Sage-Tips

How does hyperkalemia affect the cardiac action potential?

As serum potassium levels increase to greater than 6.5 mEq/L, the rate of phase 0 of the action potential decreases, leading to a longer action potential and, in turn, a widened QRS complex and prolonged PR interval. Electrophysiologically, this appears as delayed intraventricular and atrioventricular conduction.

How does hyperkalemia stop the heart?

High levels of potassium cause abnormal heart and skeletal muscle function by lowering cell-resting action potential and preventing repolarization, leading to muscle paralysis.

Why does hyperkalemia lead to depolarization?

Increased extracellular potassium levels result in depolarization of the membrane potentials of cells due to the increase in the equilibrium potential of potassium. This depolarization opens some voltage-gated sodium channels, but also increases the inactivation at the same time.

How would hyperkalemia affect neuronal excitability?

In hyperkalemia, the resting membrane potential is decreased, and the membrane becomes partially depolarized. Initially, this increases membrane excitability. However, with prolonged depolarization, the cell membrane will become more refractory and less likely to fully depolarize.

Is hyperkalemia intracellular or extracellular?

Aetiology. Hyperkalemia can be the result of psuedohyperkalemia, potassium redistribution from intracellular fluid to extracellular fluid and imbalances between potassium intake and excretion.

What causes intracellular shift of potassium?

Insulin secretion, which is stimulated by an increase in serum potassium, shifts the potassium into the liver and muscle cells. Catecholamines, through stimulation of beta-2 receptors, are also able to shift potassium into the cell.

Does hyperkalemia lead to asystole?

Severe hyperkalemia ([K+]o > 7.0 mmol/l) can lead to heart block, asystole and VT/VF. In humans, the precise level of hyperkalemia producing (or not producing) these changes varies considerably.

What are the ECG changes in hyperkalemia?

ECG changes have a sequential progression, which roughly correlate with the potassium level. Early changes of hyperkalemia include tall, peaked T waves with a narrow base, best seen in precordial leads ; shortened QT interval; and ST-segment depression.

What is the pathophysiology of hyperkalemia?

Increased plasma potassium may occur spontaneously or iatrogenically. At modest hyperkalemia (K+ ∼5 to 7 mEq. per liter) a transient and minor acceleration of cardiac conduction can be demonstrated, but profound and rapid depression of conduction occurs progressively at K > 8 to 9 mEq.

What is the normal cardiac conduction rate in hyperkalemia?

At modest hyperkalemia (K+ ∼5 to 7 mEq. per liter) a transient and minor acceleration of cardiac conduction can be demonstrated, but profound and rapid depression of conduction occurs progressively at K > 8 to 9 mEq. per liter.

Is the wide QRS complex during hyperkalemia of ventricular origin?

This suggests that the wide QRS complex during hyperkalemia was not of ventricular origin but more likely secondary to sino ventricular conduction or junctonal rhythm with significant intra ventricular conduction delay. Atrial fibrillation may disappear during severe hyperkalemia because of depressed atrial conduction-see below (1,2).

What is the difference between hyperkalemia and bundle branch block?

A clue that these EKG changes are due to hyper¬kalemia and not to bundle branch disease, is that in hyperkalemia the conduction delay persists throughout the QRS complex and not just in the initial or terminal portions as seen in left and right bundle branch block, respectively (7).