Talks
Presentation Type
Oral Presentation
Discipline Track
Patient Care
Abstract Type
Case Report
Abstract
Background: Hyperkalemia is one of the most potentially lethal electrolyte disorders. Severe hyperkalemia is defined as a serum potassium level of >6.5 mEq/L. The risk of arrhythmias increases with potassium values >6.5 mEq/L. Small elevation above this value can cause peaked T waves to quickly progress to ventricular fibrillation or asystole. The longer the patient has elevated potassium concentrations, the greater the risk of sudden deterioration. Therefore, recognizing ECG changes and acting quickly to decrease potassium concentration is important to prevent hyperkalemic cardiac arrest.
Case Presentation: A 26-Year-old man with a history of congenital hypoaldosteronism presented to the emergency department with a complaint of palpitations, lightheadedness, bilateral extremity weakness, and generalized muscle aches of 4 hours duration, culminating in collapse. He denied shortness of breath, chest pain, blurring of vision. On examination he was afebrile, tachycardic, and normotensive. Cardiac and respiratory exams were unremarkable, on neurology examination patient was alert and oriented x3, strength 0/5 in 4 extremities. Initial EKG revealed Sinus tachycardia with flattened P waves, wide and bizarre QRS morphology. On laboratory sodium was 119, potassium 9.4, chloride 87, co2 17, creatinine 1.5, and BUN of 33.
The patient was managed with emergent calcium gluconate supplementation, sodium bicarbonate, albuterol via nebulizer, insulin, and glucose. Repeat potassium after 2 hours of presentation was 9.0 mEq/L without EKG changes from baseline. Repeated administration of the above medications resulted in only partial improvement of the serum potassium, with the patient reporting improvement in motor strength, and muscle aches. Emergent hemodialysis was recommended, but delayed due to logistics, with initial medical management avoiding immediate complications. Ultimate hemodialysis resulted in rapid correction of his hyperkalemia several hours after presentation.
Conclusion: Hyperkalemia is a common electrolyte abnormality and is associated with increased mortality. It is important to recognize clinical presentation and abnormal ECG changes of severe hyperkalemia in order to prevent hyperkalemic cardiac arrest by initiating medical management to antagonize the effect of potassium on excitable membranes, rapidly shift potassium into cells, and enhance potassium elimination to preventing hyperkalemic cardiac arrest. This is more useful in small community hospitals where urgent hemodialysis is not easily accessible 24 hours a day.
Academic/Professional Position
Resident
Academic/Professional Position (Other)
PGY2
Mentor/PI Department
Internal Medicine
Recommended Citation
Burka, Semenawit B.; Flores, Eduardo; and Gyebi-Agyepong, Johnathan, "Recognizing Fatal Electrocardiography Rhythm Changes in a patient with Severe Hyperkalemia and Prevention of Cardiac Arrest with medical management in small hospitals" (2023). Research Symposium. 30.
https://scholarworks.utrgv.edu/somrs/2022/talks/30
Included in
Recognizing Fatal Electrocardiography Rhythm Changes in a patient with Severe Hyperkalemia and Prevention of Cardiac Arrest with medical management in small hospitals
Background: Hyperkalemia is one of the most potentially lethal electrolyte disorders. Severe hyperkalemia is defined as a serum potassium level of >6.5 mEq/L. The risk of arrhythmias increases with potassium values >6.5 mEq/L. Small elevation above this value can cause peaked T waves to quickly progress to ventricular fibrillation or asystole. The longer the patient has elevated potassium concentrations, the greater the risk of sudden deterioration. Therefore, recognizing ECG changes and acting quickly to decrease potassium concentration is important to prevent hyperkalemic cardiac arrest.
Case Presentation: A 26-Year-old man with a history of congenital hypoaldosteronism presented to the emergency department with a complaint of palpitations, lightheadedness, bilateral extremity weakness, and generalized muscle aches of 4 hours duration, culminating in collapse. He denied shortness of breath, chest pain, blurring of vision. On examination he was afebrile, tachycardic, and normotensive. Cardiac and respiratory exams were unremarkable, on neurology examination patient was alert and oriented x3, strength 0/5 in 4 extremities. Initial EKG revealed Sinus tachycardia with flattened P waves, wide and bizarre QRS morphology. On laboratory sodium was 119, potassium 9.4, chloride 87, co2 17, creatinine 1.5, and BUN of 33.
The patient was managed with emergent calcium gluconate supplementation, sodium bicarbonate, albuterol via nebulizer, insulin, and glucose. Repeat potassium after 2 hours of presentation was 9.0 mEq/L without EKG changes from baseline. Repeated administration of the above medications resulted in only partial improvement of the serum potassium, with the patient reporting improvement in motor strength, and muscle aches. Emergent hemodialysis was recommended, but delayed due to logistics, with initial medical management avoiding immediate complications. Ultimate hemodialysis resulted in rapid correction of his hyperkalemia several hours after presentation.
Conclusion: Hyperkalemia is a common electrolyte abnormality and is associated with increased mortality. It is important to recognize clinical presentation and abnormal ECG changes of severe hyperkalemia in order to prevent hyperkalemic cardiac arrest by initiating medical management to antagonize the effect of potassium on excitable membranes, rapidly shift potassium into cells, and enhance potassium elimination to preventing hyperkalemic cardiac arrest. This is more useful in small community hospitals where urgent hemodialysis is not easily accessible 24 hours a day.