Quinidine is ordered for a patient with recurrent atrial fibrillation. This drug:
|A||Is likely to increase blood pressure via a direct vasoconstrictor effect|
|B||Is contraindicated if the patient also requires anticoagulant therapy|
|C||Slows spontaneous S-A nodal depolarization as its predominant effect|
|D||Tends to slow electrical impulse conduction velocity through the A-V node|
a. Quinidine’s main beneficial effect in supraventricular arrhythmias is a suppression of spontaneous depolarization of the S-A node.
b. Concomitantly, the predominant effect on the A-V node is an increase of nodal electrical impulse conduction velocity (not a slowing, as noted in d).
c. This is a main reason why, when quinidine therapy is to be started and atrial rates are still high, we pretreat the patient with a dose of a drug that “blocks down” the A-V node: often digoxin. Sometimes verapamil or diltiazem, and occasionally a βeta blocker.
d. The main reason why ventricular rates aren’t identical (or close to) atrial rates during atrial fibrillation is because the A-V node cannot transmit impulses at such high rates.
e. This protective effect depends on A-V nodal refractoriness and a relative inability to transmit too many impulses per time.
f. If we did not suppress the A-V node before giving quinidine, the A-V nodal effects of the quinidine might increase A-V nodal transmission; ventricular rates might rise to dangerous levels as atrial rate slows in response to the quinidine.
g. Quinidine is not likely to increase blood pressure, or worsen preexisting hypertension. Quite the contrary: the predominant vascular effect of the drug is dilation, probably due to some α-adrenergic blocking activity