And the fact that the half-life of this drug is less than 10 seconds means that almost always (but not “always”) - adverse effects will be short-lived. That said - the potential positive effects of Adenosine far outweight the risk of adverse effects under the large maority of situations. This IS true for Adenosine, which is not a completely “benign” medication. We need to appreciate that no drug is perfect - and with ANY medication (be this a simple antibiotic or potent antiarrhythmic agents) - there is the possibility of adverse effects. Use of these medications without prior AV blockade is dangerous as it will lead to 1:1 conduction!! The atrial rate can be much slower in the setting of a sodium channel blocker such as flecainide, quinidine, or procainamide. The ventricular rate depends on AV node conduction and is usually half the atrial rate (2:1 conduction), but may become 1:1 (dangerous) or slow down to less than 2:1 in the presence of AV node blockers Here is the case: Sepsis with Pulmonary Edema and Elevated Right Sided PressuresĪtrial flutter is usually at a rate of 300, but can be anywhere between 240 and 360. Slow atrial flutter (flutter rate 240, ventricular rate 120) Thus the flutter rate is 270 with 2:1 conduction. The subsequent negative deflection of the normal P-wave in V1 is the left atrium. The positive deflection of a normal P-wave in V1 is the right atrium True P-waves are not upright in V1 they are biphasic up-down. Notice there is an extra "P-wave" at the end of each QRS in V1 The rhythm strip across the bottom is V1 (it is usually lead II) Narrow complex tachycardia at rate of 135. Notice there is a "P-wave" directly superimposed (on top of) the T-wave in V1. Notice there is a "P-wave" just before the QRS in V1 In these cases, they were misdiagnosed as sinus tachycardia (not PSVT): Here are a couple other cases of atrial flutter which were misdiagnosed. More cases of misdiagnosed atrial flutter This is primarily because patients with atrial flutter often alternate between fib and flutter, and produce thrombi during episodes of fibrillation. Similarly to atrial fibrillation, patients with atrial flutter do develop atrial thrombi, and thus cardioversion may involve a risk of thromboembolism if the onset of atrial flutter is not within 12-48 hours of ED presentation. Electrical works better (see article summary at bottom) but has a risk of thromboembolism: So atrial flutter must be treated with either:ġ) A longer acting AV nodal blocker, such as diltiazem infusion, to slow the ventricular response orĢ) Cardioversion, whether electrical or chemical. When the adenosine wears off, the impulse will continue to conduct through the AV node, still at a 2:1. The half-life of adenosine is about 10 seconds, and its effect will rapidly wear off (thankfully, otherwise this patient would be dependent on ventricular escape beats for perfusion!) Therefore adenosine will not interrupt the loop. So adenosine can help to diagnose atrial flutter, but it will not treat atrial flutter.Ītrial flutter does not use the AV node for part of its re-entrant loop, as does PSVT. This "reveals" the flutter waves, which of course continue.Īdenosine simply blocks the AV node so that there is no QRS to hide the flutter waves, and they become obvious. The AV node is blocked by adenosine and QRSs disappear. Thus, adenosine is often given.Īdenosine was given, during which this rhythm strip was recorded: The flutter rate is relatively fast at 334, such that the ventricular rate is 167 (one half the atrial rate).Īs easy as it may seem to make this diagnosis, it is often misdiagnosed as PSVT. In V1, there are upright waves that appear to be P-waves but are not: they are atrial waves and it is typical for atrial flutter waves to be upright in V1, whereas sinus P-waves are biphasic in V1. There are clear flutter waves in lead II across the bottom. It is atrial flutter with 2:1 conduction.
The computer reads supraventricular tachycardia.
A 40-something presented with palpitations and had a regular pulse at 170.
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