Question 1

A 32-year-old woman comes to the emergency department due to sudden-onset left-sided facial droop and arm weakness.  The patient also has had right leg swelling after a recent road trip.  She has no chronic medical conditions, and her only medication is an oral contraceptive.  CT scan of the head shows a right middle cerebral artery territory acute infarction.  Lower extremity ultrasound examination reveals a right femoral vein thrombus.  No obvious cardiac structural abnormalities are detected on an echocardiogram.  Agitated normal saline is injected into a peripheral vein to evaluate for abnormal right-to-left shunting.  No bubbles are seen in the left side of the heart after several minutes.  Which of the following is most appropriate to increase right-sided heart pressure to reveal an obscure intracardiac shunt?

Accepted Answer

This patient has a deep venous thrombosis and has experienced a large stroke, suggesting paradoxical embolization of thrombus (ie, passage from the venous circulation to the arterial circulation). Because thrombi are too large to pass through the pulmonary capillaries, paradoxical embolization typically occurs via an intracardiac right-to-left shunt. In this case, echocardiography did not reveal overt septal abnormalities (ie, atrial septal defect or ventricular septal defect), raising strong suspicion for a patent foramen ovale (PFO). PFO is common, affecting up to 30% of adults. It results from failure of the septum primum and septum secundum to fuse during early childhood, creating a one-way tissue valve. This valve is forced closed when left atrial pressure exceeds right atrial pressure (which is most of the time), but it opens when right atrial pressure exceeds left atrial pressure, allowing for transient right-to-left shunting. To test for the presence of a PFO, normal saline bubbles are injected intravenously, and echocardiography is performed to observe whether the bubbles pass from the right atrium into the left atrium. The release phase of a Valsalva maneuver increases venous return to the right atrium and consequently increases right atrial pressure to facilitate right-to-left shunting of saline bubbles and confirm the diagnosis (the strain phase of Valsalva maneuver decreases venous return to the RA and discourages shunting through a PFO). (Choices A, B, and C) Medications and physiologic maneuvers that reduce venous return to the right atrium discourage right-to-left shunting through a PFO. Abrupt standing from a supine position causes blood to pool in the lower extremities, amyl nitrate (an inhaled nitrate) causes venous vasodilation, and exhalation causes increased intrathoracic pressure (resulting in partial collapse of the inferior vena cava at end-expiration), all of which reduce venous return to the right atrium. (Choice D) Sustained hand grip increases systemic vascular resistance, increasing pressure in the left ventricle and left atrium and discouraging shunting through a PFO. Educational objective: Paradoxical embolization, or passage of a thromboembolism from the venous circulation to the arterial circulation, most commonly occurs through a patent foramen ovale (PFO). A PFO is a one-way tissue valve in the atrial septum that opens only when right atrial pressure exceeds left atrial pressure; venous return to the right atrium increases during the release (ie, relaxation) phase of a Valsalva maneuver and encourages opening of a PFO.

Question 2

A 46-year-old man comes to the office for an annual examination.  He has an uncomfortable heartbeat sensation at night that he tries to decrease by sleeping on his right side.  The patient has had mild shortness of breath with exertion over the last 6 months, but he has no chest pain.  He was told during a wellness check approximately 2 years ago that he had a heart murmur.  The patient has no other medical problems.  Physical examination reveals bounding femoral pulses and carotid pulsations that are accompanied by head bobbing.  Which of the following is the most likely diagnosis?

Accepted Answer

This presentation is most suggestive of aortic regurgitation. The inability of aortic valve leaflets to effectively close during diastole leads to regurgitation of blood back into the left ventricular (LV) cavity with an increase in LV end-diastolic volume and wall stress. The resultant chamber enlargement and eccentric hypertrophy increase total stroke volume, which is often felt as a sense of pounding or an uncomfortable feeling of heartbeat (especially when lying on the left side). Physical examination reveals an early "blowing" diastolic decrescendo murmur best heard at the left sternal border in the third or fourth intercostal space. The precordial impulse is hyperdynamic and displaced laterally and downward. Bounding femoral and carotid pulses, marked by abrupt distension and quick collapse ("water-hammer" pulses), are the result of the wide pulse pressure. Some patients exhibit head bobbing with carotid pulsations (de Musset sign) due to transfer of momentum from the large LV stroke volume to the head and neck. Significant systolic pulsations may also be noticed in other organs (eg, liver, spleen, retina) and the fingertips. (Choice B) Patients with severe aortic stenosis have a characteristic arterial pulse - small pulse amplitude (pulsus parvus) with a delayed peak and slower upstroke of the arterial pulse (pulsus tardus) due to diminished stroke volume and prolonged ejection time. (Choice C) The presence of atrial septal defect leads to left-to-right intracardiac shunting, which can cause a hyperdynamic right ventricular impulse. It does not cause any significant change in arterial pulse character. (Choice D) Coarctation of the aorta causes systolic hypertension in the upper extremities along with characteristic diminished and/or delayed femoral pulses (brachial-femoral delay). (Choice E) Arterial pulse, pulse pressure, and forward stroke volume remain normal in patients with chronic (compensated) mitral regurgitation. (Choice F) Arterial pulses are reduced in volume and amplitude in patients with mitral stenosis due to decreased LV end-diastolic volume and stroke volume. (Choices G and H) Tricuspid regurgitation and/or pulmonary stenosis are right-sided valvular lesions and do not cause any specific arterial pulse pattern on physical examination. Educational objective: Aortic regurgitation causes an increase in total stroke volume with abrupt distension and rapid falloff of peripheral arterial pulses, resulting in a wide pulse pressure. This leads to bounding peripheral pulses and head bobbing with each heartbeat. __________ References: Valvular heart disease: aortic regurgitation. (http://www.ncbi.nlm.nih.gov/pubmed/15998697)

Question 3

A 50-year-old man comes to the emergency department due to intermittent palpitations over the last 6 months. The patient describes them as "very uncomfortable" and says the episodes occur randomly, last for several hours, and resolve spontaneously or with sleep. The current episode started an hour ago and has been accompanied by lightheadedness. He has no medical history and says that he does not like seeing doctors. He is a lifetime nonsmoker. The patient drinks beer on weekends. He has no family history of cardiovascular disease. Temperature is normal and blood pressure is 122/75 mm Hg. BMI is 30 kg/m². Chest examination reveals no murmurs and the lungs are clear on auscultation. There is trace peripheral edema. Cardiac rhythm strip obtained in the emergency department is shown in the exhibit. Aberrant electrical activity in which of the following anatomic structures is the most likely trigger for this patient's current condition?

Accepted Answer

11ec160b_3c87_3d2c_9249_378a9ccf13cd_MD0001_00 This patient's presentation with intermittent palpitations and cardiac rhythm strip showing an irregularly irregular rhythm with varying R-R intervals and no discernible P waves is consistent with paroxysmal atrial fibrillation (AF). The development of AF involves structural and electrical changes that predispose to the initiation and maintenance of electrical reentrant circuits and/or ectopic foci. These pathologic changes, termed atrial remodeling, can occur as a result of normal aging or diseases that cause atrial dilation (eg, hypertension, mitral regurgitation). The remodeling leads to shortening of the atrial refractory period and heterogeneity in localized electrical conduction between atrial myocytes, creating a substrate for the development of AF. In predisposed patients, AF can spawn from specific triggers such as focal electrical discharges, increased atrial stretch, elevated sympathetic activity (eg, sepsis, emotional stress), and ingestion of alcohol. The most common trigger is aberrant electrical foci in the pulmonary veins near their ostia into the left atrium; therefore, catheter ablation of pulmonary vein trigger sites (pulmonary vein isolation) is used for the treatment of symptomatic, paroxysmal AF. (Choices A and F) The cavotricuspid isthmus is the area of right atrial tissue between the crista terminalis (ridge that runs along the vena cava) and the tricuspid annulus, and is usually part of the reentry circuit in atrial flutter. ECG during atrial flutter typically shows a saw-tooth pattern of flutter waves, and the ventricular rhythm can be regular or irregular. (Choices B and D) Monomorphic ventricular tachycardia most commonly originates from areas of ischemic myocardium; however, it can sometimes originate from nonischemic sites in the papillary muscles or right ventricular outflow tract. ECG of ventricular tachycardia typically demonstrates regular R-R intervals and wide QRS complexes. (Choice E) The sinoatrial node is the site of origin of sinus tachycardia; ECG shows regular rhythm with P waves and a rate >100/min. Educational objective: Atrial fibrillation is recognized by an irregularly irregular rhythm with variable R-R intervals and absence of P waves on ECG. The development of AF most commonly involves ectopic electrical foci in the pulmonary veins that trigger fibrillatory conduction in abnormal (remodeled) atrial tissue. __________ References: Atrial fibrillation: classification, pathophysiology, mechanisms, and drug treatment. (http://www.ncbi.nlm.nih.gov/pubmed/12860883)

Question 4

A 34-year-old woman comes to the office due to exertional dyspnea.  The patient has a history of IgA nephropathy; she received hemodialysis for 2 years before undergoing kidney transplantation last month.  Chest x-ray reveals cardiomegaly and pulmonary congestion.  Further evaluation determines that her symptoms are likely due to persistence of the arteriovenous fistula that was used for hemodialysis.  Which of the following physiologic changes are most likely present in this patient due to the fistula?

Accepted Answer

11ec160b_3c8a_2366_9249_55697c0f3c1d_MD0001_00 This patient with dyspnea and chest x-ray showing an enlarged heart and pulmonary edema likely has high-output heart failure due to excessive flow through her arteriovenous fistula. A surgically created arteriovenous fistula forms an enlarged vein that serves as an access point for hemodialysis (which requires a vessel with high blood flow rates); however, if the fistula becomes too large, it can lead to hemodynamic complications. A large arteriovenous fistula allows a high proportion of blood flow to bypass the resistance of the systemic arterioles, causing markedly decreased systemic vascular resistance (SVR) (ie, reduced afterload). Blood passing through the low peripheral resistance returns to the right atrium quickly and easily, resulting in increased venous return (ie, increased preload). Both the reduced afterload and increased preload facilitate increased stroke volume (ie, increased cardiac output). A baroreceptor reflex-mediated increase in contractility and heart rate in response to hypotension may also contribute to increased cardiac output. With excessively large fistulas, the left ventricle becomes unable to keep up with the increased venous return despite a persistent increase in cardiac output; left ventricular diastolic pressure gradually increases, and decompensated heart failure develops. Other common causes of high-output heart failure also involve decreased SVR as the initial disturbance. (Choice A) Hypovolemia (eg, severe dehydration) involves a marked reduction in blood volume. Venous return is decreased, leading to reduced cardiac output and a compensatory increase in SVR. (Choice B) Low-output heart failure (the typical cause of cardiogenic shock) involves left ventricular dysfunction as the initial disturbance, which leads to decreased cardiac output and a compensatory increase in SVR. Increased pressure is transmitted backward from the left ventricle, causing elevated central venous pressure (ie, increased venous return [preload]). (Choice C) The pathophysiology of sepsis is similar to high-output heart failure in that reduced SVR is the initial disturbance and is followed by a compensatory increase in cardiac output. However, in sepsis the leaky vasculature reduces intravascular volume to decrease venous return, preventing volume overload of the left ventricle. (Choice E) Stimulation of both alpha-1 and beta-1 adrenergic receptors (eg, with norepinephrine) causes arteriolar constriction to increase SVR, venoconstriction to increase venous return, and increased heart rate and contractility to increase cardiac output. Educational objective: High-output heart failure results from markedly decreased systemic vascular resistance (eg, large arteriovenous fistula) that leads to increased venous return and increased cardiac output. Despite a sustained increase in cardiac output, the left ventricle is unable to keep up with the increased venous return, and decompensated heart failure develops. __________ References: High-output cardiac failure. (http://www.ncbi.nlm.nih.gov/pubmed/30020709)

Question 5

A healthy 80-year-old man has participated in a longitudinal study over the past 30 years to study the effects of aging on overall cardiovascular status.  He has undergone annual testing with echocardiography and his left ventricular ejection fraction has remained stable throughout the 30 years.  Which of the following changes is most likely responsible for the preserved left ventricular ejection fraction in this patient?

Accepted Answer

11ec160b_3c83_e1c7_9249_13b218e4aeb4_MD0001_00 The cardiovascular system undergoes an array of age-related physiologic changes. Over time, cardiomyocytes are lost to both apoptosis and necrosis (ie, cardiomyocyte dropout), resulting in an overall reduced cardiomyocyte number. The loss of ventricular cardiomyocytes (Choice E) weakens contractile strength. In addition, the aorta and other large arteries stiffen with age, resulting in reduced arterial compliance (ie, reduced arterial reserve capacity) (Choice B) and increased left ventricular (LV) afterload. To compensate for the cardiomyocyte loss and increased afterload, cardiomyocyte hypertrophy (ie, mild concentric LV hypertrophy) occurs, allowing for maintenance of LV contractility and ejection fraction. Cardiomyocyte dropout also affects cardiac conduction cells, contributing to decreased maximal heart rate and slightly decreased resting heart rate. Decreased responsiveness to adrenergic stimuli with age also contributes to reduced maximal heart rate. (Choices C and D) The mild concentric LV hypertrophy that occurs with age results in reductions in LV compliance and LV end-diastolic volume. However, because these changes are relatively slight, stroke volume and cardiac output are mostly preserved. Educational objective: Cardiomyocyte hypertrophy (ie, concentric left ventricular hypertrophy) occurs with age to allow for maintenance of left ventricular contractility and ejection fraction despite cardiomyocyte dropout and increased left ventricular afterload (due to reduced aortic compliance).

Question 6

A 44-year-old man is hospitalized with multiple injuries following a motor vehicle collision.  An arteriovenous fistula created by an injury would most likely result in which of the following changes to the left ventricular pressure-volume loop?Solid line = preinjury
Dashed line = postinjury

Accepted Answer

11ec160b_3c89_8724_9249_3f2a007e044f_MD0001_00 The left ventricular (LV) pressure-volume loop follows the cardiac cycle. At point 1, the left ventricle is full of blood and begins isovolumetric contraction until the aortic valve opens at point 2, causing blood to eject into the aorta and LV volume to decrease. LV contraction ends at point 3, and LV pressure rapidly decreases to point 4, where the mitral valve opens and LV diastolic filling begins again. An arteriovenous fistula, which can be congenital (eg, arteriovenous malformation) or acquired (eg, traumatic injury, surgical placement for hemodialysis), allows blood to shunt from the arterial circulation to the venous circulation without passing through the high resistance of the systemic arterioles. This has the following effects on the LV pressure-volume loop: The low-resistance fistula pathway creates overall reduced systemic vascular resistance (ie, reduced afterload). Blood quickly and easily passes through the reduced peripheral resistance, resulting in increased venous return to the right atrium (ie, increased preload). Both the reduced afterload and increased preload facilitate increased stroke volume, which increases cardiac output and helps maintain blood pressure. Contractility is unchanged initially but may eventually increase via the baroreceptor reflex if there is sustained hypotension. With a large arteriovenous fistula, the left ventricle may be unable to keep up with the increased venous return despite a sustained increase in cardiac output, leading to high-output heart failure. (Choice A) This pressure-volume loop shows increased contractility with a resulting increase in stroke volume and slight increase in afterload. Such changes are expected with administration of a positive inotropic agent such as digoxin. (Choice C) This pressure-volume loop shows increased afterload with a resulting decrease in stroke volume. Contractility is unchanged. Such changes are expected with the obstruction to LV outflow that occurs with aortic stenosis. (Choice D) This pressure-volume loop shows decreased preload with a resulting decrease in stroke volume and slight decrease in afterload. Such changes are expected with administration of a primarily venous vasodilator such as nitroglycerin. Educational objective: An arteriovenous fistula allows blood to shunt from the arterial circulation to the venous circulation, bypassing the high resistance of the systemic arterioles. This leads to reduced systemic vascular resistance (ie, reduced afterload), increased venous return (ie, increased preload), and increased stroke volume. Left ventricular contractility is unchanged.

Question 7

A 56-year-old man comes to the emergency department due to chest palpitations.  He feels that his heartbeat is fast and very irregular.  The patient has no chest pain, shortness of breath, or dizziness.  Physical examination confirms the presence of an irregularly irregular rhythm with a heart rate of 120/min.  He hosted a party last night for his wife's birthday and consumed a large amount of alcohol.  The patient normally drinks only 2-3 times a year.  He is otherwise healthy and takes no medications.  Which of the following ECG findings is most likely in this patient?

Accepted Answer

This patient's presentation (palpitations, tachycardia, and irregularly irregular rhythm) is suggestive of atrial fibrillation (AF). The ECG in patients with AF typically shows an absence of P waves and irregularly irregular rhythm with varying R-R intervals. Some patients have irregular, low-amplitude, fine fibrillatory waves (f waves) between the QRS complexes that represent the chaotic atrial activation. AF is the most common tachyarrhythmia and is often precipitated by acute systemic illness or increased sympathetic tone. It is occasionally seen in patients after excessive alcohol consumption ("holiday heart syndrome"). Systemic illnesses that can precipitate AF include long-standing hypertension, heart failure, and hyperthyroidism. (Choice B) High QRS voltage in the precordial leads is a sign of ventricular hypertrophy, which most commonly results from prolonged untreated hypertension. Although hypertension can cause AF, this patient has no history of long-standing hypertension, making his acute binge drinking a more likely etiology. (Choice C) The QRS complexes are narrow in AF. Prolongation of the QRS interval occurs as a result of delay in intraventricular conduction due to fascicular or bundle branch block. The heart rhythm remains regular in patients with intraventricular conduction abnormalities. (Choice D) A prolonged QT interval can be congenital or acquired. It is associated with an increased risk of torsades de pointes (polymorphic ventricular tachycardia) and sudden cardiac death. The QT interval can be prolonged with chronic, heavy alcohol use, but this would be unlikely in a patient who drinks only a few times a year. (Choice E) ST segment elevation on an ECG is typically seen in patients with acute transmural myocardial infarction. In the absence of associated arrhythmias, the heart rhythm is typically regular. Educational objective: Palpitations refer to a subjective sensation/awareness of the heartbeat due to rapid arrhythmias or forceful ventricular contractions. Atrial fibrillation is the most common cause of an irregularly irregular rhythm and is detected on ECG by an absence of organized P waves and varying R-R intervals. __________ References: Long-term alcohol consumption and the risk of atrial fibrillation in the Framingham Study. (http://www.ncbi.nlm.nih.gov/pubmed/15019874)

Question 8

A 14-year-old girl is brought to the office to establish medical care.  The patient recently immigrated to the United States with her parents from Vietnam.  Vital signs are within normal limits.  Phonocardiogram obtained at the left upper sternal border is shown below.  Which of the following is the most likely underlying cause of this patient's heart murmur?

Accepted Answer

11ec160b_3c88_4e9f_9249_cbf10fedffa1_MD0001_00 This patient has an early-peaking systolic murmur and wide and fixed splitting of S2. These findings are characteristic of an atrial septal defect (ASD), a common congenital heart lesion involving an abnormal connection between the right and left atria. After birth, pulmonary vascular resistance decreases and systemic vascular resistance increases, creating a left-to-right shunt through the ASD. As a result, the right atrium and ventricle receive increased blood volume (ie, venous return to the heart plus blood delivered via the shunt) as compared to normal. Increased blood flow into the pulmonary arteries across the pulmonic valve creates an early-peaking, midsystolic ejection murmur best heard over the left second intercostal space (ie, pulmonic flow murmur). In addition, increased blood flow through the tricuspid valve may cause a diastolic rumble best heard at the lower left sternal border (not present in this patient). It is notable that the blood flow through the ASD itself is low velocity and does not typically cause a murmur. Increased blood flow across the pulmonic valve also accounts for the characteristic ASD finding of a widely split, fixed S2. Under normal conditions, S2 is split only during inspiration due to increased venous return to the heart, resulting in delayed pulmonic valve closure (P2) relative to aortic valve closure (A2). With ASD, increased right ventricular volume further delays P2, and the communication between the left and right atria maintains high right-sided blood volume throughout the respiratory cycle, eliminating respiratory variation of splitting. (Choice A) Aortic stenosis causes a crescendo-decrescendo systolic murmur over the right second intercostal space. A2 may be delayed until after P2 (paradoxical splitting) due to the increase in left ventricular ejection time. (Choice B) Ventricular septal defect creates a holosystolic murmur along the lower left sternal border due to a high-pressure, left-to-right shunt from the left to the right ventricle. Splitting of S2 may be widened but is usually not fixed. (Choice D) Aortic insufficiency is characterized by regurgitant blood flow through the aortic valve, resulting in a decrescendo diastolic murmur along the sternal border. Splitting of S2 is usually not affected. Educational objective: Atrial septal defects result in increased right-sided blood flow due to left-to-right shunting and characteristic findings of a systolic ejection murmur (ie, pulmonic flow murmur) and widely split, fixed S2. __________ References: Atrial septal defect (ASD). (http://www.ncbi.nlm.nih.gov/pubmed/30571061)

Question 9

Physiologists conducting research on the electrical properties of the heart measure action potential conduction velocity at 4 different points within normal cardiac tissue.  The results, expressed in terms of speed of conduction (meters per second), are as follows:Point 1 - 0.05 m/sec
Point 2 - 0.3 m/sec
Point 3 - 1.1 m/sec
Point 4 - 2.2 m/secFrom the following list of locations, which most likely corresponds to the order of points 1-2-3-4 (AV = atrioventricular)?

Accepted Answer

11ec160b_3c8b_d11c_9249_d72bba5b76a0_MD0001_00 Cardiac impulses normally originate in the sinoatrial (SA) node. SA node depolarization delivers an electrical impulse to the surrounding atrial myocardium, which carries the action potential to the atrioventricular (AV) node at a rate of 1.1 m/sec. Speed of conduction in the AV node is the slowest (0.05 m/sec), and this delay allows the ventricles to completely fill with blood during diastole. From the AV node, the action potential enters the His-Purkinje system. Impulses travel the fastest through the Purkinje fibers (2.2 m/sec), which ensures that the ventricles contract in a bottom-up fashion (necessary for efficient propulsion of blood into the pulmonary artery and aorta). From the Purkinje fibers, the action potential is transmitted to the ventricular myocardium, where it travels at a rate of 0.3 m/sec. Points 1-2-3-4 are arranged in order of increasing conduction speed (not conduction time), as follows: Point 1 - AV node (0.05 m/sec) Point 2 - Ventricular muscle (0.3 m/sec) Point 3 - Atrial muscle (1.1 m/sec) Point 4 - Purkinje system (2.2 m/sec) Educational objective: The cardiac action potential conduction speed is slowest in the atrioventricular node and fastest in the Purkinje system. Conduction speed of the atrial muscle is faster than that of the ventricular muscle.

Question 10

A 54-year-old man is admitted to the hospital due to cough, shortness of breath, and chest discomfort.  He has a known history of coronary artery disease and underwent coronary artery bypass graft surgery 3 years ago.  As a result of drug therapy, the left ventricular pressure-volume loop changes from a solid to a dashed line, as shown in the graph below (the loop is unchanged in areas where no dashed line is seen):  Which of the following parameters is most likely increased as a result of this change?

Accepted Answer

11ec160b_3c8b_34d9_9249_b17e11d7e4b7_MD0001_00 As a result of drug therapy, point 3 on this patient's left ventricular (LV) pressure-volume loop shifts up and to the left; this represents an increase in cardiac contractility that would occur with a positive inotropic agent (eg, digoxin, dobutamine). Although LV preload, represented by the volume at point 1, is unchanged (Choice E), the increase in contractility causes an increase in the fraction of LV volume ejected (ie, increased ejection fraction) and increases stroke volume (the horizontal distance between points 1 and 3). The volume remaining in the left ventricle at the end of systole (end-systolic volume represented by the volume at point 3) is consequently decreased (Choice B). LV afterload (the maximum pressure reached during blood ejection) is slightly increased due to the increase in contractility. (Choices A and D) LV end-diastolic pressure (indicated at point 1) and compliance are unchanged in this patient. Compliance is represented by the curve at the bottom of the pressure-volume loop (between point 4 and point 1) and determines the rate of LV pressure increase as LV volume increases during diastolic filling. Compliance is typically unchanged in the short term, but it can change over the long term. Decreased LV compliance (eg, due to concentric LV hypertrophy from prolonged systemic hypertension) would increase the slope of the compliance curve and increase end-diastolic pressure for a given LV end-diastolic volume. Educational objective: An increase in cardiac contractility shifts the top left corner (point 3) of the left ventricular pressure-volume loop up and to the left and increases stroke volume due to an increase in the fraction of LV preload that is ejected during systole (ie, increased ejection fraction).

Question 11

Autopsy of a 78-year-old man demonstrates decreased left ventricular cavity size and a sigmoid-shaped ventricular septum.  Light microscopy shows increased collagen content within the ventricular wall.  Some myocardial cells also have brownish perinuclear cytoplasmic inclusions.  The changes described are most consistent with which of the following conditions?

Accepted Answer

11ec160b_3c83_6c96_9249_6b87a65e20e0_MD0001_00 The morphologic changes described are consistent with normal aging of the heart. Aging is associated with decreased left ventricular chamber size, particularly in the apex-to-base dimension. This decrease in chamber length causes the ventricular septum to acquire a sigmoid shape, with the basilar portion bulging into the left ventricular outflow tract. Atrophy of the myocardium results in increased interstitial connective tissue, often with concomitant extracellular amyloid deposition. Within the cardiomyocytes, there is a progressive accumulation of cytoplasmic granules containing brownish lipofuscin pigment (the result of indigestible byproducts of subcellular membrane lipid oxidation). (Choice A) Dilated cardiomyopathy causes an increase in the left ventricular chamber size. There is an increased risk of mural thrombi with this condition due to contractile dysfunction. (Choice B) Chronic hemolytic anemia may result in the formation of hemosiderin granules containing excess iron inside cardiac myocytes (hemosiderosis), which can be visualized with Prussian-blue stain. Excessive deposition of iron within the myocytes usually leads to dilated or restrictive cardiomyopathy. (Choice C) Hypertrophic cardiomyopathy (idiopathic hypertrophic subaortic stenosis) causes asymmetric septal hypertrophy with disproportionate thickening of the ventricular septum compared to the left ventricular free wall. Microscopic examination shows extreme myocyte hypertrophy, disorganized myocyte bundles, and myofiber disarray. (Choice D) Chronic ischemic heart disease tends to result in progressive congestive heart failure and ventricular dilation. Histologically, the major findings are diffuse subendocardial vacuolization and fibrosis. (Choice E) Long-standing hypertension results in hypertensive heart disease. Although left ventricular chamber size may be reduced in this condition, the major morphologic change is concentric left ventricular hypertrophy. Educational objective: Normal morphological changes in the aging heart include a decrease in left ventricular chamber apex-to-base dimension, development of a sigmoid-shaped ventricular septum, myocardial atrophy with increased collagen deposition, and accumulation of cytoplasmic lipofuscin pigment within cardiomyocytes.

Question 12

A 56-year-old man comes to the emergency department due to palpitations that started several hours ago. He has not had similar symptoms before. The patient has had no chest pain, shortness of breath, lightheadedness, or syncope. He drinks alcohol on weekends and does not use illicit drugs. He has no family history of heart disease. Blood pressure is 145/78 mm Hg. BMI is 40 kg/m². ECG is shown in the exhibit. The patient is treated medically in the emergency department. He is then taken to the electrophysiology laboratory for radiofrequency catheter ablation to terminate his arrhythmia. The ablation procedure should create a conduction block through which of the following areas?

Accepted Answer

11ec160b_3c87_d96d_9249_ef19da037f17_MD0001_00 This patient's ECG strip shows rapid and regular atrial activity in a saw-toothed pattern (flutter or F waves), consistent with atrial flutter. Narrow QRS complexes are typically present and the ventricular rhythm appears regular. Because the atrial rate is approximately 300/min, typical ventricular rates in atrial flutter are 150/min, 100/min, or 75/min due to 2:1, 3:1, or 4:1 conduction through the atrioventricular node, respectively. Atrial flutter shares many of the same triggers as atrial fibrillation; underlying comorbidities that cause atrial dilation (eg, heart failure) are often present and alcohol intake may contribute. Typical atrial flutter is caused by a large reentrant circuit that traverses the cavotricuspid isthmus, the region of right atrial tissue between the inferior vena cava and the tricuspid valve annulus. This region is identified during electrophysiologic study and is the target for radiofrequency ablation to interrupt the reentrant circuit and abolish atrial flutter. (Choice A) An accessory pathway that bypasses the atrioventricular node is present in atrioventricular reentrant tachycardia, also known as Wolff-Parkinson-White syndrome. ECG shows the triad of short PR interval, wide QRS complex, and slurred upstroke of the QRS complex (delta wave). (Choice C) The right ventricular outflow tract is the most common origination site of idiopathic ventricular tachycardia, a repetitive monomorphic ventricular tachycardia that occurs in the absence of structural heart disease. ECG shows a wide QRS complex with uniform QRS morphology and a regular rhythm. (Choice D) The pulmonary vein ostia are often the origination site of atrial fibrillation, and catheter ablation of pulmonary vein trigger sites (pulmonary vein isolation) may be used to treat symptomatic patients. ECG reveals an irregularly irregular rhythm with varying R-R intervals and absence of P waves. (Choice E) Dual electrical pathways (a slow and fast pathway) within or near the atrioventricular node are implicated in atrioventricular nodal reentrant tachycardia; the slow pathway is targeted for radiofrequency ablation. ECG shows narrow QRS complexes with a rapid rate and regular rhythm, and sometimes retrograde P waves. Educational objective: Atrial flutter demonstrates rapid and regular atrial activity in a saw-toothed pattern (flutter or F waves) on ECG. Typical atrial flutter is caused by a large reentrant circuit that traverses the cavotricuspid isthmus of the right atrium, which is the target site for radiofrequency ablation. __________ References: Electrophysiologic studies in atrial flutter. (http://www.ncbi.nlm.nih.gov/pubmed/1395202) Electrophysiological effects of catheter ablation of inferior vena cava-tricuspid annulus isthmus in common atrial flutter. (http://www.ncbi.nlm.nih.gov/pubmed/8548901)

Question 13

A 55-year-old man undergoes an elective surgery under general anesthesia.  Two hours into the surgery, his left ventricular pressure-volume loop has changed from the solid line to the dashed line, as shown in the image below (the loop is unchanged in areas where there is no dashed line):  Which of the following is most likely responsible for this patient's hemodynamic change?

Accepted Answer

11ec160b_3c8b_82fb_9249_6fc2f3e68097_MD0001_00 The left ventricular (LV) pressure-volume loop in this patient shows a rightward shift in end-diastolic volume (point 1), indicating increased preload, which occurs with infusion of normal saline or other causes of increased blood volume (eg, blood transfusion, renal failure). Following the Frank-Starling law, the increased LV stretch from increased preload leads to increased stroke volume (the horizontal distance between points 1 and 3) and a slight increase in afterload (ie, the peak LV pressure reached during blood ejection). Contractility is unchanged. (Choice A) Clamping of the abdominal aorta increases aortic pressure to increase afterload. Stroke volume decreases because the left ventricle is unable to eject as much blood against the increased aortic pressure. Preload is unchanged. (Choice B) Blood loss decreases intravascular volume and leads to decreased preload. The decreased preload causes reduced stroke volume and a slight decrease in afterload (Frank-Starling). (Choice C) Dobutamine primarily acts as a beta 1 receptor agonist and stimulates increased contractility. The increased contractility increases stroke volume and leads to a slight increase in afterload. (Choice D) Acute myocardial infarction disrupts myocardial function and often decreases contractility. The decreased contractility decreases stroke volume and causes a slight decrease in afterload. Preload is unchanged initially but is likely to increase if the decrease in contractility is sustained. Educational objective: A rightward shift of the bottom right corner (point 1) of the left ventricular (LV) pressure volume loop indicates increased end-diastolic volume or preload, which occurs with infusion of normal saline. The increased preload causes increased LV stretching and leads to increased stroke volume and a slight increase in afterload (Frank-Starling law).

Question 14

A 34-year-old man comes to the clinic for evaluation of a heart murmur.  The patient has no chest pain, palpitations, dizziness, or shortness of breath at rest.  He also exercises regularly without any abnormal symptoms.  Cardiac auscultation in the second right intercostal space reveals an ejection click along with a soft systolic murmur radiating to the neck.  A normal volume and pressure tracing of the left ventricle is shown in the image below.  Which of the following letters corresponds to the opening of the valve most likely affected in this patient?

Accepted Answer

11ec160b_3c8c_6d5f_9249_7bf2f57512eb_MD0001_00 This young, asymptomatic patient with a soft systolic ejection murmur at the right second intercostal space most likely has a bicuspid aortic valve. The graph above depicts the normal left ventricular (LV) pressure and volume curves during the cardiac cycle. Ventricular pressure and volume curves allow one to identify the phases of the cardiac cycle and to determine the exact time of opening and closure of the cardiac valves. Aortic valve opening occurs when the LV pressure exceeds the central aortic pressure at the end of isovolumetric contraction. Subsequently, LV pressure continues to rise with forward blood flow into the aorta, until the pressure in the left ventricle falls below the aortic pressure leading to aortic valve closure. (Choice A) The initial part of the LV pressure and volume curves corresponds to atrial systole, which results in a slight increase in LV volume and pressure. This is immediately followed by mitral valve closure and the beginning of isovolumetric contraction, where the LV pressure rises rapidly while LV volume remains constant. (Choice C) This point corresponds to aortic valve closure, where LV pressure falls below the central aortic pressure. This also marks the beginning of isovolumetric relaxation, where the LV pressure rapidly falls while LV volume remains relatively constant. (Choice D) Left atrial pressure gradually increases from passive filling from the pulmonary veins and exceeds LV pressure at the end of isovolumetric relaxation, leading to the opening of the mitral valves. (Choice E) This point corresponds to passive LV filling with blood flow from the left atrium, which results in a gradual rise in LV volume and pressure. Educational objective: Ventricular pressure and volume curves allow one to identify the phases of the cardiac cycle and to determine the exact time of opening and closure of the cardiac valves. The aortic valve opens when left ventricular pressure exceeds the central aortic pressure at the end of isovolumetric contraction. __________ References: The cardiac cycle and the physiological basis of left ventricular contraction, ejection, relaxation, and filling. (http://www.ncbi.nlm.nih.gov/pubmed/18313620)

Question 15

A 46-year-old man comes to the office with chest pain and dyspnea on exertion.  He has no known medical problems and leads a sedentary lifestyle.  He is a lifetime nonsmoker.  Noninvasive cardiac testing is nondiagnostic.  Left and right heart catheterization is planned.  During the procedure, the catheter records periodic pressure changes with a maximum of 25 mm Hg and minimum of 2 mm Hg.  The catheter is advanced further, and then shows periodic pressure changes with a maximum of 25 mm Hg and a minimum of 10 mm Hg.  Assuming the results of the procedure are normal, the first set of readings was most likely obtained from which of the following locations?

Accepted Answer

11ec160b_3c8a_bfa7_9249_9738c981b705_MD0001_00 Cardiac catheterization is performed to evaluate for cardiac etiologies and obtain direct measurements of intracardiac pressures in patients with unexplained symptoms. In general, right-sided pressures are much lower than those of the left side as the right ventricle is pumping blood into a much lower resistance pulmonary vasculature. A balloon-tipped pulmonary artery (PA) catheter (attached distally to a pressure transducer) is inserted into the subclavian or internal jugular vein. When the PA catheter enters the superior vena cava (SVC), a venous waveform appears, and the balloon is inflated with air and the catheter is advanced. The location of the catheter tip is determined by the pressure readings as follows: The venous pressure waveform of the SVC appears as small-amplitude oscillations. The pressure remains unchanged as the catheter is advanced into the right atrium (RA). Normal pressure in the SVC and RA is 1-6 mm Hg (Choice D). As the catheter is advanced across the tricuspid valve into the right ventricle (RV), a pulsatile waveform appears. The peak (systolic) pressure is the strength of right ventricular contraction, and the lowest (diastolic) pressure is just below the RA pressure. RV systolic pressure is normally 15-30 mm Hg. As the catheter advances across the pulmonic valve into a main pulmonary artery, the pressure waveform shows a sudden increase in diastolic pressure with no change in systolic pressure. This rise in diastolic pressure is due to pulmonary capillary resistance and backward transmission of left atrial pressure. The PA diastolic pressure is normally 6-12 mm Hg (Choice C). When the catheter is advanced into the distal PA branches, a venous type waveform appears; this is called the PA occlusion pressure or pulmonary capillary wedge pressure (PCWP). This pressure is reflective of venous pressure in the left heart (left atrial pressure and left ventricular diastolic pressure) (Choice A). PCWP is usually equal to PA diastolic pressure (6-12 mm Hg). (Choice B) Left-sided pressures are much higher than right heart pressures in order to maintain systemic perfusion. The normal left ventricular systolic pressure is approximately 90-140 mm Hg with a left ventricular end-diastolic pressure of 6-12 mm Hg. Educational objective: Right-sided pressures in the heart are lower than left-sided pressures due to lower resistance in the pulmonary vasculature. Right ventricular diastolic pressure is similar to right atrial/central venous pressure (1-6 mm Hg), whereas pulmonary artery diastolic pressure is slightly higher (6-12 mm Hg) due to resistance to flow in the pulmonary circulation.

Question 16

A 33-year-old man comes to the office due to fatigue and decreased exercise tolerance over the past 6 months.  The patient was diagnosed with infective endocarditis in the setting of intravenous drug use a year ago and completed a course of antibiotic therapy.  He has not used drugs since then.  The patient has no other medical problems and takes no medications.  A cardiac murmur is heard on auscultation.  Both carotid arteries demonstrate a rapid rise and fall of the arterial pulse.  Partial compression of the femoral arteries by the stethoscope elicits a systolic-diastolic bruit.  Which of the following sets of pressure findings is most likely to be observed during cardiac catheterization of this patient?

Accepted Answer

11ec160b_3c85_b68b_9249_03157564f626_MD0001_00 This patient's presentation is consistent with aortic regurgitation (AR), which likely developed as a complication of infective endocarditis. AR is characterized by a rapid loss of aortic pressure during diastole due to backflow of blood into the left ventricle. The left ventricle becomes dilated with an increase in end-diastolic volume and undergoes eccentric hypertrophy that allows for a compensatory increase in stroke volume and cardiac output. The result of these effects is a characteristic high-amplitude, rapid rise-rapid fall pulsation with each ventricular contraction that manifests as widened pulse pressure, rapid distension and collapse of the carotid arteries (Corrigan sign), and a "to-and-fro" bruit appreciated over the femoral arteries (Duroziez sign). The hemodynamic changes in AR are evident on cardiac catheterization and include reduced aortic diastolic pressure and elevated left ventricular (LV) diastolic pressure due to backflow of blood during diastole. In addition, aortic and LV systolic pressures are increased due to high stroke volume and a compensatory increase in cardiac contractility. (Choice A) LV systolic pressure that is higher than aortic systolic pressure is consistent with aortic stenosis. Patients with aortic stenosis have weak and delayed pulses (pulsus parvus et tardus) and pulse pressure may be reduced due to restricted stroke volume. The LV often undergoes concentric hypertrophy (wall-thickening) due to pressure overload. (Choice B) These are normal LV and aortic pressure findings on cardiac catheterization. (Choice C) Normal LV systolic and aortic pressures but elevated LV end-diastolic pressure is consistent with compensated heart failure. The left ventricle often undergoes eccentric hypertrophy due to volume overload. (Choice E) Elevated aortic pressures with no systolic pressure gradient across the aortic valve and normal LV diastolic pressure is consistent with systemic hypertension. Concentric hypertrophy may develop due to pressure overload. Educational objective: Aortic regurgitation causes a rapid fall in aortic pressure during diastole with an increase in left ventricular end-diastolic volume and a compensatory increase in stroke volume. These hemodynamic changes create characteristic pressure changes, including reduced aortic diastolic pressure, increased aortic systolic pressure, and increased left ventricular diastolic and systolic pressures. __________ References: Clinical practice. Aortic regurgitation. (http://www.ncbi.nlm.nih.gov/pubmed/15470217)

Question 17

A 54-year-old man is being evaluated for exertional dyspnea that started 6 months ago.  The patient has no associated cough or wheezing.  There is no known history of heart disease in his family.  ECG, chest x-ray, exercise stress test, and echocardiogram are obtained to evaluate his symptoms.  He subsequently undergoes right and left cardiac catheterization, and the results are as follows:  What additional information is necessary to calculate cardiac output in this patient?

Accepted Answer

Cardiac output, expressed in liters per minute, is commonly calculated using the following formula: Cardiac output = stroke volume x heart rate Cardiac output can also be determined with a pulmonary artery (Swan-Ganz) catheter by applying the Fick principle, which uses the rate of oxygen consumption and the arteriovenous oxygen difference: Cardiac output = rate of O₂ consumption / arteriovenous O₂ content difference Arterial oxygen content is measured directly from arterial blood, and mixed venous oxygen content is measured from pulmonary arterial blood. The rate of oxygen consumption can be determined with an oxygen meter by measuring the rate of disappearance of oxygen in exhaled air. (Choice A) The arteriovenous difference in oxygen content can be calculated using the information provided in the question stem (eg, arterial blood O₂ content - venous blood O₂ content). (Choices B and C) The oxygen-binding capacity of hemoglobin and percentage of hemoglobin saturation can be used to calculate blood oxygen content using the following equation: Blood O₂ content = (O₂-binding capacity x % saturation) + dissolved O₂ Dissolved oxygen is the amount of oxygen unbound to hemoglobin and typically makes up a small fraction of the total blood oxygen content. (Choice E) The respiratory quotient is the ratio of CO₂ to O₂ across the alveolar membrane, and is used to estimate the metabolic rate. The normal value is typically 0.8. Educational objective: The Fick principle can be applied to calculate cardiac output using the rate of oxygen consumption and the arteriovenous oxygen content difference: Cardiac output = rate of O₂ consumption / arteriovenous O₂ content difference __________ References: Cardiac output monitoring: Basic science and clinical application. (http://www.ncbi.nlm.nih.gov/pubmed/18211449)

Question 18

A 39-year-old man comes to the office due to increasing fatigue for the past 2 weeks.  The patient reports no prior medical conditions, although he recently had a self-limiting upper respiratory illness.  He does not use tobacco, alcohol, or illicit drugs and has not traveled recently.  Temperature is 37.2 C (99 F), blood pressure is 116/66 mm Hg, pulse is 100/min, and respirations are 20/min.  Physical examination reveals lung crackles.  Echocardiography shows no valvular abnormalities and the following parameters:  Based on the observed findings, which of the following is most accurate about this patient?

Accepted Answer

11ec160b_3c83_1e75_9249_9db1472f5484_MD0001_00 Left ventricular stroke volume is the absolute volume of blood ejected from the left ventricle with each contraction. It is calculated by subtracting the volume of blood in the left ventricle at the end of contraction, the left ventricular end-systolic volume, from the volume of blood in the left ventricle at the beginning of contraction, the left ventricular end-diastolic volume (LVEDV). This patient's stroke volume is 50 mL (125 mL − 75 mL), which is lower than the expected normal value of approximately 70 mL. Ejection fraction, the relative volume of blood ejected from the left ventricle with each contraction, is calculated by dividing stroke volume by LVEDV. In this patient, the ejection fraction is 0.4 (50 mL / 125 mL). The fraction is typically multiplied by 100 and expressed as a percentage; therefore, this patient's left ventricular ejection fraction is 40% (0.4 × 100), which is lower than the expected normal value of ≥50%. Cardiac output, the volume of blood ejected into the aorta per unit time, is estimated by multiplying stroke volume by heart rate. This patient's cardiac output is 5 L/min (50 mL × 100/min), which is normal. Although it is not pertinent to this patient, this equation overestimates cardiac output in the setting of mitral regurgitation because a portion of the stroke volume flows backward into the left atrium with each contraction. This patient's presentation is consistent with left ventricular systolic dysfunction leading to heart failure with reduced ejection fraction. He has only mild symptoms at present because the low stroke volume is being compensated by an elevated heart rate to maintain cardiac output; however, further decompensation with reduced cardiac output is likely over time. Educational objective: Stroke volume is the absolute volume of blood ejected from the left ventricle with each contraction and is calculated by subtracting left ventricular end-systolic volume from left ventricular end-diastolic volume (LVEDV). Ejection fraction is the relative volume of blood ejected from the left ventricle with each contraction; it is calculated by dividing stroke volume by LVEDV. Cardiac output, the volume of blood ejected into the aorta per unit time, is estimated by multiplying stroke volume by heart rate.

Question 19

A 69-year-old man is brought to the emergency department with sudden onset palpitations and dyspnea.  His medical history is significant for hypertension and gastroesophageal reflux disease.  ECG reveals a heart rate of 120/min with an irregularly irregular rhythm, narrow QRS complexes, and no organized P waves.  Which of the following physiologic factors most likely determines the ventricular contraction rate in this patient?

Accepted Answer

This patient's ECG findings are diagnostic for atrial fibrillation with rapid ventricular response. Atrial fibrillation is the most common cardiac arrhythmia and is characterized by absent P waves, irregularly irregular R-R intervals, and narrow QRS complexes. Rapid, irregular, low amplitude fibrillatory waves are also frequently seen and represent chaotic, continuous atrial depolarizations. Atrial fibrillation is initiated by aberrant electrical impulses that arise within regions of heightened atrial excitability (most often the pulmonary veins). Once triggered, atrial fibrillation induces electrical remodeling of the atria with the development of shortened refractory periods and increased conductivity. This facilitates the creation and persistence of multiple ectopic foci and reentrant impulses within the atria, increasing the risk and chronicity of subsequent episodes (atrial fibrillation begets atrial fibrillation). Ventricular response in atrial fibrillation is dependent on the transmission rate of abnormal atrial impulses through the atrioventricular (AV) node. Each time the AV node is excited, it enters a refractory period during which additional atrial impulses cannot be transmitted to the ventricles; consequently, the majority of atrial impulses never reach the ventricles (Choice A). The average ventricular rate in atrial fibrillation usually ranges between 90-170/min. Because atrial excitation is chaotic, the ventricular rate is irregular with no set intervals between contractions. (Choice C) Bundle branch conductivity determines the duration of the QRS complexes, which are widened when there is bundle branch block. It does not affect the ventricular contraction rate. (Choice D) The Purkinje system can assume pacemaker activity in patients with severe bradycardia (<40 beats per minute), but it would not generate impulses in atrial fibrillation since the ventricular rate is typically elevated. (Choice E) During atrial fibrillation, the atria are in a state of chaotic, continuous depolarization that is independent of sinoatrial node activity. (Choice F) The ventricular muscle refractory period does not limit the ventricular contraction rate during AF (the ventricular heart rate can approach 300/min in ventricular tachycardia). Educational objective: Atrial fibrillation occurs due to irregular, chaotic electrical activity within the atria and presents with absent P waves, irregularly irregular R-R intervals, and narrow QRS complexes. The atrioventricular node refractory period regulates the number of atrial impulses that reach the ventricles and determines the ventricular contraction rate in conditions where the atria undergo rapid depolarization.

Question 20

A 43-year-old man is evaluated for occasional palpitations provoked by anxiety.  The patient describes a sudden-onset pounding sensation in the chest followed by lightheadedness and shortness of breath.  He has never had syncope.  The patient has no history of heart disease, and family history is unremarkable.  After initial evaluation, he is treated with verapamil and reports marked improvement in the frequency of palpitation episodes.  The tracing below shows the electrical activity of a specific type of cardiac cell in the patient's heart.  Which of the following effects would verapamil administration most likely have on these cells?

Accepted Answer

11ec160b_3c84_2fe9_9249_474ef89fd878_MD0001_00 The above tracing demonstrates the action potential of cardiac pacemaker cells in cardiac slow-response tissues such as the sinoatrial (SA) and atrioventricular (AV) nodes. The pacemaker action potential includes the following phases: Phase 4 (spontaneous depolarization) begins after hyperpolarization triggers the opening of HCN channels that allow slow influx of Na⁺ ("funny current"). T-type (transient) Ca²⁺ channels then open once the membrane potential becomes more positive, allowing Ca²⁺ influx to contribute to depolarization. As the pacemaker cell approaches threshold, L-type (long-lasting) Ca²⁺ channels begin to open, which further increases Ca²⁺ influx and significantly decreases the time until threshold is reached. Phase 0 (upstroke) is characterized by continued opening of L-type Ca²⁺ channels. In cardiac slow-response tissues, the action potential upstroke is much slower and transitions gradually from phase 4 due to the relatively slow influx of Ca²⁺ into the cell. Phase 3 (repolarization) is characterized by the opening of K⁺ channels and efflux of K⁺ from the cell in conjunction with the closure of L-type Ca²⁺ channels. This patient's anxiety-provoked episodes of sudden-onset palpitations associated with lightheadedness and shortness of breath are consistent with paroxysmal supraventricular tachycardia. Class IV antiarrhythmics (eg, verapamil, diltiazem) are commonly used to prevent recurrent nodal tachyarrhythmias such as PSVT. They work by blocking L-type calcium channels in cardiac slow-response tissues, which causes slowing of phase 4 depolarization and reduced conduction velocity in the SA and AV nodes. (Choice A) Verapamil decreases the amount of intracellular calcium available for excitation-contraction coupling within cardiac myocytes. This reduces myocardial contractility, which can be harmful in patients with impaired ventricular function. However, the tracing shown in the question stem corresponds to pacemaker action potentials, not cardiac myocyte action potentials. (Choices B and C) The threshold potential refers to the amount of depolarization required to initiate an action potential. Class I (sodium channel blockers) and class IV (calcium channel blockers) antiarrhythmics raise the threshold potential of cardiac fast- and slow-response tissues, respectively, by blocking the channels that trigger an action potential. This effect also results in reduced action potential amplitude, decreased upslope, and reduced impulse conduction speed within the respective tissues. (Choice D) Verapamil's calcium blocking activity reduces the action potential duration in nodal tissues, but it also increases the refractory period by slowing the recovery of inactivated calcium channels. Class IA (eg, quinidine) and class III (eg, amiodarone) antiarrhythmics also increase the refractory period by blocking potassium channels and prolonging repolarization. Educational objective: Class IV antiarrhythmics (eg, verapamil, diltiazem) are commonly used to prevent recurrent nodal arrhythmias (eg, paroxysmal supraventricular tachycardia). They work by blocking calcium channels in slow-response cardiac tissues, slowing phase 4 (spontaneous depolarization) and phase 0 (upstroke). This reduces impulse conduction velocity in the sinoatrial and atrioventricular nodes. __________ References: Class IV antiarrhythmic agents: new compounds using an old strategy. (http://www.ncbi.nlm.nih.gov/pubmed/25354181) Antiarrhythmic and anti-ischemic properties of calcium-channel antagonists. (http://www.ncbi.nlm.nih.gov/pubmed/8689275)

Exam 13: Physiology

A 44-year-old man is hospitalized with multiple injuries following a motor vehicle collision. An arteriovenous fistula created by an injury would most likely result in which of the following changes to the left ventricular pressure-volume loop?Solid line = preinjury Dashed line = postinjury