TABLE IV-114 Risk Factors for Active Tuberculosis Among Persons Who Have Been Infected With Tubercle Bacilli 10 page

V-17. The answer is E. (Chap. 230) Although myocardial infarction, stroke, and death are complications that have been reported with cardiac catheterization (all with a frequency of <0.1%), the more common complications are tachy- or bradyarrhythmias, acute renal failure, and vascular complications. Vascular access site bleeding is the most common complication of cardiac catheterization, occurring in 1.5–2% of patients. When catheterization is performed in an emergent fashion for acute myocardial infarction or for hemodynamically unstable patients, the complication rate may rise substantially.

V-18. The answer is A. (Chap. 230) Although right heart catheterization is no longer routinely performed at the time of left heart catheterization, there remain important indications for this procedure. These include evaluation of unexplained dyspnea, especially when there is a suspicion of pulmonary hypertension; diagnosis of valvular heart disease such as mitral regurgitation; pericardial disease; right and/or left ventricular dysfunction, particularly for determination of severity; diagnosis of congenital

heart disease; and suspected intracardiac shunts. In this case, the patient likely has an atrial septal defect with physical examination findings of a loud, fixed split second heart sound and perhaps associated dyspnea. During right heart catheterization, the pulmonary arterial pressures will be measured to assess for pulmonary hypertension, and venous saturation will be measured at the inferior vena cava, right atrium, right ventricle, and pulmonary artery to assess for evidence of an increase in saturation suggestive of intracardiac shunt. All the other patients described would be more appropriately served with a left heart catheterization and coronary angiogram.

V-19. The answer is B. (Chaps. 230 and 250) In the diagnostic algorithm for pulmonary hypertension, the right heart catheterization is important to document the presence and degree of pulmonary hypertension. The right-ventricular systolic pressure (RVSP) on echocardiography provides an estimate of pulmonary arterial pressures, but accurate determination of the RVSP relies on the presence of tricuspid regurgitation and good quality echocardiography. This patient’s body habitus is prohibitive in obtaining good windows for echocardiography. Thus, a right heart catheterization is imperative for documenting pulmonary hypertension, as well as for determining the cause. The right heart catheterization demonstrates an elevated mean arterial pressure, elevated left-ventricular end-diastolic pressure (pulmonary capillary wedge pressure), and elevated mean pulmonary artery pressure. In the presence of a normal cardiac output and an elevated left-ventricular ejection fraction, this is consistent with the diagnosis of diastolic heart failure. Systolic heart failure is associated with similar indices on right heart catheterization, but left-ventricular function is depressed in systolic heart failure. The other causes listed as options are known causes of pulmonary hypertension but would not be expected to cause an increase in the left-ventricular end-diastolic pressure. Obstructive sleep apnea is usually associated only with mild elevations in pulmonary artery pressure. This patient’s BMI puts her at risk for obstructive sleep apnea but would not be responsible for these right heart catheterization values. Both chronic thromboembolic disease and pulmonary arterial hypertension can cause severe elevations in the pulmonary arterial pressure but have a normal left atrial pressure.

V-20. The answer is B. (Chap. 232) The tachycardia-bradycardia variant of sick sinus syndrome is associated with an increased risk of thromboembolism, particularly when similar risk factors are present that increase the risk of thromboembolism in patients with atrial fibrillation. Specific risk factors associated with highest risk include age greater than 65 years and prior history of stroke, valvular heart disease, left ventricular dysfunction, or atrial enlargement. Patients with these risk factors should be treated with anticoagulation.

V-21. The answer is D. (Chap. 232) Bradycardia is frequently present in trained athletes, particularly at night, where heart rates are usually between 40 and 60 beats/min. While sleep apnea can be associated with bradycardia, no apnea was found in this patient on overnight polysomnography. Other possible causes of bradycardia in this patient such as hypothyroidism have been ruled out. Measurement of free T₄ is not indicated with a normal TSH. Pacemaker insertion is not indicated for his normal physiology.

Carotid sinus massage is likely to cause further bradycardia. Fatigue is likely due to his stressful job.

V-22. The answer is E. (Chap. 232) Sinoatrial dysfunction is often divided into intrinsic disease and extrinsic disease of the node. This is a critical distinction, as extrinsic causes are often reversible and pacemaker placement is not required. Drug toxicity is a common cause of extrinsic, reversible sinoatrial dysfunction, with common culprits including beta blockers, calcium channel blockers, lithium

toxicity, narcotics, pentamidine, and clonidine. Hypothyroidism, sleep apnea, hypoxia, hypothermia, and increased intracranial pressure are all reversible forms of extrinsic dysfunction. Radiation therapy can result in permanent dysfunction of the node and therefore is an irreversible, or intrinsic, cause of sinoatrial node dysfunction. In symptomatic patients, pacemaker insertion may be indicated.

V-23. The answer is D. (Chap. 232) When there is evidence of sinoatrial node dysfunction, as manifest in this patient with sinus bradycardia, the first approach is to search for reversible causes. In this case, excessive beta blockade is the most likely explanation for his brady-cardia and symptoms. Stopping the metoprolol at least temporarily is in order. There are no urgent indications for temporary or permanent pacemaker placement, as he does not have a high-level AV block, syncope, or shock. His heart failure should reverse when his heart rate increases. Although pharmacologic chronotropic stimulation can increase heart rate temporarily, his moderate symptoms suggest that simply waiting for the beta blocker to be metabolized will be adequate. There is no evidence of new infarction or post-infarct angina; thus the patient does not require urgent revascularization. Once the patient is stabilized, the risks and benefits of restarting the beta blocker at a lower dosage may be considered.

V-24. The answer is C. (Chap. 232) The patient presents with a classic bulls-eye lesion, or erythema migrans, consistent with Lyme disease. Cardiac conduction abnormalities are common in Lyme disease, often involving the AV node. Temporary pacing may be necessary, but the conduction abnormalities usually resolve. The most common test to diagnose this condition is an ELISA with confirmatory Western blot. Other infectious etiologies can present with heart block such as syphilis and Chagas’ disease, but these would not be associated with the characteristic Lyme rash. Autoimmune and infiltrative diseases may also present with conduction system disease such as ankylosing spondylitis, rheumatoid arthritis, scleroderma, and systemic lupus erythematosus.

V-25. The answer is B. (Chap. 232) Second-degree AV block type 1 (Mobitz type 1) is characterized by a progressive lengthening of the PR interval preceding a pause. The pause in this tracing is between the third and fourth QRS complex. First-degree AV block is a slowing of conduction through the AV junction and is diagnosed when the PR interval is greater than 200 milliseconds. Type 2 second-degree AV block is characterized by intermittent failure of conduction of the P wave without changes in the preceding PR or RR intervals. Second-degree AV block type 2 usually occurs in the distal or infra-His conduction systems.

V-26 and V-27. The answers are B and D, respectively. (Chap. 233) The patient has persistent, non– life-threatening palpitations that distress her enough to seek medical attention. A continuous Holter monitor for 24 hours is appropriate for patients in whom the symptoms happen several times a day in which an event monitor is triggered by the patient when symptoms occur and thus can be worn for a longer period of time. There is no indication of gastrointestinal triggers, so abdominal CT would not be helpful. The atrial premature contractions are uncomplicated, do not require additional diagnostic evaluation at this time, and pose no additional health risk. EP referral is indicated for patients with life-threatening or severe symptoms such as syncope.

V-28. The answer is C. (Chap. 233) The patient has physiologic sinus tachycardia related to a pneumothorax, for which he was at risk from his obstructive lung disease and volume-cycled mechanical ventilation. The increased peak inspiratory pressure on the mechanical ventilator is due to the reduced respiratory system compliance from the pneumothorax. Physiologic sinus tachycardia often

comes on slowly and responds poorly to carotid sinus massage with gradual return to original rate. Pharmacologic interventions are usually unsuccessful with correction of the underlying cause required for resolution of the tachycardia. In this case, a tension pneumothorax is confirmed by chest radiograph and, with placement of a chest tube, the tachycardia resolves. Other causes of physiologic sinus tachycardia include pain, hyperthyroidism, anxiety, anemia, hypotension, fever, and exercise.

V-29. The answer is E. (Chap. 233) Patients at the highest risk for stroke associated with atrial fibrillation include those with a prior history of stroke, TIA, or embolism, and patients with hypertension, diabetes mellitus, congestive heart failure, rheumatic heart disease, LV dysfunction, and marked left atrial dilation of greater than 5.0 cm or age greater than 65 years. Anticoagulation should be strongly considered in these patients. Increased left atrial size is a risk factor for chronic atrial fibrillation.

V-30. The answer is B. (Chap. 233) The AFFIRM and RACE trials compared outcomes in survival and thromboembolic events in patients with atrial fibrillation using two treatment strategies: rate control and anticoagulation versus pharmacotherapy to maintain sinus rhythm. There was no difference in events in the two groups, which is thought to be due to the inefficiencies of pharmacotherapy, with over half of patients failing drug therapy, and also the high rates of asymptomatic atrial fibrillation in the sinus rhythm group. Thus, when considering discontinuation of anticoagulation in patients who have maintained sinus rhythm, placing a prolonged ECG monitor is recommended to ensure that asymptomatic atrial fibrillation is not present. Because of the risk of QT prolongation and polymorphic ventricular tachycardia, initiation of dofetilide and sotalol in the hospital is recommended.

V-31. The answer is C. (Chap. 233) The patient has atrial flutter, which has a high risk of thromboembolic events and should be treated the same as atrial fibrillation. If atrial flutter has been present for more than 24–48 hours without anticoagulation, a transesophageal echocardiogram may be performed to rule out left atrial thrombus. If this is not present, cardioversion may be attempted, with anticoagulation continued for 1 month if successful. Transthoracic echocardiography is inadequate to rule out left atrial thrombus. The patient is hemodynamically stable and has no indications for acute cardioversion. Dabigatran is not currently FDA approved for atrial flutter. Intravenous heparin should be started immediately if there are no contraindications, given the greater than 12-hour duration of symptoms.

V-32. The answer is B. (Chap. 233) The ECG shows at least three different P-wave morphologies with three different PR intervals, which is the hallmark of multifocal atrial tachycardia. This is the signature tachycardia of patients with significant pulmonary disease and is commonly seen in patients with chronic obstructive pulmonary disease, as suggested by diffuse polyphonic expiratory wheezing and hyperinflation.

V-33. The answer is D. (Chap. 233) The patient has classic symptoms for an AV nodal reentrant tachycardia. The so-called frog sign (prominent venous pulsations in the neck due to cannon A waves seen in AV dissociation) on physical examination is frequently present and suggests simultaneous atrial and ventricular contraction. First-line therapy for these reentrant narrow complex tachyarrhythmias is carotid sinus massage to increase vagal tone. Often this is all that is required to return the patient to sinus rhythm. If that is not successful, IV adenosine 6–12 mg may be attempted. If adenosine fails, intravenous beta blockers or calcium channel blockers may be used (diltiazem or verapamil). Finally,

in hemodynamically compromised patients or those who have failed to respond to previous measures, DC cardioversion with 100–200 J is indicated.

V-34. The answer is D. (Chap. 233) The patient has an accessory conduction pathway, as evidenced by the delta waves on his baseline ECG. He now presents with atrial fibrillation through the accessory pathway. The wide complex is not due to ventricular arrhythmia but rather the aberrant accessory conduction through the accessory pathway. In general, this reentrant tachycardia may be treated as all others, with the exception of avoiding digoxin and verapamil, both of which may cause deterioration to ventricular fibrillation. Digoxin is thought to shorten the refractory period of the accessory pathway and thus can precipitate degeneration to ventricular fibrillation. Verapamil is thought to cause systemic vasodilation, with a resultant increase in sympathetic tone, and thus may precipitate ventricular fibrillation as well.

V-35. The answer is A. (Chap. 233) Atrial-ventricular dissociation is a classic finding in ventricular tachycardia. Physical examination may show jugular vein cannon A waves when the atria contracts against a closed tricuspid valve and the ECG will manifest this with atrial capture and/or fusion beats. Other findings on ECG of ventricular tachycardia include QRS duration greater than 140 milliseconds for right bundle branch pattern in V₁ or greater than 160 milliseconds for left bundle morphology in lead

V₁, frontal plane axis of –90 to 180°, delayed activation during initial phase of the QRS complex, or

bizarre QRS pattern that does not mimic typical right or left bundle branch block QRS complex patterns. An irregularly irregular rhythm with changing QRS complexes suggests atrial fibrillation with ventricular preexcitation. Carotid sinus massage, aimed at increasing vagal tone and slowing AV node conduction, is not effective at slowing ventricular tachycardia because the reentrant focus is below the AV node.

V-36 and V-37. The answers are C and C, respectively. (Chap. 233) The patient’s rhythm is torsade de pointes, with polymorphic ventricular tachycardia and QRS complexes with variations in amplitude and cycle length, giving the appearance of oscillation about an axis. Torsades de pointes are associated with a prolonged QT interval; thus, anything that is associated with a prolonged QT can potentially cause torsade. Most commonly, electrolyte disturbances such as hypokalemia and hypomagnesemia, phenothiazines, fluoroquinolones, antiarrhythmic drugs, tricyclic antidepressants, intracranial events, and bradyarrhythmias are associated with this malignant arrhythmia. Management, besides stabilization, which may require electrical cardioversion, consists of removing the offending agent. In addition, success in rhythm termination or prevention has been reported with the administration of magnesium as well as overdrive atrial or ventricular pacing, which will shorten the QT interval. Beta blockers are indicated for patients with congenital long QT syndrome, but are not indicated in this patient.

V-38. The answer is C. (Chap. 233) There are three main mechanisms by which arrhythmias are initiated and maintained: automaticity, afterdepolarizations, and reentry. Automaticity, such as that seen with sinus tachycardia, atrial premature complexes, and some atrial tachycardias, is due to an increase in the slope of phase 4 of the action potential. The depolarization threshold is reached more quickly and repeatedly. Afterdepolarizations are associated with an increase in cellular calcium accumulation, leading to repeated myocar-dial depolarization during phase 3 (early) and phase 4 (delayed) of the action potential. Early afterdepolarizations may be related to the initiation of torsades de pointes. Delayed afterdepolarizations are responsible for arrhythmias related to digoxin toxicity and for

catecholamine-induced ventricular tachycardia. Reentry is due to inhomogeneities in myocardial conduction and refractory periods. With reentry, conduction is blocked in one pathway, allowing slow conduction in the other. This allows for sufficient delay so that the blocked site has time for reentry and propagation of the tachycardia within the two pathways. Reentry appears to be the mechanism for most supraventricular and ventricular tachycardias.

V-39. The answer is C.(Chap. 233) The mechanisms for atrial fibrillation initiation and maintenance are still debated; however, there are anatomic structures that play a role in both of these processes. Muscularized tissue at the orifices of the pulmonary vein inlets are the predominant anatomic drivers of atrial fibrillation, although metabolic disturbances (e.g., hyperthyroidism, inflammation, infection) are also very common. Radiofrequency ablation of the tissue in the area of the pulmonary vein inlets can terminate atrial fibrillation; however, recurrences are not uncommon and other anatomic drivers may be present. The left atrial appendage is an important site of thrombus formation in patients with atrial fibrillation. Any focus within the left or right atrium can be a focus of reentry of focal atrial tachycardia, including the mitral annulus or sinus venosus. Increased automaticity of the sinus node is the mechanism for sinus tachycardia.

V-40. The answer is B.(Chap. 233) Symptoms of atrial fibrillation vary dramatically. The most common symptom is tachypalpitations; however, the hemodynamic effects account for symptoms of impaired left ventricular filling. In atrial fibrillation, there is not an effective atrial contraction to augment late-diastolic left ventricular filling. In patients with impaired ventricular diastolic function, this loss of effective atrial contraction causes impaired left ventricular filling, increased left atrial filling pressures, and pulmonary congestion. These hemodynamic effects are more common in the elderly and in patients with long-standing hypertension, hypertrophic cardiomyopathy, and obstructive aortic valve disease. The tachycardia of atrial fibrillation further compromises left ventricular filling and increases atrial filling pressures. Atrial fibrillation may occur with acute alcohol intoxication, with warming of hypothermic patients, and postoperatively after thoracic surgery. The magnitude of the hemodynamic effect and symptoms will be related to ventricular rate (a slower rate allows more time for left ventricular filling) and underlying cardiac function.

V-41. The answer is E.(Chap. 234) The patient presents with evidence of heart failure by history, and physical examination confirms this diagnosis. Physical examination also shows exophthalmos and a fine tremor, which are suggestive of hyperthyroidism Thyrotoxicosis, along with anemia, nutritional disorders, and systemic arteriovenous shunting, can all cause high-output heart failure. Although systolic and diastolic dysfunction are more common causes of heart failure, disorders associated with a high-output state are often reversible, and therefore a diagnosis should be pursued when clinical clues suggest this may be present.

V-42. The answer is C.(Chap. 234) Circulating levels of natriuretic peptides maybe a useful adjunctive tool in the diagnosis of heart failure, but they cannot replace clinical judgment. BNP or N-terminal BNP are most commonly used and are released from the failing heart, though their release is not specific to left or right heart failure; thus, elevations are commonly seen in cor pulmonale associated with pulmonary vascular disease as well as in patients with left heart failure. Additionally, there are a number of factors that may affect the level of BNP that is normally released from the failing heart. Age and renal dysfunction increase plasma BNP levels. Obesity is associated with falsely low BNP levels. Although BNP levels may normalize after therapy, serial monitoring of this peptide is not presently

recommended as a guide for heart failure therapy.

V-43. The answer is E.(Chap. 234) Several drugs have been shown to prevent disease progression in heart failure including ACE inhibitors, angiotensin receptor blockers, beta blockers, and aldosterone antagonists. ACE inhibition has been shown to improve symptoms and survival, reduce cardiac hypertrophy, and reduce hospitalizations. Its use is often complicated by cough related to kinin potentiation, which is an acceptable reason to switch to an angiotensin receptor blocker. Digoxin therapy has not been shown to improve survival, may be associated with dose toxicity, and in patients with stable disease who are not frequently hospitalized, can usually be withdrawn. Beta blocker therapy may occasionally be associated with worsening heart failure symptoms at the time of initiation, but this can usually be managed with increased diuretics. The benefits of beta blockers would far outweigh the nuisance of occasional extra diuretics in this patient. Aldosterone antagonists such as spironolactone and eplerenone are recommended for patients with EF less than 35% who are receiving standard therapy as above. There is no known benefit to one member of this class of drugs over another.

V-44. The answer is E.(Chap. 234) Although there is a wealth of information on which drugs will improve symptoms and survival in heart failure with reduced ejection fraction, little is known about heart failure with preserved ejection fraction. In fact, there are no proven or approved pharmacologic therapies for patients with heart failure and preserved ejection fraction. Therapy should be aimed at treating the predisposing factors for development of this condition, i.e., treat systemic hypertension if present, reverse ischemia if appropriate, etc. Precipitating factors, such as dietary indiscretion in this patient, atrial fibrillation, or infection, may be addressed to improve symptoms. Sildenafil is currently only approved for therapy of pulmonary arterial hypertension and is not proven to be useful for pulmonary hypertension associated with heart failure with preserved ejection fraction.

V-45. The answer is C.(Chap. 234) The New York Heart Association (NYHA) classification is a tool to define criteria that describe the functional ability and clinical manifestations of patients in heart failure. It is also used in patients with pulmonary hypertension. These criteria have been shown to have prognostic value with worsening survival as class increases. They are also useful to clinicians when reading studies to understand the entry and exclusion criteria of large clinical trials. Class I is used for patients with no limiting symptoms; class II for patients with slight or mild limitation; class III implies no symptoms at rest but dyspnea or angina or palpitations with little exertion—patients are moderately limited; class IV is used for severely limited patients in whom even minimal activity causes symptoms. Treatment guidelines also frequently base recommendations on these clinical stages. This patient has symptoms with mild exertion but is comfortable at rest; therefore, he is NYHA class III.

V-46. The answer is B.(Chap. 234) Patients with severe congestive heart failure often exhibit Cheyne-Stokes breathing, defined as intercurrent short periods of hypoventilation and hyperventilation. The mechanism is thought to relate to the prolonged circulation time between the lungs and the respiratory control centers in the brain, leading to poor respiratory control of PaC0₂. The degree of Cheyne-Stokes breathing is related to the severity of heart failure. This pattern of breathing is different from obstructive sleep apnea, which is notable for loud snoring, periods of apnea, and sudden waking. Patients are also often hypersomnolent during the day. While sleep apnea is managed with weight loss and overnight CPAP, Cheyne-Stokes breathing is difficult to address as it is often a sign of advanced systolic dysfunction and implies a poor prognosis. All efforts to further maximize heart failure management are

indicated. A sleep study would demonstrate this pattern of breathing, but this history and clinical presentation is typical. There is no role for bronchodilators or an electroencephalogram.

V-47. The answer is B.(Chap. 235) Coronary artery disease is a common late complication after cardiac transplantation and is thought to be due to a primary immunologic injury of the vascular endothelium, though it is influenced by nonimmunologic factors such as dyslipidemia, diabetes mellitus, and cytomegalovirus infection. Use of mycophenolate mofetil and the mammalian target of rapamycin sirolimus have been associated with a lower short-term incidence of coronary intimal thickening. Similarly, statin use has been shown to reduce the incidence of this complication. Because donors are generally young, the coronary artery disease after transplantation is not thought to be due to coronary lesions present pretransplantation.

V-48. The answer is E.(Chap. 234) Ventricular assist device therapy can be used either as a "bridge" to transplantation in eligible candidates or as a final destination in patients with end-stage heart failure who are not transplant candidates. There are four FDA-approved devices, all of which share common complications including thromboembolism, cerebrovascular accident, device failure, and infection.

V-49. The answer is E.(Chap. 236) Atrial septal defect (ASD) is a not uncommon simple congenital heart disease lesion that is often diagnosed in adults. Because of chronic left-to-right shunting of intracardiac blood, pulmonary arterial hypertension is a well-recognized common complication. With the development of pulmonary arterial hypertension, the potential for paradoxical embolization of either air or thrombotic material from the right atrium to the systemic circulation is increased. Similarly, with exertion in the context of pulmonary arterial hypertension and ASD, blood may shunt right to left, leading to systemic arterial oxygen desaturation. Atrial fibrillation or other supraventricular arrhythmias may occur, also as a result of atrial stretching with the lesion. While atherosclerosis and unstable angina may certainly occur in adults, is not a reported complication of ASD.

V-50. The answer is D.(Chap. 236) The patient has secondary erythrocytosis due to Eisenmenger's syndrome and chronic arterial hypoxemia. Her partially corrected left-to-right shunt resulted in chronic pulmonary circulation overflow and the subsequent development of pulmonary arterial hypertension. With a rise in pulmonary vascular pressure, the shunt reverses to become predominantly right to left, which causes systemic oxygen desaturation. Because hypoxemia is caused by shunt and not ventilation/perfusion mismatch (as in typical COPD), it is not responsive to oxygen therapy. Peripheral desaturation results in decreased oxygen delivery to the kidneys, increased erythropoietin secretion, and resultant erythrocytosis. Erythropoietin levels would be expected to be elevated in this case (in contrast to polycythemia vera rubra). Phlebotomy is only used for patients with symptomatic erythrocytosis; hyperviscosity symptoms, including neurologic symptoms such as transient ischemic attack; epistaxis or bleeding symptoms; or visual changes. Because iron depletion may worsen viscosity even at a lower hematocrit, it is considered as only a temporary therapy for management of erythrocytosis in Eisenmenger's syndrome. This patient had no symptoms referable to erythrocytosis; therefore, expectant management is most appropriate.

V-51. The answer is D.(Chap. 236) Routine antibiotic prophylaxis is indicated for bacteremic dental procedures or instrumentation through an infected site in most patients with operated congenital heart disease, particularly whenever foreign material is present. The one exception is patches that don't have a post-placement high-grade leak, where prophylaxis is only required for 6 months until

endothelialization.

V-52. The answer is E.(Chap. 236) The patient presents with dextrocardia on his chest radiograph and situs inversus, or complete mirror image situs inversus on examination. When dextrocardia occurs in isolation without situs inversus, multiple cardiac abnormalities are frequently present. Alternatively, when dextrocardia occurs with situs inversus, other cardiac defects are unlikely. Kartagener's syndrome with mucociliary dysfunction may underlie situs inversus, but it is associated with sinusitis and chronic bronchitis, which this patient did not have.

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