Correction Of Hyperkalemia Research Articles

Correction of hyperkalemia by bicarbonate despite constant blood pH

Patients having hyperkalemia often are given bicarbonate to raise blood pH and shift extracellular potassium into cells. Blood pH in many hyperkalemic patients, however, is compensated. To determine whether bicarbonate, independent of its pH action, affects plasma potassium, 14 hyperkalemic patients were treated with bicarbonate in 5% dextrose. In five patients (changed pH group), blood pH rose at least 0.08, while in nine (constant pH group), it changed less than 0.04. In the first group, pH rose 0.12, bicarbonate rose 5.9 mEq/liter, and plasma potassium fell 1.6 mEq/liter, and plasma potassium fell 1.4 mEq/liter. The correlation between changes in plasma potassium and bicarbonate was identical in the two groups and independent of urinary potassium excretion. Four additional patients, who were treated with 5% dextrose alone, did not significantly lower their plasma potassium, although subsequent treatment with bicarbonate in 5% dextrose lowered their plasma potassium. Thus, bicarbonate lowers plasma potassium, independent of its effect on blood pH, and despite a risk of volume overload, should be used to treat hyperkalemia in compensated acid-base disorders, even in the presence of renal failure, provided the plasma bicarbonate concentration is decreased.

Amelioration of metabolic acidosis with fludrocortisone therapy in hyporeninemic hypoaldosteronism.

In four patients with renal hyperchloremic acidosis and hyperkalemia, hyporeninemic hypoaldosteronism and chronic renal insufficiency (glomerular filtration rates of 13, 31, 35 and 44 ml per minute per 1.73 m2), prolonged administration of fludrocortisone increased urinary potassium and net acid excretion, corrected hyperkalemia and substantially ameliorated acidosis. Except in the patient with the lowest glomerular filtration rate, the increased net acid excretion was due mostly to increased ammonium excretion. Urine pH decreased initially in each patient, but in the three patients with the highest filtration rates, it increased subsequently as ammonium excretion increased, indicating that renal ammonia production increased. Urinary ammonium excretion correlated inversely with serum potassium concentration and did not decrease on discontinuation of therapy if hyperkalemia was prevented from recurring. In patients with renal acidosis and hyporeninemic hypoaldosteronism, administration of mineralocorticoid hormone can augment both renal hydrogen-ion secretion and, by correction of hyperkalemia, renal ammonia production, and thereby ameliorate metabolic acidosis.

Atrioventricular and intraventricular conduction in hyperkalemia

Twelve patients exhibited electrocardiographic evidence of fascicular block during hyperkalemia. Isolated left posterior hemiblock occurred in four, isolated left anterior hemiblock in two, right bundle branch block with left anterior hemiblock in two, right bundle branch block with left posterior hemiblock in one, left bundle branch block with abnormal left axis deviation in two and advanced atrioventricular block in one. In all seven patients with sinus rhythm the P-R interval shortened after correction of hyperkalemia. Electrophysiologic studies using His bundle recording and atrial pacing in one patient revealed intraatrial conduction delay and marked prolongation of conduction time in the His-Purkinje system. It is concluded that conduction defects in the specialized intraventricular conduction system are common in hyperkalemia and result in electrocardiographic patterns of fascicular block.

THE ROLE OF THE ANAESTHETIST IN THE MANAGEMENT OF ACUTE RENAL FAILURE

SUMMARY The problems encountered by the anaesthetist in the treatment of patients with acute renal failure are discussed. The diagnosis and initial treatment are reviewed, with special emphasis on the treatment of hyperkalaemia and overhydration. The treatment with mannitol in the early phase of uraemia is discussed. Uraemic patients can be safely transported over long distances provided a free airway, sufficient ventilation, a stable circulation and correction of hyperkalaemia are established. Cardiac arrest is common in patients with uraemia especially in connection with obstructive jaundice, hypoxaemia and electrolyte disturbances. The most common provocative cause of cardiac arrest is a vasovagal reflex elicited by endotracheal suction. Pulmonary complications leading to respiratory insufficiency are a major risk. Artificial ventilation should be instituted before the patient becomes exhausted, and before carbon dioxide tension rises above normal levels. The main points in the prevention of complications during and after anaesthesia are: early and active treatment of uraemia with dialysis, sufficient atropinization, the most meticulous avoidance of hypoxia and carbon dioxide retention, a careful replacement of any fluid loss and avoidance of overhydration. Postoperatively the patient must be under continuous observation until he is fully awake and the respiration is completely restored.