Pregnancy and heart disease pulmonary hypertension: Difference between revisions
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==Specific Issues with PAH and Pregnancy== | ==Specific Issues with PAH and Pregnancy== | ||
#Longterm elevation of pulmonary vascular resistance may cause right ventricular hypertrophy or dilatation, tricuspid regurgitation or arrhythmias, leading to intolerance of the increased heart rate and circulating blood volume of pregnancy. | #Longterm elevation of pulmonary vascular resistance may cause right ventricular hypertrophy or dilatation, tricuspid regurgitation or arrhythmias, leading to intolerance of the increased heart rate and circulating blood volume of pregnancy. | ||
#Cardiac output may already be reduced by pulmonary hypertension, and the heart may not be able to increase cardiac output in proportion to the reduced systemic vascular resistance that occurs during pregnancy. | |||
#Normal adaptive changes in the lungs to accommodate the increased pulmonary blood flow may be prevented by fixed vascular remodeling. | |||
#Hypercoagulability may increase the tendency for thrombus formation, which may be poorly tolerated (as above). | |||
#Patients are at risk for sudden death from pulmonary hypertensive crises, malignant arrhythmias or pulmonary thromboembolism. | |||
#Patients can develop stroke from intracardiac shunting in pre-existing [[Eisenmenger's syndrome||Eisenmenger’s syndrome]] or if there is a persistent patent foramen ovale<ref name="pmid11108754">{{cite journal| author=Jaigobin C, Silver FL| title=Stroke and pregnancy. | journal=Stroke | year= 2000 | volume= 31 | issue= 12 | pages= 2948-51 | pmid=11108754 | doi= | pmc= | url= }} </ref> | |||
==References== | ==References== | ||
Revision as of 16:45, 8 October 2011
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Anjan K. Chakrabarti, M.D. [2]
Overview
This section will review pulmonary hypertension and its association with pregnancy. For a more broad discussion, please see pulmonary hypertension.
Pulmonary hypertension, defined as mean pulmonary artery pressure of greater than 25 mmHg at rest or 30 mmHg with exercise, carries a higher mortality when it is associated with pregnancy. It carries a significant risk to mother and child during pregnancy; as a result, mothers require careful monitoring.[1]
Classification
Physiologic Considerations in Pregnancy
As reviewed in |Physiologic Changes Associated with Pregnancy, maternal blood volume increases throughout pregnancy until between 28 and 34 weeks of gestation, and circulating blood volume is increased to between 30% and 50% above the non-pregnant state. Red blood cell mass increases to approximately 25% above the non-pregnant state. Cardiac output increases through various mechanisms, and hyper coagulability is noted in the postpartum state due to relative resistance to activated protein C, reduced serum levels of protein S and increased levels of factors I, II V, VII, VIII, X and XII.[2]
All of these changes can be particularly deleterious in patients with PAH. It can be very harmful if a thrombus forms or embolises to an already compromised pulmonary circulation. Such hematological changes present a significant risk, and mortality fall between 30% and 50% for pregnant women with idiopathic PAH.[3]
Specific Issues with PAH and Pregnancy
- Longterm elevation of pulmonary vascular resistance may cause right ventricular hypertrophy or dilatation, tricuspid regurgitation or arrhythmias, leading to intolerance of the increased heart rate and circulating blood volume of pregnancy.
- Cardiac output may already be reduced by pulmonary hypertension, and the heart may not be able to increase cardiac output in proportion to the reduced systemic vascular resistance that occurs during pregnancy.
- Normal adaptive changes in the lungs to accommodate the increased pulmonary blood flow may be prevented by fixed vascular remodeling.
- Hypercoagulability may increase the tendency for thrombus formation, which may be poorly tolerated (as above).
- Patients are at risk for sudden death from pulmonary hypertensive crises, malignant arrhythmias or pulmonary thromboembolism.
- Patients can develop stroke from intracardiac shunting in pre-existing |Eisenmenger’s syndrome or if there is a persistent patent foramen ovale[4]
References
- ↑ Madden BP (2009). "Pulmonary hypertension and pregnancy". Int J Obstet Anesth. 18 (2): 156–64. doi:10.1016/j.ijoa.2008.10.006. PMID 19223169.
- ↑ PECHET L, ALEXANDER B (1961). "Increased clotting factors in pregnacy". N Engl J Med. 265: 1093–7. doi:10.1056/NEJM196111302652205. PMID 14484810.
- ↑ Weiss BM, Zemp L, Seifert B, Hess OM (1998). "Outcome of pulmonary vascular disease in pregnancy: a systematic overview from 1978 through 1996". J Am Coll Cardiol. 31 (7): 1650–7. PMID 9626847.
- ↑ Jaigobin C, Silver FL (2000). "Stroke and pregnancy". Stroke. 31 (12): 2948–51. PMID 11108754.