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![enter image description here][1]
Above picture depicts normal action potential in junctional myocardium i.e SA node.

Hypokalemia is the decrease in K+ concentration in plasma i.e. ECF (Extracellular fluid). Resting membrane potential is determined by the ratio of K+ concentration in ICF to ECF. Hence, in hypokalemia, the resting membrane potential (Stage 4) becomes more negative, moving it further away from the threshold of excitation. Thus, it takes a greater stimulus to reach threshold and open the Na+ channels that are responsible for action potential (Stage 1).

Normally, K+ leaves the cell during repolarization phase of action potential (Stage 3). Also, in hypokalemia, there is decreased permeability of cell membrane to K+ leading to decreased K+ efflux that prolongs the rate of repolarization and lengthens the relative refractory period and a decrease in the difference
of the resting membrane potential from the threshold potential during the terminal phase of the AP. Thus, cardiac tissue demonstrates increased excitability with associated ectopy for a considerable portion of the AP. Conduction slows because depolarization begins in incompletely repolarized fibers. Furthermore, hypokalemia prolongs the plateau (Stage 2) in the Purkinje fibers but shortens it in the ventricular fibers.

Both the delayed activation of Na channels and delayed rate of repolarization predispose to cardiac arrhytmias and conduction defects.

In summary, the EP effects of hypokalemia are: (1) a decrease in conduction velocity; (2) shortening of the effective refractory period (ERP); (3) prolongation of the RRP; (4) increased automaticity; and (5) early afterdepolarizations (EADs)

![enter image description here][2]

Early ECG changes include flattening or inversion of the T wave, a prominent U wave, ST-segment depression, and a prolonged QT interval. Severe K depletion may result in a prolonged PR interval, decreased voltage and widening of the QRS complex, and an increased risk of ventricular arrhythmias, especially in patients with myocardial ischemia or left ventricular hypertrophy. Hypokalemia may also predispose to digitalis toxicity.

[1]: http://upload.wikimedia.org/wikipedia/commons/thumb/c/cb/Action_potential_ventr_myocyte.gif/600px-Action_potential_ventr_myocyte.gif
[2]: http://2.bp.blogspot.com/-wxw06T-Z1to/ThBSmXhRrfI/AAAAAAAAAIM/PI5pYHeLZuY/s640/hypokalemia.jpg
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