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Hypokalemia-induced Ventricular Fibrillation
184
Letters to the Editor
debilitated, and having long-term urinary catheterization (2). The clinical course is not always benign; in fact, it can be quite complicated. Yu-Jang Su, MD Department of Emergency Medicine Mackay Memorial Hospital Taipei, Taiwan Mackay Medicine Nursing and Management College Taipei, Taiwan Research Center for Biomedical Implants and Microsurgery Devices Taipei Medical University Taipei, Taiwan doi:10.1016/j.jemermed.2010.05.083 REFERENCES 1. Lee J. Images in clinical medicine. Purple urine. N Engl J Med 2007;357:e14 2. Su YJ, Lai YC, Chang WH. Purple urine bag syndrome in a dead-on-arrival patient: case report and articles reviews. Am J Emerg Med 2007;25:861.e5– 6.
e HYPOKALEMIA-INDUCED VENTRICULAR FIBRILLATION To the Editor: Electrolyte abnormalities, including abnormal serum potassium concentration, are considered to be a correctable cause of life-threatening ventricular dysrhythmia, according to the American Heart Association/American College of Cardiology (AHA/ACC) Practice Guidelines (1). We report the case of a 61-year-old woman with ventricular fibrillation possibly related to severe hypokalemia caused by acute gastroenteritis and use of diuretics.
CASE REPORT A 61-year-old woman presented to the Emergency Department (ED) with sudden cardiac arrest. While the patient was eating her dinner, she collapsed suddenly and family members brought her to the ED within 10 min. She had a history of moderate-degree mitral failure and atrial fibrillation (AF). Her medications included carvedilol 6.25 mg, furosemide 20 mg, and lisinopril 20 mg per oral. Two weeks before her presentation, she underwent an operation for inguinal hernia repair. Preoperative evaluation of the patient demonstrated the following results: an electrocardiogram (ECG) showed left bundle branch block (LBBB), AF with normal QT interval (0.376 s), laboratory data significant for hemoglobin 9.8 mg/dL, hematocrit 29.8,
platelet count 287,000, kidney and hepatic functions within normal ranges, and an echocardiogram showed a moderate degree of mitral failure and a 65% ejection fraction. There were no complications during the operation. However, the patient’s hospital course was complicated by diarrhea three times a day. She was discharged from the hospital after 5 days. Two days later she presented to the ED in cardiac arrest and underwent cardiopulmonary resuscitation (CPR) in accordance with the AHA/ACC practice guidelines. During the resuscitation, she received three monophasic 360-j electrical shocks for ventricular fibrillation (VF). After approximately 10 min of CPR, there was return of spontaneous circulation (ROSC). At ED presentation, her vital signs were as follows: blood pressure 130/84 mm Hg, heart rate 107 beats/min, respiratory rate 20 breaths/min (mechanically ventilated), axillary body temperature 35.8°C, and oxygen saturation 100% by pulse oximeter. The Glasgow Coma Scale score was 3. The physical examination was normal except for midriatic pupils (5 mm), a sutured incision at the suprapubic area, and mitral regurgitation murmur. The ECG taken after her ROSC revealed rapid ventricular rate AF and LBBB; DII – DIII – AVF revealed approximately 1 mm ST depression. A repeat ECG 1 h later demonstrated LBBB, AF, and U-wave formation (Figure 1). Pertinent laboratory data obtained post resuscitation revealed an anemia of 7.9 mg/dL, severe hypokalemia (1.17 mmol/L), and cardiac markers that became elevated to 0.44 ng/mL at 4 h. Biochemical parameters, thyroid function, and aldosterone level were normal. Serum magnesium level was measured as 1.68 mg/dL. No free fluid was found on bedside abdominal sonography. Head computed tomography (CT) scan and multislice pulmonary CT angiography failed to detect intracranial bleeding or pulmonary embolism. These findings led us to believe that the patient had VF associated with severe hypokalemia caused by acute gastroenteritis and use of diuretics. Initially, 10 mEq potassium was administered intravenously over 5 min, and then a 40-mEq/h infusion was continued with continuous ECG monitoring (1). The patient was admitted to the intensive care unit and the electrolyte abnormalities were corrected. No neurological improvement was achieved in 2 weeks time, although vital signs and biochemical results, including electrolyte levels, were normal.
DISCUSSION We report the case of a 61-year-old woman with ventricular fibrillation associated with severe hypokalemia caused by acute gastroenteritis and use of diuretics. Electrolyte abnormalities have become an increasingly important cause of dysrhythmias due to the widespread use of high-potency diuretics. Hypokalemia is one of the common complications of diuretic use. Other factors
The Journal of Emergency Medicine
185
Figure 1. Electrocardiographic findings 1 h after resuscitation: left bundle branch block with normal ventricular rate, atrial fibrillation, and U-wave formation.
such as poor oral intake combined with vomiting and diarrhea, high insulin and aldosterone levels, and pronounced renal and gastrointestinal potassium loss resulted in severe hypokalemia (2). In this patient, the hypokalemia may have resulted from chronic diuretic use and loss of potassium via the gastrointestinal route. Hypokalemia increases the resting cardiac membrane potential and increases the duration of the action potential and the duration of the refractory period (3). All of these physiological changes increase the vulnerability and excitability of the heart, and malignant dysrhythmias may occur. The characteristic ECG findings associated with moderate to severe hypokalemia include the triad of decreased Twave amplitude, depression of the ST segment, and U-wave formation (4). These ECG findings of hypokalemia are present in approximately 80% of cases when the serum potassium concentration is ⬍2.5 mEq/L (5). The major limitation of this report is the absence of percutaneous coronary angiography. Although this wasn’t necessary for the patient’s treatment, it would have helped to exclude acute coronary syndromes. The ECG findings after ED management of VF were similar to her preoperative ECG findings. CONCLUSION In summary, hypokalemia may contribute to the occurrence of ventricular fibrillation, especially in patients with structural heart disease. We present this case to
increase awareness among emergency physicians of electrolyte disorders that may lead to cardiac arrest. Acknowledgment—This report was supported by the Akdeniz University Research Foundation and Project Unit.
Firat Bektas, MD Secgin Soyuncu, MD Department of Emergency Medicine Akdeniz University Faculty of Medicine Antalya, Turkey doi:10.1016/j.jemermed.2010.05.079 REFERENCES 1. American College of Cardiology/American Heart Association 2005 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Part 10.1: life-threatening electrolyte abnormalities. Circulation 2005;112(Suppl I):IV121–5. 2. Gibbs MA, Tayal VS. Electrolyte disturbances. In: Marx JA, Hockberger R, Walls R, eds. Rosen’s emergency medicine: concepts and clinical practice. 6th edn. Philadelphia: Elsevier; 2006;1933–55. 3. Wald DA. ECG manifestations of selected metabolic and endocrine disorders. Emerg Med Clin North Am 2006;24:145–57:vii. 4. Slovis C, Jenkins R. ABC of clinical electrocardiography: conditions not primarily affecting the heart. BMJ 2002;324:1320 –3. 5. Londer M, Hammer D, Kelen GD. Fluid and electrolyte problems. In: Tintinalli JE, Kelen GD, Stapczynski JS, eds. Emergency medicine: a comprehensive study guide, 6th edn. New York: McGrawHill:167–79.
Letters to the Editor
debilitated, and having long-term urinary catheterization (2). The clinical course is not always benign; in fact, it can be quite complicated. Yu-Jang Su, MD Department of Emergency Medicine Mackay Memorial Hospital Taipei, Taiwan Mackay Medicine Nursing and Management College Taipei, Taiwan Research Center for Biomedical Implants and Microsurgery Devices Taipei Medical University Taipei, Taiwan doi:10.1016/j.jemermed.2010.05.083 REFERENCES 1. Lee J. Images in clinical medicine. Purple urine. N Engl J Med 2007;357:e14 2. Su YJ, Lai YC, Chang WH. Purple urine bag syndrome in a dead-on-arrival patient: case report and articles reviews. Am J Emerg Med 2007;25:861.e5– 6.
e HYPOKALEMIA-INDUCED VENTRICULAR FIBRILLATION To the Editor: Electrolyte abnormalities, including abnormal serum potassium concentration, are considered to be a correctable cause of life-threatening ventricular dysrhythmia, according to the American Heart Association/American College of Cardiology (AHA/ACC) Practice Guidelines (1). We report the case of a 61-year-old woman with ventricular fibrillation possibly related to severe hypokalemia caused by acute gastroenteritis and use of diuretics.
CASE REPORT A 61-year-old woman presented to the Emergency Department (ED) with sudden cardiac arrest. While the patient was eating her dinner, she collapsed suddenly and family members brought her to the ED within 10 min. She had a history of moderate-degree mitral failure and atrial fibrillation (AF). Her medications included carvedilol 6.25 mg, furosemide 20 mg, and lisinopril 20 mg per oral. Two weeks before her presentation, she underwent an operation for inguinal hernia repair. Preoperative evaluation of the patient demonstrated the following results: an electrocardiogram (ECG) showed left bundle branch block (LBBB), AF with normal QT interval (0.376 s), laboratory data significant for hemoglobin 9.8 mg/dL, hematocrit 29.8,
platelet count 287,000, kidney and hepatic functions within normal ranges, and an echocardiogram showed a moderate degree of mitral failure and a 65% ejection fraction. There were no complications during the operation. However, the patient’s hospital course was complicated by diarrhea three times a day. She was discharged from the hospital after 5 days. Two days later she presented to the ED in cardiac arrest and underwent cardiopulmonary resuscitation (CPR) in accordance with the AHA/ACC practice guidelines. During the resuscitation, she received three monophasic 360-j electrical shocks for ventricular fibrillation (VF). After approximately 10 min of CPR, there was return of spontaneous circulation (ROSC). At ED presentation, her vital signs were as follows: blood pressure 130/84 mm Hg, heart rate 107 beats/min, respiratory rate 20 breaths/min (mechanically ventilated), axillary body temperature 35.8°C, and oxygen saturation 100% by pulse oximeter. The Glasgow Coma Scale score was 3. The physical examination was normal except for midriatic pupils (5 mm), a sutured incision at the suprapubic area, and mitral regurgitation murmur. The ECG taken after her ROSC revealed rapid ventricular rate AF and LBBB; DII – DIII – AVF revealed approximately 1 mm ST depression. A repeat ECG 1 h later demonstrated LBBB, AF, and U-wave formation (Figure 1). Pertinent laboratory data obtained post resuscitation revealed an anemia of 7.9 mg/dL, severe hypokalemia (1.17 mmol/L), and cardiac markers that became elevated to 0.44 ng/mL at 4 h. Biochemical parameters, thyroid function, and aldosterone level were normal. Serum magnesium level was measured as 1.68 mg/dL. No free fluid was found on bedside abdominal sonography. Head computed tomography (CT) scan and multislice pulmonary CT angiography failed to detect intracranial bleeding or pulmonary embolism. These findings led us to believe that the patient had VF associated with severe hypokalemia caused by acute gastroenteritis and use of diuretics. Initially, 10 mEq potassium was administered intravenously over 5 min, and then a 40-mEq/h infusion was continued with continuous ECG monitoring (1). The patient was admitted to the intensive care unit and the electrolyte abnormalities were corrected. No neurological improvement was achieved in 2 weeks time, although vital signs and biochemical results, including electrolyte levels, were normal.
DISCUSSION We report the case of a 61-year-old woman with ventricular fibrillation associated with severe hypokalemia caused by acute gastroenteritis and use of diuretics. Electrolyte abnormalities have become an increasingly important cause of dysrhythmias due to the widespread use of high-potency diuretics. Hypokalemia is one of the common complications of diuretic use. Other factors
The Journal of Emergency Medicine
185
Figure 1. Electrocardiographic findings 1 h after resuscitation: left bundle branch block with normal ventricular rate, atrial fibrillation, and U-wave formation.
such as poor oral intake combined with vomiting and diarrhea, high insulin and aldosterone levels, and pronounced renal and gastrointestinal potassium loss resulted in severe hypokalemia (2). In this patient, the hypokalemia may have resulted from chronic diuretic use and loss of potassium via the gastrointestinal route. Hypokalemia increases the resting cardiac membrane potential and increases the duration of the action potential and the duration of the refractory period (3). All of these physiological changes increase the vulnerability and excitability of the heart, and malignant dysrhythmias may occur. The characteristic ECG findings associated with moderate to severe hypokalemia include the triad of decreased Twave amplitude, depression of the ST segment, and U-wave formation (4). These ECG findings of hypokalemia are present in approximately 80% of cases when the serum potassium concentration is ⬍2.5 mEq/L (5). The major limitation of this report is the absence of percutaneous coronary angiography. Although this wasn’t necessary for the patient’s treatment, it would have helped to exclude acute coronary syndromes. The ECG findings after ED management of VF were similar to her preoperative ECG findings. CONCLUSION In summary, hypokalemia may contribute to the occurrence of ventricular fibrillation, especially in patients with structural heart disease. We present this case to
increase awareness among emergency physicians of electrolyte disorders that may lead to cardiac arrest. Acknowledgment—This report was supported by the Akdeniz University Research Foundation and Project Unit.
Firat Bektas, MD Secgin Soyuncu, MD Department of Emergency Medicine Akdeniz University Faculty of Medicine Antalya, Turkey doi:10.1016/j.jemermed.2010.05.079 REFERENCES 1. American College of Cardiology/American Heart Association 2005 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Part 10.1: life-threatening electrolyte abnormalities. Circulation 2005;112(Suppl I):IV121–5. 2. Gibbs MA, Tayal VS. Electrolyte disturbances. In: Marx JA, Hockberger R, Walls R, eds. Rosen’s emergency medicine: concepts and clinical practice. 6th edn. Philadelphia: Elsevier; 2006;1933–55. 3. Wald DA. ECG manifestations of selected metabolic and endocrine disorders. Emerg Med Clin North Am 2006;24:145–57:vii. 4. Slovis C, Jenkins R. ABC of clinical electrocardiography: conditions not primarily affecting the heart. BMJ 2002;324:1320 –3. 5. Londer M, Hammer D, Kelen GD. Fluid and electrolyte problems. In: Tintinalli JE, Kelen GD, Stapczynski JS, eds. Emergency medicine: a comprehensive study guide, 6th edn. New York: McGrawHill:167–79.