[Early recognition of malignant hyperthermia using capnometry]. / Früherkennung einer malignen Hyperthermie durch Capnometrie.

Although malignant hyperthermia is still a potentially fatal disease that was marked by a high mortality until recently, lasting damage to the patient can now be prevented by early diagnosis and treatment. The following case demonstrates the special value of capnometry in diagnosing this condition. A 34-year-old man admitted for oral surgery showed symptoms of malignant hyperthermia 5 h after induction of anesthesia. Neuroleptanalgesia had been conducted. The patient had received thiopental and fentanyl for induction of anesthesia and alcuronium and succinylcholine for intubation. The first symptom noticed was an elevation of the end-tidal pCO2 as monitored by capnometry. Additional symptoms, such as a pronounced rise in temperature, blood pressure, and heart rate did not develop until 20-25 min later. The end-tidal oxygen concentration decreased from 30 vol.-% to 26 vol.-%. The patient had to be ventilated with a volume of 25 l/min to keep end-tidal pCO2 under 6 kPa. Treatment with dantrolene was started immediately. Not until 3 h after the onset of the first symptoms did the patient's body temperature and the minute volume needed for ventilation return to normal. Postoperative laboratory findings showed only a slight elevation of creatine kinase and serum lactate. Myoglobin was not detected in serum or urine. This case indicates that capnometry permitted immediate adaptation of controlled ventilation to the patient's increased metabolic rate and early initiation of dantrolene treatment, thus preventing more severe disorders and possible consequences for the patient. Other studies have also suggested the special importance of capnometry. Since the patient refused to give his consent, the diagnosis could not be ascertained by muscle biopsy, and had to be based on symptoms.

Effects of thoracic epidural anesthesia on systemic hemodynamic function and systemic oxygen supply-demand relationship.

The effects of thoracic epidural anesthesia (TEA) on total body oxygen supply-demand ratio are complex due to potential influences on both O2 delivery (QO2) and consumption (VO2). One hundred and five patients undergoing abdominal aortic surgery were randomly assigned to one of three groups to compare the cardiovascular and metabolic responses associated with (1) thoracic epidural anesthesia plus light general anesthesia (group TEA); (2) general anesthesia with halothane (group H); and (3) neuroleptanalgesia (group NLA). Values of cardiac index (CI) and QO2 were less intraoperatively in the TEA group than in the H or NLA groups, while VO2 values were similar. VO2 during recovery was greater in both the TEA and NLA groups than in the H group. Consequently the oxygen supply-demand ratio (QO2/VO2) was less in the TEA group throughout the perioperative period and about 30% below baseline values during early recovery. At comparable VO2, CI and mixed venous O2 saturation were always less in the TEA group than in the NLA group. Heart rate was slowest intraoperatively during TEA, and stroke work was less with TEA than with NLA. As cardiac filling pressure and systemic vascular resistance did not differ among the three groups, reduced adaptation of CI to tissue O2 needs during TEA was attributed to negative inotropic and chronotropic effects of the sympathetic blockade. We conclude that in patients undergoing abdominal aortic surgery, TEA has no apparent advantage over general anesthesia.

The effect of dopamine on muscle PO2 in healthy volunteers and intensive care patients.

The effect of systemic dopamine administration (2-10 micrograms kg-1 min-1) on the Po2 distribution (histograms) and the mean Po2 in the m. vastus lateralis of m. quadriceps femoris in nine healthy volunteers and seven critically ill patients has been studied with a newly developed bedside measuring procedure. Dopamine initially raised mean muscular Po2 in both groups. In the volunteers, mean muscular Po2 thereafter decreased gradually but still remained slightly elevated after 30 min of dopamine infusion. This increase in muscle oxygenation could be abolished by the administration of a dopamine antagonist (metoclopramide). In the patients, the initial dopamine-induced increase of Po2 was significantly slower and reached a plateau within 30 min. The results are discussed with special attention given to the data available on the action of dopamine on given peripheral circulation.