Supraventricular tachycardias should be described as long RP or short RP tachycardia.
SVT is a general term and has no reference to the underlying pathophysiology or mechanism causing narrow QRS tachycardia. Short RP tachycardias, are most commonly seen in clinical practice, long RP tachycardias to a lesser extent (the latter more frequently in the ICU setting)
.
One should always look at the initiation of the tachycardia, i.e. is there warm up or ramp-up phase. How does the tachycardia terminate: is there a P before conversion to sinus tachycardia after administration of adenosine, or does the tachycardia terminate without a P-wave? What is the axis of the P-wave during narrow QRS tachycardia, i.e. is axis inferior or superior?
Adenosine should always be administered both as a diagnostic and possible therapeutic agent in the setting of sudden onset hemodynamically stable
narrow QRS tachycardia ( and regular monomorphic VT- see below) . Adenosine terminates close to 100% of short RP ( narrow QRS) tachycardias (slow-fast AVNRT as most common rhythm).
Long RP (narrowQRS) tachycardia's are seen less common but deserve some further attention (higher incidence in the ICU setting) :
1. Fast-slow AV nodal reentry tachycardia
2. AV reentry tachycardia with retrograde conduction over accessory pathway
3. Ectopic atrial tachycardia/focal atrial tachycardia
4. Sinus tachycardia
Adenosine will terminate AV nodal reentry tachycardia, but very uncommonly there is an adenosine sensitive accessory pathway. It will not terminate sinus tachycardia but can cause slowing of the rate.
However, some ectopic atrial tachycardias can be terminated by adenosine.(60-80%)
Of note, adenosine can also be administered for hemodynamically stable regular monomorphic wide complex QRS tachycardia, as it will break AV reentry tachycardia with antegrade conduction over accessory pathway as well as some forms of
ventricular tachycardia
The new ACLS guidelines now has adenosine given up to 2 times instead of 3 times. The first dose of adenosine should be 6 mg administered rapidly over 1-3 seconds followed by a 20 cc normal saline bolus (
use 3 -way stopcock). If the patient's rhythm does not convert within 1 to 2 minutes, a second 12 mg dose may be given similar fashion.
A lower initial dose of 3 mg should be used in patients taking dipyridamole or carbamazepine as these 2 medications potentiate the effect of adenosine.
Also, prolonged asystole has been seen with the use of normal doses of adenosine in heart transplant patients and central line use.
Therefore, the lower, 3 mg dose should be considered for patient's with a central venous line or history of heart transplant
Sometimes termination is followed by an immediate return of the tachycardia, even in AVNRT. In these patients, intravenous verapamil 5-10 mg slow push can be used. Diltiazem, 20 mg IV as a loading dose followed by 10 mg/min continuous infusion, can be used but is less effective than verapamil. Intravenous beta blockers i.e. metoprolol, esmolol, can be used as an alternative to verapamil or diltiazem in patients who do not not convert with or are intolerant to adenosine.
This case report in the New England Journal of Medicine is an interesting presentation of focal atrial tachycardia secondary to hyperthyroidism ( Graves' disease).
It also highlights that performing contrast studies will cause temporary suppression of thyroid production due to administration of a high iodine load and " masque" hyperthyroidism for certain period of time.
