The importance of the cardiopulmonary monitoring, particularly the right ventricular function, in patients who are suffering from COPD, pulmonary heart disease, mitral and/or aortic valve disease and coronary artery disease with emphasis on the basic consideration of the right ventricular performance characteristics are discussed. The indications, risks and complications related to the cardiopulmonary monitoring are also presented.

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It is well known that hyperthermia above 41°C rarely occures in ordinary pysiological state and that, the course of patient will be always grave with fatal outcome under high body temperature exceeding 42°C
During induced-hyperthermia above 42°C, animal (dog or monkey) evidenced respiratory depression, insufficiency of cardiovascular system, metabolic and respiratory acidosis, elevation of serum enzymes, lacticidemia and hyperkalemia.
In clinical investigations of fatal cases with hyperthermia (Malignant hyperthermia and heatstroke), thrombcytopenia and disturbances of clotting factors were observed, and autopsy findings consisted of widespread haemorrhages, congestion and cellular degeneration in numerous organs, oedema in brain and lung, and nerosis in brain and kidney.
These investigations revealed that hyperthermia exceeding about 42°C involving all organs caused multiple organ failure and irreversible changes in tissues.
So, it is suggested that body temperature of about 42°C is critical temperature for living body under hyperthermia.
These organ failure and tissue damage occuring in fatal hyperthermia might be explained by heat-induced cellular damage that, under high temperature, fat and protein in the cell undergo irreversible conformational changes.

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Evidence in now available to demonstrate that most inhalational anesthetics which were considered to be inert until early in 1960 are metabolised in the body. Biotransformation of the volatile anesthetics clinically used has become an area of interest to the anesthesiologist, since the problems of possible toxic effects produced by anesthetic metabolites on vital organ systems such as liver and kidney are generally concerned. This lecture was mainly divided into four sections:
a) Biotransformation system of drugs including anesthetics and factors influencing anesthetic-associated organ toxicity.
b) Metabolism of inhalational anesthetics.
c) Metabolism of narcotic analgesics.
d) Mechanism of toxic injury produced by anesthetics.
Firstly, some important key words such as biotransformation, cytochrome P₄₅₀ system, enzyme induction, free radical formation, and covalent binding were explained, Secondly, the metabolism of the inhalational anesthetics such as diethyl ether, trichloroethylene, chloroform, halothane, fluroxene, methoxyflurane, enflurane, and nitrous oxide associated with new volatile anesthetics such as isoflurane and sevoflurane were reviewed. In addition, author's new data regarding the metabolism of fentanyl in man, were also demonstrated, since this narcotic is now widely used in the clinical anesthesia.
Finally, mechanism of toxic injury such as nephrotoxicity, hepatotoxicity, and bone marrow disturbances associated with anesthetics were discussed.

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65-years-old male was undergone partial gastrectomy, cholecystectomy and intraoperative radiotherapy under laparotomy for the pancreas head carcinoma.
On the postoperative 11th day, the severe intraabdominal bleeding occured. At the operating room, he was already hemorrhagic shock. His abdomen was expanded and the systolic blood preessure of femoral artery was 40mmHg. Inspite of the blood and fluid transfusion and injection of vasopressors.
Before the laparotomy, the cross-clamping ata the discending aorta was done under thoracotomy. An artery on the pancreashead was injured and after its ligation, blood pressure was rised and urine flowed out even after ten minutes of the clamping.
He had smooth recovery and no complications developed.

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Severe hypotention occurred twice immediately after protamine administration in a patient who underwent coronary artery bypass graft surgery. The cause of the first hypotensive episode is not clear, but that of the second crisis was thought to be due to the spasm which occurred in the left main coronary artery. The coronary artery is said to be susceptible to spasms after extracorporeal circulation, which was the case with this patient.
Protamine or protamine-heparin interaction increases the plasma level of C_3a and C_5a, which are products of complement activation, after its administration. These two compounds induce vasospasm, increase vascular permeability and contract smooth muscles. Thus, protamine administration may have played a role in the coronary artery spasm that occurred in this patient.
After the second crisis, protamine was not administered to reverse heparin. The postoperative course was uneventful and bleeding was controlled well.
Authors suggest that, though there is a risk of postoperative bleeding, heparin may not need to be reversed in a similar situation.

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The purpose of this study was to investigate wakefulness during induction of anesthesia with high dose fentanyl by using the isolated forearm technique. Thirty six patients scheduled for elective cardiac surgery were divided into five groups according to the methods of premedication or induction of anesthesia. The patients in group I-III were premedicated with morphine (0.15mg/kg) and scoplamine (0.4-0.5mg) intramuscularly one hour before the operation, while those in group IV and V were premedicated with hydroxyzine (50-100mg) and scoplamine, and pethidine (17.5-35mg) was added to group V. Anesthesia was induced with intravenous drip injection of fentanyl (100μg/kg) over a 15 minute period in all patients. Following 10μg/kg of fentanyl, diazepam (0.1mg/kg IV) was added to group II and 50% N₂O in oxygen administrated to group III.
In group I, 7 out of 11 patients responded to verbal commands after 100μg/kg of fentanyl. One out of 5 patients in group II and 2 out of 7 patients in group III responded to verbal commands after 75μg/kg and 50μg/kg of fentanyl, respectively.
In group IV and V, none of the responses was detected after 25μg/kg of fentanyl. Most or patients in group IV, V were sedated adequately or were sufficiently sleepy before the operation. There were some complications such as tachycardia, rigidity and hypotension in proup I-III.
We conclude that patients undergoing high dose fentanyl anesthesia should be well sedated before the operation in order to obtain smooth induction and to prevent wakefulness during anesthesia.

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The effects of orally administreted atropine for the premedication of anesthesia were investigated in the children (ASA1-2). Commercically ampled atropine sulfate was given orally (0.036mg/kg) or intramuscullary (0.017mg/kg). Obviously, the drying effect on the respiratory tract was observed in the same degree in both groups treated with atropine, compared to the control group. Neither undesirable reflex during endotracheal intubation nor abnormal rise in body temprature was recognized.
In consideration of the painful stimulus and the damage to muscule due to intramuscula injection of atropine, the oral administration of commercially ampled atropine sulfate is more appropriate for the premedication of pediatric anesthesia than intramuscular injection.

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