Matters Of The Heart-Electrolyte and Drug Imballance

There are electrolyte imballances that cause certian arrhythmias:

Potassium

(acts as a partner to sodium, helps stablize the myocyte's electrical energy during repolarization)

Too much potassium is called Hyperkalemia, and results in peaked T waves, flattened P waves, and a wide QRS complex on an EKG.

Too little potassium is called Hypokalemia, and results in flat T waves as well as the creation of another wave after the T wave (called a U wave...)

These signs will increase in severity as the electrolyte imbalance increases.

Calcium

This ion functions in the AV node, his bundle, and branches. It also excellerates ventricular depolarization/repolarization.
Hyper calcemia results in a short QT interval (shortens everything except for the P wave, because that's the atria and calcium speeds up the ventricles.)

Hypocalcemia results in a prolonged QT interval.

There are also certian arrhythmias associated with drug toxicity:

Digitalis

Digoxin is a drug that treats Atrial fibrillation by slowing the SA node (it also inhibits the AV node from being receptive to the extra atrial impulses).
However, the theraputic range for this drug is narrow, and too much can cause heart block, premature beats, or both!

If the toxicity progresses, eventually the irritation and heart block will cause ventricular rhythms such as Ventricular tachycardia and fibrillation from taking over.

It's importiant to monitor drug levels in patients who take digoxin, as well as look for the charactaristic, 'dipping' ST segment depression.

Quinidine

Is another antiarrhythmic. Like Digoxin, it is for the treatment of A Fib. It works as a sodium channel blocker, it lengthens depolarization and repolarization. On an EKG strip, toxicity with this drug appears as wide, notched P and QRS waves, a depressed ST segment, and a U wave present. If not corrected, this toxicity can also lead to Torsades de Pointes.