ventricular septal defect
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Etiology
- congenital
- myocardial infarction involving the interventricular septum
- 50% of VSD result from anterior wall MI[2]
Pathology
- occurs most commonly in membranous or muscular septum
- VSD size determines the degree of left to right shunt
- may cause pulmonary hypertension
Genetics
- type 1 associated with defects in GATA4
Clinical manifestations
- small defects (most common in adults)
- loud holosystolic murmur along left lower sternal border
- murmur may obliterate S2
- murmur increases with handgrip
- murmur decreases with amyl nitrite[2]
- murmur does not radiate
- murmur intensity & duration decrease as pulmonary hypertension develops (see Eisenmenger syndrome)[2]
- thrill is often felt in the same location
- may be little blood flow through the defect
- patient may be asymptomatic
- loud holosystolic murmur along left lower sternal border
- large defects
Diagnostic procedures
- electrocardiogram:
- small VSD: normal
- large VSD:
- right ventricular hypertrophy alone or with left ventricular hypertrophy
- pulmonary artery catheter
- large v waves in wedge pressure tracing
- step-up in O2 saturation from right atrium to right ventricle
Radiology
- chest X-ray (large VSD)
- right atrial & right ventricular enlargement
- increased pulmonary vascular markings
- with pulmonary hypertension
- prominent central pulmonary arteries
- reduced peripheral pulmonary vascularity
Complications
- endocarditis (small VSD)
- right & left ventricular hypertrophy (large VSD)
- right & left atrial enlargement (large VSD)
- pulmonary hytertension (large VSD)
- Eisenmenger's syndrome[2]
Management
- indications for surgical ventricular septal closure in adults
- progressive aortic insufficiency
- progressive tricuspid regurgitation
- progressive left ventricular volume overload
- pulmonary to systemic blood flow ratio > 1.5[2] (formerly 2.0)
- recurrent endocarditis[2]
- large ventricular septal defects with cardiogenic shock due to myocardial infarction[2]
- PCI for STEMI no longer indicated after VSD diagnosis
- CABG during cardiac surgery for VSD offers only hope[2]
- large VSD with left to right shunt & pulmonary hypertension (Eisenmenger's syndrome) should not be surgically closed
- clinical deterioration will result
- heart transplantation if surgery indicated
- patients with small VSD without left heart enlargement, pulmonary hypertension, recurrent endocarditis, or cardiac valvular insufficiency may be followed clinically[2]
More general terms
More specific terms
Additional terms
References
- ↑ Mayo Internal Medicine Board Review, 1998-99, Prakash UBS (ed) Lippincott-Raven, Philadelphia, 1998, pg 46
- ↑ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 2.8 2.9 Medical Knowledge Self Assessment Program (MKSAP) 15, 16, 17, 18, 19. American College of Physicians, Philadelphia 2009, 2012, 2015, 2018, 2022.
- ↑ Poulsen SH, Praestholm M, Munk K et al Ventricular septal rupture complicating acute myocardial infarction: clinical characteristics and contemporary outcome. Ann Thorac Surg. 2008 May;85(5):1591-6 PMID: https://www.ncbi.nlm.nih.gov/pubmed/18442545
- ↑ Gabriel HM, Heger M, Innerhofer P et al Long-term outcome of patients with ventricular septal defect considered not to require surgical closure during childhood. J Am Coll Cardiol. 2002 Mar 20;39(6):1066-71 PMID: https://www.ncbi.nlm.nih.gov/pubmed/11897452
- ↑ Penny DJ, Vick GW 3rd. Ventricular septal defect Lancet. 2011 Mar 26;377(9771):1103-12. PMID: https://www.ncbi.nlm.nih.gov/pubmed/21349577