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Description : Pharmacodynamics and Mechanism of Action of Prostaglandin E1

Tags : Congenital Heart Disease

Published on : Aug 15, 2020 | Views : 2050 | Downloads : 1

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Slide 1-

Prostaglandin E 1 Brian Guenther Pharmacology Spring 2020 Vanderbilt Perfusion Program
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Prostaglandin E: Historical Perspective Discovered by Ulf von Euler in 1935 Nobel Prize winning Swedish Physiologist Prostaglandin was first isolated from seminal fluid in the prostate gland Further studies detailed the arachiodonic acid oxygenation pathway that derived prostaglandins catalyzed by cyclo-oxygenase
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Prostaglandin E (Alprostadil) Pharmacodynamics Prostaglandin E (PGE) is produced endogenously to relax smooth muscle and cause vasodilation. Used to treat erectile dysfunction and in neonates with ductal dependent congenital heart disease. Mechanism of action PGE is a vasodilator that acts directly on the smooth muscle within the PDA to keep it patent. This allows for increased pulmonary or systemic blood flow depending on the underlying cardiac lesion. In cyanotic infants this will allow for increased gas exchange and oxygen delivery to the patient.
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Patent Ductus Arteriosus Patent ductus arteriosus (PDA) is one of the most common congenital heart defects, accounting for 5%–10% of all congenital heart disease in term infants. The occurrence of PDA is inversely related to gestational age and weight, with an even greater incidence in preterm infants. Clinical signs of ductal patency include murmur, tachycardia, bounding peripheral pulses, and congestive heart failure and associated symptoms. PGE prevents or reverses the closure of the PDA allowing for temporary palliative care until a surgical procedure. This allows for further work up including cardiac catherization and other imaging in preparation for the operating room.
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Patent Ductus Arteriosus
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Pulmonary Hypertension
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Indications for Prostaglandin E Cyanotic and acyanotic congenital heart defects where presence of the patent ductus arteriosus is required for flow to either the pulmonary or systemic circulation. Especially critical for ductal dependent lesions Cyanotic: Tetralogy of Fallot, pulmonary atresia, tricuspid atresia, D-transposition of the great arteries, hypoplastic left heart syndrome Acyanotic: Critical aortic stenosis, severe coarctation of the aorta
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Pulmonary Restriction (cyanotic) vs. Systemic Restriction (acyanotic)
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Administration and Pharmacokinetics PGE is administered on a continuous intravenous drip because it is very rapidly metabolized. As much as 80% of the drug is eliminated with one pass through the lungs by beta and omega oxidation. The half life of this drug is 5 – 10 minutes. Some of the potential toxic side effects include apnea, aarhythmias, edemia, hyperemia, hypotension fever, seizures and pyrexia. Initial neonatal dose is 0.05 – 0.10 mcg/kg/min until therapeutic response is achieved. Therapeutic response is indicated by: An increase in systemic blood pressure and increase in pH in those with restricted systemic blood flow and acidosis. An increase in oxygenation (pO2) in those with restricted pulmonary blood flow.
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References: Euler, U.s. Von. “History and Development of Prostaglandins.” General Pharmacology: The Vascular System, vol. 14, no. 1, 1983, pp. 3–6., doi:10.1016/0306-3623(83)90053-8. “The Nobel Prize in Physiology or Medicine 1970.” NobelPrize.org, www.nobelprize.org/prizes/medicine/1970/euler/biographical/. Mathew, B., & Lakshminrusimha, S. (2017, July 28). Persistent Pulmonary Hypertension in the Newborn. Retrieved April 27, 2020, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5575585/ Alprostadil. (n.d.). Retrieved April 27, 2020, from https://www.drugbank.ca/drugs/DB00770