1-([Lid]pv/[Lid]pa)/([ICG]pv/[ICG]pa)¿ x 100. RESULTS: During ventilation hyperoxia, mean percent lung uptakes of lidocaine were 41-52% 1 minute after the beginning of lidocaine infusion, and decreased in time-dependent fashion to 7-12% 10 minutes later. Curves of percent lung uptake of lidocaine over time were similar for the 5 predetermined lidocaine concentration groups (5-70 micrograms/ml). There were no significant differences in percent lung uptakes of lidocaine between the ventilation hyperoxia and hypoxia conditions. CONCLUSIONS: These findings suggest that percent lung uptake of lidocaine is unaffected by hypoxic ventilation and by varying the concentration of lidocaine in the perfusion through the recipient dog lung lobe.

Lidocaine-induced hemodynamic effects are enhanced by the inhibition of endothelium-derived relaxing factor in dogs.

BACKGROUND: Lidocaine has been shown to have direct vasoconstrictive effects at low concentrations. Since lidocaine inhibits endothelium-dependent vasodilation in vitro, the vasoconstrictor effect of lidocaine may be due to inhibition of endothelium-derived relaxing factor(EDRF/NO). Therefore, the current study was designed to determine the effects of NG-nitro-L-arginine (L-NNA), a potent inhibitor of nitric oxide synthase, on systemic and pulmonary hemodynamics during lidocaine infusion. METHODS: Systemic and pulmonary hemodynamic effects of lidocaine infusion, 1 mg.kg-1.min-1, for 10 min were measured in dogs anesthetized with 1% halothane in oxygen. Dogs were studied twice with an interval of 1 week in a cross-over study, and were assigned to one of two groups that received saline or L-NNA intravenously in group 1 (n = 8), or L-NNA or L-NNA + L-arginine which reverses the nitric oxide synthesis inhibitor effect of L-NNA, intravenously in group 2 (n = 8) prior to lidocaine infusion. The free serum concentration of and protein-binding ratio for lidocaine were measured. RESULTS: With saline pretreatment in group 1, lidocaine infusion significantly decreased cardiac index (CI) and significantly increased mean pulmonary arterial pressure (MPAP), pulmonary arterial occlusion pressure (PAOP), systemic vascular resistance (SVR) and pulmonary vascular resistance (PVR). L-NNA pre-treatment in group 1 significantly enhanced the changes in CI, MPAP, PAOP, SVR and PVR during lidocaine infusion. In group 2, L-arginine infusion partially offset the additive effects of L-NNA to the depressive effects of lidocaine. There were no significant differences in free serum concentration of or protein-binding ratio for lidocaine among the groups. CONCLUSION: In contrast to in vitro study, vasoconstrictor effect of lidocaine is enhanced when a capacity for compensatory vasodilation including EDRF/NO pathway is exhausted in halothane-anesthetized dogs.

Effects of isoflurane on myocardial blood flow, function, and oxygen consumption in the presence of critical coronary stenosis in dogs.

Because isoflurane has been reported to produce coronary steal, we studied 12 open chest, anesthetized (pentobarbital) dogs with critical stenosis (CS) of the left circumflex coronary artery (LCA). Sonomicrometers were implanted to measure systolic wall thickening, myocardial blood flow (MBF) was measured with microspheres (15 microns diameter), and regional venous sampling was performed to estimate regional oxygen extraction and myocardial oxygen consumption (MVO2). Anesthetic concentrations of isoflurane reduced arterial blood pressure dramatically, resulting in a maldistribution of MBF distal to the CS consistent with the pattern characterizing a transmural coronary steal effect. Elevation of arterial blood pressure with phenylephrine during high concentration isoflurane (1.7 +/- 0.1%) augmented MBF, but the maldistribution distal to the CS persisted. Despite the maldistribution, however, there was no indication of ischemia in the LCA region because systolic wall thickening, oxygen extraction, and MVO2 were not significantly different between the LCA and left anterior descending coronary artery (LAD) (control) areas. Because wall thickening, oxygen extraction, and MVO2 were markedly reduced by isoflurane in both the LCA and control areas, it was concluded that isoflurane substantially reduced myocardial oxygen requirements by inducing myocardial depression, reducing heart rate, and decreasing afterload. Consequently, the apparent maldistribution of LCA blood flow (coronary steal) was due to the hemodynamic and vasodilatory effects of isoflurane, but did not result in ischemia because the level of blood flow was at or above the requirements of the myocardium.