A 62-year-old Caucasian man presents to the clinic for his annual physical examination. The patient has a history of hypertension, which is adequately controlled with medications and lifestyle changes. The patient reluctantly admits that he still smokes a half pack of cigarettes daily. On examination, his blood pressure is 132/88 mmHg. During the physical examination, a pulsatile abdominal mass is noted. The patient denies any symptoms from the mass. An ultrasound is ordered and reveals that the abdominal aortic diameter is 4.5 cm.
What is the next step in management?
Observation. Although abdominal aortic aneurysms (AAAs) are potentially fatal, the best evidence argues for conservative management when the aneurysm is <5.5 cm in diameter. There are some modifications to this rule based on other patient factors (e.g., patients with Marfan syndrome); however, this is a good general number to remember. These patients can be followed with serial imaging every 6 to 12 months with ultrasound or CT. Risk factors for AAAs include increasing age, male gender, Caucasian race, atherosclerosis, and most importantly smoking. Smoking cessation is the most important immediate intervention for this patient to reduce the rate of growth and the risk of rupture. In addition, he should start aspirin and a statin since an AAA is a coronary artery disease risk equivalent (others are diabetes, carotid artery disease, and peripheral vascular disease). Asymptomatic AAAs may be diagnosed on physical examination or screening (USPSTF recommends a onetime ultrasound in males aged 65 to 75 with a history of smoking). AAAs are usually not symptomatic but can present with abdominal or back pain and limb ischemia. In a patient with abdominal pain, distention, and hemodynamic instability, always consider rupture of an AAA.
(B) Blood pressure control with β-blockers and ACE inhibitors may decrease the rate of growth and risk of rupture; however, this patient’s blood pressure is at goal (<150/90 mmHg as per the most recent guidelines). Rapid reduction in blood pressure is important for patients with type B aortic dissections (involving the descending aorta); type A dissections (involving the ascending aorta) require immediate surgery. (C, D) This patient has an asymptomatic AAA <5.5 cm and therefore does not require surgery at this time.
A 68-year-old woman presents to the Emergency Department with substernal chest pain radiating to her jaw. Her medical history is significant for hypertension and hyperlipidemia. Troponins are positive, and an ECG confirms STEMI. She undergoes percutaneous coronary intervention. The rest of her hospitalization is unremarkable, and she is eventually discharged. She returns to your office 1 month later complaining of a persistent dry cough without any other symptoms. Physical examination is unremarkable.
Which of the following is the most appropriate next step in management?
Stop the patient’s lisinopril and start losartan. This is a two-part question, which tests the reader’s knowledge of (1) appropriate discharge medications after a myocardial infarction and (2) the important adverse effects of these medications. After an MI, all patients should be discharged on the following medications: aspirin, clopidogrel, β-blocker, ACE inhibitor or angiotensin receptor blocker (ARB), and statin. ACE inhibitors and ARBs improve mortality postmyocardial infarction by reducing blood pressure as well as harmful cardiac remodeling (note: ACE inhibitors and ARBs should not be used together). The most likely cause of the patient’s cough at this time is an adverse effect from the ACE inhibitor. ACE inhibits the conversion of angiotensin I to angiotensin II, which occurs primarily in the lungs. It also inactivates bradykinin, so ACE inhibition leads to the build up of bradykinin in the lungs which is responsible for the dry cough.
(A, C) Given that the patient is presenting without any other symptoms or any concerning physical examination findings, checking troponin levels and ordering a chest x-ray are unnecessary at this time. (E) Although reassurance is commonly a correct answer when seen on the shelf examination, it is inappropriate to reassure the patient if the cough is a bothersome symptom. (D) Aspirin allergy is not a true “allergy” and would not present like this; for the shelf examination, look for the classic triad of a patient with asthma, chronic rhinosinusitis with nasal polyps, and taking aspirin or other NSAIDs.
A 63-year-old woman presents to the hospital with shortness of breath and palpitations that started this morning. She has a history of coronary artery disease and takes appropriate medications. Her ECG is shown below (Figure below).
Which of the following is the most likely diagnosis?
Atrial flutter. The rhythm of atrial flutter can be diagnosed on ECG by the classic “sawtooth” pattern, which is best seen in the inferior leads (II, III, aVF). It is typically caused by a premature atrial impulse that leads to a self-perpetuating loop around the tricuspid annulus. One tip-off on an ECG is an atrial rate of 300 beats per minute with a 2:1 conduction ratio through the AV node, leading to a heart rate of 150 beats per minute.
(A) Atrial fibrillation would show an irregularly irregular rhythm on ECG with no identifiable P waves. (C) Multifocal atrial tachycardia is a rarely tested supraventricular tachycardia that is caused by multiple ectopic foci in the atria; P waves of various morphology are seen on ECG. (D) AVNRT and AV reciprocating tachycardia (AVRT) involve re-entrant circuits in either the AV node solely (AVNRT) or in the AV node with an accessory pathway (AVRT). They typically cause a heart rate >150 beats per minute with P waves that are buried within the QRS complexes.
A 59-year-old man with a history of nonischemic cardiomyopathy presents to the hospital with leg swelling and extreme shortness of breath. He reports that several weeks ago, he had trouble obtaining his medications due to losing his medical insurance. He normally takes losartan, carvedilol, nifedipine, aspirin, furosemide, atorvastatin, insulin, and omeprazole. His vitals show a blood pressure of 104/64 mmHg, a heart rate of 72 beats per minute, and a respiratory rate of 28 breaths per minute. He has an S3 on examination with bilateral rales at his lung bases and 2+ pitting edema of his lower extremities up to his sacrum. An ECG shows no acute ST elevations or depressions. A chest x-ray shows bilateral fluffy opacities, and an echocardiogram shows an estimated ejection fraction of 20%.
Which of the following medications should not be resumed at this time?
: Carvedilol. In the setting of acute decompensated heart failure, a patient’s dosage of β-blocker should be reduced or discontinued based on the severity of symptoms. This is done to help improve the rate and contractility of the heart in order to improve symptoms and aid in diuresis. (A) Furosemide should be continued, but it should be switched to IV administration in order to aggressively diurese this patient. (C) The patient’s ARB should be held if he becomes hypotensive; however, it may be continued at this time. (B, D) The rest of the medications can be resumed safely.
A 55-year-old man presents to the hospital with progressive dyspnea over the course of the last few weeks. He denies fever, cough, or chest pain. He has no significant medical or family history, but endorses drinking two 750-mL bottles of wine daily. He is afebrile with a blood pressure of 139/82 mmHg, heart rate of 98 beats per minute, and respiratory rate of 24 breaths per minute. The point of maximal impulse is displaced laterally, a 2/6 holosystolic murmur is heard at the apex, and an S3 is auscultated. There are crackles at the lung bases with pitting edema around the ankles.
Which of the following is the most important intervention for this patient?
Alcohol cessation. The patient in this vignette is presenting with symptoms and signs of heart failure from a dilated cardiomyopathy. There are many causes of dilated cardiomyopathy, but the significant history of heavy alcohol intake points to this as the underlying cause. Alcohol is directly toxic to cardiomyocytes and can cause left ventricular dysfunction with subsequent cardiac dilation. The most important first step with toxic cardiomyopathies is to stop the offending agent. If abstinence is initiated immediately, the condition may be reversible with return of normal left ventricular function. Without abstinence, these patients will continue to progress to heart failure and require the medications and devices appropriate for heart failure of any cause. Other important causes of dilated cardiomyopathy include ischemic heart disease, myocarditis (Coxsackie viruses, HIV, Lyme disease, Chagas disease, etc.), chronic valvular disease, stress-induced (Takotsubo cardiomyopathy) or chronic tachycardia, and certain metabolic conditions (hypothyroidism, pheochromocytoma, etc.). Besides alcohol, other toxins that can cause a dilated cardiomyopathy include cocaine and anthracycline chemotherapy. (A, B, C) These interventions and medications are potentially helpful in heart failure; however, the patient has a potentially reversible cause of heart failure and therefore cessation of the offending agent is the best option.
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