Adenosine is one of the “small gods” in cardiology. Where there is supraventricular tachycardia, it has its presence.
1. Learn more about “adenosine”
Adenosine, the full name of adenine nucleotides, has two main sources in the body:
ATP (adenosine triphosphate) is dephosphorylated and converted to ADP, then dephosphorylated to ADP, then dephosphorylated to AMP, and all of the phosphate is removed and converted to adenosine.
Another source is that the in vivo S-adenosyl homocysteine is converted to adenosine and homocysteine by enzymatic decomposition. In the body, most of the adenosine in the body will “snap” the phosphates that have been removed, and convert them into AMP, ADP and ATP, and enter a reverse cycle, where is the so-called where to go and where to go. A small amount of adenosine will be broken down into jaundice and hypoxanthine, which will eventually be converted into uric acid.
The action of adenosine is accomplished by binding to adenosine receptors, and there are three major adenosine receptors in the body:
The electrophysiological effects of adenosine are mainly related to the A1 receptor, including reducing the autonomicity of the sinus node and inhibiting the conduction of the atrioventricular node.
A2 type receptors are mainly related to vasodilation, and chest tightness and facial flushing caused by application of adenosine are related to this.
A3 receptors are associated with adenosine-induced asthma, which is one of the contraindications to adenosine use.
When adenosine binds to A1 receptor, it inhibits cAMP, G protein and catecholamine, promotes K+ efflux, inhibits Ca2+ influx, thereby reducing autonomic sinus node, inhibiting sinus conduction, shortening atrial action potential duration, and causing A series of effects such as atrioventricular block. Because adenosine has significant inhibitory effects on cAMP, G protein, etc., these factors are closely related to triggering activities, and some idiopathic ventricular tachycardia mechanisms act as triggering activities, so adenosine can also terminate part of ventricular tachycardia.
Of course, due to the strong and well-defined role of adenosine in the atrioventricular node, the most famous is the termination of atrioventricular node-dependent supraventricular tachycardia. For atrial tachycardia or atrial flutter, even if adenosine can not terminate its onset, it can reduce atrioventricular conduction, reveal P wave or F wave, and help to confirm the diagnosis.
2. So how to use it?
The reason why adenosine becomes a “medicine” is not only its ability to terminate the supraventricular tachycardia, but also because it works very quickly. The half-life of adenosine in the human body is only about 10s, and it needs to be completed in 5s during static pushing. The way, after pushing adenosine statically, most of the room speed can be terminated within 30s, the effect is immediate. More importantly, this drug can be applied even in special populations such as pregnant women.
Adenosine can be administered in the form of 0.1-0.25 mg/kg, but more clinical choices start from a small dose – 6 mg, if not terminated, changed to 12 mg after 1 minute, if still can not be terminated, increased to 18 mg, combined height room Ventricular conduction delay, it is not recommended to continue to add a dose of adenosine.
Adenosine is difficult to preserve. At present, ATP is used in many hospitals. The usage of ATP is similar to that of adenosine. The effect of 10 mg ATP is equivalent to that of 6 mg adenosine.
3. Although the magic medicine is good, pay special attention!
Although adenosine is good, it must be taken seriously when used. During the half-life period of about 10s, what happens is the “turning up” change.
Prepare the defibrillator and temporary pacemaker: prepare the defibrillator and pacing, the adenosine termination room is used for the atrioventricular node. Inhibition, but adenosine has an inhibitory effect on both the sinoatrial node and the atrioventricular node, and who can ensure that the heat is pinched so accurately that it will not cause excessive inhibition, and a pair of sinus node and atrioventricular node The inhibition is too strong, it is bound to produce ventricular arrest, which is not uncommon in the clinic, so preparation for pacing and defibrillation is the key to ensure the safety of patients with adenosine.
Facial flushing, chest tightness, difficulty breathing: This is mainly related to the vasodilator effect of adenosine and the transient bronchoconstriction. Most of them relieve themselves within 30s, so they can explain and comfort themselves.
Active asthma patients are banned: in addition to acting on the A1 receptor, adenosine can also act on the A3 receptor, causing and aggravating asthma, so active asthma patients, adenosine is prohibited.
Patients with severe aortic stenosis, aortic regurgitation, and hypotension should be used with caution: adenosine has a strong vasodilator effect, and the apparent dilatation of the vein can lead to a significant reduction in blood flow to the heart, in severe aortic stenosis and In patients with reflux, it can affect the attention of the coronary arteries, and the blood supply to the heart is insufficient. In patients with severe hypotension, blood pressure can be further reduced, and even shock, so in these patients, adenosine application should be extra cautious.