EFFECT
OF DIGITALIS AND CALCIUM/POTASSIUM LEVELS ON ELECTROCARDIOGRAM
DRUG EFFECTS: DIGITALIS
The effect of
common drugs such as digitalis and other antiarrhythmic agents on the ECG
depends on the dose, the rate of excretion, responsiveness of the patient, and
previous ECG abnormalities. Small doses of digitalis produce a mild digitalis
effect with sagging depression of the ST segment, negative J shifts, and
lowering of the T waves (Plate 2-28, A). The QT interval may be
shortened slightly because of increases in the rate of ventricular
repolarization. Digitalis usually slows the cardiac rate and A-V conduction
because of vagal depression of the SA and AV nodes. With large doses a further
depression of J occurs, with sagging of the S-T segments and a distinct
decrease in the Q-T intervals, which fall outside of normal limits (Plate 2-28, B). With toxic doses
there is a depression of the A-V conduction tissue, with prolonged P-R
intervals, and a state of ventricular irritability, with ventricular ectopic
beats, which may be single or multiple and multifocal (Plate 2-28, C). Coupling is
common, and atrial fibrillation or flutter, with paroxysmal atrial tachycardia,
and block or variable degrees of A-V block may occur.
Drugs such as
procainamide (Pronestyl) and lidocaine (Xylocaine), tend to depress the
electric activity of the atria and ventricles. Characteristically, the P waves
increase in duration, with a slight increase in amplitude. Drugs such as
ibutilide often cardiovert the AF to sinus rhythm, but the patient should
receive intravenous magnesium sulfate before treatment, to prevent torsades de
pointes. Intravenous amiodarone also prolongs the Q-T interval and frequently
will cardiovert the patient to sinus rhythm.
Hypercalcemia
may be
encountered in patients with hyperparathyroidism. The ECG is characterized by
shortening of the Q-T intervals, often with increased amplitudes of the T waves
(Plate 2-28, H). The T waves begin
immediately after the ending of the QRS complexes, so the QRS complexes and T
waves appear compressed.
Hypocalcemia
increases
the duration of the S-T and Q-T intervals (Plate 2-28, J). The QRS complexes and T waves merely appear to be
widely separated from each other by long S-T segments, which often are
isoelectric.
Hyperkalemia
depresses
the atria, the A-V node, and the ventricles but has less effect on the sinus
node.
Consequently,
increases in potassium concentration produce prolonged P-R intervals (Plate 2-28, L), high T waves, SA block
with small or absent mechanical contractions of the atria, tenting of the T
waves (tall and narrow at base), intraventricular block with widening of QRS
complexes, abnormal shifts of the S-T segment, and ventricular standstill or
ventricular fibrillation (Plate 2-28, K).
Hypokalemia frequently results from
administration of diuretics or cortisone or from vomiting, diarrhea, surgical
suction, or low intake of potassium. Hypokalemia causes an amplitude loss in
the T waves (Plate 2-28, N) and a prominence of the U waves, with easily measured Q-U intervals. T
and U waves are clearly separated in some leads but may fuse in others,
causing a T-U complex. Deviations of the S-T segment (depression or elevation)
may occur. It is difficult to recognize hypokalemia associated with other
abnormal states, such as myocardial ischemia or infarction, or with cardiac
drugs.
