EKG Case - A 72 year old female with shortness of breath
Brian Strickler, MD
BRIEF CLINICAL BACKGROUND
The patient is a 72 year-old female who was transferred to the Emergency Department from her nursing home due to shortness of breath and dizziness. She denied other complaints.
Her past medical history is significant for end stage renal disease on hemodialysis (last dialysis treatment was on the day prior to presentation), COPD, type II diabetes, hypertension, atrial fibrillation, congestive heart failure, and an abdominal aortic aneurysm.
Her vital signs and physical exam on admission were unremarkable.
An electrocardiogram (EKG) shows:
What is the diagnosis?
ANSWER: Hyperkalemia
DISCUSSION
The EKG shows a ventricular rate of 90 beats per minute. The rhythm is sinus, as P waves are visible in leads I, aVL, V1, and V2. The most obvious abnormality in the EKG is widening of the QRS complex. The QRS duration in this EKG is 0.48 seconds, which is markedly prolonged compared to the normal value of less than 0.1 seconds. This indicates delayed conduction within the ventricles.
There are many causes of intraventricular conduction delay, including ischemic conduction system damage, age-related conduction system degeneration, and iatrogenic conduction delay secondary to a ventricular pacemaker. Hyperkalemia is also an important cause of delayed intraventricular conduction and, in extreme cases, widening of the QRS complex.
In our patient, it is vital to recognize that she has end stage renal disease on hemodialysis, and is thus at very high risk for developing hyperkalemia. Her serum potassium concentration was ultimately found to be 8.2 mEq/L. The abnormal appearance of her EKG is secondary to hyperkalemia.
Hyperkalemia causes cardiac toxicity by causing partial depolarization of myocyte cell membranes. This reduces the excitability of the myocytes and delays the passage of electrical impulses through the ventricular conduction system. As the severity of the hyperkalemia increases, cardiac toxicity worsens in a predictable manner. The electrocardiogram findings parallel the worsening toxicity. Initially, peaked T waves develop as elevated extracellular potassium levels cause prolongation of ventricular repolarization. As potassium levels increase, the PR interval and QRS duration both increase, reflecting delayed depolarization secondary to decreased membrane excitability. Eventually, a "sine-wave" results when the QRS complex widens enough that it fuses with the T wave. Once a sine wave pattern results, the patient is at the maximum serum concentration of potassium that is still compatible with life. If potassium levels increase further, the result can be ventricular fibrillation, asystole, and death. The EKG of this patient very closely resembles a sine-wave pattern.
Treatment of hyperkalemia has three goals: reverse the myocyte membrane toxicity, immediately reduce the serum potassium concentration by shifting potassium into the intracellular space, and removing potassium from the body. To reverse membrane toxicity, the patient should be given calcium gluconate 1000mg intravenously over 2-3 minutes. This should result in membrane stabilization within minutes, and if the EKG changes have not resolved within 10 minutes, this dose may be repeated. To rapidly reduce serum potassium concentration, the patient should be given 10 units of regular insulin IV, 50 grams of intravenous dextrose, and a beta-2 agonist such as nebulized albuterol. Both insulin and beta-2 agonists work by driving potassium into the cells by increasing the activity of the sodium-potassium ATPase channel. Each of these interventions should reduce plasma potassium by 1.5 mEq/L, with peak effect arriving in thirty minutes to one hour after the initial dose is given. Ultimately, the patient should undergo emergent hemodialysis for effective potassium removal from the body. For patients with functioning kidneys, a loop diuretic such as furosemide can be used for potassium removal. If her hyperkalemia were less severe, an oral cation-exchange resin such as sodium polystyrene sulfonate would be a reasonable alternative as well.
REFERENCES
- Rose, Barton D."Clinical Manifestations and Treatment of Hyperkalemia. " Up to Date. 2007.
- Singer, Gary G and Brenner, Barry M."Fluid and Electrolyte Disturbances. "Harrison's Principles of Internal Medicine. 2001.
- Podrid, Philip J."Approach to the Diagnosis and Treatment of Wide QRS Complex Tachycardias." Up to Date. 2007.