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  #1  
Old 10-21-2011
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You are seeing a 24-year-old G1P0 woman brought to the emergency department for acute shortness of breath. She is at 26 weeks' gestation and has no other past medical history. The patient was born in Malaysia and moved to the United States with her family at age 12 years. She now lives with her family and husband and works in retail. She has been seen twice by a local obstetrician since being told she was pregnant and has been taking multivitamin and folate supplements. She reports having a fetal ultrasound done at 3 months’ gestation and was told, “Everything looked fine.” The patient reports she has felt fine throughout the pregnancy until 2 days ago when she was feeling increasing fatigue and breathlessness with minimal exertion. She at first thought that this was related to her normal pregnancy, until early this evening when she became acutely short of breath while sitting down. Her blood pressure is 160/90 mm Hg, pulse is 120/min, respirations are 26/min, and jugular venous pressure is 15 cm H2O. Physical examination shows bibasilar crackles and a high-pitched early diastolic “snap” followed by a diastolic rumble at the apex. Chest x-ray shows increased peripheral vascular markings and an elevated left mainstem bronchus. Electrocardiogram shows sinus tachycardia and a large negative P wave in lead V1. Which of the following is the most appropriate management?
A. Refer her for prosthetic valve replacement
B. Started her on an ACE-inhibitor for afterload reduction
C. Start her on a beta-blocker for rate control
D. Administer antibiotic prophylaxis during delivery
E. Explain that usually patients with this diagnosis present with symptoms in early pregnancy


A 76-year-old man with a long-standing history of congestive heart disease has been successfully maintained on a regimen of diuretics, beta-blockers, digoxin, and ACE-inhibitors. He reports occasional palpitations and his beta-blocker regimen is changed; atenolol is increased to 50 mg per day. Two weeks later, the patient comes to the clinic complaining of increased shortness of breath and leg swelling. His medications now include furosemide, 20 mg daily, digoxin, 0.25 mg daily, lisinopril, 40 mg daily, and atenolol, 50 mg daily. His blood pressure is 100/60 mm Hg and his pulse is 48/min. He has crackles in both lungs. Jugular venous distention is 12 cm of water. He has 2+ edema. Which of the following is appropriate management at this time?
A. Advise the patient to reduce his salt intake
B. Decrease the dose of atenolol
C. Increase the dose of digoxin
D. Increase the dose of furosemide
E. Increase the dose of lisinopril
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Old 10-22-2011
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B. Started her on an ACE-inhibitor for afterload reduction
B. Decrease the dose of atenolol
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Old 10-22-2011
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Case of Mitral Stenosis, so
E. Explain that usually patients with this diagnosis present with symptoms in early pregnancy, because of Increase plasma volume in pregnancy


D. Increase the dose of furosemide
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Old 10-22-2011
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Quote:
Originally Posted by pass7 View Post
Case of Mitral Stenosis, so
E. Explain that usually patients with this diagnosis present with symptoms in early pregnancy, because of Increase plasma volume in pregnancy


D. Increase the dose of furosemide
hey.....bt wen the bp is already 100/60 do u think furosemide can b increased??
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Old 10-23-2011
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The correct answer is C. This patient is presenting with acute pulmonary edema secondary to mitral stenosis. Although cardiac disease complicates 2 to 4% of all pregnancies in the United States, it remains a major cause of obstetric morbidity and mortality. Congenital heart disease has become the most common form of heart disease complicating pregnancy in the United States, but rheumatic heart disease is still the most common cardiac problem in immigrant populations and women born in third world countries. Mitral stenosis is the most common valvular lesion of rheumatic origin found in women of childbearing age. Pregnancy is associated with many important cardiocirculatory changes that can affect any underlying cardiac disease. These changes include a 30 to 50% increase in cardiac output. This increase in cardiac output is caused by (1) an increase in overall ―preload‖ as blood volume is increased, (2) reduction in afterload as systemic vascular resistance declines, and (3) an increase in maternal pulse by 15-20 bpm. These changes reach their peak during late second trimester and thus often cause patients with underlying asymptomatic cardiac disease to decompensate during the latter half of pregnancy. This patient is found to have many of the physical findings characteristic of mitral stenosis. The cardiac examination is significant for the early diastolic ―opening snap‖ followed by a diastolic rumble radiating toward the apex. The ECG shows evidence of left atrial enlargement (P. mitrale), and the chest x-ray demonstrates a dilated left atrium consistent with a straightening of the left heart border and left mainstem bronchus elevation. This patient likely had rheumatic fever as a child and has had an insidious progression of calcification of the mitral valve leaflets. When mitral stenosis reaches hemodynamic significance (valve area <1.5 cm2), flow across the valve is maintained by two factors: an increase in pulmonary wedge filling pressures (because of increased resistance by stenotic valve) and prolonged diastolic filling time (to fill the left ventricle). During pregnancy, an increase in cardiac output and pulse result in reduced diastolic filling time and an increase in wedge pressure, resulting in pulmonary congestion. For patients with pulmonary edema and decompensated congestive heart failure during pregnancy for mitral stenosis, management includes gentle diuresis and beta-blockers to lower pulse (and increase diastolic filling time).
Prosthetic valve replacement should be avoided (choice A).
ACE-inhibitors (choice B) are contraindicated in pregnancy for their teratogenic potential and should not be used. Mitral balloon valvuloplasty has been performed successfully during pregnancy in patients who fail medical management. Valve replacement with prosthetic heart valves requires long-term anticoagulation and thus presents an increased bleeding risk and presents teratogenic risks for the fetus.
The need for antibiotic prophylaxis during routine delivery in patients with cardiac disease is not recommended by current American Heart Association (AHA) guidelines,
because there is a very small incidence of bacteremia during normal delivery (choice D). Antibiotic prophylaxis is optional for high-risk patients including those with bioprosthetic valves and homografts. Antibiotic prophylaxis is recommended for women who have a vaginal delivery in the presence of an infection or who undergo urethral catheterization; however, many clinicians provide prophylaxis to all cardiac patients. Patients with rheumatic heart disease or mitral valve prolapse are considered to be moderate risk.
Not uncommonly, women with ―occult‖ mitral stenosis who have lived in a compensatory state first present with pulmonary edema during late pregnancy (choice E), demonstrating how the altered hemodynamics of pregnancy can result in cardiac decompensation.

2.
The correct answer is D. Given this patient’s history of heart failure, he is on an appropriate medical regimen. Because he was having palpitations, however, it was appropriate to increase the dose of beta-blocker. In this situation, however, the patient became bradycardic with a decrease in stroke volume. It seems the patient does need the increased dose of atenolol. Given his increased volume status, it would be appropriate to increase diuresis by increasing the dose of furosemide.
If the patient has a higher salt diet that has changed recently, he certainly should be advised to reduce his salt intake (choice A). If this is not the case, however, he needs an increase in the diuretic regimen.
Decreasing the atenolol dose (choice B) may be necessary if the patient becomes dangerously hypotensive and bradycardic. The first step, however, must be decreasing the fluid overload.
Increasing the dose of digoxin (choice C) may be necessary to increase inotropy. The level must be measured first, however.
Increasing the dose of lisinopril (choice E) would not be appropriate given this patient’s borderline blood pressure. Furthermore, the patient is already on a high dose of the medication.
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