Concentrated potassium chloride infusions in critically ill patients with hypokalemia.

Although concentrated infusions of potassium chloride commonly are used to treat hypokalemia in intensive care unit patients, few studies have examined their effects on plasma potassium levels. Forty patients with hypokalemia were given infusions of 20 mmol of potassium chloride in 100 mL of normal saline over 1 hour; 26 patients received the infusions through the central vein and 14 patients through the peripheral vein. Plasma potassium ([K]p) was measured at 15-minute intervals during and after the infusion in 31 patients. delta K was defined as the difference between each potassium determination and baseline plasma potassium concentration. Continuous electrocardiographic recording was carried out during the infusion and during the 1-hour period immediately preceding the infusion. Mean baseline [K]p was 2.9 mmol/L and all subsequent plasma concentrations significantly increased from baseline. Mean peak [K]p was 3.5 mmol/L, [K]p (1 hour postinfusion) was 3.2 mmol/L, and mean postinfusion delta K was 0.48 mmol/L (range -0.1-1.7 mmol/L). Arrhythmias, changes in cardiac conduction intervals, and other complications did not occur. The frequency of premature ventricular beats decreased significantly during the infusion compared with that of the control period. The high concentration (200 mmol/L) and rate of delivery (20 mmol/hr) of the potassium chloride infusions were well tolerated, decreased the frequency of ventricular arrhythmias, and did not cause transient hyperkalemia.

A direct relationship between ionized calcium and arterial pressure among patients in an intensive care unit.

Serum ionized calcium (Ca+2), creatinine, magnesium, phosphate, and arterial pH were measured in patients on admission to the medical ICU (MICU). Patients were classified into three groups: a) hypotensive (n = 38), those who received vasopressor support for frank hypotension; b) hypertensive (n = 21), those who required vasodilator therapy; and c) normotensive (n = 53), those who required neither vasopressor nor vasodilator therapy. Analysis of variance revealed that only Ca+2, creatinine, and arterial pH differed among the three groups. The difference in Ca+2 persisted when analysis of variance was repeated with creatinine as a covariate. Hypotensive patients had a significantly (p less than .05) lower mean Ca+2 (1.04 +/- 0.13 mmol/L) than normotensive patients (1.13 +/- 0.10 mmol/L), who in turn had a significantly (p less than .05) lower Ca+2 than hypertensive patients (1.18 +/- 0.09 mmol/L). Ca+2 correlated with mean arterial pressure at the time of serum collection (n = 118; r = .43; p less than .01), independent of any other variable. Vasopressor support was required in 41% of hypocalcemic patients in comparison to 14% of normocalcemic patients (p less than .01). Vasodilator therapy was required for 34% of normocalcemic patients, compared to 7.5% of hypocalcemic patients (p less than .01). There appears to be a clinically significant association between hypotension and hypocalcemia. This association may or may not be causal.

Prevalence and clinical implications of hypocalcemia in acutely ill patients in a medical intensive care setting.

The incidence and the clinical implications of hypocalcemia were evaluated in acutely ill patients admitted to the Medical Intensive Care Unit of the Detroit Receiving Hospital. Total and ionized calcium levels were prospectively evaluated upon admission for all patients over a three-month interval. A high proportion of patients (62 of 88, 70 percent) were found to have decreased levels of both total and ionized calcium. Known causes of hypocalcemia could be identified in only 28 patients (45 percent). These included hypomagnesemia (17, 28 percent), renal insufficiency (five, 8 percent), alkalosis (four, 6 percent), and acute pancreatitis (two, 3 percent). In the remaining 34 patients (55 percent), no readily identifiable cause could be found. These 34 patients had a lower mean albumin level than did the 23 normocalcemic patients (p less than 0.01), but there were no differences in age, pH, serum creatinine, magnesium, or phosphate between the two groups. Serum albumin correlated directly with ionized calcium levels (n = 82, r = 0.33, p less than 0.01), as well as with total calcium levels (n = 76, r = 0.70, p less than 0.01). There was a strong association between sepsis and hypocalcemia. Patients who survived the hospitalization had higher mean ionized calcium, total calcium, and albumin values than did nonsurvivors, but there were no differences in age, serum creatinine, magnesium, and phosphate between the two groups. The mortality of the hypocalcemic patients (44 percent) was significantly greater (p less than 0.05) than the mortality of the normocalcemic patients (17 percent). These findings suggest that hypocalcemia is a very common abnormality in acutely ill patients and is associated with a poor prognosis.

Clinical approach to the hyperosmolar patient.

The successful evaluation and treatment of the hypertonic patient depends on a clear understanding of the differences between effective and noneffective solute and the consequences of changes in these solutes for water distribution. Measured osmolality, calculated osmolality, tonicity, and sodium concentration must be evaluated in the approach to these patients.

Hypocalcemia and hypophosphatemia in acutely ill patients.

Hypocalcemia and hypophosphatemia have recently been recognized as common metabolic complications in acutely ill patients. The diagnostic and therapeutic approaches to these abnormalities are described in this article.

Demeclocycline-induced natriuresis and renal insufficiency: in vivo and in vitro studies.

We examined renal function and Na+ balance in a patient with congestive heart failure who was treated with demeclocycline (DMC) on three separate occasions under strict metabolic balance conditions. Natriuresis and reversible renal insufficiency, which could not be explained solely on the basis of negative Na+ balance, developed on each occasion. In contrast to reports of an association between elevated serum DMC levels and renal insufficiency in patients with cirrhotic edema, the renal insufficiency in this patient with cardiac edema occurred in the absence of high DMC levels. Consequently, markedly elevated serum DMC levels do not appear to be a prerequisite for the development of natriuresis or renal insufficiency in edematous patients receiving this drug. In an attempt to clarify the mechanism of the natriuresis, we also examined the effects of DMC on Na+ transport in an in-vitro model system, the toad urinary bladder. DMC inhibited aldosterone-stimulated Na+ transport, but had no effect on Na+ transport when the latter was jointly stimulated by ADH and theophylline. Despite this selective inhibition of the natriferic effect of aldosterone in vitro, it is unlikely that such a mechanism completely accounts for the natriuresis observed in-vivo since the natriuresis is generally of large magnitude and is usually accompanied by some degree of kaliuresis, and DMC had no consistent effect on urinary aldosterone excretion. Consequently, other mechanisms must be sought to explain the natriuretic effect of DMC in edematous patients. Likewise, mechanisms other than negative Na+ balance (perhaps primary alterations in renal hemodynamics) must underly the development of renal insufficiency in such individuals.