Akito Ohmura

Anesthetic management for separation of craniopagus twins.

In 1967 Keats et all reviewed the published data on anesthetic management for separation of conjoined twins. Of the 21 cases reported, five were for separation of craniopagus twins. Since the incidence of births of conjoined twins is estimated at 1:50,000 live births with a distribution of thoracopagus (including xiphopagus and omphalopagus) 73%, pygopagus 19%, ischiopagus 6%, and craniopagus 2%, the review of Keats et all suggested a surprisingly large number of craniopagus twins who had been subjected to surgical separation. A more recent review of anesthetic management of conjoined twins reported 17 cases from 1965-1974 including two cases of craniopagus twins,2 but there were no specific comments on anesthetic management referable to these two cases performed in South Africa (Cywes, 1966) and in France (Pertuiset, 1974).2 We report our experience in the management of craniopagus twins that finally led to their successful separation on May 29, 1979.

Effects of Hypocarbia and Normocarbia on Cardiovascular Dynamics and Regional Circulation in the Hypothermic Dog

The effects of carbon dioxide on the cardiovascular system, cerebral, mesenteric, and renal blood flows, and total-body oxygen consumption under surface-induced hypothermia to 24 C were evaluated in 12 dogs. In Group I (six dogs), PaCO, was allowed to decrease from 35 to 18 torr during cooling without the addition of CO2 to the inspired gas mixture. In Group II (six dogs), CO2 was added to the inspired gases to maintain Paco, 34–38 torr during cooling. Arterial blood pH increased in Group I (7.39 to 7.50), while it decreased in Group II (7.35 to 7.27). Cardiac index decreased markedly with cooling in Group II, from 3.37 to 1.18 1/min/m2, while it showed an initial increase in Group I at 34 C, followed by a decrease to 1.62 1/min/m2 at 24 C. Stroke index did not change significantly, but heart rate decreased significantly in either group, with Group II showing a greater decrease. Mean arterial pressure was significantly decreased in either group from about 120 to 80 torr, but there was no significant differences in mean arterial pressures between groups at the same hypothermic temperatures. Mean pulmonary arterial and pulmonary capillary wedge pressures were essentially unchanged in both groups. Pulmonary vascular resistance showed significantly greater increases in Group II than in Group I. Internal carotid arterial blood flow was significantly greater in Group II than in Group I, but there was no difference in renal or superior mesenteric arterial blood flows between the two groups. Total-body oxygen consumption in either group decreased from about 127 ml/min/m2 at 37 C to 41 at 24 C, and there was no significant difference between groups. These results suggest that adding CO2 to the inspired gases to maintain normal Paco2 during hypothermia may be desirable for cerebral perfusion but harmful to the cardiovascular system.

Epinephrine-induced arrhythmias: effect of exogenous prostaglandins and prostaglandin synthesis inhibition during halothane-O2 anesthesia in the dog.

Prostaglandins (PG) modify sympathetic and parasympathetic neurotransmission and have antiarrhythmic properties. Inhibitors of PG synthesis sensitize the heart to certain experimentally induced arrhythmias. This study examined the arrhythmogenic dose (AD) of epinephrine n dogs during halothane-O2 anesthesia as modified by the infusion of PG and by treatment with an inhibitor of PG synthesis.Dogs were anesthetized with 1.25 MAC halothane. The AD of epinephrine was established by a series of 3-minute epinephrine infusions at 10-minute intervals. The AD of epinephrine was then redetermined during infusions of PG (PGE1—1 μg/kg/min and PGF2 alpha—1 μg/ kg/min), after indomethacin, 3 mg/kg, and after aminophylline, 10 mg/kg. The AD remained unchanged from control during both of the PG infusions and following indomethacin. Only Following aminophylline did the AD decrease significantly.Our study suggests that pretreatment of surgical patients with nonsteroidal antiinflammatory drugs which inhibit PG synthesis does not increase the likelihood of ventricular arrhythmias during halothane-O2 anesthesia.

Centrally induced sympathetic dystrophy of the upper extremity.

a right atrial catheter, in order to ensure that the catheter has not moved into the right ventricle. Furthermore, it should be anticipated that neck flexion also might result in caudad displacement of other catheters that pass through the neck, such as those used for administration of blood, drugs, or hyperalimentation solutions. Intracardiac catheters, such as a Swan-Ganz catheter, might also be subjected to displacement into a wedge position within the pulmonary circulation. Central venous and right atrial catheters introduced via peripheral veins in the extremities would not be subject to the effects of neck flexion. However, it is possible that cephalad movement of the diaphragm and mediastinal contents, resulting from surgical packs within the abdomen, or the extreme head-down position, also might produce the relative caudad displacement of such catheters. Reports 373

Deep hypothermia and circulatory arrest: effect on cerebrospinal fluid electrolytes in newborn lambs.

Abstract Cerebrospinal fluid (CSF) Na, K, and acid-base changes were studied in 13 new-born lambs anesthetized with α-chloralose (60 mg/kg) or diethylether during 90 min of normothermic (37 °C) or hypothermic (20 °C) circulatory arrest. CSF K concentration increased linearly from 3.1 to 23.2 meq/liter during 90 min of normothermic circulatory arrest. During hypothermic circulatory arrest, animals anesthetized with α-chloralose exhibited an exponential increase in CSF K concentration from 3.1 to 13.6 meq/liter and animals anesthetized with diethylether had an exponential increase in CSF K concentration from 3.3 to 12.7 meq/liter. The rate of increase in CSF K concentration in hypothermic and normothermic animals between 60 and 90 min of circulatory arrest was the same. CSF Na concentration decreased slightly in both hypothermic and normothermic animals, with a greater decrease in the normothermic group. Although CSF pH and bicarbonate were significantly decreased during normothermia as well as hypothermia, both CSF pH and bicarbonate showed greater decreases during normothermia. Mean pH values after 90 min of circulatory arrest were 6.34, 6.87, and 6.77, respectively, in the normothermic, α-chloralose-hypothermic, and diethylether-hypothermic groups; corresponding values for bicarbonate were 7.7, 13.8, and 12.2 meq/liter. CSF pCO2 increased linearly from 40.2 to 190.0 Torr during 90 min of normothermic circulatory arrest, from 28.6 to 92 Torr in the ether-hypothermic group, and from 28 to 81 Torr in the α-chloralose-hypothermic group.

Hypoxic pulmonary vasoconstriction and the pharmacologically denervated lung

The roles of the autonomic nervous system and cardiac output on hypoxic pulmonary vasoconstriction were studied in 15 mongrel dogs anaesthetised with intravenous pentoharbitone (30 mg/kg) and the lungs mechanically ventilated to maintain normal arterial blood gases. After a hypoxic challenge in Group I (n =6) and Group II (n =3) animals, autonomic denervation was achieved by total spinal block with tetracaine (20 mg) injected into the cisterna magna. Group I animals received a large volume of intravenous fluid (80 ml/kg normal saline) before the block while Group II animals were given minimum fluid. When Group I animals were exposed to 10% inspired oxygen, mean pulmonary arterial pressure increased by 88 and by 72% before and after the block, respectively. The cardiac output increased by 27% with hypoxia before the block while it did not change significantly with hypoxia after the block. The pulmonary vascular resistance increased by 65 and by 152% with hypoxia before and after the block. Group II animals were also exposed to 10% inspired oxygen. They showed a similar response to Group I animals before the block. However, after the block irreversible hypotension developed with hypoxia.

CARDIAC EFFECTS OF SUCCINYLDICHOLINE AND SUCCINYLMONOCHOLINE

SummaryThe present study evaluated possible contribution of succinylmonocholine in producing serious cardiovascular effects with or without succinyldicholine, using albino rabbits as the experimental animal. Forty-eight experiments were performed, 22 in vivo and 26 in vitro (Langendort heart).Succinyldicholine and succinylmonocholine administered separately or together, produced an immediate bradycardia in vivo as well as in vitro. The combination of these drugs had a direct arhythmogenic effect as well as an indirect reflex mediated cardiac effect. When succinyldicholine was given within five minutes following a dose of succinylmonocholine there was significant nodal and ventricular ecto-pic beats, but no bradycardia. Dysrhythmias in in vivo hearts were abolished by cord trans-section, trimethaphan and reserpine pretreatment. There was no evidence in vivo that succinylmonocholine produced more serious bradycardia, dysrhythmias or hypotension than succinyldicholine.RésuméNous avons étudié les effets cardiovasculaires de la succinylmonocholine employée isolément ou en association à la succinyldicholine, ceci chez le lapin albinos.En tout 48 expériences ont été faites, soit 24 in vivo et 24 in vitro (cœur de Langendort).In vivo et in vitro, la succinyldicholine et 1a succinylmonocholine utilisées séparément ou en association produisaient une bradycardie immédiate. L’association des deux agents, en plus des effets indirects réflexes, était suivie fréquemment d’extra-systoles. Une injection de succinyldicholine donnée en dedans de cinq minutes après une dose de succinylmonocholine était fréquemment suivie d’extrasystoles ventriculaires ou de rythme jonctionnel mais ne produisait pas de bradycardie.L’on pouvait abolir les troubles du rythme in vivo, soit par une section médullaire, soit par l’administration préalable de trimethapan ou de réserpine. In vivo, la succinyldicholine ne semblait pas produire plus de troubles du rythme, d’hypotension ou de bradycardie que le succinylmonocholine.