Week 5 Flashcards
A 42-year old man presents to the clinic with 1 week of chest pain, shortness of breath, and worsening leg swelling. He reports that, prior to the development of his symptoms, he had a brief illness characterized by a fever, sore throat, and occasional attacks of sharp, stabbing chest pain. Physical exam is notable for jugular venous distension, bilateral pitting edema in the feet and lower legs, a weak and laterally displaced point of maximal impulse, and an S3 gallop. An echocardiogram reveals enlargement of all four chambers with a left ventricular ejection fraction of 15 percent.
The infectious agent responsible for this patient’s symptoms is most likely:
a. A fungus with broad-based budding yeast
b. A positive-sense RNA virus
c. A Gram-positive bacterium that ferments mannitol
d. A double-stranded DNA virus
e. A mosquito-borne parasite
The correct answer is b, a positive-sense RNA virus. This patient is presenting with signs and symptoms consistent with a dilated cardiomyopathy (diffuse chamber enlargement, systolic dysfunction, edema, shortness of breath). Given this patient’s recent illness and chest pain, it is likely that this cardiomyopathy is secondary to myocarditis. The most common cause of myocarditis is viral infection, with coxsackie B virus being the classic etiology (pleurodynia, characterized by attacks of stabbing chest pain, is a symptom typical of coxsackie B virus infection).
Apart from viral infection, infection by parasites can be a cause of myocarditis, particularly in patients with a history of travel to Latin America (Chagas’ Disease, Trypanosoma cruzi parasite transmitted by the reduviid bug) or who are immunocompromised (toxoplasmosis is an important cause in this population). Myocarditis can also be seen in patients with diphtheria.
Additional, non-infectious causes of myocarditis include acute rheumatic fever, systemic lupus erythematosus, and transplant rejection. In all of these cases, in addition to causing dilated cardiomyopathy, myocarditis can also produce ventricular arrhythmias that can result in sudden cardiac death (myocarditis is one of the leading causes of SCD in young and middle-aged adults).
A 51-year old woman presents to the emergency room with 1 day of chest pain. She describes the pain as sharp and stabbing and notes that it is worsened when she breathes in or lies down. Physical exam is notable for a triphasic friction rub that is audible throughout the precordium. Electrocardiogram is notable for ST-segment elevation in leads II, III, aVL, aVF, V2, V3, V4, and V5.
Which of the following is most appropriate for managing this patient?
a. Emergent percutaneous coronary intervention
b. Administration of a beta-blocker
c. Administration of a class III antiarrhythmic agent
d. Administration of an NSAID
e. Administration of a fibrinolytic agent
The correct answer is d, administration of an NSAID. This patient’s presentation is most consistent with acute pericarditis, which is generally managed with NSAIDs and colchicine. Because the presentation of this condition can be very similar to an acute myocardial infarction, it is important to know the clinical features that distinguish them. First, pericarditis is generally characterized by a sharp, stabbing pain in contrast to the “crushing”, pressure-like pain associated with an MI. Additionally, the pain of pericarditis is generally relieved when the patient sits upward and leans forward, as this reduces pressure on the pericardium, while there is typically no positional variation in the pain of an MI. A classic physical exam finding in pericarditis is a pericardial friction rub, which is typically triphasic. With respect to EKG changes, pericarditis can be associated with diffuse ST-segment elevation throughout almost all leads, while the ST-segment changes in an MI are typically restricted to the leads overlying the infarct.
Pericarditis is most commonly caused by a viral infection (coxsackievirus and ECHO are classic causes), though other infectious agents can also be a cause. Non-infectious causes of pericarditis include systemic lupus erythematosus and other collagen vascular diseases, like rheumatoid arthritis. Pericarditis can also occur as a complication of a myocardial infarction, in which it is known as Dressler’s syndrome. Pericardial effusion and cardiac tamponade are potential complications of pericarditis.
Which of the following is associated with the development of hypertrophic cardiomyopathy?
a. Excessive alcohol intake
b. Pregnancy
c. Radiation exposure
d. Viral infection
e. None of the above
The correct answer is e, none of the above. While dilated and restrictive cardiomyopathies can be acquired as a result of various environmental exposures, hypertrophic cardiomyopathy generally occurs as a genetic condition (typically there is an inherited defect in one or more sarcomere proteins).
With respect to the other cardiomyopathies, dilated cardiomyopathy can be acquired by excessive alcohol intake, pregnancy (peripartum cardiomyopathy), or as a sequela of myocarditis. A restrictive cardiomyopathy generally arises as a result of conditions that lead to infiltration of the myocardium, including amyloidosis, sarcoidosis, hemochromatosis, and post-radiation fibrosis.
Which set of hemodynamic changes is expected in the heart of a patient with a dilated cardiomyopathy as compared to a normal heart? (LVEDP = left ventricular end-diastolic pressure, LVEDV = left ventricular end-diastolic volume, SV = stroke volume)
a. LVEDP increased, LVEDV increased, SV decreased
b. LVEDP decreased, LVEDV increased, SV decreased
c. LVEDP increased, LVEDV decreased, SV decreased
d. LVEDP decreased, LVEDV decreased, SV decreased
e. LVEDP increased, LVEDV increased, SV increased
The correct answer is b, LVEDP decreased, LVEDV increased, SV decreased. In a patient with dilated cardiomyopathy, there is diffuse dilatation of the chambers of the heart. This dilatation increases the volume of the chambers while also increasing their compliance, enabling the chambers to hold a larger volume of blood at a lower pressure. However, this dilatation also leads to systolic dysfunction, reducing the stroke volume.
Which set of hemodynamic changes is expected in the heart of a patient with a restrictive cardiomyopathy as compared to a normal heart? (LVEDP = left ventricular end-diastolic pressure, LVEDV = left ventricular end-diastolic volume, SV = stroke volume)
a. LVEDP increased, LVEDV increased, SV decreased
b. LVEDP decreased, LVEDV increased, SV decreased
c. LVEDP increased, LVEDV decreased, SV decreased
d. LVEDP decreased, LVEDV decreased, SV decreased
e. LVEDP increased, LVEDV increased, SV increased
The correct answer is c, LVEDP increased, LVEDV decreased, SV decreased. In a restrictive cardiomyopathy, infiltration of the myocardium causes the compliance of the chambers to be reduced and, as a result, the pressure within the chambers increases. Moreover, because of increased filling pressures, filling of the left ventricle during diastole is impaired, resulting in a decreased left-ventricular end-diastolic volume. Systolic function is typically close to normal, resulting in a normal to near-normal ejection fraction, but because of the reduced LVEDV, stroke volume is reduced.
Which of the following blood vessels in the fetal circulation contains the most oxygenated blood?
a. Aorta
b. Superior Vena Cava
c. Inferior Vena Cava
d. Ductus Arteriosus
e. Right Common Carotid Artery
The correct answer is c, the inferior vena cava. In the fetus, blood is oxygenated at the placenta and then returns to the body through the umbilical vein. Blood from the umbilical vein is shunted through the liver and into the inferior vena cava by the ductus venosus, where it mixes with deoxygenated blood returning from the lower part of the body. When this blood returns to the heart, it mixes with deoxygenated blood from the SVC in the right atrium; thus, blood in all locations subsequent to the right atrium have a lower oxygen content than blood in the IVC.
Which congenital heart defects are initially associated with cyanosis?
The T’s: Tetralogy of Fallot Transposition of the Great Arteries Truncus Arteriosus Total Anomalous Pulmonary Venous Return Tricuspid Atresia/Pulmonary Atresia (Also: Hypoplastic Left Heart Syndrome)
All are characterized by the presence of a right-to-left shunt
A patient with pulmonary hypertension secondary to a ventricular septal defect is undergoing evaluation to determine whether it would be beneficial to surgically close the defect. A cardiac catheterization is performed, and the following data is obtained:
Pulmonary Artery Pressure = 47 mmHg
Pulmonary Capillary Wedge Pressure = 12 mmHg
Cardiac Output = 5 L/min
Is surgical closure of the defect permissible?
The answer depends on the pulmonary vascular resistance, which is determined as follows:
PVR = Change in Pressure / Flow Rate = PAP – PCWP / CO
Thus, in this case, PVR is equal to:
(47 – 12) / 5 = 35 / 5 = 7 Wood units
It has been found that, if the PVR is greater than 6 Wood units, closure of the ventricular septal defect is likely to precipitate right-sided heart failure. Thus, in this patient, surgical closure of the defect is not indicated.
The following oxygen saturation data is obtained from a patient with a ventricular septal defect:
Right Atrium O2 Saturation: 75%
Pulmonary Artery O2 Saturation: 85%
Pulmonary Vein O2 Saturation: 100%
Systemic Artery O2 Saturation: 100%
What is the Qp/Qs ratio?
Qp/Qs = (Systemic Artery Sat – Systemic Vein Sat) / (PV sat – PA sat)
Thus, the Qp/Qs ratio in this patient is:
(100-75) / (100-85) = 25 / 15 = 1.67 (the cardiac output through the pulmonary circuit is 1.67 times the cardiac output through the systemic circuit)
Which chambers of the heart would be expected to enlarge over time in a patient with a patent ductus arteriosus?
The left atrium and left ventricle would be expected to enlarge. The right side of the heart would not enlarge, as it does not receive extra volume in the left-to-right shunt generated by a PDA.
Which chambers of the heart would be expected to enlarge over time in a patient with an atrial septal defect?
The right atrium, right ventricle, and possibly the left atrium would enlarge. The left ventricle would not enlarge, as it does not receive extra volume in the left-to-right shunt generated by an ASD.
Which chambers of the heart would be expected to enlarge over time in a patient with a ventricular septal defect?
The left atrium and left ventricle would enlarge. The right ventricle may enlarge, but this is variable, as the left ventricle can effectively pump blood directly into the pulmonary artery, sparing the right ventricle of a volume overload. The right atrium would not enlarge.
What hemodynamic changes underlie the reversal of shunt direction in Eisenmenger Syndrome?
Large left-to-right shunts lead to significantly increased blood flow through the pulmonary circuit; over time, this will cause a rise in the pulmonary vascular resistance, which will force the right ventricle to pump at a higher pressure to maintain flow. Eventually, this can result in the pressure on the right side of the heart becoming greater than the pressure on the left side of the heart, which will cause reversal of the shunt.
What gross pathologic features can help distinguish aortic stenosis that occurs due to rheumatic heart disease from aortic stenosis that occurs due to calcification?
A hallmark pathologic characteristic of aortic stenosis in rheumatic heart disease is fusion of the valve commissures. In calcific aortic stenosis, there is no fusion of the commissures, but calcified nodules may be visible on the valve leaflets.
A 24-year old man presents to the clinic with one week of fever, fatigue, and worsening swelling in his legs and abdomen. Prior to the onset of these symptoms, the patient had no health concerns. Social history reveals that the patient is a regular user of heroin. Physical exam is notable for pitting edema in the feet and legs, jugular venous distension, and a grade III/VI holosystolic murmur best heard in the fourth intercostal space on the left sternal border.
What infectious agent is most likely responsible for this patient’s symptoms?
a. A Gram-positive, coagulase-positive bacterium
b. A Gram-positive, novobiocin-sensitive bacterium
c. A Gram-positive, optochin-resistant bacterium
d. A non-enveloped DNA virus
e. A Gram-negative encapsulated bacterium
The correct answer is a, a Gram-positive, coagulase-positive bacterium. This patient’s presentation is most consistent with infective endocarditis affecting the tricuspid valve. This can be classically seen in users of injectable drugs, such as heroin, in which the typical causes are Staphylococcus aureus and Candida albicans. Once the infectious agent enters a vein, it travels back to the heart and adheres to the tricuspid valve, the first valve that is encountered. In the case of S. aureus, acute bacterial endocarditis can result, in which the valve is very quickly eroded with significant tricuspid regurgitation occurring as a result.
