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Old 10-21-2011
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Default Cardiology

A 58-year-old man with known congestive heart failure (CHF) comes to the clinic complaining of painful, swollen breasts. Over the last couple of months he has noticed small, tender nodules on both of his breasts that appear to lie just below the skin. He is concerned because, aside from the pain, he finds the growth of his breasts embarrassing. Other than this new growth, the patient has been doing well. His heart failure has been stable on his current medical regimen, and he has been carefully following a low-salt diet. He denies any weight changes, and reports only mild orthopnea and dyspnea on exertion. Past medical history is significant for a myocardial infarction 3 years prior, hypertension, and diabetes mellitus type 2, diagnosed 5 years ago. Current medications include fosinopril, aspirin, atenolol, spironolactone, furosemide, metformin, and a stool softener. Vital signs are: blood pressure 133/84 mm Hg, pulse 62/min, respirations 20/min, and temperature 37 C (98.6 F). Chest examination shows nodular, enlarged breasts, which are mildly tender to palpation. Cardiac examination reveals a diffuse point of maximal impulse but is otherwise unremarkable. Lower extremities display 1+ pitting edema bilaterally. The rest of the examination is normal. Which of the following is the most likely cause of his chief complaint?
A. ACE inhibitor effect on fibroblast proliferation
B. Fluid retention
C. Idiosyncratic side effect of beta-blockers
D. Sex hormone–like effects of spironolactone
E. Undiagnosed liver disease caused by right heart failure

A 62-year-old woman with a past medical history of hypertension, hyperlipidemia, and left-sided breast carcinoma status post a left lumpectomy and radiation therapy 3 years ago now presents with increased lethargy, weakness, and shortness of breath for 4 days. The patient is unable to answer questions appropriately due to her mental status changes, but according to her family the patient was in her usual state of good health until 1 week ago. At that time the patient had started complaining of increasing dyspnea on minimal exertion and vague chest discomfort until 3 days ago, when the patient became increasingly somnolent and fatigued. The family also notes that the patient has not been urinating as frequently as her normal baseline. The patient’s vital signs on presentation are: blood pressure 95/50 mm Hg, pulse 105/min, respirations 24/min,and temperature 37 C (98.6 F). Physical examination shows an increased jugular venous pressure, distant heart sounds with a rub that is heard throughout the cardiac cycle, and dullness to percussion over the right lower lung field. Which of the following additional clinical findings would you expect to find associated with this patients’ current condition?
A. Increased pulmonary congestion on chest x-ray
B. An increase in systolic blood pressure with inspiration
C. Increased voltage on electrocardiogram across precordial leads.
D. Inspiratory increase in venous distention
E. A raised central venous pressure with prominent “x descent” and blunted “y descent” on right-heart catheterization
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Old 10-22-2011
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D. Sex hormone–like effects of spironolactone
D. Inspiratory increase in venous distention
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Old 10-22-2011
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D. Sex hormone–like effects of spironolactone

D. Inspiratory increase in venous distention (kausmaul sign???)
Is it a case of Constrive pericarditis post radiation??
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Old 10-23-2011
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Default Answer

The correct answer is D. Spironolactone is proven to reduce mortality in patients with CHF by inhibiting cardiac remodeling and fibrosis. However, a common side effect of chronic spironolactone, even if given at the low doses necessary to maintain cardiac function, is gynecomastia. Spironolactone chemically resembles some of the sex steroids and thus has minimal hormonal activity, inducing gynecomastia in some males and menstrual irregularities in some females.
Some ACE inhibitors (choice A) have demonstrated a beneficial effect on the severity of heart failure. ACE inhibitors may significantly decrease peripheral (systemic vascular) resistance, blood pressure (afterload), pulmonary capillary wedge pressure (preload), pulmonary vascular resistance and heart size and increase cardiac output and exercise tolerance time. ACE inhibitors do not cause gynecomastia.
Fluid retention (choice B) occurs from homeostatic responses to a decreased cardiac output. This explains the patient’s peripheral edema, but not gynecomastia.
Beta-blockers (choice C) cause a host of side effects, including bronchospasm, cardiac decompensation, and, arguably, depression and sexual dysfunction. They do not cause gynecomastia.
Right heart failure (choice E) can cause hepatic congestion, which may manifest as elevated liver transaminases. However, hepatic congestion usually does not cause synthetic liver dysfunction, certainly not to the degree necessary to see gynecomastia, which is associated with the hyperestrogenic state of end-stage liver disease

The correct answer is E. This patient presents with cardiac tamponade, which is characterized by elevated intrapericardial pressure with impairment of cardiac diastolic filling and ultimately a reduction in cardiac output. Any cause of pericarditis can lead to a large enough effusion and then tamponade, but the most common etiologies are malignancy, uremia, proximal aortic dissection with rupture, postcardiac surgery, and idiopathic. The signs and symptoms of cardiac tamponade are all reflective of a low cardiac output and can vary from nonspecific mental status changes such as restlessness, agitation, and lethargy to other low-perfusion signs as decreased urine output, dyspnea, chest pain, or liver failure. Other physical findings of tamponade include tachypnea, tachycardia, pericardial rub, diminished heart sounds, and signs of right-heart failure, including hepatomegaly and peripheral edema. A raised central venous pressure with prominent ―x descent‖ and blunted ―y descent‖ on right-heart catheterization is associated with cardiac tamponade. Since the pericardial effusion is in a finite space around all four heart chambers, diastolic pressures are equal (―equalization of diastolic pressures‖). When the tricuspid valve opens at the beginning of diastole, the pressure in the right ventricle equals the pressure in the right atrium; thus there is no rapid exit of blood from right atrium to right ventricle (no pressure gradient); and thus there is a ―blunted y descent‖ seen on a Swan Ganz right-heart cath. This patient very likely has a recurrence of breast carcinoma that has metastasized to invade the pericardium, causing tamponade. Both right-heart catheterization (Swan Ganz catheter) and cardiac echo are diagnostic, and this patient needs to be treated with urgent pericardiocentesis to drain the pericardial effusion.
Increased pulmonary congestion on chest x-ray (choice A) is incorrect because tamponade presents with signs of right-heart failure as opposed to left-heart failure. Pulmonary edema on chest radiography is characteristic of congestive heart failure from left ventricular dysfunction and is not seen with tamponade.
An increase in systolic blood pressure with inspiration (choice B) is incorrect. One of the hallmark physical findings of cardiac tamponade is a ―pulsus paradoxus,‖ which is an inspiratory decrease in systolic blood pressure greater than 10 mm Hg. The mechanism of pulsus paradoxus is still uncertain. Arterial pressure normally falls a little with inspiration because the intrathoracic pressure drops. This fall is also more obvious in patients with obstructive lung disease. Arterial paradox is thus an accentuation of the normal response and not, in fact, paradoxical. Overall stroke volume falls, and the interventricular septum shifts from right to left. Right ventricular stroke volume is thus maintained only by almost complete obliteration of the left ventricular cavity during inspiration.
Increased voltage on electrocardiogram across precordial leads (choice C) is incorrect because with the increased pericardial fluid surrounding the heart, the EKG will often show a reduction in voltage across the precordial leads.
Kussmaul's sign (choice D) refers to an inspiratory increase in venous distention. Abnormal filling is reflected in the venous pressure. The pressure is always raised; if it is not, the diagnosis of tamponade must be questioned. Usually, it is very high, and it may be difficult to see the top; if a central venous line is in place, a further increase may occur with inspiration (Kussmaul's sign). This is a nonspecific finding and merely reflexts the inability of the right heart to deal with an increase in stroke volume, so it is seen in a variety of conditions including right ventricular disease (right ventricular hypertrophy; right ventricular infarction) and pulmonary hypertension. Usually this sign is present in constrictive pericarditis but may be present in patients with cardiac tamponade.
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