74) A 75 year-old man with history of hypertension presents to the emergency room with complaints of shortness of breath and palpitations. His vital reveal a heart rate 142/min, blood pressure 130/86, temperature 98.6 and oxygen saturation of 89% on room air. On auscultation, there are no rhonchii or crepitations, the heart rate was irregular and rapid with out any murmurs. The patient is placed on oxygen by nasal cannula. An urgent EKG is obtained which reveals rapid atrial fibrillation with no evidence of significant ST-T changes. The patient is started on diltiazem. Chest x-ray is normal and a brain natriuretic peptide is 80ng/L. Electrolytes, TSH and complete blood count are with in normal limits. Cardiac enzymes are drawn. Arterial blood gases reveal a pH of 7.48, po2 of 58, pco2 of 20 on room air ( Fio2 of 21%). The next step in evaluating the etiology of his atrial fibrillation :
A) Cardiac catheterization
B) Spiral CT scan of the chest
C) Venos doppler of lower extremities
D) 2D Echocardiogram
E) D-Dimer
75) What is the most likely etiology of atrial fibrillation in Case 1?
A) Acute ST elevation MI
B) Acute pulmonary embolism
C) Pneumothorax
D) COPD exacerbation
E) Congestive heart failure
Archer USMLE Step 3 Blog 
d and e
B
B
B and B: tachypnea leading to resp alkalosis and explaining the low O2 Sat of 89%. There are no rales/crackles to suggest CHF on physical exam.
B and B
D-dimer testing is most reliable for excluding pulmonary embolism in younger patients who have no associated comorbidity or history of venous thromboembolism and whose symptoms are of short duration.[40] However, it is of questionable value in patients who are older than 80 years, who are hospitalized, who have cancer, or who are pregnant, because nonspecific elevation of D-dimer concentrations is common in such patients. D-dimer testing should not be used when the clinical probability of pulmonary embolism is high, because the test has low negative predictive value in such cases
Chest radiographs are abnormal in most cases of pulmonary embolism, but the findings are nonspecific. Common radiographic abnormalities include atelectasis, pleural effusion, parenchymal opacities, and elevation of a hemidiaphragm. The classic radiographic findings of pulmonary infarction include a wedge-shaped, pleura-based triangular opacity with an apex pointing toward the hilus (Hampton hump) or decreased vascularity (Westermark sign). These findings are suggestive of pulmonary embolism but are infrequently observed.
V/Q scanning of the lungs is an important modality for establishing the diagnosis of pulmonary embolism. However, V/Q scanning should be used only when CT scanning is not available or if the patient has a contraindication to CT scanning or intravenous contrast material.
A negative ultrasonographic scan does not rule out DVT, because many DVTs occur in areas that are inaccessible to ultrasonographic examination. Before an ultrasonographic scan can be considered negative, the entire deep venous system must be interrogated using centimeter-by-centimeter compression testing of every vessel. In two thirds of patients with pulmonary embolism, the site of DVT cannot be visualized with ultrasonography, so a negative duplex ultrasonographic scan does not markedly reduce the likelihood of pulmonary embolism.
b, b
B,B
Correct answer is D, B. Hypoxia can precipitate atrial fibrillation. ABGs reveal hypoxic respiratory failure and a large A-a gradient. Since CXR is normal and BNP at 80, there is no reason to suspect pulmonary edema. No pneumonia on CXR either. While pulmonary embolism is a strong suspect here, other causes that could cause atrial fibrillation including right heart failure, structural cardiac anomalies/ valvular disorders can be best evaluated by a 2D echocardiogram. Moreover, a 2D echo showing acute cor-purmonale is also strongly supportive of Pulmonary embolism. Therefore, a 2D echo not only gives information regarding a possible PE but also differential diagnosis such as cardiac causes for atrial fibrillation
BNP in normal. So it is not CHF
tricky tricky.
This is probably a stupid question but can a right atrial fibrillation cause a pulmonary embolism? (i.e. clot from rightt afib emboli to pulmonary arteries) If yes, how does one finds out which comes first? Is the PE causing the Afib? Or the Afib is causing the PE? Chicken or egg?
b b