Adenosine in Pregnancy and Breastfeeding

Risk Factor: CM
Class: Cardiovascular drugs / Cardiac drugs

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Fetal Risk Summary

Adenosine, an endogenous purine-based nucleoside found in all cells of the body, is used for the treatment of paroxysmal supraventricular tachycardia. Adenosine phosphate and adenosine triphosphate have been used as vasodilators. Ordinarily, adverse fetal effects secondary to adenosine would not be expected because of the widespread, natural distribution of this substance in the body and its very short (<10 seconds) half-life after IV administration. However, the maternal administration of large IV doses of adenosine may potentially produce fetal toxicity, as has been observed with other endogenous agents (e.g., see Epinephrine).

A reproduction study in chick embryos did not observe teratogenicity (1). Injection into the fourth cerebral ventricle of fetal sheep resulted in depressed fetal respiratory drive (2). In pregnant sheep, constant infusions and single injections of adenosine produced alterations in maternal heart rate and a decrease in diastolic pressure, but no changes in maternal systolic pressure or arterial blood gases, and had no effect on fetal heart rate, arterial pressure, or arterial blood gases (3,4). Another experiment using near-term sheep demonstrated that angiotensin II-induced maternal-placental vasoconstriction could not be reversed by a high-dose infusion of adenosine (5).

Endogenous adenosine cord blood levels, measured in 14 fetuses of 1934 weeks' gestation, were not related to gestational age, but were significantly increased in anemic fetuses and were positively associated with blood oxygen tension (6). The investigators concluded that the results were compatible with a fetal response to tissue hypoxia.

The first case describing the use of adenosine in human pregnancy appeared in 1991 (7). Recurrent narrow complex tachycardia occurred suddenly in a 40-year-old woman in her 39th week of gestation. She had been hospitalized 6 months before the current episode for a similar condition secondary to mitral valve prolapse and had been taking atenolol for tachyarrhythmia prophylaxis since that occurrence. Maternal blood pressure was 80 mm Hg systolic with a pulse of 240. Fetal heart rate was 140. Two IV bolus doses of adenosine (6 mg and 12 mg) were administered resulting in conversion to sinus rhythm with a rate of 80. A nonstress test, conducted after stabilization of the mother, was normal. Two weeks later, a healthy 3.6-kg infant was delivered. Both mother and baby were doing well 1 month postpartum.

Since the above case, a number of reports have described the safe use of adenosine to treat maternal or fetal supraventricular tachycardia (8,9,10,11,12,13,14,15,16,17 and 18) during all phases of gestation, including one woman in active labor (15), eight during the 1st trimester (16), and one case of direct fetal administration (18). The first three of the maternal reports and the fetal case are described below.

A 19-year-old woman was treated at 38 weeks' gestation for the arrhythmia during labor (8). Conversion to a normal sinus rhythm required two IV bolus doses (6 and 12 mg). No effect was observed on uterine contractions, fetal heart rate, or variability. A cesarean section was required for failure of the labor to progress. The second case occurred in a 34-year-old woman with onset of supraventricular tachycardia at 30 weeks' gestation (9). She responded within 30 seconds to a single 6-mg IV adenosine dose with no changes observed in the fetal heart rate tracing. A normal infant was delivered at term. The third woman was a 26-year-old patient with a history of Wolff-Parkinson-White syndrome who was initially treated successfully with 6 mg IV adenosine at 7 months' gestation (10). She was subsequently treated with atenolol and eventually admitted at term for labor induction. During labor the supraventricular tachycardia recurred and two doses (6 and 12 mg) of adenosine were required to convert to a normal sinus rhythm. During the mother's arrhythmia, fetal distress demonstrated by recurrent, deep variable decelerations with loss of short-term variability was observed, but fetal bradycardia resolved with a return to a fetal heart rate of 130 beats/minute on conversion of the mother. A third recurrence of the mother's tachycardia occurred shortly before a cesarean section and this was successfully converted with a 12-mg dose of adenosine. A male infant was delivered with Apgar scores of 1 and 5 at 1 and 5 minutes, respectively. No adverse effects in the fetus or newborn attributable to adenosine were observed in any of the above cases or in the other cited cases.

A 1995 Reference described the direct fetal administration of adenosine for the treatment of persistent supraventricular tachycardia with massive hydrops at 28 weeks' gestation (18). Treatment with digoxin and flecainide for 5 weeks had not been successful in reversing the condition. Based on estimated fetal weight, 0.2 mg/kg of adenosine was given by bolus injection into the umbilical vein and a normal rhythm occurred within seconds. The umbilical serum levels of digoxin and flecainide were determined at the same time and further loading of the fetus with digoxin (0.05 mg/kg) and flecainide (1.0 mg/kg) were administered via the umbilical vein (18). After about 20 minutes of intermittent atrial arrhythmia and tachycardia, the fetal heart converted to a stable, normal rhythm. One week later, the fetus died in utero from what was thought to be a recurrence of the tachycardia or the onset of a drug-induced arrhythmia (18). Massive hydrops fetalis with a structurally normal heart was found at autopsy.

Breast Feeding Summary

Because adenosine is used only by IV injection in acute care situations, it is doubtful that any reports will be located describing the use of adenosine during human lactation. Moreover, the serum half-life is so short, it is unlikely that any of the drug will pass into milk.

References

1. Shepard TH. Catalog of Teratogenic Agents. 6th ed. Baltimore, MD: Johns Hopkins University Press, 1989:194.
2. Bissonnette JM, Hohimer AR, Knopp SJ. The effect of centrally administered adenosine on fetal breath movements. Respir Physiol 1991;84:27385.
3. Mason B, Ogunyemi D, Punla O, Koos B. Maternal and fetal cardiovascular effects of intravenous adenosine (abstract). Am J Obstet Gynecol 1993;168:439.
4. Mason BA, Ogunyemi D, Punla O, Koos BJ. Maternal and fetal cardiorespiratory responses to adenosine in sheep. Am J Obstet Gynecol 1993;168:155861.
5. Landauer M, Phernetton TM, Rankin JHG. Maternal ovine placental vascular responses to adenosine. Am J Obstet Gynecol 1986;154:11525.
6. Ross Russell RI, Greenough A, Lagercrantz H, Dahlin I, Nicolaides K. Fetal anaemia and its relation with increased concentrations of adenosine. Arch Dis Child Fetal Neonatal 1993;68:356.
7. Podolsky SM, Varon J. Adenosine use during pregnancy. Ann Emerg Med 1991;20:10278.
8. Harrison JK, Greenfield RA, Wharton JM. Acute termination of supraventricular tachycardia by adenosine during pregnancy. Am Heart J 1992;123:13868.
9. Mason BA, Ricci-Goodman J, Koos BJ. Adenosine in the treatment of maternal paroxysmal supraventricular tachycardia. Obstet Gynecol 1992;80:47880.
10. Afridi I, Moise KJ Jr, Rokey R. Termination of supraventricular tachycardia with intravenous adenosine in a pregnant woman with Wolff-Parkinson-White syndrome. Obstet Gynecol 1992;80:4813.
11. Leffler S, Johnson DR. Adenosine use in pregnancy. Lack of effect on fetal heart rate. Am J Emerg Med 1992;10:5489.
12. Propp DA, Broderick K, Pesch D. Adenosine during pregnancy. Ann Emerg Med 1992;21:4534.
13. Adair RF. Fetal monitoring with adenosine administration. Ann Emerg Med 1993;22:1925.
14. Matfin G, Baylis P, Adams P. Maternal paroxysmal supraventricular tachycardia treated with adenosine. Postgrad Med J 1993;69:6612.
15. Hagley MT, Cole PL. Adenosine use in pregnant women with supraventricular tachycardia. Ann Pharmacother 1994;28:12412.
16. Elkayam U, Goodwin TM Jr. Adenosine therapy for supraventricular tachycardia during pregnancy. Am J Cardiol 1995;75:5213.
17. Hagley MT, Haraden B, Cole PL. Adenosine use in a pregnant patient with supraventricular tachycardia. Ann Pharmacother 1995;29:938.
18. Kohl T, Tercanli S, Kececioglu D, Holzgreve W. Direct fetal administration of adenosine for the termination of incessant supraventricular tachycardia. Obstet Gynecol 1995;85:8734.

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Questions and Answers

What is adenosine and why does its blockage cause the heart to pound?, I'm doing an experiment write up about the affects of caffeine on a daphnia's heart rate. Apparently, one reason for this, is that caffeine blocks adenosine receptors on heart muscle cells, which causes the heart to pound. What exactly is adenosine and why does its blockage cause the heart to pound??
Thanks in advance.

AN ADENOSINE IS A...
nucleoside composed of a molecule of adenine attached to a ribose sugar molecule, there are differnts types of adenosine such as A1, A2a, A2b, and A3.
As a drug, adenosine is used to treat some types of arrhythmias (abnormal heart rhythms), such as too slow or too fast.

WHY ITS BLOCKAGES CAUSES HEART TO POUND...
SOZ CULDNT FIND ANY INFO 4 DIS ONE :/



COMPLICATED AND CONFUSIN STUFF! :P

Is adenosine given in private family practice or only in the hospital?, I know why the drug is given--I'm wondering if general family practice physicians give the drug for supraventricular tachacardia or if someone would only be given adenosine in the ER or as an admitted patient.
thanks!

Most FP doc's wouldn't stock it. It would go bad before it was used.

In my past experience as a medic, most FP docs want the emergency patients out of the office ASAP.

What is ATP, otherwise known as adenosine triphosphate?, What is ATP, also known as adenosine triphosphate?

-Thank you so much, I am very confused and no internet definition is very clear, or simple.

its the energy your body uses, everything you do takes ATP

How much does an Adenosine nuclear stress test cost?, My grandma is having one done and just want to know the scope of cost for her. She has medicare but that's all. Thanks for your help!

Here is the total cost in US $:
Adenosine. $36. Fujisawa Healthcare. Professional fee. $175. Cost of nuclear stress imaging. $1093. $700-$1300.
If you are living in UK I can recommend you for a lower than above.
Anyway you can write me the country, may be I have some one over there to help you out.

What kind of bonds does caffeine form with the adenosine receptor?, What anchors it there to that receptor? Salt bridges? Hydrogen bonds? What kind of chemistry bonds? A source would be awesome as well.

Do you know that consume 500 to 600 milligrams of caffeine a day, or about four to seven cups of coffee, can cause restlessness, anxiety, headaches and other problems.
For information on Caffeine Content of Food & Drugs please visit the link @ http://www.yourinsomniacure.com/Caffeine...

what materials are needed for a cell to produce a molecule of adenosine triphosphate?, also, how do adenosine diphosphate and adenosine triphosphate differ in structure? in energy content?

compare oxidation and reduction

a) mitochondria, adp, p, O2, glucose, water, etc
b) adenosine TRIphosphate has one more phosphate than adenosine DIphosphate. ATP has a higher energy content.
c) Oxidation means to increase the oxidation number of a molecule, to make it more positive, to make it lose electrons, for example, to make it unite with a highly electronegative atom such as oxygen who would steal the electrons. Reduction (reducing ON) is the opposite process.

What are the consequences of adenosine deaminase in mammals?, (1)what the enzyme does? (2)causes of over activity? (3)role in diagnosis?

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How do plant and animal cells obtain their supply of adenosine triphosphate?,

animal cells use cellular respiration via the oxidation of glucose. Plant cells use photosynthesis reactions.

Why does caffeine prevent adenosine from working?, Why do methylxanthines prevent binding of adenosine at receptor sites?

Also,
Does adenosine only dilate the blood vessels in the brain or the whole body?

Since caffeine and other methyxanthines act as competitive antagonists to adenosine. This means that they bond to the same receptor site but fail to activate it. As they are bound to the receptor, the true agonist is unable to bind and activate that receptor. Similar to carbon monoxide, caffeine could have a higher affinity to the receptor thus attaching to the receptor longer and/or displacing adenosine from the receptor to attach.

As for the role of adenosine in dilation of blood vessels, I have only found that it dilates coronary arteries and constricts the the afferent arterioles of the glomerulus.

What are the components of adenosine in Cellular Respiration?,

how do you mean this, do you mean what does adenosine look like in the cell, its structure? or do you mean what does it function as within the cell?

charlie