BACKGOUND: During apnea, as in any other acid-base disturbance, ion exchanges between intra- and extracellular compartments are expected, but few studies have reported such findings. The purpose of this study was to observe serum sodium, potassium, chloride and bicarbonate concentrations during apnea until death. METHODS Seventeen New Zealand White Rabbits (weight 2.0~3.0 kg) were subjected to apneic oxygenation. Then we measured heart rate, blood pressure, intracranial pressure, arterial blood gas analyses and serum electrolytes (sodium, potassium, chloride and bicarbonate) concentrations during apnea until death. RESULTS Heart rate decreased because of sinus bradyarrythmia at 10 minutes after apnea and thereafter continued to increase. Blood pressure increased up to 30 minutes after apnea and thereafter continued to decrease.
Intracranial pressure consistently increased during apnea.
Serum bicarbonate and chloride ion concentrations showed reciprocal changes, but there was no significant correlation. Serum sodium and potassium concentrations increased up to 40 minutes and 30 minutes respectively, and thereafter decreased until death. All serum ion concentrations were within normal limits. CONCLUSION The serum sodium, potassium, chloride and bicarbonate concentrations were maintained within normal limits during apneic oxygenation until death.
Malignant hyperthermia (MH) is an inherited skeletal muscle disorder characterized by hypermetabolism, muscle rigidity, rhabdomyolysis, fever, metabolic acidosis and death if untreated. The syndrome is believed to result from abnormal control of intracellular calcium ions in the skeletal muscle: on exposure to certain anesthetics, calcium level is increased, and then it activates contractile processes and biochemical events that support muscle contraction. We experienced a MH of 2 years-old male who had release of sternocleidomastoid muscle due to torticolis under general anesthesia. Anesthesia was induced with thiopental and succinylcholine, maintained with enflurane, nitrous oxide and oxygen (2 volume%: 2 L/min: 2 L/min). After induction of anesthesia, his heart rate, end-tidal CO2 tension and body temperature had been gradually increased and then those were reached to maximal value of heart rate (160~170 BPM), end-tidal CO2 tension (60~70 mmHg) and body temperature (41degrees C) 55 minutes later. He was immediately managed with symptomatic treatment such as hyperventilation with oxygen, cooling, beta-blocker, sodium bicarbonate and diuretics, so he was survived without any sequelae.