Serum potassium levels during prolonged hypothermia

Hypokalemia (mean serum potassium 2.3 +/- 0.4 mEq/l) was observed in six hypothermic patients (30 degrees - 32 degrees C) with head injuries or brain hypoxia. In the first three patients, potassium was administered to maintain serum levels above 3.5 mEq/l and on rewarming after 48 h of hypothermia hyperkalemia (peak serum potassium = 7.1 +/- 0.5 mEq/l) associated with cardiac arrhythmias developed. The remaining three patients received sufficient potassium to approximately replace measured losses during the hypothermic period. These patients did not become hyperkalemic on rewarming. Clinically insignificant sinus bradycardia, premature atrial contractions and junctional rhythms were seen during hypothermia with hypokalemia. We conclude that hypothermia produces hypokalemia by a shift of potassium from the extracellular to intracellular or extra vascular spaces. Potassium therapy during controlled hypothermia in the range 30 degrees - 32 degrees C should only replace measured losses.     

The Cardiac Electrophysiology of Postresuscitation Hypokalemia in Dogs

Hypokalemia has been observed in man after out-of-hospital ventricular fibrillation and after cardioversion from ventricular tachycardia in the electrophysiology laboratory, and also in dogs following ventricular fibrillation (maximal effect 45-60 minutes after resuscitation). Since the electrophysiological effects of postresuscitation hypokalemia are unknown, we evaluated the effects of this hypokalemia on ventricular fibrillation thresholds (group 1) and on right ventricular effective refractory periods (group 2). In both groups, anesthetized dogs with normal hearts were divided into experimental animals that had 2 minutes of ventricular fibrillation followed by cardioversion without medications and control animals without ventricular fibrillation. In group 1, we measured serum potassium before ventricular fibrillation (or time 0 in control dogs) and then measured potassium and ventricular fibrillation threshold at 45, 60, 75, and 90 minutes after baseline. In group 2 animals we measured right ventricular effective refractory periods and serum potassium at baseline and sequentially from 7 to 180 minutes after resuscitation. In group 1, the maximum change in potassium from baseline was -0.8 +/- 0.3 mEq/L at 60 minutes after resuscitation as compared to -0.1 +/- 0.3 mEq/L in control animals at 60 minutes (P less than 0.01). At 60 minutes, ventricular fibrillation threshold was 8 +/- 3 mA in ventricular fibrillation animals and 7 +/- 3 mA in control animals (P = NS). In group 2 animals, the maximum change in serum potassium also occurred 60 minutes after resuscitation and was -0.8 +/- 0.3 mEq/L as compared to -0.2 +/- 0.2 mEq/L in control animals (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of pretreatment with propranolol on potassium, calcium, and magnesium shifts after ventricular fibrillation in dogs

Hypokalemia and other electrolyte changes have been observed after resuscitation from ventricular fibrillation. We studied the effect of propranolol on postresuscitation electrolytes in a canine model of ventricular fibrillation and cardiac resuscitation by randomizing 40 anesthetized dogs to four groups: ventricular fibrillation--no drug (VF), ventricular fibrillation--propranolol pretreatment (VF-prop), control-no drug (NoVF), control--propranolol (NoVF-prop). We measured serum electrolytes at baseline and periodically for 3 hours. In VF dogs, serum potassium decreased from 3.9 +/- 0.4 to 3.2 +/- 0.2 mEq/L 60 minutes after resuscitation (p less than 0.001). The decrease in potassium was prevented (p less than 0.001) by propranolol. Serum calcium decreased from 10.6 +/- 0.8 to 10.2 +/- 0.8 mg/dl in VF dogs 15 minutes after resuscitation (p less than 0.05); this decrease was not blocked by propranolol (p = NS). Serum magnesium increased from 1.5 +/- 0.2 to 1.8 +/- 0.1 mEq/L in VF dogs 7 minutes after resuscitation (p less than 0.001); this rise was partially blocked by propranolol (p less than 0.01). Serum glucose increased from 105 +/- 6 to 183 +/- 27 mg/dl in VF dogs 7 minutes after resuscitation (p less than 0.001); this increase was diminished by propranolol (p less than 0.001). Thus propranolol prevents the decrease in serum potassium after ventricular fibrillation in this canine model, providing evidence that postresuscitation hypokalemia is caused by the beta-adrenergic effects of catecholamines secreted in response to cardiac arrest. Propranolol blocks the rise in magnesium and glucose but does not block the decrease in calcium after resuscitation.     

Effect of Bilateral Stellectomy on Electrical Instability of the Atrium in the Dog with Hypokalemia

To investigate the effect of sympathetic nerve activity on electrical instability of the atrium in the presence of hypokalemia, open chest electrophysiological study was performed before and after bilateral stellectomy (BS) in 15 dogs with hypokalemia (hypokalemia group) and in 15 dogs with normokalemia (control group). Hypokalemia was created by infusion of 5.0 g/kg of polystyrene sulfonic acid calcium into the colon. Serum level of potassium was significantly lower in the hypokalemia group (2.94 +/- 0.52 mEq/L) than in the control group (4.86 +/- 0.51 mEq/L, P less than 0.01) before BS. There was no significant change in serum level of potassium in the two groups after BS. Incidence of electrically induced atrial fibrillation (AF) was significantly higher in the hypokalemia group (80%) than in the control group (13%, P less than 0.001) before BS. It was significantly reduced in the hypokalemia group (40%, P less than 0.05), but not in the control group (6%) after BS. Dispersion of effective refractory period of the atrium (delta ERP) was significantly greater in the hypokalemia group (26.1 +/- 2.8 msec) than in the control group (22.0 +/- 3.3 msec, P less than 0.005) before BS. It was significantly decreased to 23.1 +/- 3.2 msec in the hypokalemia group (P less than 0.001) and to 20.6 +/- 2.5 msec in the control group (P less than 0.01) after BS. Maximum conduction delay in the atrium (MaxCD) was 36.1 +/- 3.5 msec before and 36.2 +/- 4.1 msec after BS in the hypokalemia group and 31.1 +/- 4.2 msec before and 32.3 +/- 4.9 msec after BS in the control group. There was a significant difference in MaxCD between the two groups before BS. Atrial fibrillation threshold (AFT) was significantly lower in the hypokalemia group (3.9 +/- 0.7 mA) than in the control group (13.8 +/- 3.1 mA, P less than 0.001) before BS. It was significantly increased both in the hypokalemia group (6.5 +/- 1.3 mA, P less than 0.001) and in the control group (15.0 +/- 2.7 mA, P less than 0.005) after BS. It is concluded that sympathetic nerve activity may play some role in the increase in electrical instability of the atrium in the presence of hypokalemia.     

Incidence and causes of hypokalemia associated with cardiac resuscitation

To further investigate the incidence and etiology of hypokalemia during cardiac arrest, the authors compared data on 74 adult nontrauma cardiac arrest patients (44 men, 30 women, age 65 +/- 13 years) who had a serum potassium (K+) level documented during or immediately following resuscitation with data on 53 adult controls with life-threatening medical emergencies presenting to the emergency department who did not experience arrest. Hypokalemia (serum K+ less than 3.6 mEq/l) occurred in 25 arrest patients (34%) compared with nine controls (17%). Serum K+ was not significantly different shortly before (3.7 +/- 0.4) versus immediately after arrest (3.6 +/- 0.8) in a small subgroup of patients, making intracellular shifting of K+ because of metabolic events during resuscitation an unlikely etiology. Hypokalemia was associated with a 2.5-fold increase in relative risk for cardiac arrest. Patients who were receiving diuretics without K+ supplementation had the highest risk of arrest (4.4-fold increase). Supplementation of K+ appeared to be protective in patients on diuretics. The authors confirm the association between hypokalemia and cardiac arrest and suggest that this metabolic abnormality may be an important risk factor for cardiac arrest.     

Hypokalemia, hyperglycemia, and acidosis after intentional theophylline overdose

Three cases of intentional theophylline overdose in adult patients are described. Among these, hypokalemia, hyperglycemia, and acidosis were found, and markedly elevated initial serum theophylline concentrations (106, 76.2, and 41.4 micrograms/ml) were measured. All patients recovered completely with conservative management. The observed biochemical abnormalities rapidly resolved during maintenance fluid therapy and modest potassium supplementation. In addition, seizures, ventricular arrhythmias, and other serious toxic effects were notably absent.     

急性心肌梗死早期低血钾与心衰的关系

目的 探讨急性心肌梗死（AMI）患者早期低钾血症的变化以及与心力衰竭的关系。方法收集200例急性心肌梗死的患者,发病时间小于24小时,所有患者均为首次入院。根据血钾浓度分为低钾血症组和正常血钾组,其中低钾血症组又分为重度低钾组（〈2．50mmol／L）、中度低钾组（2．51mmol／L-3．0mmool／L）和轻度低钾组（3．01-3．50mmol／L）。所有患者予以常规积极治疗,观察心力衰竭发生情况。结果AMI患者低钾血症的发生率为73．5％,低钾血症组心力衰竭的发生率为51．7％,明显高于正常组（22．6％）,其中重度低钾组心衰的发生率78．2％,中度低钾组为58．3％,轻度低钾组为38．9％。结论急性心肌梗死早期易出现低钾血症,并且随着血钾浓度的降低,心力衰竭的发生率也明显增高。     

Hyponatremia during carbamazepine therapy

Sixty patients receiving carbamazepine and 61 age-matched controls were studied to determine the prevalence of hyponatremia. There was a significant difference between the mean (+/- SE) serum sodium levels of the subjects (138.8 +/- 0.6 mEq/L) and the controls (141.7 +/- 0.4 mEq/L). Thirteen (21.7%) of the subjects, but none of the controls, had sodium levels less than 135 mEq/L. The risk of hyponatremia increased with age (subjects greater than 30 years old had four times the prevalence of hyponatremia as those less than 30 years old) and carbamazepine serum level (those with levels greater than 6 micrograms/ml had three-and-a-half times the prevalence as those with lower levels).     

Oral potassium chloride and amiloride in hydrochlorothiazide-induced potassium loss

To compare the effect of amiloride with that of oral potassium chloride (KCl) in hypokalemia, metabolic balance studies were carried out in hospitalized subjects with mild hypertension without edema who developed negative potassium balance after 4 days on hydrochlorothiazide (HCTZ). Subjects' diets contained measured amounts of sodium and potassium. While HCTZ treatment continued, oral preparations of either KCl solution or amiloride was added for 5 additional days. Potassium balance in the KCl-treated group further decreased by -44.9 +/- 32.3 mEq K+, while subjects on amiloride went into positive balance that averaged +51.7 +/- 24.1 mEq K+. Hypokalemia after HCTZ did not respond to KCl, while K+ levels rose from 3.32 +/- 0.22 to 3.67 +/- 0.26 mEq/l after amiloride.     

A role for epinephrine in post-traumatic hypokalemia

We have previously described a high incidence of admission hypokalemia in trauma patients at our institution. We subsequently performed a prospective study of 112 trauma patients to examine the possible etiologies of post-traumatic hypokalemia. Trauma patients >or=5 years old were evaluated within 6 h of injury with a variety of studies including catecholamines, cortisol, and insulin levels, with studies repeated 24 to 36 h after admission. No potassium replacement was given during this time. Demographic factors such as age, types of injury, and severity of injuries were collected. We found that the mean age of those with post-traumatic hypokalemia (相似文献   

Serum magnesium concentrations after repetitive magnesium cathartic administration

Severe hypermagnesemia has been reported by several authors after multiple doses of magnesium-containing cathartic are administered during management of a toxic ingestion. To evaluate the frequency and magnitude of serum magnesium elevations after the use of repetitive magnesium catharsis, we prospectively evaluated 102 patients who received multiple doses of magnesium citrate as a part of treatment of an overdose. Commonly ingested substances for which repetitive cathartic was administered were tricyclic antidepressants in 47%, aspirin in 17%, and phenytoin in 10%. For each case, serial electrolytes, blood urea nitrogen, creatinine, calcium and magnesium were obtained. Mean initial serum magnesium concentration was 1.8 +/- .03 mEq/L. After a mean 960 mL of magnesium citrate (9.22 g magnesium), final mean serum magnesium concentration was 2.5 +/- .05 mEq/L. Forty-seven patients (47%) developed an elevated (greater than 2.4 mEq/L) serum magnesium concentration, with 12 greater than 3.0 mEq/L. No correlation was found between total quantity of magnesium citrate administered and the increment in serum magnesium concentration. Our data indicate that serum magnesium concentrations consistently rise after repetitive magnesium citrate use. However, the magnitude of this rise appears modest. The elevation in serum magnesium concentration does not correlate with the quantity of magnesium administered. We conclude that with close monitoring, repetitive magnesium citrate can be administered without inducing severe hypermagnesemia (serum magnesium concentration greater than 5.0 mEq/L).     

Low-dose diuretic therapy for hypertension

The efficacy of low dosages of diuretics was evaluated in two studies. In one, 62 (48%) of 130 patients became normotensive with 2.5 mg/day of metolazone. In the other, 28 (49%) of 57 patients became normotensive with 25 mg of chlorthalidone, compared with 12 (22%) of 55 patients given placebo. There was a marked variation in blood pressure response and the occurrence of hypokalemia (less than 3.5 mEq/L of potassium) from center to center and within patient groups in both studies. The mean decrease in serum potassium was between 0.5 and 0.6 mEq/L in the metolazone group and 0.44 mEq/L in the chlorthalidone-treated patients. This degree of hypokalemia is only slightly less than that noted when larger dosages of thiazide diuretics are used (0.6 to 0.7 mEq/L). It is concluded that 2.5 mg/day of metolazone or 25 mg/day of chlorthalidone are effective antihypertensive agents but that blood pressure lowering may be inconsistent at these dosage levels. It is reasonable, therefore, to begin diuretic therapy with low dosages, but larger dosages (5 mg of metolazone or 50 mg of chlorthalidone) should be tried before adding another drug or concluding that diuretic therapy is ineffective if an acceptable blood pressure response is not obtained. The degree of hypokalemia that occurs at lower-dose therapy is variable but may be of less clinical significance than that noted with higher dosages of diuretics in some patients.(ABSTRACT TRUNCATED AT 250 WORDS)     

Poor tolerance of oral activated charcoal with theophylline overdose

Vomiting is a common manifestation of theophylline toxicity and may limit the tolerance of orally administered activated charcoal (OAC). However, this potentially important interaction has received little attention. The records of 33 consecutive patients who presented to the emergency department with serum theophylline concentrations greater than 30 micrograms/ml and toxic symptoms and who were treated with OAC were reviewed. Seventeen (22%) of the 76 OAC doses were vomited. Six patients who had ingested theophylline as a single acute overdose vomited all 11 OAC doses administered, whereas 27 patients receiving chronic theophylline therapy vomited only six (11%) of 65 OAC doses. Vomited doses were associated with higher serum theophylline concentrations. Although theophylline-related vomiting preceded OAC intolerance in all acute toxicity patients, this condition was not predictive of OAC vomiting for chronic toxicity patients.     

Blood pressure lowering and potassium conservation by triamterene-hydrochlorothiazide and amiloride-hydrochlorothiazide in hypertension

Effects of once-daily doses of 50 mg triamterene with 25 mg hydrochlorothiazide and 5 mg amiloride with 50 mg hydrochlorothiazide were compared in a randomized, multicenter study of 84 adult subjects with mild to moderate hypertension (diastolic blood pressure 90 to 114 mm Hg). After a 3-wk placebo lead-in period, the subjects entered a 6-wk treatment period. The two drug regimens were compared with respect to antihypertensive effects and effects on serum potassium and magnesium levels during the final week of drug therapy, with the use of the last week of placebo therapy as a covariate. Both drug regimens substantially reduced mean supine systolic and diastolic blood pressures to well within normal limits; there was no significant difference the two groups. Twenty-four of the 41 subjects receiving triamterene-hydrochlorothiazide (59%) and 29 of the 43 patients receiving amiloride-hydrochlorothiazide (67%) had diastolic blood pressure less than 90 mm Hg at week 9. Five subjects receiving amiloride-hydrochlorothiazide (12%) and two subjects receiving triamterene-hydrochlorothiazide (5%) had hypokalemia (serum potassium level less than 3.5 mEq/l) at week 9. The average decrease in serum potassium levels during amiloride-hydrochlorothiazide therapy (-0.33 +/- 0.08 mEq/l) was greater than that after triamterene-hydrochlorothiazide (- 0.08 +/- 0.07 mEq/l). Serum magnesium levels were not changed by either regimen. Weight loss was greater in the amiloride-hydrochlorothiazide group than in the triamterene-hydrochlorothiazide group.(ABSTRACT TRUNCATED AT 250 WORDS)     

Theophylline overdose: acute single ingestion versus chronic repeated overmedication

Currently available guidelines for managing theophylline intoxication do not distinguish between acute single ingestion and chronic repeated overmedication and do not reliably predict which patients should undergo hemoperfusion. Although hemoperfusion is widely recommended when serum concentrations exceed 40-60 mg/l, many patients with acute overdose tolerate much higher levels without serious toxicity. Because manifestations of toxicity might be dependent on the chronicity of the overdose, the authors retrospectively compared the clinical features of 15 patients with chronic repeated overmedication with those of 27 patients suffering acute single overdose. Patients suffering chronic repeated overmedication developed seizures (7/15) and serious arrhythmias (4/15) with serum levels of 28-70 mg/l. By contrast, only one of 19 patients suffering acute single overdose with peak levels less than 100 mg/l had seizures, and only two of 19 with levels less than 100 mg/l had serious arrhythmias. However, of the eight single-overdose patients with levels over 100 mg/l, seven had seizures and three had serious arrhythmias. Single-overdose patients were easily recognized by the presence of hypotension, hypokalemia, and low serum bicarbonate, features not present in chronic-type patients. Thus, while patients with theophylline overdose caused by chronic repeated overmedication frequently develop seizures and arrhythmias with serum levels of 40-70 mg/l, those with acute single ingestion are highly unlikely to suffer serious complications unless serum levels exceed 100 mg/l. Management of the intoxication, especially selection of patients for hemoperfusion, should be based on whether the overdose is caused by an acute single ingestion or chronic repeated overmedication.     

Model for theophylline overdose treatment with oral activated charcoal

The effect of repeated oral doses of activated charcoal on theophylline kinetics was studied in six subjects with hepatic cirrhosis and five patients with moderate theophylline poisoning to determine whether an activated charcoal regimen would be a useful strategy in patients with theophylline poisoning who did not require hemoperfusion. Six subjects with cirrhosis were injected IV with 6 mg/kg aminophylline followed by either water or water with activated charcoal (140 gm) in divided doses over 12 hr. In these subjects, treatment with activated charcoal decreased the mean (+/- SE) serum theophylline t1/2 from 12.7 +/- 4.0 hr to 4.0 +/- 0.7 hr. Subjects with the longest control t1/2s demonstrated the greatest charcoal effect. We developed a mathematical model that predicts that treatment with repeated oral doses of activated charcoal would result in an average serum theophylline t1/2 of 7.1 hr or less even if the subject's endogenous theophylline t1/2 is very long. In a pilot study of five patients with moderate theophylline poisoning, treatment with repeated oral doses of activated charcoal was well tolerated and led to a mean (+/- SE) t1/2 that was shorter than expected (4.9 +/- 0.8 hr, range 3.1 to 7.1 hr). We conclude that repeated oral doses of activated charcoal are relatively more effective in decreasing the serum theophylline t1/2 in persons with long endogenous t1/2s and that this may be useful for certain patients with mild or moderate theophylline poisoning.     

Hyaluronan: relationship to hemodynamics and survival in porcine injury and sepsis.

BACKGROUND AND METHODS: Hyaluronan is a polysaccharide normally present in low concentrations in the blood, and is rapidly cleared from the blood by the liver. Increased plasma hyaluronan concentrations have been found in patients with sepsis. We studied changes in serum hyaluronan concentrations and their relationship to hemodynamics and survival in a 48-hr porcine model of injury and sepsis. RESULTS: Circulating hyaluronan concentrations increased to high values after induction of experimental sepsis (from mean baseline values of 242 +/- 26 [SEM] to mean maximum concentrations of 964 +/- 255 micrograms/L [p less than .01]) compared with controls (199 +/- 38 to 303 +/- 32 micrograms/L). A weak negative correlation between mean arterial pressure (MAP) and serum hyaluronan values was found (r2 = .47; p less than .01). Nonsurvivors had higher mean serum hyaluronan concentrations than survivors (603 +/- 147 vs. 285 +/- 43 micrograms/L [p less than .05]). CONCLUSIONS: Experimental sepsis is associated with an increase in serum hyaluronan values. The relationship between decreased MAP and increased serum hyaluronan concentrations could point to reduced liver perfusion as a cause. An association between high hyaluronan values and nonsurvival in sepsis is possible.     

Inadequate aldosterone response to hyperkalemia during angiotensin converting enzyme inhibition in chronic renal failure

To assess the mechanism involved in hyperkalemia during angiotensin converting enzyme inhibition with captopril in chronic renal failure, captopril, 150 mg/day, was administered to 16 patients with hypertension with plasma creatinine levels between 1.6 and 12.4 mg/dl. After 4 weeks of therapy, plasma potassium levels increased from 3.9 +/- 0.1 to 5.5 +/- 0.2 mEq/L (P less than 0.001) and the final plasma potassium levels correlated with plasma creatinine levels (r = 0.67; P less than 0.01). In six patients with plasma creatinine levels greater than or equal to 3 mg/dl, aldosterone excretion decreased after 4 weeks of captopril, from 7.5 +/- 3.1 to 1.8 +/- 0.5 micrograms/24 hr, whereas plasma renin activity increased from 0.6 +/- 0.2 to 4.4 +/- 1.1 ng/ml/hr (P less than 0.05). This was associated with increases in plasma potassium levels from 3.9 +/- 0.2 to 5.4 +/- 0.4 mEq/L (P less than 0.005) and a significant reduction in fractional excretion of potassium from an average of 34% to 25%. No significant changes in plasma creatinine levels were observed during therapy. There was a significant positive correlation between aldosterone excretion and the potassium excretion fraction (r = 0.53; P less than 0.01). Increases in plasma potassium levels were not able to increase aldosterone excretion, although the greater the plasma potassium level attained, the smaller the reduction in aldosterone excretion (r = 0.47; P less than 0.05). Our results indicate that adequate aldosterone production is essential to preserve potassium homeostasis in chronic renal failure. Moreover, angiotensin II appears necessary for an adequate aldosterone response to potassium stimulation.     

Clinical perspectives on the rationale for potassium supplementation

Hypokalemia is a common electrolyte disturbance, observed in > 20% of hospitalized patients. Hypokalemia, although not formally defined, is generally considered to be when serum potassium levels fall below the normal value of 3.6 mmol/L. In contrast to other electrolytes, potassium is primarily an intracellular ion: only 2% of all potassium in the body is present in the extracellular fluid, so a small decrease in serum potassium may represent a significant decrease in intracellular potassium. Individuals with mildly decreased potassium levels (3.0–3.5 mmol/L) may be asymptomatic, but patients with more pronounced decreases may report symptoms including muscle weakness, fatigue, and constipation. Very low serum potassium levels (≤ 2.5 mmol/L) can lead to muscle necrosis, paralysis, cardiac arrhythmias, and impaired respiration, which can be life-threatening. Absent comprehensive and robust treatment guidelines, strategies for the prevention or treatment of hypokalemia, such as how to diagnose hypokalemia, when to treat patients, what dosage regimen of potassium supplementation to use and for how long, are often based on the experience of the physician and empirical evidence. However, proper evaluation and treatment of hypokalemia in patients is essential because of associated morbidities. Because small potassium deficits in serum represent large body losses, potassium repletion requires substantial and prolonged supplementation. For patients with known risk factors for hypokalemia (e.g. hypertension, heart failure, or diabetes), careful monitoring is crucial to avoid the adverse sequelae associated with potassium deficits and to ensure that adequate and timely preventive measures can be taken. In this review, we provide practical insights into the etiology, differential diagnosis, and treatment of hypokalemia, including treatment strategies for patients with known risk factors.     

Relationship of potassium and magnesium concentrations in serum to cardiac arrhythmias

Low concentrations of potassium and magnesium in serum have been implicated in cardiac arrhythmias; the importance of mild hypokalemia or hypomagnesemia is uncertain. To investigate possible associations among use of diuretics, the concentration of these ions in serum, and the onset of clinically important arrhythmias, we reviewed records of 103 patients admitted to our Coronary Care Unit during three months and found mild to moderate hypokalemia and hypo- magnesemia in 18 and 24%, respectively. The significant correlation between the concentrations of magnesium and potassium in serum at admission (r = 0.27, p less than 0.007) remained constant in patients, whether they were receiving diuretics or not. Potassium concentrations were significantly lower (p less than 0.05) in patients receiving diuretics (3.93 mmol/L) than in those who were not (4.21 mmol/L), but the mean concentrations of magnesium did not differ significantly. Except for myocardial infarction, no single variable or combination of variables was highly predictive of cardiac arrhythmias in these patients. We conclude that there is no strong predictive relationship between mildly decreased concentrations of magnesium or potassium in serum and onset of cardiac arrhythmias.