This patient's ECG demonstrated changes consistent with profound hypokalemia. The patient's history of intractable vomiting occurring for many weeks raised a clinical suspicion for hypokalemia, which was confirmed by the ECG findings. The ECG demonstrated a markedly prolonged QT interval, with the ECG computer interpretation calculating a corrected QT interval (QTc) of 590 msec (which is greatly prolonged). Additionally, the ECG showed slight "thumbprint-like" ST depressions in many leads, including II, III, aVF, and V4-V6, which represented another sign of hypokalemia. ST elevations were seen in V1 and V2; however, the patient's clinical presentation was not consistent with myocardial ischemia or infarction.
Hypokalemia is a common clinical problem. It is estimated that less than 1% of people on no medications have a serum potassium less than 3.5 mEq/L (3.5 mmol/L)[1]; however, up to 21% of hospitalized patients, 50% of patients on non–potassium-sparing diuretics, and 19% of patients with eating disorders may have hypokalemia.[1] Given the prevalence of these conditions and other causes of hypokalemia, many people are affected. In the majority of patients, the degree of hypokalemia is not of clinical significance; however, since symptoms of hypokalemia may be vague or absent, potassium levels should be monitored in patients at risk for developing hypokalemia. The definition of hypokalemia is a serum potassium level of less than 3.5 mEq/L (3.5 mmol/L). Bedside potassium measurements are now available in many facilities. If an immediate test is needed and a delay is anticipated, an ECG can serve as a surrogate marker. If acute hypokalemia is a concern, a normal ECG can be reassuring, while an abnormal ECG can suggest hypokalemia, but not a specific level.
There are numerous causes of hypokalemia, which can be generally divided into poor intake, increased excretion, and shifting potassium from the extracellular to intracellular spaces.[1] Poor intake can be caused by mechanical problems (eg, inability to swallow), eating disorders (eg, bulimia), and hospitalization (eg, inappropriate potassium in parenteral nutrition).[1] Increased excretion occurs in multiple settings. Some examples are an excess of endogenous mineralocorticoids causing increased renal losses, congenital disorders that affect the kidney's distal tubule (such as Bartter and Gitelman syndromes), medications (particularly diuretics), and diarrhea, among other causes.[1] Finally, potassium can shift intracellularly and cause hypokalemia. Potassium shift occurs with alkalosis, albuterol or insulin administration, and during refeeding syndrome.
Clinical manifestations of hypokalemia are wide ranging. For mild hypokalemia (potassium levels above 3.0 mEq/L [3.0 mmol/L]), patients are typically asymptomatic, unless the level falls rapidly or there are other comorbidities.[4] Once the levels are below 3 mEq/L (3 mmol/L), patients may experience various symptoms that can be difficult to link directly to a particular level and depend more on the individual patient and their medications and comorbidities. Muscle weakness typically manifests below levels of 2.5 mEq/L (2.5 mmol/L), and it tends to begin slowly in the lower extremities and progress to the trunk and upper extremities.[4] Decreased gastrointestinal motility leading to ileus may occur and, if severe, respiratory depression or failure can occur.[4] In addition, rhabdomyolysis can develop as a result of potassium depletion. Potassium release from muscle cells during exertion normally mediates blood flow to muscles during exercise. Decreased potassium release causes less blood flow to the muscles. This decreased blood flow can lead to rhabdomyolysis and the associated cascade of metabolic problems.[4]
The most potentially serious complications from hypokalemia involve cardiac dysrhythmia. These may be relatively benign abnormalities, such as premature atrial and ventricular beats, or they can be life-threatening problems, such as atrioventricular block, ventricular tachycardia, or ventricular fibrillation.[4] Since hypokalemia is typically associated with concomitant hypomagnesemia, torsades des pointes can occur.[4] Also, hypokalemia occurring with digitalis toxicity or underlying illnesses (such as coronary ischemia) can make these illnesses more severe.[4] Potassium levels below 3.0 mEq/L (3.0 mmol/L) are associated with a 2-fold increase in ventricular dysrhythmia.[4]
Determining the etiology of hypokalemia depends upon the clinical context. A history of diuretic use is suggestive of causation. For a patient on no medications, without vomiting or diarrhea and who has normal food intake, establishing the cause may be much more difficult. A diagnostic evaluation may include looking for surreptitious diuretic use in the patient's urine or measuring 24-hour aldosterone and cortisol levels, among many other possibilities.[4] Mild fluctuations in potassium levels are common, and an extensive work-up of the cause in the setting of mild hypokalemia is not typically necessary. Instead, repeat levels can be performed to monitor for correction or progression.
Hypokalemia is treated with potassium repletion and correction of the underlying problem causing the hypokalemia. A large amount of potassium may be required to replace severe hypokalemia, as serum potassium reflects total body potassium stores. For example, a drop in serum potassium of just 1 mEq/L (1 mmol/L) in a patient without an acute acid-base disorder may represent a 370 mEq (370 mmol) deficit of total body potassium.[6] The potassium level can increase as much as 1-1.5 mEq/L (1-1.5 mmol/L) transiently after an oral dose of 40-60 mEq (40-60 mmol), so laboratory monitoring and care must be used to avoid hyperkalemia.[4] Potassium replacement can be accomplished via enteral or intravenous replacement. Oral replacement is preferred to intravenous replacement because of the lesser risk of iatrogenic hyperkalemia, the ability to give larger doses of potassium replacement quickly, and burning at the infusion site if potassium is given via peripheral IV.[6] For mild-to-moderate hypokalemia (potassium between 3.0 and 3.5 mEq/L [3.0 and 3.5 mmol/L]), potassium can usually be replaced orally. Replacing the lost potassium can be accomplished with 10-20 mEq (10-20 mmol) of potassium chloride dosed 2-4 times daily.[4] For severe hypokalemia (potassium less than 3.0 mEq/L [3.0 mmol/L]), oral doses of 40-60 mEq (40-60 mmol) can be given 3-4 times daily.[4]
For patients who cannot tolerate oral medications or are acutely ill, intravenous replacement can be considered. Generally, the rate of repletion should be no more than 10-20 mEq/hour (10-20 mmol/hour) to prevent complications related to hyperkalemia or burning at the infusion site.[4,6] Replacement rates exceeding 20 mEq/hour (20 mmol/hour) require cardiac monitoring and central venous access.[6] Patients with hypokalemia almost always have concurrent hypomagnesemia, so empiric magnesium repletion is also recommended. If the magnesium deficit is not corrected, the hypokalemia may persist.[4] It should be noted that serum magnesium levels may not accurately reflect total body stores, so correction should be done empirically even in the setting of a normal laboratory reading.
Most hypokalemic patients can be safely discharged to home with primary care follow-up to manage potassium repletion and potassium level monitoring. Severely hypokalemic or symptomatic patients will require admission and, possibly, cardiac monitoring.
The laboratory studies for the patient in this case were notable for a potassium level of less than 2.0 mEq/L (2.0 mmol/L), as well as a chloride level of 66 mEq/L (66 mmol/L), a creatinine of 1.5 mg/dL (132.6 μmol/L), a total bilirubin of 3.7 mg/dL (63.27 μmol/L), and negative cardiac enzymes. The potassium level was confirmed on a repeat study. Treatment began simultaneously with both oral and intravenous potassium chloride replacement, and oral and intravenous magnesium replacement. The patient was admitted to the intensive care unit for cardiac monitoring, fluid and electrolyte resuscitation, and further evaluation of the etiology of the gastric mass.A patient with a history of bulimia and recent recurrent vomiting presents to the ED with generalized weakness and dehydration, raising suspicion of hypokalemia. Which of the following ECG findings would be expected in a patient with severe hypokalemia?
The hallmark findings of severe hypokalemia on an ECG are diminished T-waves and prominent U-waves. Peaked T-waves are a characteristic finding in hyperkalemia, with sine waves seen in cases of severe hyperkalemia. Osborn waves are seen in severe hypothermia, not hypokalemia.
You are treating a patient with known hypokalemia with potassium repletion. A deficit of which of the following can cause refractory hypokalemia, despite potassium replacement?
