Adenosine is the drug of choice for paroxysmal supraventricular tachycardia (PSVT) and is once again Advanced Cardiac Life Support-approved for differentiating PSVT with aberrancy from ventricular tachycardia (v tach) in patients with monomorphic wide complex tachycardias.1 Adenosine is a potent and safe antiarrhythmic when used appropriately. However, its use in the wrong patient or rhythm can prove fatal. This article focuses on how to expertly use adenosine and to know when this “safe” antiarrhythmic can be dangerous and contraindicated.
Pharmacology & Mechanisms of Action
Adenosine’s mechanism of action can be thought of as a “temporary paralyzing” of supraventricular tissue. Pharmacologically, adenosine hyperpolarizes the cell by stimulating an inward potassium current and temporarily inhibiting calcium migration.2 In doing so, the pacemaker activity of the sinoatrial (SA) node, spontaneous atrial activity and conduction through the atrioventricular (AV) node are dramatically slowed or temporarily stopped.
Adenosine has no effects on accessory pathways, such as those seen in the Wolf-Parkinson White Syndrome (WPW). Mild side effects of adenosine are common. They include a transient sinus pause that usually lasts less than five seconds, chest pressure or tightness, dyspnea, facial flushing and the feeling of impending doom (see Table 1).2–4
Rare, benign side effects reported include anxiety and dizziness. In one large prehospital trial, 11% of patients had a minor transient complaint, with chest pain being the most common complaint seen in 4% of patients.4 Chest tightness was induced by adenosine administration in 83% of patients in one large in-emergency department (ED) study.5
Side effects from adenosine administration that are serious are extremely rare when used in healthy patients with PSVT (see Table 1). Adenosine may cause mild bronchospasm, which is almost always short lived. However, adenosine can also cause severe bronchospasm and should be given carefully to those with a history of asthma or chronic obstructive pulmonary disease (COPD).6 It shouldn’t be given to patients who are already wheezing. Adenosine has also been reported to cause prolonged sinus pauses, syncope, seizures and even asystole, although this rare side effect has been described almost solely in older patients with preexisting conduction disease and/or second- or third-degree heart block.7–9 Adenosine is the drug of choice for PSVT in pregnant patients.1
The biggest dangers with adenosine are seen in two groups of patients: 1) those with atrial fibrillation or atrial flutter, and 2) those in sinus tachycardia and not PSVT.
Numerous studies in the literature report serious rhythm degeneration and even death when adenosine has been inadvertently given to patients with either atrial fibrillation or atrial flutter. Adenosine can convert relatively stable atrial flutter with 2:1 conduction and a heart rate of 150 to 1:1 conduction with a heart rate of 300 and cause rapid clinical decompensation.10
Adenosine slows or blocks antegrade (atrial to ventricular) conduction through the AV node but doesn’t affect accessory or bypass tracts like those seen in WPW syndrome. Because of this, adenosine can be dangerous when given to patients with atrial fibrillation, especially if they have a bypass track. Numerous reports show patients degenerating into rapid atrial fibrillation with rates at 250 or greater and becoming hemodynamically unstable.10–13
Thus, an absolute contraindication to adenosine exists in patients who have either atrial flutter or an irregular rhythm in atrial fibrillation. Because rapid atrial fibrillation may seem regular on ECG monitor, paramedics are urged to run a rhythm strip and verify true regularity.
We find this easiest by making marks on a piece of paper that match the peaks of the QRS then moving the QRS-marked paper a few beats over to compare it to three to four new beats on the rhythm strip. If they line up, then the rhythm is regular; if they don’t, then the rhythm is irregular (and likely atrial fibrillation), and adenosine shouldn’t be used (see Figures 1a, 1b, 1c).
The other absolute contraindication to adenosine is in sinus tachycardia. Dehydrated patients, especially the elderly with fever, failure to thrive and/or an infection may appear to be in PSVT when in fact they’re barely compensated with a sinus tachycardia with a rate that may be greater than 150. These patients are at high risk for morbidity and mortality if adenosine is administered, and they have a prolonged sinus pause (see Table 2).
In cases for which there’s any chance that sinus tachycardia is the etiology of the patient’s elevated heart rate, a rapid fluid bolus of 250 cc should be administered. Any slowing by just a few beats per minute (rather than a dramatic conversion to a normal sinus rhythm) confirms the diagnosis of sinus tachycardia due to volume depletion.
This is also true in heat stroke victims with PSVT at rates approaching 180 beats per minute. EMS providers should rapidly hydrate and cool these patients before administering adenosine. If the patient’s pulse begins to fall with therapy, the diagnosis of sinus tachycardia due to heat illness and dehydration is confirmed, and adenosine is contraindicated. Table 2 lists the rhythms, rates and patient types in which the diagnosis of PSVT should be considered unlikely.
Administration & Dosage
Once adenosine is administered, its effectiveness lasts only between five and 10 seconds because it’s rapidly metabolized by cellular uptake. Because of the ability of blood vessel endothelium to metabolize adenosine, it’s imperative for EMS providers to give adenosine by rapid bolus followed by a 10–20 cc rapid flush.2,3
Larger, more proximal IV lines are preferred because small-bore IVs don’t routinely allow fast flow or rapid transit to the heart. The dosage of adenosine should be reduced to 3 mgs if injected into a central line, and it shouldn’t be used in heart transplant patients.1,14
The standard initial recommended dosage of adenosine is 6 mg, followed by a rapid saline flush. If this dose isn’t effective, EMS providers should double the dose to 12 mg, repeat the bolus and rapidly flush the line.1–15 These recommendations come from the original article that compared adenosine with verapamil in PSVT and used a variety of adenosine doses. In this article, the investigators found that 6 mg of adenosine converted 62.3% of patients and that 12 mg converted 91.4% of patients without increase in toxicity.15,16
Because there doesn’t appear to be any increased toxicity in a 12 mg initial dose and it’s more effective, others have recommended starting at 12 mg.4,17 Some have recommended doses as high as 18 mg, which can convert 95% of PSVT patients vs. 65% with 6 mg and 90% with 12 mg.18
Thus, paramedics and their medical directors should have pre-established protocols beginning with 6–12 mg. These protocol should conclude that a second 12 mg dose should be attempted if 12 mg is ineffective,. This is because reports show a second repeat dose of 12 mg may convert up to 10–31% of patients.4,5
Treating Wide Complex Tachycardia
Adenosine was initially considered useful in helping distinguish wide complex tachycardias due to aberrantly conducted PSVT vs. true v tach. However, based on cases of patients deteriorating, many cautioned against trying this drug in any patient with wide complex tachycardia.14,16
We now know that adenosine is safe and can help distinguish supraventricular arrhythmias from those originating in the ventricle for monomorphic wide complex tachycardias that are regular in rate (and by definition, have the same QRS size and shape).1
In the largest recent study of adenosine in wide complex tachycardias, 197 patients were studied.16 Of these, 116 had SVT and 81 had v tach. Ninety percent of the SVTs responded to escalating doses of adenosine (i.e., administering 6 mg, then 12 mg, then repeating 12 mg if no response, and even administering 18 mgs to one patient). Only one patient with proven v tach responded to adenosine, and a second patient may have transiently slowed.
The authors concluded that adenosine was safe as long as patients had regular monomorphic wide complexes and that adenosine was useful in helping distinguish between PSVT and v tach. In fact, they noted a 36-fold increase in the likelihood of a supraventricular origin if the wide complex tachycardia converted to sinus with adenosine and a nine-fold increased likelihood of v tach if it didn’t respond to escalating doses of adenosine.
Another thing is absolutely clear: Never give adenosine to a wide irregular tachycardia or a polymorphic (multiple different QRS configurations) tachycardia, such as Torsades de Pointes. It’s in these patients that adenosine might be lethal.1,16
Summary, Conclusion & Recommendations
Adenosine is a safe and effective agent in PSVT. It’s currently the EMS drug of choice for regular tachycardias about 150–160 beats per minute, believed to be PSVT—whether wide or narrow. The side effects of adenosine are usually mild and transient, lasting just a few seconds. They include chest tightness, shortness of breath and a short sinus pause. Although more serious side effects can occur, such as hypotension, bradycardias and seizures, these side effects are rare in healthy patients with no underlying heart disease.
Adenosine is contraindicated in patients who are likely to be harmed by its inappropriate use. Patients with irregular heart rates, especially atrial fibrillation, patients with PSVT mimics such as atrial flutter with 2:1 conduction or sinus tachycardia in a dehydrated or stressed patient should never receive adenosine.
Adenosine should never be used in wide irregular tachycardias. Providers who are going to use adenosine must be experts in cardiac rhythm interpretation. They also must carefully review a rhythm strip prior to drug administration.
Our recommended starting dosage is 12 mgs via IV push followed by a 10–20 cc rapid flush of saline. If the first 12 mg dose isn’t effective after one minute, we recommend repeating 12 mgs a second time. EMS services and their medical directors should decide whether 6 or 12 mgs should be initially used because there’s no national consensus on which is optimal.
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17. Slovis CM, Kundencheck PJ, Wayne MA, et al., Prehospital management of acute tachyarrhythmias. Prehosp Emerg Care. 2003;7(1):2–12.
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