Emergency Medicine Q & A, 2009, Pg

Emergency Medicine Q & A, 2009, Pg


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can be dif\ufb01cult to differentiate from normal variants with early repolarization. In stage two,
ST segments become isoelectric and T-wave amplitude decreases. In stage three, T-wave inversion occurs in leads
that showed ST elevation. In stage four, there is resolution of the repolarization abnormalities. CXR is of limited
value, although some patients will have effusions.
58 Emergency Medicine Q & A: Pearls of Wisdom ...
36. A 50-year-old woman complains of acute chest pain and shortness of breath. She describes the pain as sharp
and \u201cmuch worse than childbirth.\u201d Heart rate 100/min; blood pressure 190/110 mmHg. You hear bibasilar
rales and a grade 3/6 systolic murmur with a short diastolic component. Chest radiograph shows a left
pleural effusion, mild mediastinal widening, and mild pulmonary vascular congestion. EKG shows 2 mm of
ST depression in the lateral leads and voltage criteria for LVH. Her history is remarkable for hypertension,
for she has refused therapy. Which statement about her diagnosis is true?
a. Treatment with a \ufb01brinolytic agent within an hour of presentation signi\ufb01cantly prolongs survival.
b. A ventilation\u2013perfusion scan will probably show mismatched defects.
c. CPK isoenzymes and troponin levels will be positive.
d. Emergency angiogram or transesophageal echocardiography is indicated.
e. The mean 1-year survival of untreated patients is 50%.
The answer is d. Acute, severe chest pain, aortic insuf\ufb01ciency, hypertension, ischemic EKG changes, and a left
pleural effusion with mediastinal widening are consistent with acute aortic dissection. Ninety percent of these
patients present with EKG changes, but MI patterns are rare. Unlike the case in acute MI, the chest radiograph is
usually abnormal. An aortic knob with an abnormal amount of soft tissue density projecting beyond the aortic
calci\ufb01cation may be seen. Emergency aortography (or in some centers contrast enhanced CT scan) con\ufb01rms the
process. Patients may also present with stroke or paraplegia from involvement of the carotid arteries. The diagnosis
should be entertained in patients presenting with chest pain and neurologic \ufb01ndings. Differences in extremity blood
pressure should be sought. Untreated aortic dissection has a mortality of 28% at 24 hours and 90% at 3 months.
37. A 21-year-old woman in her 16th week of pregnancy complains of 2 days of right chest pain approximately
1 week after she underwent a successful appendectomy. Vital signs: temperature 37.8\u25e6C (100.1\u25e6F); heart rate
100/min; respiratory rate 35/min. She appears mildly anxious. You can hear a few wheezes at the right lung
base. She has a well-healing scar on her abdomen. The remainder of the examination is negative. A chest
radiograph (with her abdomen appropriately shielded) shows subsegmental atelectasis of the right lower
lobe with elevation of the right hemidiaphragm. Complete blood count and basic metabolic panel are
unremarkable, and quantitative beta-HCG is appropriate to her pregnancy. Your next step is to:
a. Prescribe an albuterol inhaler and incentive spirometer with assurances that the lung effects of general anesthesia
(atelectasis) will resolve soon.
b. Obtain lower extremity duplex ultrasonography to rule out deep vein thrombosis (DVT).
c. Obtain a ventilation\u2013perfusion scan to rule out pulmonary emboli.
d. Prescribe ibuprofen for the chest pain and refer to gynecology for follow-up.
e. Presume venous thromboembolic disease and begin warfarin therapy.
The answer is c. The diagnosis of exclusion is pulmonary embolism. This patient has risk factors for DVT, and
presents with chest pain, subsegmental lung atelectasis, and tachypnea. Appropriate radiologic investigations should
not be withheld from pregnant patients. A ventilation\u2013perfusion lung scan or a pulmonary angiogram is an
appropriate choice. Negative venograms occur in up to 30% of documented cases of pulmonary embolism.
Warfarin is contraindicated during pregnancy, as it crosses the placental barrier.
38. Choose the appropriate statement about alcohol ingestion and heart disease:
a. Chronic alcohol ingestion can lead to a restrictive cardiomyopathy.
b. If heart failure does develop, discontinuing alcohol will not change the prognosis.
c. High-output congestive heart failure may be due to a thiamine de\ufb01ciency.
d. If a patient with alcoholic cardiomyopathy continues to drink, mortality rate is greater than 70% over the next
3 years.
e. The most common dysrhythmia associated with a drinking binge is ventricular tachycardia.
... CHAPTER 3 Cardiovascular Emergencies 59
The answer is d. Chronic alcoholics may develop a clinical picture identical to that of dilated cardiomyopathy.
Stopping the consumption of alcohol can halt the progression of disease. With continued alcohol use, mortality
rate approaches 75% within the next 3 years. While beriberi heart disease leads to a high-output congestive heart
failure, alcoholic cardiomyopathy is associated with a low-output state. Binge drinking, or \u201choliday heart
syndrome,\u201d causes atrial \ufb01brillation more than any other dysrhythmia.
39. Choose the true statement regarding the progression to complete atrioventricular block (AVB) in the setting
of myocardial infarction:
a. The risk of complete AVB is the same regardless of the region of myocardium involved in the infarction.
b. Mobitz I second-degree block is an indication for prophylactic insertion of a pacemaker.
c. Mobitz II second-degree block infrequently progresses to complete AVB, and if it does, a stable infranodal
pacemaker with an adequate rate is usually maintained.
d. A \ufb01rst-degree AVB with a new left bundle-branch block (LBBB) is an indication for prophylactic insertion of a
pacemaker.
e. Infarctions that cause Mobitz II blocks are usually small and patients do well regardless of therapy.
The answer is d. The risk of complete AVB in an AMI depends on the site of infarction and the appearance of new
conduction disturbances. Patients with AMI are at risk for profound bradycardia if complete AVB develops because
the ventricular escape pacemaker is often slow and unreliable. Increased vagal tone impairing AV conduction is
often seen in inferior wall MI with \ufb01rst-degree AVB or Mobitz I (Wenckebach) second-degree AVB and usually
requires no treatment. Symptomatic patients usually respond to simple measures such as administration of atropine.
40. Choose the correct statement regarding acute myocardial infarction:
a. Elderly patients are more likely to present with nonspeci\ufb01c symptoms than younger ones.
b. An S4 is rare and is probably the result of increased ventricular compliance.
c. Inferior infarctions frequently cause tachycardia.
d. A new systolic murmur usually represents tricuspid regurgitation.
e. Acute fever precludes the diagnosis of myocardial infarction.
The answer is a. New systolic murmurs in acute myocardial infarction require careful investigation. The most
likely causes are acute papillary muscle dysfunction/rupture with mitral regurgitation or ventricular septal rupture.
Mild fever in AMI is common. Elderly patients may present with symptoms related to decreased cardiac output,
such as confusion or shortness of breath.
41. Captopril:
a. Decreases plasma renin activity.
b. Increases degradation of circulating bradykinin.
c. Increases formation of angiotensin II.
d. Cannot be safely used in combination with a beta-blocking agent.
e. Is contraindicated in patients with bilateral renal artery stenosis.
The answer is e. Captopril is an inhibitor of angiotensin converting enzyme and impairs production of angiotensin
II, which is a potent vasoconstrictor. Through removal of the feedback mechanism, renin secretion is increased.
There are additional antihypertensive effects from reduction of bradykinin degradation and stimulation of
vasodilating prostaglandin production. Converting enzyme inhibitors such as captopril can be added to
beta-adrenergic blockade