cardiology2016

cardiology2016 241-250,Q 1,A 65-year-old immigrant from Eastern Europe comes to the physician because of a four-week history of low-grade fever multiple joint pains, and a well-demarcated erythematous rash on his face and trunk. The patient denies hair loss, mucosal ulceration, or photosensitivity. His serum test is positive for the presence of antinuclear antibody (ANA) in very high titers. The patient reports a past medical history of coronary artery disease, congestive heart failure, and cardiac rhythm abnormalities.This patient should be specifically questioned about the intake of which of the following medications?A. Amiodarone B. Propranolol C. Lidocaine D. Procainamide E. Verapamil O F. Adenosine,A 1,Correct answer:DFeatures of drug-induced lupus erythematosus New onset lupus symptomsAnti-nuclear antibodies (ANA) and antihistone antibodies present in 95% of casesAnti-dsDNA antibodies are rarely seenExposure to implicated drugsHydralazine Procainamide IsoniazidMinocycline QuinidineDrug-induced lupus erythematosus (DILE) should be considered in patients presenting with signs and symptoms of systemic lupus erythematosus (SLE). Both hydralazine and procainamide are categorized as high-risk drugs for the development of DILE. Procainamide is metabolized via hepatic acetylation. Individuals who are “slow acetylators” are at greatest risk for DILE. while individuals who metabolize the drug more rapidly are less likely to experience this adverse effect. Drug-induced lupus erythematosus occurs in up to 20% of patients taking procainamide.The presence of autoantibodies can be used to help differentiate DILE from SLE. Although anti-histone antibodies are very common in DILE, they are seen in only 50% of SLE patients. Likewise. anti-dsDNA antibodies are present in 80% of SLE patients, but are rarely seen in DILE. Anti-nuclear antibodies are frequently positive in both diseases.(Choice A) The most notable side effects of amiodarone include thyroid dysfunction, lung fibrosis, and liver toxicity, as well as a blue or grey discoloration of the skin.(Choice B) The most frequently encountered adverse effects of nonselective beta-blockers are negative inotropy and bronchoconstriction in patients with asthma or COPD.(Choice C) The adverse effects of lidocaine are characteristically nonfocal neurologic signs such as tremor, drowsiness, and change in mental status, although lidocaine can also lead to generalized seizures.(Choice E) Verapamil is a calcium channel blocker and class 4 antiarrhythmic. The most frequently noted adverse reactions include negative inotropy, constipation, and gingival hyperplasia.(Choice F) Adenosine is used as a vasodilator in chemical cardiac stress tests and as a fast acting antiarrhythmic for stopping acute supraventricular tachycardias. Adenosine has an extremely short half-life, and its immediate adverse effects include chest burning, flushing, and transient hypotension.Educational objective:Procainamide and hydralazine have the highest risk of causing drug-induced lupus erythematosus (DILE), which is characterized by the development of lupus-like symptoms in addition to positive ANA and anti-histone antibodies. Unlike with SLE, anti-dsDNA antibodies are rarely seen.,Q 2,A 55-year-old man comes to the emergency department with recurrent episodes of retrosternal chest pain. The episodes occur during physical activity, usually when he climbs stairs or walks uphill. The patient has no known medical problems and does not use tobacco, alcohol, or illicit drugs. He is given a sublingual tablet and reports rapid relief of the pain. This daig most likely improved this patients symptoms by causing which of the following hemodynamic changes?A Decrease in arteriolar resistance B. Decrease in heart rate C Decrease in left ventricular volume D. Increase in coronary blood flow E. Increase in coronary perfusion pressure,A 2,Correct answer:CThis patient has a classic presentation of chronic stable angina, with rapid symptom relief with sublingual nitroglycerin. Nitrates exert their effect by direct vascular smooth muscle relaxation that results in:Vasodilation of the peripheral veins and arteries, predominantly venodilationDecreased myocardial oxygen demand due to decreased preload (decreased left ventricular end-diastolic volume and pressure)Modest reduction in afterloadMild coronary artery dilation and reduction of coronary vasospasmThis results in decreased left ventricular systolic wall stress and myocardial oxygen demand, leading to improved exercise tolerance and relief of angina symptoms.(Choice A) Nitrates have only a modest effect on arteriolar dilation and cause minimal or no change in systemic vascular resistance at low doses. Higher doses can cause a drop in systemic blood pressure, thereby reducing cardiac afterload and left ventricle wall stress, and leading to a further decrease in myocardial oxygen demand.(Choice B) Beta blockers and calcium channel blockers exert their antianginal effect in part via a decrease in heart rate (negative chronotropic effect). Nitrates do not have a direct effect on cardiac chronotropy and/or inotropy.(Choices D and E) The increase in coronary blood flow is limited with nitrates as they dilate the large epicardial arteries more than the smaller resistance vessels (eg, arterioles). Furthermore, coronary arterioles in an area of flow-limited stenosis are typically maximally dilated to maintain resting blood flow. Medications that cause dilation of arterioles within the normal myocardium (eg, dihydropyridine calcium channel blockers) can divert blood away from the ischemic area (coronary steal phenomenon).Educational objective:Sublingual nitroglycerin is used as a first-line agent for rapid symptom relief in patients with stable angina pectoris. The primary anti-ischemic effect of nitrates is mediated by systemic vasodilation with a decrease in left ventricular end-diastolic volume and wall stress, resulting in decreased myocardial oxygen demand and relief of angina symptoms.,Q 3,A new antiarrhythmic medication, Drug A, is tested in several animal experiments. The action potentials of ventricular muscle cells are recorded before and after administration of the drug.Black curve - before administration of Drug A Red curve - after administration of Drug 。The action of Drug A most closely resembles the effect of which of the following antiarrhythmic drugs?A. Disopyramide B. Lidocaine C. Propranolol D. Diltiazem E. Flecainide F. Adenosine G. Digoxin,A 3,Correct answer:AAdministration of this drug has slowed phase 0 depolarization and prolonged phase 3 repolarization of the ventricular myocyte. (Recall that cardiac pacemaker cells have different action potential curves where there is phase 4 depolarization and phases 1 and 2 do not exist). Disopyramide (Choice A) is a class IA antiarrhythmic and is the only drug listed that prolongs the action potential in cardiac muscle cells.(Choice B) Lidocaine is a class IB antiarrhythmic. a sodium channel blocking drug that is highly selective for rapidly depolarizing cardiac myocytes. It has little effect on phase 0 depolarization (due to rapid binding and rapid release), but it does shorten phase 3 repolarization (by blocking sodium window current) and the action potential duration. These effects are illustrated by the red curve seen below.(Choice C) Propranolol is a beta-adrenergic blocking agent that slows conduction through the AV node and prolongs phase 4 depolarization in cardiac pacemaker cells. Beta-blockers do not affect the ventricular myocyte action potential; their primary site of action is on the AV node and cells with automaticity.(Choice D) Diltiazem is a calcium channel blocker and therefore a class 4 antiarrhythmic drug. Calcium channel blockers act primarily on tissues in the AV node and on pacemaker cells (cells with automaticity) and are most selective for rapidly depolarizing cells (“use-dependent”). They do not have an appreciable effect on the ventricular myocyte action potential.(Choice E) Flecainide. a class 1C antiarrhythmic, blocks sodium channels and exhibits a slow rate of dissociation during diastole (thus being more effective at rates of deoolarizati(Choice F) Adenosine does not modulate the ventricular myocyte action potential. It primarily acts on the AV node where it slows conduction and decreases automaticlty by hyperpolarizing the cells.(Choice G) Digoxin exerts its antiarrhythmic effects by increasing vagal output to the AV node and conduction system, thereby slowing conduction in these tissues. It does not alter the ventricular myocyte action potential, but it does increase intracellular calcium in ventricular myocytes leading to increased cardiac contractility.Educational objective:The class IA antiarrhythmics (quinidine, procainamide, and disopyramide) are sodium channel blocking agents that slow phase 0 of the ventricular myocyte action potential and prolong re polarization as well as the refractory period of these cells.,Q 4,A 76-year-old woman is brought to the emergency department by her son due to lethargy and confusion over the past 2 days. The patient has persistent atrial fibrillation and congestive heart failure and is on multiple medications. Recently, she has had nausea and decreased appetite. Today, she had 3 episodes of vomiting. The patient also reports vision difficulties. Temperature is 36.7 C (98 F) and blood pressure is 133/80 mm Hg. Laboratory results are as follows:Sodium 140 mEq/LPotassium 5.7 mEq/LCalcium 9.3 mg/dLCreatinine 1.2 mg/dLGlucose 85 mg/dLECG shows junctional escape rhythm at a rate of 48/min with occasional ventricular premature beats. Increased blood level of which of the following medications is most likely responsible for her symptoms?A. Amiodarone B. Aspirin C. Digoxin D. Diltiazem E. Furosemide F. Metoprolol G. Spironolactone H. Valsartan,A 4,Correct answer:CThis patient with atrial fibrillation and congestive heart failure has signs and symptoms of digoxin toxicity. Although calcium channel blockers and beta blockers are the preferred treatments for patients with atrial fibrillation with rapid ventricular response, digoxin is a common second-line treatment that is particularly useful in patients with underlying systolic cardiac dysfunction. Its major effects are:1.Increased vagal tone, causing slowing of conduction through the atrioventricular (AV) node (rate-control effect)2.Na-K-ATPase inhibition, causing increased intracellular sodium and calcium (increases cardiac contractility)Digoxin has a narrow therapeutic index, making toxicity relatively common. Symptoms of digoxin intoxication are fairly nonspecific and include nausea, abdominal pain, fatigue, dizziness, confusion, blurred vision, and abnormal color perception. Digoxin toxicity can cause a wide range of cardiac arrhythmias, including bradycardia and junctional escape beats due to increased AV nodal block. Hypokalemia can precipitate toxicity by increasing digoxin binding to Na-K-ATPase. However, elevated potassium is a sign of digoxin toxicity as inhibition of Na-K-ATPase pumps increases extracellular potassium.(Choice A) Amiodarone can cause pulmonary toxicity, thyroid dysfunction, cardiac arrhythmias, elevated liver enzymes, and visual disturbances. However, it does not cause hyperkalemia.(Choice B) Acute aspirin overdose presents with vertigo, tinnitus, vomiting, and diarrhea, whereas severe intoxication can lead to coma, hyperpyrexia, pulmonary edema, and death.(Choices D and F) Beta blocker and/or calcium channel blocker overdose usually cause profound bradycardia and hypotension (absent in this patient). In addition, nausea and vomiting are more common in digoxin overdose than in beta blocker overdose, which typically causes bronchospasm and hypoglycemia.(Choice E) Furosemide overdose causes volume depletion, along with electrolyte abnormalities such as hypokalemia and hypomagnesemia.(Choice G) Excess spironolactone can cause hyperkalemia, gynecomastia, impotence, and decreased libido.(Choice H) Valsartan is an angiotensin II receptor blocker. Overdose usually causes hypotension, renal failure, and hyperkalemia.Educational objective:Digoxin toxicity typically presents with cardiac arrhythmias and nonspecific gastrointestinal (nausea, vomiting), neurological (confusion, weakness), and visual symptoms. Elevated potassium is another sign of digoxin toxicity and is caused by inhibition of Na-K-ATPase pumps.,Q 5,The cardiac output and venous return curves of a healthy person are shown below with solid lines.Right atrial pressureWhich of the following is the most likely cause of the change depicted by the dashed lines?A. Excessive hydration B. Acute hemorrhage C. Chronic anemia D. Myocardial infarction E. Anaphylaxis,A 5,Correct answer: DThe graph above combines cardiac and vascular function curves. The cardiac function curve, labeled as cardiac output, illustrates the Frank-Starling effect. The Frank-Starling effect states that as cardiac muscle is increasingly stretched, the cardiac output increases (up to a limit, as illustrated by the flat portion of the curve). This is essentially the same length-tension relationship that is seen in skeletal muscle.The venous return curve represents how venous return changes with variations in right atrial pressure. Where the venous return curve intersects with the x-axis, it indicates a venous return of zero. At this point, all circulatory flow ceases, and the pressure throughout the circulatory system equalizes. This average pressure is termed the mean systemic filling pressure, which is a measure of the degree of filling of the circulatory system relative to the circulatory capacity. Increases in blood volume (such as with excessive hydration, dashed line) shift the x-intercept to the right, while decreased blood volume (acute hemorrhage, dashed line) shifts it to the left (Choices A and B). Total peripheral resistance (TPR) affects the slope of both the venous return and cardiac output curves. Increases in the TPR decrease the slope of both curves, as higher vascular resistance restricts venous return and increases afterload.The dashed lines in the question image depict decreased cardiac output and an unchanged venous return (unchanged blood volume and TPR). An isolated decrease in cardiac output indicates decreased contractility that is not the result of decreased preload (because the venous return line is unchanged). This indicates inhibited contraction either from the action of a negative inotropic drug or an injury to the myocardium, such as a myocardial infarction.(Choice C) Chronic anemia causes an increase in cardiac output in an effort to meet the metabolic demands of the tissues. This causes an increase in the slope and height of the cardiac output graph. Venous return also increases somewhat due to decreased blood viscosity.(Choice E) Anaphylaxis causes widespread venous and arteriolar dilation along with increased capillary permeability and third-spacing of fluids. This results in a serious drop in venous return (shifted down and leftward). Cardiac contractility also increase as the body attempts to maintain blood pressure.Educational objective:Myocardial infarction causes a sharp decrease in cardiac output due to loss of function of a zone of myocardium. On a cardiac function curve, myocardial infarction would decrease both the slope and the maximal height of the line.,Q 6,Electrophysiologists conduct a study in which they record the membrane potential changes of atrial cells while exposing them to various agents. A tracing from one of the experiments is shown below.Which of the following substances was most likely applied to the cells at the point indicated by the arrow?A. Adenosine B. Aldosterone C. Angiotensin II D. Glucagon E. Glycine F. Norepinephrine,A 6,Correct answer: AThe membrane potential changes shown above are typical of cardiac pacemaker cells, which are primarily located in the sinoatrial node on the wall of the right atrium. These specialized cells demonstrate slow spontaneous depolarization at regular intervals (automaticity) and have an action potential that differs from that of cardiomyocytes. The action potential of pacemaker cells proceeds as follows:1.Phase 0 (upstroke) begins once the cell crosses the depolarization threshold (about -40 mV). It is characterized by the opening of voltage-gated L-type (long-lasting) Ca：- channels with a large influx of Ca:* into the cell.2.Phase 3 (repolarization) begins with closure of L-type Ca - channels in conjunction with the opening of K+ channels and the efflux of K+ ions from the cell.3.Phase 4 (pacemaker potential) is characterized by the slow influx of Na- that begins at the end of repolarization. During this time, there is also a slow decrease in K+ efflux as the K+ channels continue to close. Once the membrane potential reaches approximately -50 mV, the T-type (transient) Ca：4 channels open and allow Ca - to enter the cell and contribute to depolarization. As the action potential approaches -40 mV, the L-type (long-lasting) Caz+ channels open and trigger an action potential.Adenosine and acetylcholine affect phase 4 of the action potential, reducing the rate of spontaneous depolarization in cardiac pacemaker cells. Adenosine interacts with A1 receptors on the surface of cardiac cells, activating potassium channels and increasing potassium conductance, causing the membrane potential to remain negative for a longer period. Adenosine also inhibits L-type Ca+ channels, further prolonging the depolarization time. These actions result in a transient slowing of the sinus rate and an increase in atrioventricular (AV) nodal conduction delay Adenosine is useful in the termination of paroxysmal supraventricular tachycardia. Acetylcholine behaves similarly by increasing outward conductance while decreasing inward Ca+ and Na- currents during phase 4.(Choices B and C) Angiotensin II is a potent vasoconstrictor that increases both systolic and diastolic blood pressure. Aldosterone acts on collecting duct epithelium in the kidneys; this increases Na+ reabsorption and urinary excretion of and However, neither process directly affects phase 4 of pacemaker action potential.(Choices D and E) Glycine is an inhibitory neurotransmitter, and glucagon is a pancreatic hormone that increases blood sugar levels. Neither affects phase 4 of pacemaker action potential.(Choice F) Norepinephrine facilitates opening of L-type Ca:+ channels and Na-channels in phase 4 of the nodal action potential. This leads to more rapid depolarization.Educational objective:The phase 4 slow depolarization in cardiac pacemaker cells occurs due to the closure of repolarizing K* channels, the slow influx of Na+ through funny channels, and the opening of T-type Ca+ channels. Acetylcholine and adenosine reduce the rate of spontaneous depolarization in cardiac pacemaker cells by prolonging phase,Q 7,A 44-year-old man with non-ischemic cardiomyopathy experiences fatigue and exertional dyspnea. He has no symptoms at rest, but his daily activities are significantly limited by dyspnea. He is compliant with dietary and exercise recommendations and takes his medications regularly. The patients blood pressure is 132/78 mm Hg and pulse is 88/min. Physical examination shows no signs of fluid overload. A medication that selectively decreases the heart rate but has no effect on myocardial contractility or relaxation is added to this patients regimen. Which of the following ion transporters does this medication most likely inhibit?A Funny sodium channels during phase 4 B. L-type calcium channels during phase 2 C. Rapid sodium channels during phase 0 D. Slow delayed rectifier potassium channels during phase 3 E. Sodium potassium pump,A 7,Correct answer:ASeveral classes of drugs, including beta blockers, non-dih