Effect Of Low Potassium Research Articles

A propensity-matched study of the association of low serum potassium levels and mortality in chronic heart failure

Potassium homeostasis is essential for normal myocardial function, and low serum potassium may cause fatal arrhythmias. However, the association of low potassium and long-term mortality and morbidity in heart failure (HF) is largely unknown. We studied 6845 HF patients in the Digitalis Investigation Group trial with serum potassium levels < or =5.5 mEq/L. Of these, 1189 had low potassium (<4 mEq/L). Propensity scores for low potassium were calculated for each patient and were used to match 1187 low-potassium patients with 1187 normal-potassium (4-5.5 mEq/L) patients. Effects of low potassium on outcomes were assessed using matched Cox regression analyses. All-cause mortality occurred in 379 (rate, 1103/10 000 person-years) normal-potassium and 441 (rate, 1330/10 000 person-years) low-potassium patients, respectively, during 3437 and 3315 years of follow-up [hazard ratio (HR), 1.25; 95% confidence interval (CI), 1.07-1.46; P = 0.006]. Cardiovascular mortality occurred in 297 (864/10 000 person-years) normal-potassium and 356 (1074/10 000 person-years) low-potassium patients (HR, 1.27; 95% CI, 1.06-1.51; P = 0.009). Cardiovascular hospitalization occurred in 610 (rate, 2553/10 000 person-years) normal-potassium and 637 (rate, 2855/10 000 person-years) low-potassium patients (HR, 1.13; 95% CI, 0.99-1.29; P = 0.082). In a cohort of ambulatory chronic systolic and diastolic HF patients who were balanced in all measured baseline covariates, serum potassium <4 mEq/L was associated with increased mortality, with a trend towards increased hospitalization.

Effects of low potassium or magnesium concentrations on isolated cardiac tissue

Low potassium and magnesium concentrations not only cause cardiac arrhythmias, but also interfere with the efficacy or enhance the toxicity of drugs commonly used to treat patients with heart disease. Arrhythmias may develop in hypokalemia due to enhanced normal automaticity, abnormal automaticity, or slowed conduction; moreover, hypokalemia is associated with enhanced digitalis toxicity, quinidine-related Torsades de pointes, and interference with the antiarrhythmic activity of quinidine. Hypomagnesemia, especially in the presence of other electrolyte abnormalities, also affects automaticity and is associated with decreased efficacy of digitalis and with quinidine-related Torsades de pointes. Therefore, treatment that controls hypertension without causing electrolyte abnormalities is preferable for patients who are at risk of arrhythmias, or who are receiving drugs such as digitalis or quinidine.

Effect of restricted potassium intake on its excretion and on physiological responses during heat stress.

The effect of low potassium (K+) intake on its excretion, concentration in sweat and on physiological responses during heat stress was evaluated on eight Indian male soldiers in winter months at Delhi. After a stabilization period of 3 days on each diet, i.e., 85 mEq of K+/d (diet I, normal), 55 mEq of K+/d (diet II), and 45 mEq of K+/d (diet III), the physiological responses and the sodium and potassium concentrations in sweat, plasma, RBC, and urine were measured when the subjects were exposed to heat for 3 h daily in a climatic chamber maintained at 40 degrees C DB and 32 degrees C WB. The subjects worked in the chamber at the rate of 465 W/h for 20 min periods with 40 min rest between each period of exercise. The whole body sweat was collected after the spell of work and was analysed for sodium and potassium levels. Throughout the study the subjects remained on positive sodium balance except on day 4 in diet III. Fluid balance also remained positive while potassium balance was negative in subjects on diet II and diet III. There was no significant change in heart rate, sweat volume, oral temperature, sodium, and potassium concentrations in plasma and RBC during the entire period of the study. Even in the subjects with negative potassium balance there was no change in the sodium and potassium concentrations in sweat during exercise in heat. The only evidence of potassium conservation was a reduced excretion in urine. Out of the eight subjects, in one subject there was a flattening of the 'T' wave in the ECG and reduction in amplitude of the 'T' wave in two more subjects. As there is no reduction in sweat potassium concentration and the urine volume is low, the marginal level of reduced excretion of potassium in urine with a high rate of sweating (7-81) in subjects doing work in the tropics, there is every likelihood of potassium deficiency if a liberal intake is not ensured. In our earlier studies (Malhotra et al. 1976) we found that the concentration of potassium (K+) in sweat is much higher than in plasma even in acclimatised subjects. A large amount of K+ is therefore likely to be lost in sweat during exposure to heat. In that study there was no evidence of a reduction in K+ concentration in the sweat or urine upon repeated exposure of the subjects to heat, indicative of a compensatory mechanism for conservation of K+ losses. However, these earlier studies were done on subjects who were on a normal diet which contained 75-80 mEq of K+ per day. Since a compensatory mechanism may be triggered only when the body K+ becomes dificient and not earlier, as is the case with sodium (Malhotra et al. 1959), we have now investigated the effects of a sequential reduction of reduced dietary K+ on the dermal and urinary losses of K+. The effects of K+ deficiency on the physiological responses to heat have also been studied. The results of these studies are reported here.