Chest pain in pregnancy: Difference between revisions
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*Physiologically, cardiac output and blood volume increase during pregnancy, both of which may increase the risk of cardiovascular events. | *Physiologically, cardiac output and blood volume increase during pregnancy, both of which may increase the risk of cardiovascular events. | ||
===Diagnosis=== | ===Diagnosis=== | ||
*Diagnosis similar to the general population by: Symptoms, ECG changes, and cardiac | *Diagnosis similar to the general population by: Symptoms, ECG changes, and troponin. | ||
*CK-MB concentrations may markedly increase during labor and post-delivery due to non-cardiac causes, namely placental and uterine leaks. | |||
:*To view common normal physiological changes on ECG in pregnancy (may mimic AMI), click [[The electrocardiogram#EKG Abnormalities in Normal Pregnancy (Physiological Changes)|'''here''']]. | |||
:*To view normal physiological changes in biomarker concentrations during labor and delivery: for troponin, click [[Creatine kinase|here]] | for CK-MB, click here. | |||
*Echocardiography is safe and may be performed to evaluate wall motion abnormalities. | *Echocardiography is safe and may be performed to evaluate wall motion abnormalities. | ||
*Fetal monitoring is recommended. | *Fetal monitoring is recommended. | ||
Revision as of 16:24, 8 February 2016
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Chest pain in pregnancy On the Web |
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Risk calculators and risk factors for Chest pain in pregnancy |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Causes
Life-threatening Causes
Life-threatening causes of chest pain among pregnant women include the following:
- Acute MI
- Atherosclerotic plaque rupture: Common in antepartum period
- Coronary dissection: Common in peripartum or postpartum period
- Aortic dissection and other aortic syndromes
- Pulmonary embolism
- Amniotic fluid embolism
- Tension pneumothorax
Other Causes
Other causes of chest pain of pregnancy include the following:
- Asthma exacerbation
- Pneumonia
- Pneumothorax
- TB reactivation
- Gastroesophageal reflux disease
- Vasospasm
- Myocarditis
- Pericarditis
- Endocarditis
- Trauma
- Sarcoidosis
- Severe kyphoscoliosis
- Chest expansion (usually physiological change)
- Breast tenderness (usually physiological change)
Acute MI in Pregnancy
- Incidence: 1 per 35,000 deliveries
- Maternal mortality rate: 5% to 18%, fetal mortality rate: 9%
- Common in third trimester until 1-2 months post-delivery
- Antepartum: Atherosclotic plaque rupture is the most common cause
- Perpartum or postpartum: Coronary artery dissection (LAD > RCA > LC > LM)
Risk Factors
- It is unknown if pregnancy itself is a risk factor in development of acute MI
- The most important risk factors in the development of AMI in pregnancy are generally similar to those in the general population. Risk factors include:
- Age > 35 years
- Diabetes mellitus
- Hypertension
- Smoking
- Connective tissue diseases (e.g. Ehler Danlos syndrome)
- Vasculitis (e.g. Takayasu arteritis)
- Thrombophilia (e.g. antiphospholipid syndrome)
- Acute post-partum stress:
- Severe post-partum hemorrhage
- Post-partum infection
Pathophysiology
- During pregnancy, progesterone release results in structural changes in the vascular intima and media.
- Physiologically, cardiac output and blood volume increase during pregnancy, both of which may increase the risk of cardiovascular events.
Diagnosis
- Diagnosis similar to the general population by: Symptoms, ECG changes, and troponin.
- CK-MB concentrations may markedly increase during labor and post-delivery due to non-cardiac causes, namely placental and uterine leaks.
- Echocardiography is safe and may be performed to evaluate wall motion abnormalities.
- Fetal monitoring is recommended.
Treatment
- Percutaneous coronary intervention
- If spontaneous coronary artery dissection occurs, a more thorough investigation for connective tissue diseases and vasculitis is wawrranted.
Coronary Spasm
Pathophysiology
- It is thought that there an increased concentrations of RAAS hormones in pregnancy, as well as increased vascular reactivity to angiotensin II and norepinephrine.