Bbc: Practice Questions Part E

Front 1

What is a blowing murmur?

Back 1

blood flowing the wrong way across a valve

Front 2

A 48-year-old Asian female who is taking an angiotensin-converting enzyme (ACE) inhibitor for hypertension is brought for evaluation secondary to sporadic and transient palpitations and progressively worsening muscle weakness. What is the likely cause and what must be done, respectively?

A. Hypokalemia; prescribe potassium supplements
B. Hypokalemia; advise for a high protein diet
C. Hyperkalemia; prescribe kayexalate
D. Hyperkalemia; administer IV calcium immediately, and then administer insulin and glucose
E. Hyperkalemia; administer heparin and spironolactone

Back 2

D. Hyperkalemia; administer IV calcium immediately, and then administer insulin and glucose

However, ACE-Is (ACE inhibitors) work to inhibit angiotensin converting enzyme. When that enzyme is inhibited, the metabolism of angiotensin I to angiotensin II is inhibited. The result is decreased levels of angiotensin II. Among other things, angiotensin II NORMALLY promotes adrenal cortical production of aldosterone. The aldosterone then works on the late distal convoluted tubule (late DCT) and the collecting duct in promoting the exchange of potassium for sodium; for every sodium absorbed from the renal tubule, back into the body, a potassium is released to the renal tubule. Hence, when the production of angiotensin II is inhibited, resulting in a decrease in aldosterone, more potassium is retained in the body. Thus, a possible side effect to ACE-I therapy is hyperkalemia. Hyperkalemia can cause muscle weakness and palpitations. In most cases, it does not cause just arrhythmias that feel like palpitations, such as tachycardia or PVCs (although it is possible, like in this case). The most common cardiac outcome to severe hyperkalemia is ventricular fibrillation or asystole, both being life-threatening events that always cause syncope. Muscle weakness is also an outcome to hyperkalemia, and is one of the most common complaints even in mild hyperkalemia. Because of the possibility of sudden death due to cardiac causes in any case of hyperkalemia, it must be addressed aggressively. In fact, if it is severe enough to cause EKG changes (peaked T waves initially), treatment is started emergently. As this patient is already experiencing arrhythmias, we know that cardiac effects are already underway. So, she is immediately managed by providing IV calcium. The calcium is not used to reduce the serum potassium levels. Instead, it is used to stabilize the cardiac cell membranes, thus reducing the chance for life-threatening arrhythmia while the hyperkalemia is in existence. After the heart has been stabilized, then the high potassium levels are managed. This is done by administrating insulin. Insulin drives potassium into cells, thus reducing serum potassium levels, and resolving the hyperkalemia. Likewise, glucose must be given concomitantly so as to eliminate the possibility of insulin-induced hypoglycemia.

Front 3

A patient presents with acute onset extreme pyrexia, chills, and a new onset cardiac murmur. What is the most likely site affected, as seen on echocardiogram?

A. Tricuspid valve
B. Mitral valve
C. Aortic valve
D. Damaged mitral valve
E. Posterior urethral valve

Back 3

A. Tricuspid valve, Acute infective endocarditis features acute onset high fever (pyrexia), chills, and, like most any endocarditis, a new onset cardiac murmur. Acute infective endocarditis most often affects the right heart. The reason for that is that it is generally due to blood contamination with high numbers of particularly virulent bacteria. They attach to the endocardium (including valves) at the first chance presented; the first chance is at the area where blood enters the heart: the right heart. Either the tricuspid or pulmonic valves are the most affected valves in acute infective endocarditis, with the former being the more common one being affected. The mitral valve and the aortic valve are in the left heart. They are the most common valves to have pathologies in the human body (e.g., mitral valve regurgitation, mitral valve stenosis, aortic regurgitation, aortic stenosis). Thus, the valves to most often have pre-existing pathology are those in the left heart. That is why subacute infective endocarditis is most likely to occur in the left heart, since it only occurs on valves that have been previously damaged. Thus, the mitral valve and the aortic valve, due to their high rate of pre-existing pathology, are the valves most likely to be affected by subacute infective endocarditis

Front 4

A 34-year old construction worker complained of sudden, tearing chest pain that radiated to his back. He was unconscious by the time medics arrived. At presentation to the hospital, he is found to have a BP of 70/40. Physical exam reveals jugular venous distention and distant heart sounds. What accounts for the findings on physical exam?

A. Cardiac tamponade
B. Aortic dissection
C. Myocardial infarction
D. Pericarditis
E. Nutcracker esophagus

Back 4

A. Cardiac tamponade, Sudden, tearing chest pain radiating to the back is a classic finding for aortic dissection. As the aorta dissects, it can occlude branching vessels. The result can be lack of perfusion to many tissues, including the brain. The latter results in loss of consciousness and, often times, cerebral vascular accident (CVA). However, the dissection can also move proximally, tearing into the pericardium and causing blood to enter the pericardial sac. If it does so, hemopericardium occurs. Hemopericardium can, with increasing amounts of blood entry, cause tamponade (outside compression of heart causing chambers to collapse). While this can cause tamponade, realize that a more common cause of tamponade is idiopathic pericarditis wherein ever-increasing amounts of non-sanguinous fluid enter the pericardial sac, gradually, as a result to inflammation. However, in this case, the tamponade is due to blood. As the chambers collapse, cardiac output falls, causing hypotension. Likewise, as the chambers collapse, venous blood cannot enter the right heart, causing jugular venous distention (JVD). Lastly, tamponade causes the heart to sounds to be distant or muffled; it is because the heart is encased in a fluid-filled sac that serves to dampen the sounds of the heart. Thus, it is cardiac tamponade that is responsible for the physical exam findings. Aortic dissection is responsible for the tamponade.

Front 5

A 63-year old African American female presents to the emergency department with shortness of breath. She admits to increasing fatigue for the past 6 months. Which heart sound is the most common manifestation of her condition?

A. S1
B. A2
C. S3
D. S4
E. S2

Back 5

C. S3, This patient is demonstrating features of congestive heart failure: fatigue (due to poor cardiac output and, thus, poor perfusion to tissues) and dyspnea (due to pulmonary edema, secondary to backup of blood in the pulmonary vessels from a failed left ventricle). Due to the back-up, we can think of it as a situation, promoted by the failed ventricle, in which there is abundant blood and pressure just “waiting” to get into the ventricular chamber. The result is that, when the valve allowing entry of blood into that ventricular chamber is opened, the blood fills the ventricle rapidly and vigorously and hits walls of the failed heart. It is that vigorous and rapid filling of the somewhat non-compliant ventricle chamber that produces the third heart sound, otherwise known as S3. It is appreciated in early diastole (just as the mitral valve is opening), and manifests as a low-pitched, dull sound heard best with the bell of the diaphragm held against the apex of the heart. Another term for it is ventricular gallop and, when heard, IS congestive heart failure until proven otherwise.

Front 6

A 53-year-old American Indian female is diagnosed with unstable angina. What did her laboratory results demonstrate?

A. Elevated CK-total, CK-MB, and AST with no elevation in troponin or CK-MM
B. Elevated CK-total and CK-MB with no elevation in troponin
C. Elevated CK-total and LDH, with no elevation in CK-MB and troponin
D. Elevated CK-total, CK-MB, and troponin
E. Elevated troponin and BNP, with dramatic elevations in cardiac enzymes

Back 6

A. Elevated CK-total, CK-MB, and AST with no elevation in troponin or CK-MM


Unstable angina is a type of coronary artery disease (CAD; coronary heart disease; CHD; coronary heart disease). Since it shares the same pathology as that for myocardial infarctions, it is grouped along with MIs into a class of CADs known as acute coronary syndromes. All acute coronary syndromes (ACS) start with the deposition of cholesterol on the walls of coronary arteries. This is encouraged by elevated levels of LDL or low levels of HDL. The deposited cholesterol is immunologically stimulating to the vessel walls, causing the attraction and accumulation of macrophages to the area. The macrophages phagocytose the cholesterol, but, being unable to metabolize or digest it, the cholesterol accumulates as thousands of tiny lipid droplets in the macrophage cytoplasm. The result is macrophages in that area that look like they are full of foam – hence, the term foam cells is applied to those macrophages. Because they are macrophages and are immunologically stimulated, they release inflammatory mediators like IL-1 and TNF. The result is an inflammatory lesion, filled with thousands of macrophages. That lesion is known as an atheroma or an atherosclerotic lesion. It develops a calcium cap, and becomes and atherosclerotic plaque, all on the inner lining of the blood vessels well. Additionally, the immune mediators released by the macrophages work to slowly damage the muscle layer of the vessel wall, too. In any case, the atherosclerotic plaque sticks out into the lumen of the vessel, partially occluding it. That decreases perfusion downstream. When in the coronary arteries, this can result in stable angina. Stable angina features chest pain when the heart works harder, such as during exercise or sex. When the heart works harder, it requires more oxygen, which requires more blood perfusion. However, because of the atherosclerotic plaque, the perfusion is inadequate to meet the increased oxygen demands. Hence, pain is generated. Since there is no significant injury done to the heart tissue during such an event, no measurable serum levels of CK-total or CK-MB (CK = creatine kinase = CPK = creatine phosphokinase). Because there is no death of tissue, there is no elevation of troponin. However, if the plaque becomes disrupted, platelets quickly adhere to the site, providing FULL occlusion of the vessel. This can occur at any time, so can occur as much at rest as it can during activity. The full occlusion means that there is no perfusion of tissues downstream to the lesion. Initially, that results in unstable angina, which presents with chest pain that occurs at any time. As there is NO perfusion to the affected tissues, there is injury to the heart tissue. The result is the release of CK-MB from the injured cardiac tissue, resulting in increased serum CK-MB (cardiac-specific CK) as well as increased CK-total (which is a measure of CK-MB, CK-MM, and CK-BB). However, since there is no death of tissue, troponin does not become elevated.

Front 7

A 6-year old boy presents with fever, erythema of the palms and soles, and erythematous conjunctivae. On physical exam, you also appreciate lymphadenopathy. What will you administer first?

A. Aspirin and IV immunoglobulins
B. Acetaminophen and IV immunoglobulins
C. Corticosteroids, PO and IV
D. Salicylic acid, PO
E. Vitamin A

Back 7

A. Aspirin and IV immunoglobulins. This patient has Kawasaki’s disease: child, fever, red palms and soles, red conjunctivae, +/- cervical lymphadenopathy. It is imperative to start treatment immediately; the longer that treatment is delayed, the higher the risk for the eventual development of coronary artery aneurysm (which can result in sudden death when it ruptures). First-line treatment (e.g., the first treatment given) is IV immunoglobulins and aspirin.

Front 8

A 24-year old male is diagnosed with narcotic endocarditis. What is the most likely causative agent?

A. Streptococcus bovis
B. Staphylococcus aureus
C. Gram-negative bacilli
D. Escherichia coli
E. Streptococcus viridans

Back 8

B. Staphylococcus aureus.

Front 9

A 71-year old female presents with complaints of recurrent chest pain, shortness of breath, and syncopal events. What maneuver will increase the sound you expect to appreciate on cardiac auscultation?

A. Suddenly standing up, and auscultation at the very moment he rises
B. Valsalva during maximal strain
C. Sudden squatting
D. Passive leg raising
E. Expiration

Back 9

D. Passive leg raising. This patient has the classic triad for advanced aortic stenosis: dyspnea, angina, and syncope. The most common cause for aortic stenosis is age-related calcification of the valve leaflets wherein the disorder is termed senile aortic stenosis. In fact, more than one-third of all persons in the US who are greater than 65 years of age have this stenosis (although not all of them are symptomatic yet). Passive leg raising increases the sound of aortic stenosis. With this maneuver, the patient lies supine and the physician passively raises the straight leg. This causes passive return of blood to the heart (by draining the veins of the legs). That causes a high pre-load, yielding heart filling. The resulting high volume of blood in the heart increases the murmur sound since such a high volume eventually is thrust against the stenotic aortic valve as the heart attempts to pump it out.

Front 10

Valsalva during maximal strain augments the sounds ...2

Back 10

of hypertrophic obstructive cardiomyopathy (HOCM) and mitral valve prolapse (MVP).

Front 11

Sudden squatting increases the sounds of...2

Back 11

aortic regurgitation and mitral regurgitation

Front 12

. Expiration increases the sounds of....3

Back 12

1. hypertrophic obstructive cardiomyopathy (HOCM)
2. mitral valve prolapse (MVP)
3. aortic regurgitation