Pulmonary regurgitation medical therapy: Difference between revisions
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==Overview == | ==Overview == | ||
Revision as of 20:19, 7 August 2020
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Pulmonic regurgitation Microchapters |
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Diagnosis |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Aravind Kuchkuntla, M.B.B.S[2], Aysha Anwar, M.B.B.S[3], Javaria Anwer M.D.[4]
Overview
Treatment of pulmonic regurgitation may be divided into medical and surgical treatment. Medical management of pulmonic regurgitation may include use of diuretics in patients with RV dysfunction. ACE inhibitors and beta blockers may be used to reverse neurohormonal activation and improve symptoms. Antibiotic prophylaxis may be indicated in certain conditions such as patients with cyanotic heart disease, prosthetic heart valves, rheumatic heart disease, and patients previously having sustained bacterial endocarditis. Among patients with carcinoid heart disease subcutaneously administered octreotide in 2–4 divided doses (50–1500 μg/day) provides symptomatic and biochemical benefit.
Medical Therapy
- There are no specific medical measures for the management of PR.
- Diuretics are recommended in patients with RV dysfunction or PAH for maintenance of fluid balance.[1]
- Among patients with repaired tetralogy of fallot, ACE inhibitors or beta-blockers are used to reverse the neuroharmonal activation and improve the symptoms.[2][3]
Antiobiotic prophylaxis
The American Heart Association Recommendations on Prevention of Bacterial Endocarditis indicate that antibiotic prophylaxis is not necessary for pulmonic regurgitation in those patients with otherwise structurally normal pulmonic valves, particularly if there is no diastolic murmur. It should be noted, though, that those patients with the following conditions may warrant antibiotic prophylaxis:[4]
- Complex cyanotic heart disease
- Prosthetic heart valves
- Patients with congenital heart disease and pulmonic regurgitation
- Acquired pulmonic valve regurgitation as the result of rheumatic heart disease
- Patients with complex cyanotic heart disease
- In patients who have previously sustained bacterial endocarditis
- Among patients with severe acute PR due to the large duct (such as in neonatal Ebstein's anomaly or post balloon dilation of pulmonary stenosis or perforation of valvar pulmonary atresia)[5][6]:
- If TR accompanies the situation, a circular shunt may occur leading to poor systemic blood flow. The treatment involves stopping the prostaglandins and urgent duct ligation among unstable patients.
- If tricuspid valve is competent, increasing ventilation, oxygen, and nitric oxide to cause pulmonary vasodilatation can reduce PR.
Heart failure therapy
- General measures for the treatment of heart failure include[7]:
- Diet: Salt and water restriction
- Monitoring: Weight and fluid balance monitoring
- Mobility: Mobility and compression stockings help prevent the development of deep venous thrombosis and leg edema.
- Right heart failure: A combination of loop diuretics and digoxin (may help with right ventricular contractility). Often, loop diuretics alone are enough to achieve sufficient fluid loss, but if additional diuresis is required, the judicious coadministration of a Thiazide diuretic may be administered with loop diuretics to achieve optimal fluid balance.
- To read more about the medical therapy utilized in heart failure, click here.
Carcinoid heart disease[7][8]
Subcutaneously administered octreotide in 2–4 divided doses (50–1500 μg/day) provides symptomatic and biochemical benefit. Octreotide (somatostatin analog) binds to somatostatin receptors, and reduces the vasoactive peptides that provoke carcinoid syndrome. Concomitant monitoring of BSL and blood glucose levels is required. Lanreotide (BIM23014, angiopeptin and somatuline) is a newer somatostatin analog, has an advantage of less frequent administrations, and can be used as an alternative to octreotide.
References
- ↑ Fauci, Anthony (2008). Harrison's principles of internal medicine. New York: McGraw-Hill Medical. ISBN 978-0071466332.
- ↑ Bolger AP, Sharma R, Li W, Leenarts M, Kalra PR, Kemp M; et al. (2002). "Neurohormonal activation and the chronic heart failure syndrome in adults with congenital heart disease". Circulation. 106 (1): 92–9. PMID 12093776.
- ↑ Davos CH, Davlouros PA, Wensel R, Francis D, Davies LC, Kilner PJ; et al. (2002). "Global impairment of cardiac autonomic nervous activity late after repair of tetralogy of Fallot". Circulation. 106 (12 Suppl 1): I69–75. PMID 12354712.
- ↑ Seiler C (2004). "Management and follow up of prosthetic heart valves". Heart. 90 (7): 818–24. doi:10.1136/hrt.2003.025049. PMC 1768319. PMID 15201262.
- ↑ Wald RM, Adatia I, Van Arsdell GS, Hornberger LK (September 2005). "Relation of limiting ductal patency to survival in neonatal Ebstein's anomaly". Am. J. Cardiol. 96 (6): 851–6. doi:10.1016/j.amjcard.2005.05.035. PMID 16169376.
- ↑ Chaturvedi RR, Redington AN (July 2007). "Pulmonary regurgitation in congenital heart disease". Heart. 93 (7): 880–9. doi:10.1136/hrt.2005.075234. PMC 1994453. PMID 17569817.
- ↑ 7.0 7.1 Fox DJ, Khattar RS (October 2004). "Carcinoid heart disease: presentation, diagnosis, and management". Heart. 90 (10): 1224–8. doi:10.1136/hrt.2004.040329. PMC 1768473. PMID 15367531.
- ↑ Janmohamed S, Bloom SR (April 1997). "Carcinoid tumours". Postgrad Med J. 73 (858): 207–14. doi:10.1136/pgmj.73.858.207. PMC 2431281. PMID 9156122.