CV cases Step 1 QandA Flashcards
A physician decides to place a patient on a calcium channel blocker for treatment of her angina. Calcium channel blockers can relax the smooth muscle of blood vessels and can also have various effects on cardiac contractility, conduction, and heart rate. Which calcium channel blocker would be most effective in reducing heart rate and contractility?
Verapamil
The calcium channel blockers verapamil and diltiazem are both effective in slowing the rate and contractility of
the heart. Both drugs decrease the magnitude of inward calcium current through L type calcium channels and also decrease the rate of recovery of the channel. It is this latter effect that depresses the sinus node pace-maker and slows atrioventricular conduction. Verapamil is a stronger negative inotrope than diltiazem, and therefore is more effective in decreasing heart rate and contractility.
A 28-year-old African-American man presents to the physician with fever, weight loss, and abdominal pain. His blood pressure is 168/92mm Hg, his pulse is 83/min, and his respiratory rate is 18/min. On physical examination,
there is palpable purpura on his lower extremities; a fundoscopic examination reveals fluffy, white spots on his retina. His past medical history is significant for a previous hepatitis B infection. What is the most prominent morphologic feature of the affected arteries in this patient’s disease process?
This individual is likely suffering from polyarteritis nodosa
(PAN), which is characterized by necrotizing immune complex inflammation of small or medium-sized arteries. PAN is typically associated with fever, malaise, weight loss, abdominal pain, headache, myalgias, and hyper-tension. There are no diagnostic serologic tests
specific for PAN. Patients with classic PAN are ANCA-negative and may have low titers of rheumatoid factor or antinuclear antibodies, both of which are nonspecific findings. In patients with PAN, appropriate serologic tests for active hepatitis B infection must be performed
as up to 30% of patients with PAN are positive for hepatitis B surface antigen. Histologically, the intense inflammatory infiltrate in the arterial wall and surrounding connective tissue is associated with fibrinoid necrosis and disruption of the vessel wall.
A 50-year-old man with diabetes receives the results of a fasting lipid profile that reveals hypercholesterolemia.
To reduce the patient’s mortality risk, his physician recommends lifestyle changes and initiates therapy with a statin. What mechanism describes the action of statins in reducing serum levels of LDL cholesterol?
3-Hydroxy-3-methylglutaryl coenzyme A reductase (HMG-CoA reductase) catalyzes the rate-limiting step in the synthesis of cholesterol. The enzyme converts
3-hydroxy-3-methylglutaryl coenzyme A (HMGCoA) to mevalonic acid, a cholesterol precursor. Statins competitively inhibit HMGR by obstructing part of the enzyme’s active site and preventing sufficient interaction with HMGCoA to produce mevalonate. The consequent
decrease in intrahepatic cholesterol causes upregulation
of hepatic LDL cholesterol receptors, ultimately lowering plasma LDL cholesterol levels. Diabetes mellitus is considered a cardiac heart disease equivalent, and by the ATP III recommendations, the target LDL cholesterol of a diabetic patient is 130 mg/dL.
A 45-year-old man who takes spironolactone and digoxin for his congestive heart failure is admitted to the hospital because he is experiencing an altered mental status. Urinalysis would most likely reveal what?
The key to answering this question is realizing that it asks for electrolyte levels in urine, not serum. The ECG
shows peak T waves and widened QRS interval, which are classic changes seen in hyperkalemia. Spirono-lactone is the most likely medication to affect urinary electrolytes. As an inhibitor of aldosterone receptors in the collecting tubule and an inhibitor of Na+ channels, spironolactone greatly decreases the excretion of K+ and mildly increases the excretion of Na+. Urine volume
will be high-normal because the diuretic will increase
saltwater wasting.
A medical student working in the emergency department sees a female baby, born 2 weeks ago, who is brought in by her anxious mother.The mother tells the student that her baby seems “purple,” especially her fingers and toes, and looks extremely blue when crying. On physical examination the sleeping baby has mild cyanosis of the face and trunk, but moderate cyanosis of the extremities. What is the most common cause of cyanosis within the first few weeks of life?
Tetralogy of Fallot.
It’s is the most common cause of cyanosis within the first few weeks of life. The skin becomes bluish because of the malformed right-to-left shunt. Infants also have worsening cyanosis with agitation, difficulty feeding, and failure to gain weight. Patients may also have clubbing of the fingers and toes or even polycythemia. The four components of the teratology are (1) ventricular septal defect, (2) overriding aorta, (3) infundibular pulmonary stenosis, and (4) right
ventricular hypertrophy.
A 48-year-old man presents to the emergency department 1.5 hours after the onset of severe substernal chest pain radiating to his left arm. The pain is accompanied by diaphoresis and shortness of breath. His blood pressure is 165/94 mm Hg, pulse is 82/min, and respiratory rate is 18/min. Which test is the most important tool in the initial evaluation of patients in whom acute myocardial infarction (MI) is suspected?
ECG.
ECG is the gold standard for diagnosing MI within the first 6 hours of symptom onset. ECG changes will include ST-segment elevation (signifying transmural infarct), ST-segment depression (signifying subendocardial infarct), and Q waves (signifying transmural infarct).
A 56-year-old woman arrives in the emergency department complaining of dizziness and headache. Her blood pressure is 210/140 mmHg. She is currently not taking any medications and has not seen a doctor for several years. The physician decides to address her hypertension urgently. Which drug is contraindicated in this patient?
Nifedipine.
Nifedipine is a dihydropyridine class calcium channel blocker that could be used in the long-term control of hypertension. However, in the case of a hypertensive emergency, nifedipine used sublingually can cause dangerous fluctuations in blood pressure that are difficult to control and can lead to more harm than good.
A 55-year-old man with hypertension is prescribed an antiarrhythmic agent that alters the flow of cations in myocardial tissue. What would be affected by an agent that affects phase 2 of the myocardial action potential?
Voltage-gated Ca2+ channels open slowly in response to the Na+ upstroke as increasing K+ conductance during phase 2 gradually depolarizes the cell. The result is a slow conduction velocity that prolongs the transmission from the atria to the ventricles.
A 56-year-old woman arrives in the emergency department complaining of dizziness and headache. Her blood pressure is 210/140 mmHg. She is currently not taking any medications and has not seen a doctor for several years. The physician decides to address her hypertension urgently. Which drug is contraindicated in this patient?
Nifedipine is a dihydropyridine class calcium channel blocker that could be used in the long-term control of hypertension. However, in the case of a hypertensive emergency, nifedipine used sublingually can cause dangerous fluctuations in blood pressure that are difficult to control and can lead to more harm than good.
A 65-year-old man presents to the emergency department with chest pain that he noticed after climbing a set of stairs. The emergency physician sends him for an exercise stress test. What physiologic mechanism does the heart use to deal with increased work demand during an exercise stress test?
An increase in myocardial contractility due to exercise leads to increased oxygen demand by the cardiac muscle and increased oxygen consumption, causing local hypoxia. This local hypoxia causes vasodilation of the coronary arterioles, which then produces a compensatory increase in coronary blood flow and oxygen delivery to meet the demands of the cardiac muscle. Oxygen extraction from heart muscle is maximized. Increased demand can be met only by increasing blood flow.
A 16-year-old Japanese exchange student presents to the physician with a history of fevers, joint pain, night sweats, and muscle pain. On physical examination, the patient has extremely weak pulses in her upper extremities. Which laboratory abnormalities are most likely?
Erythrocyte sedimentation rate.
This individual is most likely suffering from Takayasu’s arteritis, which is also known as “pulseless disease.” It typically affects medium and large arteries, resulting in thickening of the aortic arch and/or proximal great vessels. Symptoms include
fevers, arthritis, night sweats, myalgias, skin nodules, ocular disturbances, and weak pulses in the upper extremities. It is most common in young Asian females and is associated with an elevated erythrocyte sedimentation rate.
A 72-year-old African-American man undergoes hip surgery. On his third hospital day he experiences chest pain, tachycardia, dyspnea, and a low-grade fever. The man goes into cardiac arrest, and efforts to resuscitate him are unsuccessful. On autopsy a massive pulmonary embolus is discovered. What would most likely predispose the patient to this event?
Mutation in the Factor V gene.
A mutation in the Factor V gene, also known as Factor V Leiden, causes resistance to deactivation of Factor V by protein C. Uninhibited Factor V activity leads to a hypercoagulable state, which can lead to deep vein thrombosis and subsequent pulmonary embolism.
A 70-year-old woman with a history of type 2 diabetes mellitus, a body mass index of 30 kg/m2, and an MI 10 years prior presents to the emergency department with crushing substernal chest pain radiating to her neck and jaw. Emergency cardiac catheterization with percutaneous coronary intervention (PCI) shows a 99% occlusion of her left anterior descending artery, and an ECG reveals an anterior wall ST segment elevation MI. The patient remains stable after PCI, and echocardiography shows a mildly impaired ejection fraction (EF) of 45%. Three days later, the patient becomes acutely hypotensive and dyspneic, and physical examination reveals a high-pitched holosystolic
murmur, loudest at the apex and radiating to the axilla, that had not been heard on previous exams. An emergency echocardiogram shows an EF of 25%. This patient has developed?
Ruptured papillary muscle.
This patient has suffered rupture of one of the two left ventricular papillary muscles, a complication that may occur 3–10 days after an acute MI, when the infarcted
area of myocardium is replaced with granulation tissue and thus is the most weak. Without the anchor of the papillary muscle, there is severe acute mitral valve regurgitation, diagnosed by a new holosystolic “blowing murmur” that is loudest at the apex and radiates to the axilla, a severely reduced stroke volume (hypotension with EF of 25%), and evidence of pulmonary edema (dyspnea).
A 67-year-old woman presents to the ED with dizziness, syncope, and palpitations. She states she is taking a medication for “heart troubles” but cannot remember its name. Results of an ECG are shown in the image (Torsades de Pointes). Which of this patient’s current medications might have caused this abnormal ECG
pattern?
Quinidine.
The ECG shows torsades des pointes. Quinidine is a class IA antiarrhythmic agent used in the treatment of supraventricular arrhythmias. Quinidine slows conduction and can increase the QT interval, leading to torsades de pointes.
A 35-year-old man with no significant medical history presents to his primary care physician with a 2-week history of progressive shortness of breath that occurs with activity. He previously exercised regularly and has never had symptoms like this before, but now he finds that he can walk only one block before becoming symptomatic. He has also noticed a 7-lb (3.2-kg) weight gain during this time. He does not smoke or use alcohol or illicit drugs and has not traveled recently. In addition, he has no family history of cardiac disease and does not have any sick contacts, but recalls having an upper respiratory infection about a month ago that improved on its own. Physical examination reveals crackles in his lungs bilaterally and an S3 gallop. X-ray of the chest reveals cardiomegaly. What is the most likely mechanism
causing this patient’s heart failure?
Direct cytotoxicity via receptor-mediated entry of virus into cardiac myocytes.
This patient is most likely experiencing congestive heart failure (CHF) secondary to dilated cardiomyopathy (DCM), which is characterized by dilation and impaired contraction of one or both ventricles. Symptoms of CHF include dyspnea (especially on exertion), orthopnea, paroxysmal nocturnal dyspnea, and peripheral edema with weight gain. DCM may also present with arrhythmias
such as atrial fibrillation, or sudden cardiac death. DCM has a variety of etiologies including idiopathic, myocarditis, ischemic, drug induced, hypertension, infiltrative disease, HIV infection, connective tissue disease, and the chemotherapeutic agent doxorubicin. In this case the most likely cause of the patient’s DCM is viral myocarditis following his upper respiratory infection several weeks ago. Viruses known to cause myocarditis include coxsackievirus, influenza virus, adenovirus, echovirus, cytomegalovirus, and HIV. These viruses cause myocarditis with subsequent DCM by inflicting direct cytotoxicity via receptor-mediated entry of the virus into cardiac myocytes. Patients with myocarditis may present initially with symptoms of chest pain or arrhythmias with ECG changes; in others, symptoms of
heart failure may be the initial manifestation, as in this patient.
