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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3063_Библиотеки_им_академика_М_И_Перельмана
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Case 9
Chief Complaint
“I’m having a hard time breathing.”
History and Physical Examination
A 36-year-old woman from Ecuador comes to the office because of progressive dyspnea
on exertion over the last several months. Although she has been symptomatic for several
months, she now comes at the insistence of her employer because she is starting to cough
up blood on a regular basis. The dyspnea is occurring with progressively smaller amounts
of exercise. She also complains of occasional palpitations.
Vital signs are T 37 C (98.6 F), BP 110/70 mm Hg, and pulse 90/min. Examination shows
jugular venous distension with prominent a-waves. Mild bibasilar rales are present upon
auscultation. She has a regular heart rate and rhythm with a 2/6 diastolic murmur at the
lower left sternal border and a loud S1 and snap after S2. The rest of the physical
examination is unremarkable.
Differential Diagnosis
Mitral stenosis1.
Left atrial myxoma2.
Atrial septal defect3.
Primary pulmonary hypertension4.
Tuberculosis5.
161
CLINICAL PEARL
Although electrocardiogram and chest x-ray should be part of any initial evaluation in
shortness of breath, do not expect them to show much on valvular disorders.
Initial Management
Setting: outpatient
Diagnostic/Therapeutic Plan
Test Results
Assessment
Although there are numerous possibilities for the cause of hemoptysis, a young patient with the
physical findings above suggests a cardiac etiology. The patient is young for aortic stenosis,
Chest x-ray
Electrocardiogram
Oximeter
Echocardiogram
X-ray: straightening of left heart border, some elevation of left main stem bronchus, and a
density is visible behind the heart; prominent pulmonary arteries are seen
Electrocardiogram: normal sinus rhythm with biphasic P waves in V1
Oximeter: 94% saturation on room air
Echocardiogram: Left atrial enlargement with moderate mitral stenosis
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and the cardiac exam does not support this form of lesion in which you would expect to find a
systolic murmur at the right second intercostal space.
In addition, the patient has a snap after S2, which is characteristic of the opening snap of mitral
stenosis. The patient is from Ecuador and may have a history of rheumatic fever. Mitral
stenosis is the most common valvular abnormality after rheumatic fever. The electrocardiogram
shows the biphasic P wave in V1, characteristic of left atrial hypertrophy, and the chest x-ray
shows the same.
The symptoms imply that the stenosis is becoming severe, but only cardiac catheterization from
the arterial side can give a precise estimate.
All left-sided valvular disorders increase in intensity and become louder with squatting and
leg-raises. Squatting and leg-raising increase the amount of venous return to the heart. Valsalva
will decrease their intensity. The opposite happens with mitral valve prolapse and obstructive
cardiomyopathy.
Basic Science Correlate
Rheumatic fever causes fibrosis of the mitral valve.
Mechanism of opening snap happening earlier in worsening disease:
Mechanism of hemoptysis: pulmonary hypertension
Mechanism of atrial fibrillation: dilation of left atrium
Mechanism of opening snap: mitral valve leaflets suddenly stopping
Mitral valve opens when left atrial pressure exceeds left ventricular pressure
When stenosis worsens, left atrial pressure increases
163
Why does dysphagia occur in MS?
Further Management Plan
Test Results
Discussion
Symptoms of mitral stenosis usually develop in the fourth decade of life. This is usually about
20 years after the episode of acute rheumatic fever. Because symptoms are based on an
inability to handle the forward flow of blood through a narrowed orifice, anything that
increases the amount of blood that has to flow through (i.e., exertion, excitement, infection,
pregnancy, or thyrotoxicosis) will increase symptoms. Anything that decreases the amount of
plasma volume, like salt restriction or diuretics, will decrease symptoms. Any cause of
tachycardia will also increase symptoms because the atria empty only during diastole, and
tachycardia shortens diastole.
When the orifice of the mitral valve becomes severely narrow (<1.0 cm
2
), some form of
surgical repair will result in not only a dramatic reduction in symptoms but also a decrease in
mortality.
Most posterior structure in the heart is left atrium
Left atrial enlargement presses against the esophagus
Left heart catheterization
Salt restriction
Diuretics
Left heart catheterization: mitral stenosis with 1.3 cm
2
outlet
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Endocarditis prophylaxis before dental or surgical procedure is not indicated. Atrial
fibrillation is very common in mitral stenosis because of the dilation of the atria. Control of the
rate of atrial fibrillation and anticoagulation to prevent thrombus formation is usually central to
the management of mitral stenosis because a rapid rate worsens symptoms of pulmonary
congestion. Digoxin is generally used for its effect on heart rate. If the rate is not sufficiently
controlled with digoxin, a small dose of a beta-blocker is useful.
Surgical therapy should be implemented before the onset of pulmonary hypertension.
Follow-up Management and Prevention
Basic Science Correlate
Mechanism of frequent stroke in MS: dilated left atrium, frequent atrial fibrillation.
Mechanism of hoarseness: left atrial pressure on recurrent laryngeal nerve
Mechanism of metoprolol improving symptoms: slowing heart rate allows greater time for
ventricular filling
Balloon valvuloplasty or commissurotomy if symptoms persist after salt restriction and
diuretics are tried
Valvular replacement if the balloon valvuloplasty fails
Metoprolol orally decreases symptoms of dyspnea
If atrial fibrillation develops only warfarin is truly effective for clot prevention
Transesophageal echo is better than transthoracic echo for mitral stenosis because
the mitral valve is the most posterior valve in the heart.
You can balloon mitral stenosis (MS) but not aortic stenosis (AS); that is because the
mechanism of MS is fibrosis while the mechanism of AS is calcification (you cannot
balloon open calcification).
165
Final Diagnosis
Mitral stenosis
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Case 10
Chief Complaint
“I have cramping pain in my right calf while walking.”
History and Physical Examination
A 71-year-old man with a long history of cardiovascular disease comes to your office
complaining of cramping pain in the right calf while walking. In recent months he has had
increased difficulty walking because of pain in the right calf, which starts after walking
approximately 2 blocks. When he stops, the pain goes away, and then it begins again if he
continues another 3 blocks. He experiences no pain while at rest. He had a myocardial
infarction 20 years ago. He is a 40-pack-year smoker. Current medications include oral
nitrates and a beta-blocker.
Vital signs are stable. Examination of the extremities shows left leg with strong pulses
throughout. Right leg has diminished femoral pulse compared with the left, and there are
no popliteal or pedal pulses palpable. There is an absence of hair with smooth, shiny skin
in the right lower leg. Motor and sensory examination is equal bilaterally in both
extremities.
Differential Diagnosis
Leg claudication1.
Spinal stenosis2.
Peripheral neuropathy3.
167
Initial Management
Setting: outpatient
Diagnostic/Therapeutic Plan
Test Results
Assessment
Most often, no further diagnostic evaluation is necessary. This patient’s history is quite
characteristic of peripheral arterial disease. He has a history of myocardial infarction, which
already indicates arterial disease, and he is a long-term smoker. Atrophic changes such as
diminished peripheral pulses on the side of the pain and the absence of hair with smooth, shiny
skin also contribute to the diagnosis.
Normally, the ratio of the ankle-brachial arterial pressures should be >1.0. The femoral and
popliteal arteries are the most commonly involved in artherosclerosis of the extremities.
Further Management Plan
Ankle/brachial arterial pressure index (ABI)
ABI: 0.5 on right, 1 on left (normal ≥1)
Stop smoking
1.
Aspirin or other antiplatelet drugs such as clopidogrel
2.
Graded exercise program
3.
Meticulous foot care (keep clean and dry with well-fitting shoes)
4.
Cilostazol
5.
Lipid panel; if LDL >100 mg/dL, then statins
6.
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CLINICAL PEARL
CCBs do not help peripheral vascular disease.
Discussion
The patient should be advised to stop smoking and continue on an exercise program, to be
followed up with serial ankle-brachial indices every 3–6 months. Most patients who stop
smoking and maintain an exercise program will remain stable or improve their claudication
and will not require surgery. If the clinical situation deteriorates, however, to the point where
the patient develops rest pain or becomes incapacitated (to the point of not being able to
function), then arteriography and consideration for surgical revascularization will be
necessary. Arteriography is not necessary for routine evaluation. It is useful only for planning
surgical bypass or angioplasty by helping to determine the exact site of the lesion.
Cilostazol is an agent used in peripheral arterial disease:
In the past there has been concern about the use of beta blockers in those with peripheral
arterial disease. Metoprolol and beta-1 specific agents do not worsen claudication. If a patient
needs beta blockers for ischemia, arrhythmia of CHF you can safely give them in peripheral
arterial disease.
Possible revascularization with angioplasty or surgery7.
Both a vasodilator and an antiplatelet agent
Has been shown significant effects in prolonging exercise tolerance and for decreasing
symptoms
Is clearly superior to pentoxifylline (there is no clear benefit of pentoxifylline)
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Follow-up Management and Prevention
Final Diagnosis
Peripheral arterial disease (PAD)/claudication
Check-ups at 1-month intervals to confirm adherence to diet and exercise programs
Smoking cessation counseling; varenicline or bupropion to help stop smoking
ACE inhibitors (e.g., enalapril or lisinopril) for hypertension in peripheral arterial disease
Statins for LDL >100 mg/dL
Combination of both aspirin and clopidogrel for severe disease
Beta blockers as needed for other indications when peripheral arterial disease is present
Metoprolol is not dangerous in peripheral arterial disease
—
Revascularization for persistent symptoms
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