Cardiac disease in pregnancy Flashcards
General management principle for cardiac disease in pregnancy
General Management Points:
- Avoid spinal
- Most do NOT need SBE prophylaxis; reserve CD for OB reasons
- CD exceptions:
o Dilated aortic root > 4cm
o Aortic aneurysm
o Acute severe CHF
o Recent MI
o Severe symptomatic aortic stenosis
SBE prophylaxis (indications) and types of antibodies
Updated in 2007
What are the maternal mortality rates associated with groups and types of cardiac disease?
Mitral stenosis in pregnancy - critical area, management
KEEP DRY!
- Can present with arrhythmia (A fib) beta blocker
- watch out for pulmonary edema in mitral stenosis patients, especially postpartum
- L atrium can become large
- PCWP not accurate reflection of LV filling pressure
- Most common rheumatic valvular lesion
- L atrial obstruction enlarged atrium ultimately PHTN and RVH fixed CO
- Problem:
o Gravidas who can’t accommodate the increasing volume and heart rate of pregnancy decompensate pulmonary edema
o Balloon valvuloplasty has been used in pregnancy for refractory cases to medical therapy
o Most hazardous time is post-delivery volume shifts
With severe MS, PCWP can increase by 16mmHg
o PCWP will increase right after delivery - Treatment: need to diurese just before delivery; need to accommodate for the auto-transfusion
- Intrapartum management:
o Avoid tachycardia
Decreases LV filling time
B blockers for HR > 90-100
o Keep PCWP approx 14 Accommodate postpartum volume load
o May need diuretics
Aortic stenosis: critical stenosis definition, risks, management in pregnancy
- Critical stenosis = valve area < 1-1.5cm2 LVH CHF
- Fixed CO in severe cases may not be adequate to perfuse coronary and cerebral systems angina, MI, syncope, death
o Coronaries are first vessels to branch off aorta - Management:
o AVOID HYPOTENSION
Decreased venous return will decrease CO
Avoid hemorrhage
Avoid conduction anesthesia
Avoid supine block
Hypovolemia more dangerous that pulmonary edema - Keep on the wetter wise
- PCWP 114-17mmHg to maintain margin of safety
o Moderate lesion should undergo pregnancy prior to valve replacement
o Balloon valvuloplasty can be considered in severe cases that require intervention prior to delivery
o Limit physical activity in those with fixed CO
o All left sided obstricve lesions need to keep more “wet”
Pulmonary HTN, definition and management in pregnancy
- PHTN = PAP > 30mmHg
- AVOID HYPOTENSION
o Hypotension decrease RV filling pressure decreased pulmonary perfusion in fase of PHTN profound hypoxemia sudden death - Labor in LLD position
- In pulmonary HTN fluid overload the patient
Marfan syndrome: genetics, pathophysiology, delivery options
- AD, variable expression
- Mutation on fibrillin gene on 15q21
- Connective tissue weakness; can lead to aneurysms, rupture, dissection
- 60% also have mitral or aortic regurgitation
- risk in pregnancy surrounds aortic root dissection or rupture
- Delivery Route:
o < 4cm root: vaginal + assisted 2nd stage
o > 4cm root: CD
What are the risk of dissection or rupture and mortality with aortic root diameters in pregnancy? What is the treatment and prophylaxis?
Peripartum cardiomyopathy
- cardiomyopathy in last month of pregnancy or 1st 5 months postpartum with exclusion of other causes
- peak incidence is within 1 month pp
- greater risk: older, multips, blacks, twins, PIH
- manifests as biventricular failure and didlation
- 50% will develop chronic dilated cardiomyopathy; the rest recover; ultimately 10% need transplant
o all women who “recovered” showed permanent damage when stress test done
o EF > 40% = 29% had worsening cardiac symptoms
o EF < 25% = 57% end stage cardiac disease - Acute treatment:
o Reduce preload
Lasix 20-40mg daily
o Reduce afterload if hypertension (hydralazine)
o Improve contractitlity – digoxin - Reduce myocardial demand and remodeling (beta blocker – metoprolol)
High risk heart disease in pregnancy:
- Aortic regurge or mitral regurge with NYHA Class III or IV
- Marfan with aortic regurgitation
- Severe aortic stenosis with vlave area < 1.5cm2 or gradiant > 30mmHg
- Severe mitral stenosis < 2cm2
- LVEF < 40% or severe PHTN (PAP > 75% of systemic pressure)
- Mechanical valves that require chronic anticoagulation
- Poor functional class or cyanosis (III or IV)
Low risk heart disease in pregnancy
- asymptomatic aortic stenosis with LVEF > 50% and a mean gradient < 25mmHg
- aortic or mitral regurgitation with no or mild symptoms (I or II)
- mild to moderate pulmonary valve stenosis
What is the natural course of chock
- Initially, blood flow restricted to preserve vital organs
- Sympathetic stimulation increases cardiac oxygen deman
- Ongoing hypovolemia leads to anaerobic metabolism and acidosis
- This can lead to LV failure and irreversible shock
- Immunologic and metabolic response to injury is SIRS which leads to endothelial damage, ARDS, DIC and MOF
- Beyond 4 hrs, death is most likely outcome secondary to irreversible sympathetic induced cellular changes
What is the treatment of shock in pregnancy
- first line therapy is crystalloid: NS or LR
- improve BP
- Vasopressors: temporary adjuvants
o Spiral arterioles are sensitive and can results in perfusion compromise - Presentation: fever, tachycardia, tachypnea, leukocytosis, lactate elevation, Cr>1
- Treatment:
o Hydrate, intubate
o If MAP < 50mmHg vasopressors (norepinephrine)
o Steroids for refractory shock
Cardiac output in pregnancy
CO: increases by 30-50%; peaks at 20-24 weeks
- CO = HR x SV
- SV increases early (increased plasma and LV dilation)
- HR increases by 15-20 bpm by 32 weeks
o Tachycardia maintains CO in late pregnancy
Cardiovascular adaptations in pregnancy, by trimester