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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 7
Chief Complaint
“My breath is short and my vision is blurry. I can’t think straight.”
History and Physical Examination
A 47-year-old man comes to the emergency department complaining of several hours of
dyspnea, blurry vision, and difficulty thinking. He has never had symptoms like this
before. They came on while he was at his sedentary office job. He also has a worsening
headache, dizziness, and mild palpitations. The patient has never had a myocardial
infarction in the past, but he has high BP for which he is on a thiazide diuretic.
Vital signs are T 36.9 C (98.4 F), BP 230/150 mm Hg, pulse 88/min, and respirations
18/min. Physical examination of the head, eyes, ears, nose, and throat shows arteriolar
narrowing and AV nicking. A few hemorrhages are visible, and there is no jugular venous
distention. Upon auscultation, there are very few scattered rales. He has a regular heart
rate and rhythm, with an audible S4 gallop. His abdomen is soft and nontender, and his
extremities are not edematous.
Differential Diagnosis
Hypertensive emergency1.
Acute myocardial infarction2.
Intraparenchymal brain hemorrhage3.
Subarachnoid hemorrhage4.
151
CCS NOTE
Move the clock forward only 15 min at a time for an unstable patient.
Initial Management
Setting: emergency department
Diagnostic/Therapeutic Plan
Test Results
Assessment
The patient’s most obvious problem on physical examination is a profoundly high BP; the
dyspnea, blurring of vision, dizziness, and headache can all be the result of that. Often, these
Electrocardiogram
BUN/creatinine
CBC
IV labetalol, nitroprusside, or enalaprilat
Oxygen
Oximeter
Sinus rhythm, S in V1 + R in V5 = 42 mm, mild down-sloping of ST segment in V2–V4
BUN/creatinine mildly elevated
Hematocrit 37%, few schistocytes visible, platelets 110,000/mm
3
Oximeter 98% saturation on room air
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complaints can be hard to differentiate from the headache and dizziness that accompany an
intracranial bleed such as a subarachnoid hemorrhage. We know that it can be characterized by
disseminated intravascular coagulation, fibrinoid necrosis of arteriolar walls,
microangiopathic hemolytic anemia, and dilation of cerebral blood vessels, but the root cause
is unknown.
Further Management Plan/Results
Test Results
CCS NOTE
The most important issue in a hypertensive emergency is to use an IV medication. On
the exam you will not be asked for doses. The specific agent is not as important as the
route of administration.
Discussion
Head CT scan1.
Chest x-ray2.
Continue IV antihypertensive: labetalol, nitroprusside, or enalaprilat3.
Transfer to ICU for critical care consult4.
Reduction of BP by approximately 1/3, but not <95 mm Hg diastolic5.
Head CT normal
Cardiomegaly with clear lung fields
153
There are various medications that can be used to treat a hypertensive emergency. Because of
the emergent nature of the crisis and the potential for myocardial infarction, stroke, and
blindness, an IV agent that works in minutes is preferable. The best agents are as follows:
Hypertensive emergency (or “malignant” or “accelerated” hypertension or “crisis”) is not
defined on the basis of any specific blood-pressure number; it describes the development of
end organ damage. The most common causes of death from hypertensive emergency are stroke,
renal failure, and CHF. Other manifestations of the syndrome include retinal changes (such as
in this patient) and confusion from altered cerebral blood flow. In this case the
electrocardiogram abnormalities are the findings consistent with left ventricular hypertrophy
(SV2 + RV5 >35 mm). ST segment depression can also result from hypertrophic
cardiomyopathy.
Scleroderma-induced malignant hypertension is preferentially treated with ACE inhibitors.
Cocaine-induced hypertensive crisis is treated with the alpha blocker phentolamine.
Labetalol works through the nonspecific beta-1 and -2 blockade and is also an alpha-
blocking agent. It has the added advantage of being available intravenously and orally.
There are few serious side effects with emergent use. This drug can be safely used in
pregnancy as well.
Nitroprusside is both an arterial and venous dilator, and has the most rapid onset of action
(seconds) and shortest duration of action (minutes). Because of its potency, it should be
given only in an ICU setting where an arterial line can establish very direct monitoring of
pressure. Cyanide poisoning, however, may develop from its metabolites.
Nitroglycerin works predominantly through venous dilation. This agent is ideal for those
patients in hypertensive crisis in whom an MI may be occurring.
Other agents are enalaprilat (IV ACE inhibitor), nicardipine, fenoldopam, and
hydralazine. About 1% of patients with hypertension will develop a hypertensive crisis at
some point, and very rarely is it the first manifestation of hypertensive disease.
The calcium blocker nicardipine can also be used to lower pressure acutely.
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CCS NOTE
Patients with BP problems severe enough to cause chest pain or altered mental status
should go to the ICU.
Follow-up Management and Prevention
Final Diagnosis
Hypertensive emergency
When symptoms resolve, transfer patient to floor
Stop IV medication, start oral medication
Labetalol or enalapril orally is acceptable
Expect to use 2–3 oral medications
155
Case 8
Chief Complaint
“I fainted in ballet class.”
History and Physical Examination
A 17-year-old girl comes to the office for evaluation of recurrent syncope. Each episode
occurred following vigorous exertional activity. The day before she came in, she had been
jogging around the school track and suddenly passed out. She was reportedly unconscious
for less than a minute and felt fine afterwards. She had no associated palpitations, seizure
like movements, or incontinence. She reports regular menses since age 12 and has noted
no association between the syncopal episodes and her menstrual cycle.
Vital signs are T 36.7 C (98.0 F), BP 110/60 mm Hg, pulse 80/min, and respirations
16/min. Cardiovascular examination shows prominent apical impulse, S4 gallop, and a
2/6 systolic murmur at the lower left sternal border. The murmur worsens with Valsalva
and improves with squatting. The rest of the physical examination is unremarkable.
Differential Diagnosis
Vasovagal syncopal episode
1.
Seizure disorder
2.
Cardiac arrhythmia
3.
Hypertrophic obstructive cardiomyopathy (HOCM)
4.
Aortic stenosis
5.
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CLINICAL PEARL
The most important feature of a case of syncope is whether the loss of consciousness
occurred suddenly or gradually. A sudden loss of consciousness is caused by cardiac
and neurologic problems.
Initial Management
Setting: emergency department
Diagnostic/Therapeutic Plan
Test Results
Assessment
Hypoglycemia6.
Electrolyte disorder7.
Pulmonary hypertension8.
Electrocardiogram
Telemetry
Left ventricular hypertrophy; nonspecific ST- and T-wave abnormalities; small Q waves in
inferior and lateral leads
Telemetry normal; no arrhythmias detected
157
The differential diagnosis of syncope in a young patient is quite broad. In this patient, the
prominent findings on physical examination point to a cardiac etiology. Although dyspnea is the
most common presenting complaint with hypertrophic obstructive cardiomyopathy, it’s possible
for patients to have angina or syncope. Most commonly, these symptoms are related to exertion.
Characteristic findings on physical exam include sustained left ventricular apical impulse,
prominent S4 gallop, and harsh systolic ejection murmur, loudest at the left lower sternal
border and often associated with a thrill. A brisk carotid upstroke is often present.
Valsalva maneuver results in augmentation of the murmur, whereas squatting diminishes it. The
Valsalva maneuver decreases venous return to the heart, which results in a smaller ventricular-
chamber size. Anything that decreases ventricular-chamber size increases the outflow tract
obstruction and therefore increases the murmur. Echocardiogram is the diagnostic procedure of
choice.
Further Management Plan
Test Results
Patient Safety Note
Echocardiogram
Troponin
Thickened ventricular septum, which is hypertrophied disproportionately to the posterior
wall of the left ventricle. Anterior displacement of the mitral valve apparatus during systole.
Diastolic dysfunction.
Troponin normal
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Patients with syncope should be placed on continuous cardiac monitoring. The most
important aspect of a syncope case is to exclude a cardiac etiology; 80–85% of the
mortality has a cardiac etiology.
Discussion
Although HOCM may present in young adults, it does not often become clinically apparent until
later in life. Asymmetric septal hypertrophy leads to outflow tract obstruction. Diastolic
abnormalities with decreased compliance and delayed relaxation are not uncommon.
When symptomatic, the most common symptom of HOCM is dyspnea. Life-threatening
arrhythmias, myocardial ischemia, and sudden death are all complications. Initial management
usually involves giving a beta-blocker or calcium-channel blocker to enhance diastolic filling.
Verapamil is preferable because of its negative inotropic effects. (In general, positive
inotropes including digitalis and beta-agonists should be avoided.)
The major concern with treatment in HOCM is the associated risk of malignant arrhythmia and
sudden death. Beta-blocker therapy helps to reduce this risk, though amiodarone is an option.
Surgical therapy is reserved for those refractory to medical therapy.
Diuretics should be avoided, as should digoxin, nitrates, vasodilators, and ACE inhibitors.
They all help reduce the left ventricular-chamber size and therefore worsen the obstruction.
HOCM is the best example of diastolic dysfunction. With diastolic dysfunction, the mainstay of
therapy is beta blockers. Digoxin has no value here, and in fact may worsen symptoms.
Follow-up Management and Prevention
Oral beta blocker, e.g., metoprolol
159
Final Diagnosis
Syncope due to hypertrophic obstructive cardiomyopathy (HOCM)
Telemetry monitoring for 24–48 hrs in hospital
Electrophysiology evaluation
Cardiology consult to evaluate patient for implantable defibrillator
Avoidance of extreme exertional activity and volume depletion
Alcohol infusion via a catheter into myometrium of the septum to cause microinfarctions of
septal perforator arteries
Surgical myomectomy when not responsive to medical management
Possible defibrillator placement
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