Cardiomegaly case 1

Cardiomegaly case 1

A 45-year-old woman presents to her primary care physician complaining of fatigue, weight gain, and shortness of breath. She has always been an active athlete, but in the past 2 weeks, has found it impossible to jog for more than a few minutes, after which she feels tired and
winded. She feels like her appetite is normal or has even declined, but she notices that she has gained 15 pounds and her pants and shoes no longer fit welI. She has very little energy, and is sleeping poorly, with occasional difficulty breathing at night. She denies any pain, fever, or
chills. Review of her chart reveals an up-to-date health screening including a normal baseline mammogram, a normaI Pap smear in the last year, and total cholesterol of 165 mg/dL two years ago. On physical examination, she appears comfortable, has a temperature of 36.8 C
(98.2. F), blood pressure of 135/68 mm Hg, pulse of 90/min, and respiratory rate of 24/min. She appears fatigued but not in acute distress, and her skin appears normal. Expiratory wheezes are heard at the bases of both lungs. Her heart has a normal-sounding S1 and S2, with a
II/IV soft holosystolic murmur heard best at the apex of the heart. Her abdomen is modestly distended, and her ankles are edematous. A chest x-ray film reveals cardiomegaly as well as increased vascular markings in the lung beds and bilateral small pleural effusions.

Q 1
Which of the following is the most likely diagnosis?
/ A. Acute leukemia
/ B. Cardiomyopathy
/ C. Fibromyalgia
/ D. Hypothyroidism
/ E. Major depressive disorder

Q 2
Which of the following is the most likely cause of the patient's murmur?
/ A. Aortic insufficiency
/ B. Aortic stenosis
/ C. High-output flow murmur
/ D. Mitral regurgitation
/ E. Mitral stenosis
/ F. Pulmonic insufficiency
/ G. Pulmonic stenosis
/ H. Tricuspid regurgitation
/ I. Tricuspid stenosis

Q 3
BIood in the pulmonary veins is at the same pressure (during all phases of the cardiac cycle) as blood in which of the following?
/ A. Aorta
/ B. Left atrium
/ C. Left ventricle
/ D. Right atrium
/ E. Right ventricle

Q 4
To improve her shortness of breath, the patient is given furosemide. What is the molecular mechanism and site of action of this drug?
/ A. ADH antagonism of in the collecting ducts
/ B. AIdosterone antagonism in the distal tubule
/ C. BIockade of sodium reabsorption in the proximal tubule
/ D. BIockade of sodium transport in the distal tubule
/ E. Inhibition of carbonic anhydrase in the proximal tubule
/ F. Inhibition of sodium-potassium-chloride cotransport in the loop of Henle

Q 5
What important physiologic effect will starting this patient on an angiotensin-converting-enzyme inhibitor achieve?
/ A. Decrease in arteriolar resistance, resulting in less resistance to forward cardiac output
/ B. Decrease in cardiac filling pressures, resulting in less pulmonary congestion
/ C. Increase in arteriolar resistance, resulting in improved blood pressure
/ D. Increase in left-ventricular end-diastolic volume, improving stroke volume via Starling forces
/ E. Increase in myocardial contractility, resulting in improved stroke volume
/ F. Stabilization of myocardial membranes, resulting in reduced risk of arrhythmia

____________________________________________________________________


Cardiomegaly Case 1 Answers

A1
The correct answer is B. This woman has many of the classic symptoms of heart failure, with symptoms of both poor forward cardiac output (fatigue, poor appetite) and of vascular congestion in both the right and left atria (edema, abdominal distension that may be ascites, cardiomegaly, pulmonary vascular congestion and effusions seen on chest x-ray, dyspnea with exertion, and paroxysmal nocturnal dyspnea.)
Acute leukemia (choice A) is a potential cause of fatigue, poor energy, and poor nutritional status (which can cause edema and pleural effusion). Usually some abnormality will be apparent, most commonly pancytopenia, due to replacement of bone marrow with leukemic cells; the leukocyte count may be elevated due to the presence of leukemic cells in the peripheral blood. They often present with bleeding or infectious complications of pancytopenia. Anemia could potentially cause a murmur due to elevated cardiac output, but an acute leukemia would not typically cause cardiomegaly or pulmonary edema.
Fibromyalgia (choice C) is a potential cause of fatigue, poor energy, and poor sleep, especially in women ages 25-45: its principal sign, however, is diffuse musculoskeletal pain and stiffness, with characteristic tender trigger points. It is not consistent with this patient's chest x-ray abnormalities or cardiac and lung findings.
Based on examination, this patient could certainly have hypothyroidism (choice D). Symptoms are usually insidious in onset and include fatigue, poor appetite with weight gain, poor sleep and possibly, obstructive sleep apnea. Patients often complain of constipation, cold intolerance, stiffness and muscle cramping, as well as decreased intellectual activity. Severe hypothyroidism can result in cardiomegaly, pericardial effusion, and symptoms of cardiac failure. The skin often appears dry, rough, and doughy in texture. The normal TSH, however, makes hypothyroidism in this patient very unlikely: The TSH is nearly always elevated, as most hypothyroidism is primary, which means the pituitary is secreting maximal TSH in an attempt to stimulate a hypofunctional thyroid gland. Rarely, TSH may be normal or depressed (even undetectable) in pituitary or hypothalamic failure. To rule this out, one might test first for T4 and T3 levels. Normal levels of these, in conjunction with the normal TSH, would rule out hypothyroidism as a cause of this clinical presentation.
Major depression (choice E) should always be in the differential for a patient who presents with disturbances in sleep, appetite, and energy, and can also result in weight loss or gain. These "vegetative signs" of depression may be the presenting abnormality in a depressed patient who does not note a mood disturbance themselves. One should also ask about depressed mood, anhedonia (loss of interest in or inability to take pleasure in activities the person normally enjoys), an inability to concentrate and carry on usual intellectual activities, feelings of worthlessness or guilt, and suicidal ideation. Depression cannot, however, on its own, produce the physical findings this patient has, which taken together, are worrisome for some physiologic abnormality.

A2
The correct answer is D. Mitral regurgitation is characterized by a holosystolic murmur heard best at the apex, often with a blowing sound, which may radiate to the axilla.
The murmur of aortic insufficiency (choice A) is a decrescendo diastolic murmur. Remember that the aortic valve is open during systole; a systolic murmur, then, cannot represent regurgitant aortic flow due to an improperly closed valve.
Aortic stenosis (choice B) does produce a systolic murmur caused by turbulent flow across a narrowed aortic valve during systole. This murmur is usually a crescendo-decrescendo murmur, often with a harsh quality, and is characteristically heard best at the base of the heart; it may radiate to the carotids as well.
High-output states (choice C) can cause a similar soft systolic murmur to that described here. However, this patient's history is most consistent with cardiac failure, which is a low-output state.
Mitral stenosis (choice E) causes a murmur due to turbulent low-velocity flow during diastolic filling of the left ventricle through a narrowed mitral orifice. This results in a soft diastolic murmur heard best at the apex. Remember that the mitral valve is closed during systole, therefore, an abnormal mitral sound in systole must be the sound of abnormal regurgitant flow through a closed valve.
The right-sided murmurs are less common, similar in quality, and usually less loud than the left-sided murmurs (given that pressures on the right are usually lower):
Pulmonic insufficiency (choice F), when audible, therefore causes a soft diastolic murmur at the right upper sternal border.
Pulmonic stenosis (choice G) causes a crescendo-decrescendo systolic murmur also heard at the base of the heart.
Tricuspid regurgitation (choice H) causes a holosystolic murmur at the left lower or right lower sternal border.
Tricuspid stenosis (choice I) when audible, is a diastolic murmur heard best at the same location

A3
The correct answer is B. The pressures in two chambers, which are not separated by a closed valve, will be equal. The pulmonary vein empties into the left atrium, and no valve separates the two chambers, therefore the pressures are equal in all phases of the cardiac cycle. This patient's pulmonary vascular congestion is likely due to elevated pulmonary venous pressure, which is, in turn, likely due to elevated left atrial pressures.
Pressures in the aorta (choice A) will be higher than pressures in the pulmonary veins during the cardiac cycle.
The left ventricle (choice C) is separated from the left atrium and the pulmonary veins by the mitral valve. The pulmonary veins and the left atrium are at the same pressure as the left ventricle during diastole, when the mitral valve is open. With complete mitral insufficiency, the pulmonary veins are completely exposed to left ventricular pressures during systole, resulting in severe pulmonary edema.
The right atrium (choice D) is not in communication with the pulmonary veins, being separated from them by, in sequence, the tricuspid valve, the right ventricle, the pulmonic valve, the pulmonary arterial system, and the pulmonary capillary bed.
The right ventricle (choice E), during systole, is at the same pressure as the pulmonary artery, not the pulmonary veins. During diastole, the pulmonary arterial pressure exceeds right ventricular pressure, and the valve is closed.

A4
The correct answer is F. The Na-K-2Cl cotransporter in the loop of Henle operates via an ATP-dependent sodium-potassium exchange pump in the cell that creates a gradient for sodium diffusion from the urine space into the cell. This maintains the sodium concentration gradient of the renal medulla. Furosemide is the most commonly used loop diuretic; it acts by blocking the action of the cotransporter in the thick ascending limb of the loop of Henle.
ADH antagonism (choice A) is not an important diuretic drug mechanism, however, certain drugs, most notably lithium, inhibit ADH's action, resulting in nephrogenic diabetes insipidus.
Aldosterone promotes the reabsorption of sodium in the late distal tubule and collecting system and promotes the excretion of potassium. Aldosterone receptor antagonism (choice B) is the mechanism of action of potassium-sparing diuretics such as spironolactone.
Sodium reabsorption in the proximal tubule (choice C) is a largely passive process, which is coupled to the transport of organic solutes and anions and also to chloride transport, via both transcellular and paracellular mechanisms.
The thiazide diuretics work primarily by blocking sodium transport in the early portion of the distal tubule (choice D).
Acetazolamide inhibits carbonic anhydrase (choice E), preventing the luminal transformation of bicarbonate into CO2, which diffuses back into the cell. Inhibition of this enzyme increases both bicarbonate and sodium concentrations in the urine, resulting in high urine pH and metabolic acidosis.

A5
The correct answer is A. In cardiac failure, the juxtaglomerular apparatus releases renin in response to low blood pressure or low flow states. Renin cleaves angiotensinogen into angiotensin I, which is then cleaved by angiotensin-converting enzyme (ACE) into angiotensin II. Angiotensin II is a potent vasoconstrictor and increases blood pressure. This, however, increases the resistance against which the heart must pump, thereby reducing cardiac output. By reducing angiotensin II activity, systemic vascular resistance (normally high in cardiac failure, in an attempt to maintain blood pressure in the presence of low flow) is reduced, permitting the heart to eject more volume against a lower aortic pressure. This is often described as "afterload reduction" and is the mainstay of therapy in congestive heart failure. Paradoxically, blood pressure may not change: the reduced resistance, by permitting increased flow, may result in no net change in pressure. This is most easily understood as a physiologic manifestation of Ohm's law: V = IR. In electricity, this law means that voltage is equal to current times resistance. Blood pressure is analogous to voltage, cardiac output to current flow, and the resistance in this case is the resistance of the systemic vasculature.
Reduction of cardiac filling pressures (choice B) or "preload," is also an important aspect of the treatment of heart failure. In heart failure, the heart operates at high filling pressures and high left ventricular end-diastolic volume (LVEDV) because both aldosterone and ADH promote the retention of fluid in response to low forward flow and decreased effective circulating volume. The result is vascular congestion in the pulmonary veins due to the high LV diastolic pressure, resulting in symptomatic pulmonary edema. By reducing this preload, congestive symptoms can be relieved, and LVEDV can be reduced without significant loss of stroke volume. ACE inhibitors, however, do not reduce preload: drugs that do this are nitrates (which act as venodilators) and diuretics.
Increasing arteriolar resistance (choice C) in heart failure increases the "afterload" against which the heart must eject and does not improve cardiac output.
Increasing LVEDV (choice D) is usually helpful in hypovolemia or other states in which inadequate volume is available to the heart, thereby limiting cardiac output. This happens in the portion of the Starling curve at low LVEDV, where an increase in LVEDV results in a large increase in stroke volume. Patients in symptomatic heart failure like this patient operate at very high LVEDV and benefit from its reduction.
Increasing myocardial contractility (choice E) is beneficial in heart failure, and is the mechanism of action of inotropic drugs. This is not a mechanism of ACE inhibitors.
Prevention of arrhythmia (choice F) is also important in heart failure, as the dilated heart is vulnerable to both atrial and ventricular arrhythmias. This is not a direct action of ACE inhibitors, however.