Runner’s new diet, his collapse, and his ECG

Case description

A 58-year-old man was brought to the emergency department by emergency medical services (EMS). He was found unresponsive by his wife at home. When EMS arrived, he was pulseless and the automated external defibrillator indicated a nonshockable rhythm. Cardiopulmonary resuscitation was started and the patient was intubated. Return of spontaneous circulation was achieved after a single dose of epinephrine. Upon arrival in the emergency department, measurement of his vital signs revealed the following: heart rate of 95 beats/min, oxygen saturation of 99%, respiratory rate of 12 breaths/min (ventilated), blood pressure of 110/78 mm Hg, temperature of 37°C, and a glucose level of 6.8 mmol/L. An electrocardiogram (ECG) was obtained (Figure 1).

The patient had a history of hypertension and had been taking 5 mg/d of ramipril orally for 1 year. He was not taking any other medications and had no other medical problems. He recently started a vigorous exercise and diet regimen that included a commercial nutritional supplement.

• Download figure
• Open in new tab

Figure 1.

Electrocardiogram of a 58-year-old patient: Note the prolonged PR interval, peaked T waves, and widened QRS characteristic of the acute and unstable hyperkalemic state.

Hyperkalemia is a potentially fatal condition and is associated with various nonspecific clinical findings, including nausea, vomiting, abdominal pain, muscle weakness, cardiac conduction abnormalities, and arrhythmias. Multiple factors contribute to the development of hyperkalemia. Medications, especially in the setting of impaired renal function, are a common culprit (Box 1).

The ECG findings

An ECG is a rapid test that can provide the putative diagnosis long before results of laboratory work are available. The initial ECG features of hyperkalemia include tall peaked T waves and a shortened QT interval. This is followed by a lengthening of the PR interval and widening of the QRS complex. Late manifestations include an absent P wave and widening of the QRS complex. A sine-wave pattern of the QRS, ventricular fibrillation, and asystole¹ are the terminal ECG manifestations of hyperkalemia.

It is noteworthy that although the probability of ECG changes increases with increasing potassium concentration, there is no direct correlation between serum potassium levels and ECG findings.² It is also essential that emergency care providers recognize that peaked T waves can be present in other acute medical conditions such as acute myocardial infarction.³

Rapid-acting therapies

The ECG changes of hyperkalemia are a result of sodium-potassium adenosine triphosphatase (ATPase) pump disruption and disordered cardiac membrane depolarization.² Calcium, which stabilizes the cardiac membrane, is the only effective treatment of the cardiovascular insults of the hyperkalemic state. Essential treatment of hyperkalemia in individuals with ECG changes requires the rapid administration of calcium, an insulin-glucose combination, and β₂-adrenergic agonists (Table 1).^4–7 Sodium bicarbonate might also be required in certain patients.

Calcium

Calcium has no effect on potassium concentration, but it antagonizes cardiac membrane excitability. Calcium is indicated in patients with ECG changes or arrhythmias. It is administered in the form of either 1000 mg of calcium chloride (10 mL of a 10% solution) or 1000 mg of calcium gluconate (10 mL of a 10% solution). Figure 2 shows the patient’s ECG immediately after the administration of calcium gluconate. Calcium gluconate can be given through a peripheral intravenous line. Calcium carbonate is a sclerosing agent (it contains 6.8 mmol of calcium vs 2.2 mmol of calcium in the gluconate form) and requires central venous access for administration. Cardiac membrane stabilization is apparent on the ECG almost immediately but only lasts 30 to 60 minutes. Concurrent treatment to lower the potassium concentration is essential.⁸ Repeat doses of calcium might be required.

• Download figure
• Open in new tab

Figure 2.

Patient’s electrocardiogram (ECG) immediately after administration of calcium gluconate: Although not a completely normal ECG, note the cardiac membrane stabilization effects of calcium administration in the hyperkalemic patient. The ECG now has a narrowed QRS complex and shortened PR interval.

Elimination therapies

Administering rapid-acting therapies only transiently lowers serum potassium levels. Ultimate treatment of hyperkalemia requires elimination. Elimination therapies used in the past include diuretics, cation-exchange resins (CERs), and dialysis.

Case resolution

Based on the ECG findings and the collateral history suggestive of hyperkalemia, empiric treatment with calcium gluconate (Figure 2), insulin and glucose, and salbutamol was started. The patient’s potassium level returned to 7.3 mmol/L. Thankfully the EMS crew did not use succinylcholine for the rapid sequence intubation. Succinylcholine can increase serum potassium levels between 0.5 and 1.0 mmol/L.

Further consideration revealed an increased dietary potassium load in the nutritional supplement the patient had been taking. The combination of increased dietary potassium, ramipril use, and exercise-induced volume depletion resulted in this patient’s hyperkalemic state.

The patient stopped taking his angiotensin-converting enzyme inhibitor during hospitalization and use of the nutritional supplement was discontinued. He was counseled to avoid volume depletion by drinking more fluid after exercise.