CARDIOVASCULAR QUIZ SET 1 Flashcards
A 30-year-old woman comes to the emergency department because of a 1-day history of sharp chest pain radiating to the left shoulder. The pain worsens when she coughs, breathes deeply, or lies down. She has had a mild fever and a cough for the past 2 days. She takes ibuprofen for hip and knee pain, which started 4 months ago. Examination shows a symmetric, erythematous rash on her nose and cheeks, and erythematous patches with scaling and plugged follicles over her hands. Cardiovascular evaluation of this patient is most likely to show which of the following findings?
Increased distension of jugular veins during inspiration
18 mm Hg decrease in systolic blood pressure during inspiration
High-pitched pericardial sound occurring slightly earlier than a third heart sound
Triphasic scratchy heart sound of varying intensity
Jugular venous pulsation visible 9 cm above the sternal angle
Holosystolic blowing murmur heard best at the apex
Joint pain, malar rash, and a discoid rash (erythematous patches with scaling and follicular plugging) should immediately raise suspicion of systemic lupus erythematodes (SLE). The acute onset of low-grade fever and pleuritic chest pain that is aggravated by lying down (and thus improved by sitting up) is suggestive of acute pericarditis, the most common cardiovascular manifestation of SLE.
Answer is Triphasic scratchy heart sound of varying intensity
A triphasic scratchy or squeaky heart sound on auscultation suggests a pericardial friction rub, which is highly specific for pericarditis. Acute pericarditis typically manifests with fever and pleuritic chest pain that is usually sharp in nature, improves on sitting and leaning forward, and often radiates to the shoulder. It is the most common cardiac manifestation of SLE, occurring in ∼ 25% of patients.
Increased distension of jugular veins during inspiration11%The Kussmaul sign is classically seen in right ventricular infarction, restrictive cardiomyopathy, constrictive pericarditis, and tricuspid stenosis. Constrictive pericarditis may occur with SLE but would be characterized by signs of decreased cardiac output such as fatigue and tachycardia. It would also take months to years to develop. The patient’s acute presentation with pleuritic chest pain, cough, and fever is more consistent with acute pericarditis, in which case the Kussmaul sign would not be expected.
B
18 mm Hg decrease in systolic blood pressure during inspiration
9%
A decrease of 18 mm Hg in systolic blood pressure during inspiration suggests pulsus paradoxus, which may be seen in cardiac tamponade, constrictive pericarditis, and in noncardiac diseases such as asthma, COPD, and tension pneumothorax. Although SLE-associated pericarditis can be associated with a pericardial effusion, it rarely progresses to tamponade. Furthermore, other findings of cardiac tamponade, including dyspnea, hypotension, tachycardia, and jugular venous distention, would be expected. Constrictive pericarditis is also rarely associated with SLE and would cause signs of decreased cardiac output (fatigue) and fluid overload (jugular venous distention, Kussmaul sign).
C
High-pitched pericardial sound occurring slightly earlier than a third heart sound
19%
Pericardial knock is a high-pitched, early-diastolic sound in patients with constrictive pericarditis. Constrictive pericarditis may occur with SLE but would be characterized by signs of decreased cardiac output such as fatigue and tachycardia. It would also take months to years to develop. The patient’s acute presentation with pleuritic chest pain, cough, and fever is more consistent with acute pericarditis, in which case the Kussmaul sign would not be expected.
D
Triphasic scratchy heart sound of varying intensity
43%
A triphasic scratchy or squeaky heart sound on auscultation suggests a pericardial friction rub, which is highly specific for pericarditis. Acute pericarditis typically manifests with fever and pleuritic chest pain that is usually sharp in nature, improves on sitting and leaning forward, and often radiates to the shoulder. It is the most common cardiac manifestation of SLE, occurring in ∼ 25% of patients.
E
Jugular venous pulsation visible 9 cm above the sternal angle
4%
Elevated jugular venous pulsation can be seen in cardiac tamponade or constrictive pericarditis, both of which are uncommon in SLE. Furthermore, other findings of cardiac tamponade, including dyspnea, hypotension, tachycardia, and jugular venous distention, would be expected. Constrictive pericarditis would cause signs of decreased cardiac output (fatigue) and fluid overload (jugular venous distention, Kussmaul sign).
F
Holosystolic blowing murmur heard best at the apex
14%
Holosystolic blowing murmur best heard at the apex suggests mitral regurgitation. Libman-Sacks endocarditis, which is caused by noninfectious verrucous vegetations and is seen in SLE, favors the mitral valve and can result in mitral regurgitation. Most patients, however, are asymptomatic. This patient’s fever, cough, and pleuritic chest pain are more consistent with acute pericarditis, which is also the most common cardiac manifestation of SLE.
A 59-year-old man is brought to the emergency department one hour after developing shortness of breath and “squeezing” chest pain that began while he was mowing the lawn. He has asthma, hypertension, and erectile dysfunction. Current medications include salmeterol, amlodipine, lisinopril, and vardenafil. His pulse is 110/min and blood pressure is 122/70 mm Hg. Physical examination shows diaphoresis. An ECG shows sinus tachycardia. Sublingual nitroglycerin is administered. Five minutes later, his pulse is 137/min and his blood pressure is 78/40 mm Hg. Which of the following is the most likely mechanism of this patient’s hypotension?
Bradykinin accumulation
Calcium channel antagonism
Alpha-1 receptor antagonism
Cyclic GMP elevation
Decreased nitric oxide production
Histamine release
Beta-2 receptor agonism
The correct answer is Cyclic GMP elevation
Vardenafil is a PDE-5 inhibitor and should not be used in combination with nitrates.
Nitrates (e.g., sublingual nitroglycerin) and PDE-5 inhibitors (e.g., vardenafil) both work by increasing the intracellular concentration of cGMP. Nitrates increase intracellular NO, which is responsible for activating guanylate cyclase, leading to increased synthesis of cGMP. PDE-5 inhibitors, as their name implies, inhibit phosphodiesterase (PDE), which leads to a decreased breakdown of cGMP. Accumulation of cGMP leads to activation of myosin-light-chain phosphatase (MLCP), which dephosphorylates the light chains of myosin. This results in smooth muscle cell relaxation in blood vessels with subsequent vasodilation. Life-threatening hypotension can occur if these two drugs are taken in combination.
Bradykinin accumulation3%
ACE inhibitors (e.g., lisinopril) can lead to the accumulation of bradykinin, which can cause hypotension (due to vascular dilation). However, an acute, life-threatening drop in blood pressure is unlikely. Furthermore, if an accumulation of bradykinin had occurred in this patient, symptoms such as bronchoconstriction, angioedema, and dry cough would also be expected.
Calcium channel antagonism3%
Calcium channel antagonists (e.g., amlodipine) can cause vascular smooth muscle relaxation, which may lead to a drop in blood pressure. However, this class of drugs rarely causes acute, severe hypotension, even when taken in conjunction with nitroglycerin.
Alpha-1 receptor antagonism5%
Alpha-1 antagonists (e.g., prazosin) cause peripheral vasodilation by inhibiting the alpha-1 receptor in smooth muscle cells. This can also cause hypotension, which is why this class of drugs is contraindicated in patients who take nitrates. However, this patient is not currently taking any alpha-1 antagonists.
Decreased nitric oxide production5%
Nitroglycerin, a nitric oxide (NO) donor, causes vasodilation, which leads to smooth muscle relaxation via a process that starts with the activation of guanylyl cyclase. So NO production would be increased rather than decreased in this patient.
Histamine release2%
A release of histamine, which acts as a peripheral vasodilator, is the mechanism underlying hypotension in anaphylactic shock. Anaphylactic shock could account for this patient’s hypotension and tachycardia, but he lacks other typical features of anaphylactic reactions, such as urticaria, angioedema, wheezing, nausea, and vomiting. Furthermore, allergic reactions to nitroglycerin are rare.
Beta-2 receptor agonism3%
Beta-2 receptor agonists (e.g., salmeterol) cause relaxation of the smooth muscle in bronchial tubes and blood vessels. They are primarily used as bronchodilators in the management of asthma and other obstructive pulmonary diseases (e.g., COPD). Although smooth muscle cell relaxation leads to vasodilation, severe hypotension is rare, even when beta-2 receptor agonists are taken in combination with nitrates.
A 65-year-old man comes to the physician for a routine examination. He feels well. His pulse is 80/min and blood pressure is 140/85 mm Hg. Cardiac examination shows a holosystolic murmur in the 4th intercostal space along the left sternal border that gets louder during inspiration. The increase of this patient’s murmur is best explained by which of the following hemodynamic changes?
Increased peripheral vascular resistance
Increased right ventricular stroke volume
Decreased pulmonary vessel capacity
Decreased left ventricular venous return
Increased systemic venous compliance
The correct answer is Increased right ventricular stroke volume
A holosystolic murmur that becomes louder on inspiration hints at a right-sided murmur. The auscultation site suggests tricuspid valve regurgitation.
A holosystolic murmur in the 4th intercostal space along the left sternal border that gets louder during inspiration is classic for tricuspid regurgitation. Tricuspid regurgitation, unlike other holosystolic murmurs (e.g., mitral regurgitation or ventricular septal defects), increases during inspiration. Inspiration causes a period of negative intrathoracic pressure, allowing for increased venous return to the heart, ultimately producing increased right ventricular stroke volume. This excess blood volume must be entirely ejected through the tricuspid valve, producing the increased intensity of the murmur. The left ventricle stroke volume is affected in the opposite manner with inspiration decreasing venous return from the pulmonary veins, leading to a reduction in left ventricular stroke volume. Consequently, the left-sided holosystolic murmurs of mitral regurgitation and ventricular septal defects do not augment with inspiration.
Increased peripheral vascular resistance
9%
Increased peripheral vascular resistance (afterload) does not occur during inspiration. Asking a patient to squat can effectively increase afterload, though. Increased afterload leads to enhanced murmur intensity in mitral regurgitation, aortic regurgitation, and ventricular septal defect. In all these instances, increased afterload augments the pathological, retrograde blood flow across the mitral valve, aortic valve, or ventricular septal defect, respectively. Increased blood flow is appreciated as a more intense murmur.
Decreased pulmonary vessel capacity
9%
During inspiration, the intrathoracic pressure is negative. This reduces the barometric compressive force on the outer surface of the pulmonary vessels, permitting an increase in the vessel capacitance. This increase in vessel capacity is part of the explanation for the augmented murmur intensity during inspiration.
Decreased left ventricular venous return
12%
Decreased left ventricular venous return occurs during inspiration but does not impact right-sided heart murmurs such as tricuspid regurgitation. Left-sided murmur intensity, such as in mitral regurgitation, is typically unaffected or minimally reduced by this phenomenon.
Increased systemic venous compliance
6%
Increased systemic venous compliance, such as immediately following a change from supine to standing, leads to decreased preload as a result of blood pooling in the peripheral venous circulation. The majority of cardiac murmurs become softer in this scenario as a result of diminished blood flow across valves. The one notable exception is the murmur of hypertrophic cardiomyopathy, which increases. Altered systemic venous compliance does not have a role in explaining this patient’s examination findings.
