From the Guidelines
The pathophysiology of ECG changes in hyperkalemia involves the effect of elevated potassium levels on cardiac cell membrane potential and excitability, leading to a predictable sequence of ECG changes, including peaked T waves, flattened or absent P waves, prolonged PR interval, widened QRS complex, and eventually a sine-wave pattern or asystolic cardiac arrest. The sequence of ECG changes in hyperkalemia is well described in the 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care 1. Hyperkalemia reduces the resting membrane potential difference between the inside and outside of cardiac cells, making them less negative (less polarized), which occurs because the normal potassium gradient across the cell membrane is diminished when extracellular potassium rises.
As potassium levels increase, characteristic ECG changes develop, initially with T waves becoming tall and peaked (often the earliest sign) due to accelerated repolarization, as noted in the guidelines 1. Further increases in potassium levels lead to a prolongation of the PR interval and a decrease in P wave amplitude because of slowed atrial conduction. With worsening hyperkalemia, QRS complexes widen as ventricular depolarization slows. In severe cases, P waves disappear completely, and the QRS complex continues to widen, eventually merging with the T wave to create a sine wave pattern, which can ultimately lead to ventricular fibrillation or asystole, as described in the guidelines 1.
Key ECG changes associated with hyperkalemia include:
- Peaked T waves (tenting) on the electrocardiogram (ECG)
- Flattened or absent P waves
- Prolonged PR interval
- Widened QRS complex
- Deepened S waves
- Merging of S and T waves
- Sine-wave pattern
- Idioventricular rhythms
- Asystolic cardiac arrest, all of which are critical indicators of the need for immediate intervention to prevent life-threatening cardiac complications, as emphasized in the guidelines 1.
From the Research
Pathophysiology of EKG Changes in Hyperkalemia
The pathophysiology of EKG changes in hyperkalemia is complex and involves various mechanisms.
- Hyperkalemia can lead to changes in the electrocardiogram (ECG), including peaking of the T waves, wide QRS, and bradycardia 2, 3.
- These changes are thought to be due to the effects of hyperkalemia on the cardiac action potential, including shortening of the action potential duration and alterations in the profiles of potassium currents 4.
- The inward rectifier potassium current (IK1) is significantly increased in hyperkalemia, which can contribute to the shortening of the action potential duration 4.
- Hyperkalemia can also lead to a reduction in the driving force for potassium efflux, which can affect the rapid and slow delayed rectifier potassium currents (IKr and IKs) 4.
ECG Alterations in Hyperkalemia
ECG alterations in hyperkalemia can be variable and may include:
- Peaked T waves 2, 3
- Wide QRS 3
- Bradycardia 3
- First-degree AV block 3
- Prolonged QTc interval 3
- These alterations can be seen in both normokalemic and hyperkalemic patients, although they are more common and severe in patients with hyperkalemia 3.
Clinical Implications
The clinical implications of EKG changes in hyperkalemia are significant, as they can indicate a life-threatening condition that requires prompt intervention 2, 5, 6.
- Treatment of hyperkalemia typically involves administration of intravenous calcium salts to stabilize the cardiac membrane potential, as well as measures to lower the potassium concentration, such as insulin and glucose infusion, and nebulized β-2 adrenoceptor agonists 5.
- In severe cases, hemodialysis may be necessary to rapidly lower the potassium concentration 6.