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Spontaneous Circulation: Curious Consequences of the Lessor Metals

Bruen, Charles MD

doi: 10.1097/01.EEM.0000462406.49048.ed
Spontaneous Circulation

Dr. Bruenis a fellow in critical care medicine and emergency cardiology at Hennepin County Medical Center in Minneapolis. He has special interest in stabilization, resuscitation, hemodynamic evaluation, and emergency cardiovascular care. Visit his website,http://resusreview.com, follow him @resusreview, and read his past columns athttp://bit.ly/SponCirc.

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Figure. EC

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The potassium level in the body is closely regulated, but hypokalemia can still develop by several mechanisms, including gastrointestinal loss, renal potassium wasting, or shifting potassium into the intracellular space with an alkalosis. Characteristic changes in the ECG are associated with hypokalemia, which become more prominent as the hypokalemia worsens. The T waves flatten, and may disappear. A U wave may develop, which is seen as a small deflection after the T wave and in the same direction. Its magnitude is usually <0.5mm, but it is inversely proportional to the pulse, becoming larger at a slower heart rate. It is most prominent in V2 and V3. It is important not to mistake the QU interval for a prolonged QT interval.

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Table EC

The myocardium is very sensitive to hypokalemia, with its largest effect on inhibiting the action of the delayed rectifier potassium channels (IKr) reducing the outward potassium current. Even though the cardiac action potential is prolonged, the refractory period remains unchanged, which dramatically increases the chance after depolarizations that can lead to ventricular arrhythmias. These effects may be exacerbated by ischemia or digoxin toxicity. Hypokalemia also increases the hyperpolarization in the AV node, which increases the effects of acetylcholine suppression on AV conduction (negative dromotropic).

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