A random sampling of 160 patients in a chronic disease facility showed that 36 patients (22.5 percent) had chronic hyponatremia. Their mean age was 72 years (range, 42–94 years); 75 percent of the patients were more than 65 years old. Women comprised 57 percent of the group. The mean serum sodium level was 120 mEq/L (range, 109–135 mEq/L). The mean serum osmolarity was 270 mOsm/L (range, 251–294 mOsm/L). Of the 36 patients, 9 were asymptomatic. Symptoms were associated with underlying disorders rather than with hyponatremia, although in 9 patients the hyponatremia appeared to have intensified existing symptoms. The most common cause of hyponatremia (in 41.6 percent of 20 overhydrated patients) was inappropriate secretion of antidiuretic hormone (IADH syndrome). Factors accounting for the high incidence of IADH were the age of the patient and the nature of the underlying disorders, particularly diseases associated with aging. Simple measures were used to manage the hyponatremia, e.g., water restriction for patients who were overhydrated; replacement of sodium chloride for patients who were losing salt excessively and had a low sodium intake; and control of hyperglycemia in the pseudohyponatremic patients with hyperglycemia. No treatment was required for pseudohyponatremia associated with hyperlipidemia. When hyponatremia was due to drug‐induced ADH excess, the involved drug was discontinued. Emphasis on management of the patients' primary disorders also ameliorated the hyponatremic state.

No abstract

The APS Journal Legacy Content is the corpus of 100 years of historical scientific research from the American Physiological Society research journals. This package goes back to the first issue of each of the APS journals including the American Journal of Physiology, first published in 1898. The full text scanned images of the printed pages are easily searchable. Downloads quickly in PDF format.

Alternans of the elevated ST segment (STEA) was found in 8 of 21 patients (38%) with Prinzmetal's variant angina. In addition to STEA, all eight patients had varying cardiac arrhythmias: multiple premature ventricular depolarizations in eight, ventricular tachycardia in five, and ventricular fibrillation in three. There was no consistent temporal relationship between the occurrence of STEA and the cardiac arrhythmias. Alternans occurred during periods when no arrhythmias were present. All eight patients underwent coronary angiography. Spontaneous coronary artery spasm was documented angiographically in three patients including two who had minimal or no coronary atherosclerotic disease. Six patients had severe, fixed, occlusive coronary artery disease. Possible mechanisms for STEA include: 1) failure of regions of myocardium to depolarize on alternate beats due to variation in conduction and refractoriness between ischemic and nonischemic zones of myocardium, and 2) electrical alternans of the transmembrane action potential during phase 2 and 3 (repolarization) caused by changes in the rate and extent of electrolyte transfer across cell membranes during ischemia. It is postulated that STEA is an electrocardiographic sign in the surface ECG of a dysequilibrium of refractory periods during ischemia and reflects an unstable electrical state of the myocardium.