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Cardiovascular Medicine Echocardiogram may show regional wall motion abnormalities in ACS when the diagnosis is not clear. Unstable Angina/NSTEMI In patients with unstable angina/NSTEMI, immediate angiography is indicated if any of the following are present . hemodynamic instability .HF . recurrent rest angina despite therapy . new or worsening MR murmur . sustained VT Risk stratification: In patients with unstable angina and NSTEMI, risk stratification is used to determine whether the patient should receive early angiography or predischarge stress testing with angiography if significant ischemia is present. Several risk scoring systems are available. One is the Thrombolysis in Myocardial Infarction (TIMI) risk score. The risk of death from MI significantly increases with a higher TIMI risk score. Do not memorize the scoring system, but understand the difference in approach for a patient with a low risk score, such as a TIMI score of 0 to 2, compared with the approach for a patient with a higher score (3 7). STUDY TAELE; Unstable Angina or NSTEMI Risk Stratification TlMl Risk Score Strategy 0-2 Low risk. Begin aspirin, F-blocker, nitrates, heparin, statin, clopidogrel. Predischarge stress testing and angiography if testing reveals significant myocardial ischemia aa lntermediate to high risk. Begin aspirin, p-blocker, nitrates, heparin, statin, clopidogrel, and early revascularization DON'T BE TRICKED o STEMI is not the only cause of ST-segment elevations. Consider acute pericarditis, LV aneurysm, stress (takotsubo) cardiomyopathy, coronary vasospasm, acute stroke, or normal variant. STEMI For patients with STEMI, percutaneous coronary intervention (PCI) is the preferred strates/. PCI should be performed as soon as possible, with first medical contact to PCI time <90 minutes in a PCI capable hospital and <120 minutes if transferred from a non PCl-capable hospital to a PCI capable hospital. --\ Other indications for PCI are:

STEMI For patients with STEMI, percutaneous coronary intervention (PCI) is the preferred strates/. PCI should be performed as soon as possible, with first medical contact to PCI time <90 minutes in a PCI capable hospital and <120 minutes if transferred from a non PCl-capable hospital to a PCI capable hospital. --\ Other indications for PCI are: o failure of thrombolytic therapy . new HF or cardiogenic shock Thrombolytic agents: Administer thrombolytic agents when PCI is not available and cannot be achieved within 120 minutes with transfer. The most commonly encountered contraindications include active bleeding or high risk lor bleeding (recent major surgery). BP >180/110 mm Hg is a contraindication, but if the blood pressure is lowered, treatment is possible. STUDY TABLE: Drug Therapy for ACS Drug lndication Aspirin ASAP for all patients with ACS Continue indefinitely as secondary prevention P2Y,, inhibitor (clopidogrel, ASAP for all patients with ACS ticagrelor, or prasugrel in pati ents with ACS treated with PCI) Prasugrel contraindicated in patients age >75 years or history of CVA,/TIA Continue for at least 1 year following Ml (Continued on the next page) 2

Cardiovascular Medicine STUDY TABLE: Drug Therapy lor ACS (Continued) Drug lndication t p-B lockers ( metoprolol, carved i lol) AdministerforACS within 24 hours Continue indefinitely as secondary prevention Anticoagulant (UFH, LMWH, ASAP for definite or likely ACS. Choice depends on reperfusion strategy. Any can be used with fondaparinux) thrombolytic therapy. UFH is preferred for PCl, and fondaparinux shouid be avoided. ACE inhibitors Administer within 24 hours Continue indefinitely in patients with reduced LVEF or clinical HF, diabetes, hypertension, or CKD ARB Administer if intolerant of ACE inhibitor Nitroglycerin Administer in presence of ongoing chest pain or HF Statin Administer high-intensity statin early, even in patients with low LDL levels Continue indefinitely as secondary prevention Eplerenone Administer 3 to 14 days after Ml if LVEF <40% and clinical HF or diabetes t DO]I'T BE TRICKED . Do not choose thrombolytic therapy for patients with NSTEMI or for asymptomatic patients with onset of pain >24 hours ago. Pacing in Acute Ml Recommendations for temporary pacing in the setting oflacute MI are: o symptomatic bradycardia (including complete heart block) o alternating LBBB and RBBB . new or indeterminate-age bifascicular block with first degree AV block Complications of Acute MI Right ventricular ffiarction: Patients with a right ventricular/posterior infarction may present with hypotension or may develop hypotension following the administration of nitroglycerin or morphine. Look for JVD with clear lungs, hypotension, and tachycardia. The most predictive ECG finding is ST-segment elevation on right sided ECG lead V.R. Treat with IV fluids.

Complications of Acute MI Right ventricular ffiarction: Patients with a right ventricular/posterior infarction may present with hypotension or may develop hypotension following the administration of nitroglycerin or morphine. Look for JVD with clear lungs, hypotension, and tachycardia. The most predictive ECG finding is ST-segment elevation on right sided ECG lead V.R. Treat with IV fluids. Mechanical complications (VSD, papillary muscle rupture, and LV free wall rupture) may occur 2 to 7 days after an MI. Emergency echocardiography is the initial diagnostic study. Patients with VSD or papillary muscle rupture develop abrupt pul monary edema or hypotension and a loud holosystolic murmur and thrill. LV free wall rupture causes sudden hypotension or cardiac death associated with pulseless electrical activity. Patients with papillary muscle rupture and VSD should be stabilized with an intra aortic balloon pump, afterload reduction with sodium nitroprusside, and diuretics followed by emergency surgical intervention. Cardiogenic shock: Emergency revascularization supported by intra aortic balloon pump and LVAD may be necessary. Postinfarction angina: Cardiac catheterization is indicated. In patients with recurrent ventricular arrhythmias, an underlying cause, such as recurrent ischemia, should be sought. ICDs are indicated in post-MI patients meeting all of the following criteria: . >40 days since MI or >3 months since PCI or CABG o LVEF <35% and NYHA functional class II or III or LVEF <30'7, and NYHA functional class I Depression: Al1 post MI patients should be screened for depression, because it is associated with increased hospitalization and death. 3

1 t I 1 I Cardiovascular Medicine TESTYOURSEIF A 56-year-old woman has a 3-hour history of chest pain. BP is 80/60 mm Hg, respiration mte is 30/min, and pulse rate is 120/min' Physical examination shows JVD, inspiratory crackles, and an S, gallop. ECG shows 2-mm ST-segment elevation in leads V2 to V6' ANSWER: For diagnosis, choose STEMI and cardiogenic shock. For management, choose cardiac catheterization and PCI' A S8-year-old man with acute chest pain has ST-segment elerration in leads II' III, and aVE BP is 82/52 mm Hg, and pulse rate is 54/min. Physical examination shows IVD, clear lungs, and no murmur or Sr. AIISWER: For diagnosis, choose RV MI. For management, select IV fluids, ECG lead VrR tracing, and cardiac catheterization' llon-ST-Elcvadon tlyoodlal lnhrdon: The ECG demonstrates a non-Sf-elevation myocardial infarction. A 1-mm Sl-segment depression is seen in leads Va to V6 (asterisk) and nonspecific 5[-T wave changes are seen in leads ll, lll, and aVF. Sl-Elevrtlon t{yoodlal lnhntlon: Ihe ECG shows abnormal 0 waves in leadsV3 to V5 and Sl-segment elevation in leads V2 to V5.TheT waves are begin- ning to invert in leads V, to Vu. This pattern is most consistent with a recent anterolateral Ml. 4

Cardiovascular Medicine DOil'T BE TRICKED . Stress testing is of little diagnostic value in patients with a very low (e.g., <10%) or very high (e.g., >90%) pretest probability of CAD. In patients with very high pretest probability, stress testing may provide prognostic information. Treatment Intensive lifestyle modiflcation is selected for all patients with chronic stable angina. Treatment is indicated to achieve the following goals: BP <130/80 mm Hg and glucose control in those with diabetes. Tlpe 2 diabetes treatment should include an SGLI2 inhibitor (e.g., empagliflozin) or a GLP I receptor agonist (e.g., liraglutide). The four major classes of antianginal medications for stable angina are p blockers, nitrates, calcium channel blockers. and ranolazine. Most patients with stable angina will require combination therapy. Cardioselective p-blockers are first-line therapy. Dosage should be adjusted to achieve a resting HR of approximately 60/min. Absolute contraindications to p-blockers include severe bradycardia, advanced AV block, decompensated HF, and severe reactive airways disease (wheezing present). Calcium channel blockers should be initiated as first line therapy for patients with absolute contraindications to p blockers. In the setting of continued angina despite optimal doses of p blockers and nitrates, calcium channel blockers can be added. Avoid short-acting calcium channel blockers. Nondihydropyridine calcium channel blockers (diltiazem, verapamil) should not be used in patients with LV dysfunction. Bradycardia and heart block can occur in patients with significant conduction system disease, especially when combined with B blockers. Nitrates are as effective as p-blockers and calcium channel blockers in reducing angina. Prevent nitrate tachyphylaxis by estab lishing a nitrate-free period ofB to 12 hours per day (typically overnight), during which nitrates are not used. For patients using nitrates, sildenafil, vardenafil, and tadalafil are contraindicated. Ranolazine should be considered in patients who remain symptomatic despite optimal doses of p blockers, calcium channel blockers, and nitrates. Cardioprotective drugs reduce the progression of atherosclerosis and subsequent cardiovascular events.

Nitrates are as effective as p-blockers and calcium channel blockers in reducing angina. Prevent nitrate tachyphylaxis by estab lishing a nitrate-free period ofB to 12 hours per day (typically overnight), during which nitrates are not used. For patients using nitrates, sildenafil, vardenafil, and tadalafil are contraindicated. Ranolazine should be considered in patients who remain symptomatic despite optimal doses of p blockers, calcium channel blockers, and nitrates. Cardioprotective drugs reduce the progression of atherosclerosis and subsequent cardiovascular events. o Aspirin reduces the risk of stroke, MI, and vascular death in patients with CAD. . ACE inhibitors reduce cardiovascular and all-cause mortality in patients with diabetes, hypertension, CKD, LVEF <40,X,, HF, or a history of MI. . High intensit5z statins reduce cardiovascular events, including MI and death. Revascularization therapy with PCI or CABG should be considered in patients with persistent symptoms despite maximal medical therapy. Revascularization with CABG for mortality reduction may also be recommended in patients at high risk, par ticularly those with triple-vessel disease or left main disease with LV dysfunction. DOil'T BE TRICKED . Do not select hormone replacement therapy (in women), antioxidant vitamins (vitamin E), or treatment of elevated serum homocysteine levels with folic acid or vitamin B,r. TESTYOURSETF A 69 year-old man has a 3-month history of burning retrosternal discomfort related to exertion that is relieved by rest. physical examination is unremarkable, and the resting ECG is normal. ANSWER: For treatment, choose aspirin, sublingual nitroglycerin, and a p-blocker, and follow up with an exercise stress test. 6

Cardiovascular Medicine Heart Failure I Diagnosis HFrEF is defined by an LVEF of <40'1,. Common causes include CAD, hypertension, diabetes, and valvular heart disease. HFpEF is commonly defined by an LVEF of >50'1,. Hypertension is the most common cause. Patients with HFrEF often have dilated ventricles, and patients with HFpEF have normal systolic contraction and normal sized ventricles or concentric hypertrophy. Symptoms are the same for HFrEF and HFpEE Symptoms and signs that increase the likelihood of HF include: . paroxysmal nocturnal dyspnea (>2 fold likelihood) o an S.r (li-fold likelihood) The likelihood of HF is decreased 50'1, by: . absence ofdyspnea on exertion . absence of crackles on pulmonary auscultation Disease classification systems are part of the diagnosis and can help guide treatment decisions. STUDY TAB[E: Classification Schemes of Heart Failure That Guide Therapy NYHA Functional Classifi cation ACC/AHA Stages of Heart Failure l: No limitations of physical activity A: At risk for heart failure but without structural heart changes (e.g., patients with diabetes mellitus, coronary artery disease, hypertension, vascular disease) ll: Slight limitation of physical activity B: Structural heart disease (e.g., reduced ejection fraction, left ventricular hypertrophy, chamber enlargement) but without heart failure symptoms lll: Marked limitation of physical aaivity C: Structural heart disease with current or prior heart failure symptoms lV: Unable to carry on any physical activity D: Refractory heart failure requiring advanced intervention (e.g., biventricular without symptoms pacemakel leftventricular assist device, transplantation) Testing A BNP level >400 pglml is compatible with HF, and a level <100 pg/ml argues against HF as a cause of acute dyspnea. The ECG may show a previous MI, ventricular hypertrophy, arrhythmias, or conduction abnormalities. Chest x rays may show cardiomegaly, pulmonary edema, or pleural effusion. Echocardiography will estimate EF and may detect valvular heart disease, HCM, and regional wall abnormalities suggesting CAD.

Testing A BNP level >400 pglml is compatible with HF, and a level <100 pg/ml argues against HF as a cause of acute dyspnea. The ECG may show a previous MI, ventricular hypertrophy, arrhythmias, or conduction abnormalities. Chest x rays may show cardiomegaly, pulmonary edema, or pleural effusion. Echocardiography will estimate EF and may detect valvular heart disease, HCM, and regional wall abnormalities suggesting CAD. Other studies include stress testing or coronary angiography to detect myocardial ischemia, depending on the patient's symp toms and risk factors, and measurement of serum TSH level. CMR imaging can assess for myocarditis and infiltrative processes, such as hemochromatosis, sarcoidosis, and amykridosis. Routine CMR imaging should be used only when clinical suspicion warrants. Endomyocardial biopsy is rarely indicated but can assist in the diagnosis ofgiant cell myocarditis and sarcoidosis. A sleep study should be performed on symptomatic patients with NYHA class IIIV HFrEF and excessive day'time sleepiness. Obstructive and central sleep apneas can be treated with CPAP if conditions persist despite guideline-directed medical therapy. 7

Cardiovascular Medicine DOil'T BE TRICKED o Routine testing for unusual causes of HF, including hemochromatosis, multiple myeloma, amyloidosis, and myocarditis, should not be performed. . Don't order serial BNPs in ambulatory patients to monitor HF or guide therapy. . Kidney failure, older age, and female sex all increase BNP; obesity reduces BNP. Treatment of HFrEF For making treatment decisions, NYHA functional classification provides guidance. SYtJ*Y '1"&8lS: Treatment of HFrEF Therapy lndication ACE inhibitors For all NYHA stages of HF to reduce mortality ARBs are acceptable if ACE inhibitor cannot be tolerated Va lsa rta n-sacu bitril lnitiate or substitute for an ACE inhibitor or ARB in HFrEF (NYHA class ll-lV and EF <40%) Hydralazine plus nitrates Given in addition to standard therapy for NYHA class lll-lV and EF <40% in Black and select non-Black patients (low output syndrome, hypertension)to reduce mortality For patients who cannot tolerate ACE inhibitors or ARBs B-Blockers (only metoprolol For NYHA class l-lV to reduce mortality succinate, carvedilol, and bisoprolol) Aldosterone antagonist For NYHAclass lll-lV HFto reduce mortality (spironolactone or eplerenone) Digitalis Used predominantly in patients who continue to experience symptoms despite guideline- directed medical therapy Diuretics Given to improve symptoms of volume overload lvabradine EF <35% who are in sinus rhythm with a heart rate >70lmin despite maximal p-blocker therapy

B-Blockers (only metoprolol For NYHA class l-lV to reduce mortality succinate, carvedilol, and bisoprolol) Aldosterone antagonist For NYHAclass lll-lV HFto reduce mortality (spironolactone or eplerenone) Digitalis Used predominantly in patients who continue to experience symptoms despite guideline- directed medical therapy Diuretics Given to improve symptoms of volume overload lvabradine EF <35% who are in sinus rhythm with a heart rate >70lmin despite maximal p-blocker therapy Sodium-glucose cotransporter-2 To reduce the risk of cardiovascular events and HF hospitalization regardless of the presence inhibitors oftype 2 diabetes lron therapy Treatment of iron deficiency anemia improves functional capacity and quality of life rcD For ischemic and nonischemic cardiomyopathy in patients with an EF <35% and NYHA functional class ll-lll or with an EF <30% and NYHA functional class I to improve survival Cardiac resynchronization therapy For NYHA class ll-lv LVEF <35%, LBBB with ORS duration >150 ms, and sinus rhythm to improve LVEF and reduce symptoms and mortality Exercise training Recommended in all patients with newly diagnosed HF Lower BP to <130/80 mm Hg; encourage weight loss and smoking cessation; and offer vaccination for COVID 19, pneumonia, and influenza. DOil'T BE TRTCKED . Do not begin p-blocker therapy in patients with decompensated HF. o Continuous IV infusion of furosemide provides no advantage vs. bolus therapy in decompensated HF. . Do not prescribe or continue NSAIDs or thiazolidinediones because they worsen HF. . Nondihydropyridine calcium channel blockers (diltiazem or verapamil) may be harmful to patients with HFTEF. . Do not implant ICD until guideline-directed medical therapy has been administered for 3 months (or 40 days after MI) to assess potential recovery ofLVEF.

DOil'T BE TRTCKED . Do not begin p-blocker therapy in patients with decompensated HF. o Continuous IV infusion of furosemide provides no advantage vs. bolus therapy in decompensated HF. . Do not prescribe or continue NSAIDs or thiazolidinediones because they worsen HF. . Nondihydropyridine calcium channel blockers (diltiazem or verapamil) may be harmful to patients with HFTEF. . Do not implant ICD until guideline-directed medical therapy has been administered for 3 months (or 40 days after MI) to assess potential recovery ofLVEF. TESTYOURSELF A 64 year old woman with previously stable HF now has increasing orthopnea. Medications are lisinopril l0 mg/d and furosemide 20 mg/d. BP is 140/68 mm Hg, and HR is 102/min. Pulmonary crackles and increased JVD are present. ANSWER: For treatment, increase the furosemide and lisinopril dosages and add a p-blocker when the patient is stable. I

Cardiovascular Medicine STUDY TABLE: Differential Diagnoses of Nonischemic Dilated Cardiomyopathy (Continued) Condition Distin gu ishin g Cha racteristics Drug-induced lllicit use of cocaine and amphetamines has been associated with myocarditis and dilated cardiomyopathy, cardiomyopathy as well as Ml, arrhythmia, and sudden death. Choose standard HF treatment. ln patients with stimulant-induced acute myocardial ischemia, p-blockers may exacerbate coronary vasoconstriction; labetalol, a p-blocker with cr-blocker activiry is preferred. Giant cell myocarditis Rare disease characterized by biventricular enlargement, refractory ventricular arrhythmias, and rapid progression to cardiogenic shock in young to middle-aged adults. Histologic examination demonstrates the presence of multinucleated giant cells in the myocardium. Choose immunosuppressant treatment and/or LVAD placement or cardiac transplantation. Hemochromatosis Caused by excess iron deposition in the myocardium. Characterized by symptoms of HF and by conduction defects. Peripartum Presence of HF with an LVEF <45% diagnosed between 1 month before and 5 months after delivery. cardiomyopathy Management includes early delivery (when identified before parturition) and HF treatment. ACE inhibitors, ARBs, and aldosterone antagonists (e.9., eplerenone)should be avoided (teratogenicity) during pregnancy. Anticoagulation with heparin or warfarin is recommended for women with peripartum cardiomyopathy with LVEF <35%. The choice of anticoagulant depends on whether the patient is still pregnant and the time since delivery. Women with persistent LV dysfunction should avoid subsequent pregnancy. Stress-induced Characterized by acute LV dysfunction in the setting of intense emotional or physiologic stress. May mimic (takotsubo) acute STEMI. Dilation and akinesis of the LV apex occur in the absence of CAD. Resolves in days to weeks cardiomyopathy with supportive care. Tachyca rd ia-med iated Occurs when myocardial dysfunction develops as a result of chronic tachycardia. Primary treatment is to slow or eliminate the arrhyhmia. ilardiomvoqilly

Drug-induced lllicit use of cocaine and amphetamines has been associated with myocarditis and dilated cardiomyopathy, cardiomyopathy as well as Ml, arrhythmia, and sudden death. Choose standard HF treatment. ln patients with stimulant-induced acute myocardial ischemia, p-blockers may exacerbate coronary vasoconstriction; labetalol, a p-blocker with cr-blocker activiry is preferred. Giant cell myocarditis Rare disease characterized by biventricular enlargement, refractory ventricular arrhythmias, and rapid progression to cardiogenic shock in young to middle-aged adults. Histologic examination demonstrates the presence of multinucleated giant cells in the myocardium. Choose immunosuppressant treatment and/or LVAD placement or cardiac transplantation. Hemochromatosis Caused by excess iron deposition in the myocardium. Characterized by symptoms of HF and by conduction defects. Peripartum Presence of HF with an LVEF <45% diagnosed between 1 month before and 5 months after delivery. cardiomyopathy Management includes early delivery (when identified before parturition) and HF treatment. ACE inhibitors, ARBs, and aldosterone antagonists (e.9., eplerenone)should be avoided (teratogenicity) during pregnancy. Anticoagulation with heparin or warfarin is recommended for women with peripartum cardiomyopathy with LVEF <35%. The choice of anticoagulant depends on whether the patient is still pregnant and the time since delivery. Women with persistent LV dysfunction should avoid subsequent pregnancy. Stress-induced Characterized by acute LV dysfunction in the setting of intense emotional or physiologic stress. May mimic (takotsubo) acute STEMI. Dilation and akinesis of the LV apex occur in the absence of CAD. Resolves in days to weeks cardiomyopathy with supportive care. Tachyca rd ia-med iated Occurs when myocardial dysfunction develops as a result of chronic tachycardia. Primary treatment is to slow or eliminate the arrhyhmia. ilardiomvoqilly Treatment In addition to reversal ol the underlying cause (alcohol, drug, and tachycardia-mediated cardiomyopathies), if possible, choose standard medical therapy for HFi,

Drug-induced lllicit use of cocaine and amphetamines has been associated with myocarditis and dilated cardiomyopathy, cardiomyopathy as well as Ml, arrhythmia, and sudden death. Choose standard HF treatment. ln patients with stimulant-induced acute myocardial ischemia, p-blockers may exacerbate coronary vasoconstriction; labetalol, a p-blocker with cr-blocker activiry is preferred. Giant cell myocarditis Rare disease characterized by biventricular enlargement, refractory ventricular arrhythmias, and rapid progression to cardiogenic shock in young to middle-aged adults. Histologic examination demonstrates the presence of multinucleated giant cells in the myocardium. Choose immunosuppressant treatment and/or LVAD placement or cardiac transplantation. Hemochromatosis Caused by excess iron deposition in the myocardium. Characterized by symptoms of HF and by conduction defects. Peripartum Presence of HF with an LVEF <45% diagnosed between 1 month before and 5 months after delivery. cardiomyopathy Management includes early delivery (when identified before parturition) and HF treatment. ACE inhibitors, ARBs, and aldosterone antagonists (e.9., eplerenone)should be avoided (teratogenicity) during pregnancy. Anticoagulation with heparin or warfarin is recommended for women with peripartum cardiomyopathy with LVEF <35%. The choice of anticoagulant depends on whether the patient is still pregnant and the time since delivery. Women with persistent LV dysfunction should avoid subsequent pregnancy. Stress-induced Characterized by acute LV dysfunction in the setting of intense emotional or physiologic stress. May mimic (takotsubo) acute STEMI. Dilation and akinesis of the LV apex occur in the absence of CAD. Resolves in days to weeks cardiomyopathy with supportive care. Tachyca rd ia-med iated Occurs when myocardial dysfunction develops as a result of chronic tachycardia. Primary treatment is to slow or eliminate the arrhyhmia. ilardiomvoqilly Treatment In addition to reversal ol the underlying cause (alcohol, drug, and tachycardia-mediated cardiomyopathies), if possible, choose standard medical therapy for HFi, TEST YOURSELF A 35 year old man develops abdominal discomfort and swelling in both legs. He has an lS-pack-year smoking history and drinks a six-pack of beer daily but has no other significant medical history. Physical examination shows JVD, a displaced apical impulse, distant heart sounds, a grade 21 6 apical holosystolic murmur, an enlarged and tender liver, and peripheral edema. ANSWER: For diagnosis, choose alcoholic cardiomyopathy. For management, select echocardiography and alcohol cessation.

TEST YOURSELF A 35 year old man develops abdominal discomfort and swelling in both legs. He has an lS-pack-year smoking history and drinks a six-pack of beer daily but has no other significant medical history. Physical examination shows JVD, a displaced apical impulse, distant heart sounds, a grade 21 6 apical holosystolic murmur, an enlarged and tender liver, and peripheral edema. ANSWER: For diagnosis, choose alcoholic cardiomyopathy. For management, select echocardiography and alcohol cessation. Hypertro p h ic Ca rd io myo pathy Diagnosis HCM is an uncommon primary cardiac disease characterized by diffuse or focal myocardial hypertrophy. The disease is geneti- cally inherited in an autosomal dominant pattern. Most patients are asymptomatic but may present with HF, palpitations, syncope, or sudden cardiac death (SCD). HF symptoms are attributable to abnormal diastolic dysfunction and dynamic left ventricular outflow tract (LVOT) obstruction. STUDY TABLE: Distinguishing HCM from AS ; Assessment/Finding HCM AS Carotid pulse Rises briskly and then declines, followed by a Rises slowly and has low volume (pulsus parvus second rise (pulsus bisferiens) et tardus) Murmur Ejection quality murmur usually best heard at Ejection quality murmur usually best heard at left lower sternal border right upper sternal border Valsalva maneuver lncreased murmur intensity No change or decreased murmur intensity Squatting to standing position lncreased murmur intensity No change or decreased murmur intensity Carotid radiation None Usually present beat "Triple ripple" Sustained single 1o

Cardiovascular Medicine 1 li I ll \ ^"t : vl- t1 ii : tl i .l !1 ! 1: 1: ll t l-i il i' I l_| \ !- -_. .. --)1 1 tr I il j1i ll t i ,:J, il li il rz' \ '-.---*- ,.;l ;/r' 1 t'5 Complete Heail Bloct: Ihe rhythm strip shows third-degree heart block with three nonconducted atrial impulses and a pause of 3.5 seconds li Bifascicutar Block: Ihe ECG shows RBBB and left anterior hemiblock characteristic of bifascicular block. \ I 16

Cardiovascular Medicine DOil'T BETRICKED o Don't place a pacemaker for asymptomatic bradycardia in the absence of second- or third degree heart block. Atrial Fibrillation Diagnosis Findings of AF include an irregularly irregular ventricular rhythm with absence of p waves in all ECG leads. Do not confuse AF with: o sinus tachycardia with premature atrial beats e MAT in patients with COPD o Mobitz type 1 second-degree AV block (Wenckebach) with characteristic group beating . arrhythmia caused by digitalis toxicity (atrial tachycardia with block) o atrial flutter with variable conduction AF can appear as irregular, wide complex tachycardia mimicking VF in the setting of underlying intraventricular conduction delay or in the presence ofan accessory pathway. Diagnostic studies include serum TSH and digoxin level measurement (if appropriate), pulse oximetry sleep apnea evaluation, and echocardiography. Treatment Perform emergency electrical or pharmacologic cardioversion for patients with hemodynamically unstable AF. If duration is unknown or >48 hours, institute immediate anticoagulation and continue for at least 4 weeks. Rhythm control is an appropriate management for younger patients with persistent symptomatic AF and select patients with numerous cardiovascular comorbidities. Rhythm control may be achieved with medications, synchronized cardioversion, or both. If r$thm control is unsuccessful or not tolerated, catheter based AF ablation is a more effective option. Rate control for chronic AF or AF and normal LV function (resting HR <110/min) is achieved with calciurn channel blockers or p-blockers. Almost all patients with AF require chronic anticoagulation. The risk of stroke in patients who have nonvalvular AF plus one other risk factor (other than sex) exceeds the risk of hemorrhage from anticoagulation. The recommended method of assessing stroke risk in patients with nonvalvular AF is by calculating the CIIA2DS2-VASc score. 1 point each is given for: oHF o hlpertension . diabetes . vascular disease (previous MI, PAD, aortic plaque) r female sex o age 65 toT4years 17

Cardiovascular Medicine 2 points each are given for: o previous stroke, TIA, or thromboembolic disease . age >75 years Provide anticoagulation for a score >2 in men or >3 in women. 5f UtrY ?ABtE; Anticoagulants Approved for Stroke Prevention in Atrial Fibrillation Medication Type of AF Cautions Warfarin (vitamin K antagonist) Nonvalvular Avoid in pregnancy Dabigatran (direct thrombin inhibitor) Nonva lvular Caution with P-glycoprotein inhibitors Reduce dose with CrCl 15-30 mUmin Rivaroxaban (factor Xa inhibitor) Nonvalvular Avoid with CrCl <30 mUmin, moderate hepatic impairment, strong P-glycoprotein inhibitors, and strong cytochrome P-450 inducers and inhibitors Reduce dose with CrCl 30-50 mUmin Apixaban (factor Xa inhibitor) Nonvalvular Avoid with strong P-glycoprotein inhibitors or strong cytochrome P-450 inducers and inhibitors Reduce dose with >2 of the following: creatinine >1.5 mg/dL, age >80 years, weight <60 kg Edoxaban (factor Xa inhibitor) Nonvalvular Avoid with strong cytochrome P-450 inducers and inhibitors Avoid with CrCl >95 mUmin (reduced effectiveness in stroke prevention) Reduce dose with CrCl 30-50 mUmin, weight <60 kg, or concomitant use of verapamil or quinidine (potent P-g lycoprotein i n hi bitors)

5f UtrY ?ABtE; Anticoagulants Approved for Stroke Prevention in Atrial Fibrillation Medication Type of AF Cautions Warfarin (vitamin K antagonist) Nonvalvular Avoid in pregnancy Dabigatran (direct thrombin inhibitor) Nonva lvular Caution with P-glycoprotein inhibitors Reduce dose with CrCl 15-30 mUmin Rivaroxaban (factor Xa inhibitor) Nonvalvular Avoid with CrCl <30 mUmin, moderate hepatic impairment, strong P-glycoprotein inhibitors, and strong cytochrome P-450 inducers and inhibitors Reduce dose with CrCl 30-50 mUmin Apixaban (factor Xa inhibitor) Nonvalvular Avoid with strong P-glycoprotein inhibitors or strong cytochrome P-450 inducers and inhibitors Reduce dose with >2 of the following: creatinine >1.5 mg/dL, age >80 years, weight <60 kg Edoxaban (factor Xa inhibitor) Nonvalvular Avoid with strong cytochrome P-450 inducers and inhibitors Avoid with CrCl >95 mUmin (reduced effectiveness in stroke prevention) Reduce dose with CrCl 30-50 mUmin, weight <60 kg, or concomitant use of verapamil or quinidine (potent P-g lycoprotein i n hi bitors) In patients with AF undergoing PCI for ACS, anticoagulant and antiplatelet therapies are necessary. A P2Yr2 inhibitor plus an oral anticoagulant is preferred to a P2Y,, inhibitor, oral anticoagulant, and aspirin (double therapy, not triple therapy). In patients with AF and stable CAD, treatment with rivaroxaban alone is noninferior to rivaroxaban plus aspirin. Bridging anti- coagulation is discussed in the General Internal Medicine section.

In patients with AF undergoing PCI for ACS, anticoagulant and antiplatelet therapies are necessary. A P2Yr2 inhibitor plus an oral anticoagulant is preferred to a P2Y,, inhibitor, oral anticoagulant, and aspirin (double therapy, not triple therapy). In patients with AF and stable CAD, treatment with rivaroxaban alone is noninferior to rivaroxaban plus aspirin. Bridging anti- coagulation is discussed in the General Internal Medicine section. DOil'T BETRICKED . Only warfarin is indicated for valvular AF. o Antiplatelet therapy alone is no longer routinely used for stroke prevention in AF. . Do not begin calcium channel blockers, B-blockers, or digoxin in patients with AF and WPW syndrome; use procainamide instead. . Adenosine is not effective for cardioversion of AF. TEsTYOURSELF A S5-year old woman has dyspnea and chest pain of 12 hours' duration. BP is 75144 mm Hg, and bibasilar crackles are heard. ECG shows a wide complex tachycardia of 160/min. ANSWER: For management, always choose cardioversion in patients with any arrhythmia who are hemodynamically unstable. 18

Cardiovascular Medicine II III aVF I Atdal Fibilllation: The rhythm strip (bottom) shows two sinus beats followed by AF. The AF rhythm is inegular, and fibrillatory waves are clearly seen. RBBB is also present. Atrial Flutter Diagnosis Atrial flutter is a reentrant arrhythmia with atrial rates typically between 250 and 300/min. ECG typically shows a saw-tooth pattern on the inferior leads and a positive deflection in lead V,. The ventricular response is often regular, although it may be irregular and can be confused with AF: Classically, patients have 2:1 conduction resulting in a ventricular response close to 150/min. Atrial flutter may be seen interspersed with AF or may follow treatment of AF. Treatment Catheter ablation is the definitive treatment for tlpical atrial flutter. Guidelines for anticoagulation for atrial flutter are similar to those for AF. aW III Atrial tlutter: The ECG shows a "saw{ooth" pattern in leads ll and lll characteristic of atlial flutter 19

Cardiovascular Medicine i I I ll I Atrial lachycardia: Ihe ECG shows a narrow-complex tachycardia with P waves most clearly seen in lead V1 and atthe end oftheTwave in other leads. ! ! I i I ! I i, iV5' ! I ii Multifo(al Atrial Iathyordia: Ihe ECG shows an irregular tachycardia with three distinct P,wave morphologies characteristic of MAT(arows). Wolff- Pa rkinson-Wh ite Synd rome Diagnosis WPW syndrome is a symptomatic AVRT caused by an accessory AV conduction pathway that is: . usually antegrade to the ventricles, resulting in the delta wave that indicates ventricular preexcitation (WpW is "manifest") o occasionally retrograde; ventricles are depolarized over the normal AV node-His-purkinje network, resulting in a normal surface ECG (WPW is'concealed") 22

Gardiovascular Medlcine ECG findings include a short PR interval, delta wave, and normal or prolonged QRS. Treatment Begin procainamide or another class I or class III agent for patients with wide-complex tachycardia, especially when AF and preexcitation are present. Ablation of the accessory bypass tract is first-line therapy for patients with preexcitaton and symptoms. DOT'? BE TNIC(ED . Asymptomatic WPW conduction without arrhythmia (WPW pattern) does not require investigation or treatment. o Do not select calcium channel blockers, p-blockers, or digoxin for patients who have AF with WPW syndrome; such treatment may convert AF to VT or VF. TEs?YOURSEI} A 28-year-old woman has a 4-hour history of palpitations. Physical examination shows a BP of 132/80 mm Hg, an irregularly irregular HR of 140/min, and no other abnormal findings. The ECG shows AF with a ventricular rate of 180 to 270lmin. QRS com- plexes are broad and bizarre. ANSWER: The diagnosis is WPW syndrome with AE Begin IV procainamide. A 30-year-old woman has an episode of palpitations and syncope. ECG shows WPW pattern. AI\ISWER: Refer for ablation of the accessory tract. Wolff-Pr*inson-t{hlte tyndrcmo: A WPW pattern is identified by a short PR interval, prolonged 0R5, and a slurred onset of the ORS (delta wavel. Ventricu la r Tachyca rd ia Diagnosis Prrernature ventrlcular ctmplexes (PVCs) can be single, in pairs (couplets), or alternating with sinus beats. In healthy adults, occasional PVCs are benign. Ventricular taclryrrrh5rthmias consist of VI, VF, and torsades de pointes. Ventricular tachyarrhythmias are characterized by: o QRS >0.12 s . AVdissociation 23

Cardiovascular Medicine VT can be further classified as sustained or nonsustained. Nonsustained VT lasts <30 s' VT is also categorized by the morphologi of the QRS complexes: . Monomorphic VT: QRS complexes in the same leads do not vary in contour. o Polymorphic VT: QRS complexes in the same leads do vary in contour. Differentiating VT from SVT with aberrant conduction is important because the treatment differs markedly. VT is more com mon than SVT with aberrancy, particularly in persons with structural heart disease. Any wide QRS tachycardia should be considered to be VT until proven otherwise. In the presence of known structural heart disease, especially a previous MI, the diagnosis of VT is almost certain. Torsades de pointes is a specific form of polymorphic VT associated with long QT interval. Torsades de pointes episodes are typicaily short lived and terminate spontaneously, but multiple successive episodes may result in syncope or VF. Testing Evaluation with resting ECG, exercise treadmill testing (to provoke arrhythmias), and cardiac imaging (to identifi/ structural heart disease) is indicated in all patients with VT. Treatment Patients without identifiable structural heart disease: First line treatment for symptomatic PVC suppression is p-blocker or calcium channel blocker therapy. Calcium channel blockers, especially verapamil, and B-blockers are first-line therapy for idiopathic VT. Patients with structural heart disease: Patients with ischemic cardiomyopathy who present with VT should be considered for angiography and revascularization, if appropriate. In patients with recurrent VT despite p blocker therapy, antiarrhythmic drug therapy or catheter ablation may be considered. ICD placement is indicated for prevention of SCD in patients with structural heart disease or cardiomyopathy who have sustained VT/VF, if reversible causes have been excluded. Acute treatment of sustained VT: . For unstable patients, immediate electrical cardioversion is indicated. Pulseless VT is treated in the same way as VF. . For hemodynamically stable patients, IV procainamide, amiodarone, and sotalol are therapeutic options. DON'T BE TRICKED r In patients with structural heart disease, therapy to suppress PVCs does not alTect outcomes

. For unstable patients, immediate electrical cardioversion is indicated. Pulseless VT is treated in the same way as VF. . For hemodynamically stable patients, IV procainamide, amiodarone, and sotalol are therapeutic options. DON'T BE TRICKED r In patients with structural heart disease, therapy to suppress PVCs does not alTect outcomes TEST YOURSELF A 65 year-old woman with chronic stable angina and a history of an anterior MI is evaluated in the emergency department for palpitations and lightheadedness. Vital signs are stable. ECG shows a wide complex tachycardia with an RBBB pattern. No previous ECGs are immediately available. ANSWER: The diagnosis is most likely sustained VT. The acute treatment is IV lidocaine or amiodarone. 24

Cardiovascular Medicine llonomorphic yI: Approximately one of the way into this ECG rhythm strip (botrom) Polymoryhlc tachycardia 25

Cardiovascular Medicine STUDY TAB!E: ECG Features Differentiating Acute Pericarditis from Myocardial lschemia Feature Acute Pericarditis Myocardial lschemia ST-segment contour Concave upward Convex upward ST-segment lead i nvolvement Diffuse Localized Reciprocal ST-T changes No Yes PR-segment abnormalities Yes (depression in limb leads, elevation in aVR) No Pathologic O waves No Yes DON'T BE TRICKED o Cardiac enzyme values may be slightly elevated in patients with pericarditis (myopericarditis) . Absence ofa pericardial effusion on echocardiography does not rule out pericarditis. Treatment First-line treatment is colchicine plus aspirin (preferred after MI) or an NSAID. Add glucocorticoids to first line treatment for pericarditis that is: . recurrent (second orthird recurrence), incessant (>+ to O weeks), chronic (>3 months) o uremic. unresponsive to dialysis o autoimmune TESTYOURSELF A 57 year old man has a 2-day history of chest pain that worsens when he lies flat. Cardiac examination sho'o's a three-component friction rub. ANSWER: For diagnosis, choose pericarditis. Look for diffuse ST-segment elevation and PR-segment depression. Ignclre slight elevation of cardiac troponin tempting you to answer "acute Ml." I aVR v1 II v2 v5 1r1 v3 Atute Perirarditis: The ECG shows sinus rhythm with diffuse ST'segment elevation and PR-segment depression in lead ll, characteristic of acute pericarditis. 28

Cardiovascular Medicine TESTYOURSELF A 44 year old woman with a history of ovarian cancer presents with fatigue, dyspnea, and peripheral edema. Examination shows IVD that increases with inspiration, reduced heart sounds, BP of 94150 mm Hg, and HR of 132/min. A 20 mm Hg pulsus paradoxus is present. ANSWER: For diagnosis, choose acute pericardial tamponade, probably secondary to metastatic disease. For management, select pericardiocentesis. Constrictive Pericard itis Diagnosis Pericardial thickening, fibrosis, and sometimes calcification that impair diastolic filling and limit total cardiac volume are seen. Typically, it is associated with slowly progressive symptoms of right sided HF with clear lungs and may include hepatomegaly, ascites, and peripheral edema. Findings may include o elevated jugular venous pressure, increasing with inspiration . pericardial knock . ECG showing low voltage o pericardial calcification (CT, MRI more sensitive than x ray) Absence ofa pericardial effusion excludes a diagnosis ofcardiac tamponade. Treatment Pericardiectomy is the most effective treatment, but it is unnecessary in patients with early disease (NYHA functional class I) and is unwarranted in many patients with advanced disease (NYHA functional class IV). Cardiac Physical Diagnosis Heart Murmurs Important pearls regarding auscultation of heart murmurs: . Right-sided heart murmurs increase in intensity during inspiration. . HCM murmurs increase in intensity with Valsalva maneuver and on standing from a squatting position. o MVP clicks move closer to S,, and the murmur lengthens with Valsalva and on standing from a squatting position. . Fixed splitting occurs with RBBB, pulmonary valve stenosis, VSD, and ASD (both with left to right shunts). . Paradoxical splitting (split 52 with expiration) occurs with LBBB, HCM, and severe AS. o Innocent heart murmurs are midsystolic, located at the base of the heart, grade 1/6 to 2/6 without radiation, and associ ated with normal splitting of Sr. Signs of serious cardiac disease include an So, murmur grade >3/6 intensity, any diastolic murmur, continuous murmurs, and abnormal splitting of Sr. TTE is indicated in symptomatic patients, in those with a systolic murmur grade >3/6 intensi$/, and in those with a diastolic murmur or any continuous murmur (a murmur that begins after S, and extends beyond Sr). 30

Cardiovascular Medicine DOil'T BE TRICKED r An increased Pr, an 53, and an early peaking systolic murmur over the upper left sternal border are normal flndings during pregnancy. TESTYOURSETF A 19-year-old asymptomatic woman has a heart murmur first heard during a college sports physical examination. A nonradiating grade 21 6 midsystolic murmur is heard over the upper left sternal border. Physiologic splitting of S, is present, and a soft S, is heard at the cardiac apex. ANSWER: For diagnosis, choose an innocent heart murmur. Do not order echocardiography. Valvular Lesions

TESTYOURSETF A 19-year-old asymptomatic woman has a heart murmur first heard during a college sports physical examination. A nonradiating grade 21 6 midsystolic murmur is heard over the upper left sternal border. Physiologic splitting of S, is present, and a soft S, is heard at the cardiac apex. ANSWER: For diagnosis, choose an innocent heart murmur. Do not order echocardiography. Valvular Lesions Cardiac Characteristic Location Radiation Associated Findings Severity and Pitfalls Condition Murmur Aortic stenosis Mi dsystolic, RUSB Right clavicle, Enlarged, nondisplaced Severe aortic stenosis ha rsh, carotid; apex apical impulse; Sa; findings may include crescendo- bicuspid valve without decreased 42; high- decrescendo calcification will have pitched, late-peaking systolic ejection click murmur; diminished and followed by murmur delayed carotid upstroke; radiation of murmur to both clavicles and carotids Radiation of murmur down the descending thoracic aorta may mimic mitral regurgitation Aortic Diastolic, LLSB (valvular) or None Enlarged, displaced Acute severe regurgitation regurgitation decrescendo RLSB (dilated apical impulse; 53 or So; murmur may be masked aorta) (heard best increased pulse pressure; by tachycardia and short sitting and bounding carotid and duration of murmur leaning forward) peripheral pulses Severity in chronic regurgitation is difficult to assess by auscultation

Cardiac Characteristic Location Radiation Associated Findings Severity and Pitfalls Condition Murmur Aortic stenosis Mi dsystolic, RUSB Right clavicle, Enlarged, nondisplaced Severe aortic stenosis ha rsh, carotid; apex apical impulse; Sa; findings may include crescendo- bicuspid valve without decreased 42; high- decrescendo calcification will have pitched, late-peaking systolic ejection click murmur; diminished and followed by murmur delayed carotid upstroke; radiation of murmur to both clavicles and carotids Radiation of murmur down the descending thoracic aorta may mimic mitral regurgitation Aortic Diastolic, LLSB (valvular) or None Enlarged, displaced Acute severe regurgitation regurgitation decrescendo RLSB (dilated apical impulse; 53 or So; murmur may be masked aorta) (heard best increased pulse pressure; by tachycardia and short sitting and bounding carotid and duration of murmur leaning forward) peripheral pulses Severity in chronic regurgitation is difficult to assess by auscultation Mitral stenosis Diastolic; Apex (heard best None Loud 51, tapping apex lnterval between 52 and low-pitched, in left lateral beat, opening snap after opening snap is short in rumble; decubitus 52 if leaflets mobile, severe mitral stenosis decrescendo position) irregular pulse if AF lntensity of murmur present correlates with transvalvular gradient P2 may be loud if pulmonary hypertension present Mitral Systolic; holo- Apex Axilla or back, Systolic click in mitral valve Acute severe regurgitation regurgitation mid-, or late occasionally prolapse; 53; apical may have soft or no systolic; anteriorly to impulse hyperdynamic holosystolic murmur, mitral blowing or precordium and may be displaced if inflow rumble, or 53 musical dilated left ventricle; in mitralvalve prolapse, Valsalva maneuver moves onset of clicks and murmur closerto 51; handgrip maneuver increases murmur intensity (Continued on the nert page)

Mitral stenosis Diastolic; Apex (heard best None Loud 51, tapping apex lnterval between 52 and low-pitched, in left lateral beat, opening snap after opening snap is short in rumble; decubitus 52 if leaflets mobile, severe mitral stenosis decrescendo position) irregular pulse if AF lntensity of murmur present correlates with transvalvular gradient P2 may be loud if pulmonary hypertension present Mitral Systolic; holo- Apex Axilla or back, Systolic click in mitral valve Acute severe regurgitation regurgitation mid-, or late occasionally prolapse; 53; apical may have soft or no systolic; anteriorly to impulse hyperdynamic holosystolic murmur, mitral blowing or precordium and may be displaced if inflow rumble, or 53 musical dilated left ventricle; in mitralvalve prolapse, Valsalva maneuver moves onset of clicks and murmur closerto 51; handgrip maneuver increases murmur intensity (Continued on the nert page) 31

Cardiovascular Medicine STUDY TABLE: Valvular and Other Cardiac Lesions and TheirAssociated Examination Findings (Continued) Cardiac Characteristic Location Radiation Associated Findings Severity and Pitfalls Condition Murmur Tricuspid Holosystolic LLSB LUSB Merged and prominent c Right ventricular impulse regurgitation and v waves in jugular below sternum venous pulse; murmur Pulsatile, enlarged liver increases during with possible ascites inspiration Murmur may be high- pitched if associated with severe pulmonary hypertension Tricuspid Diastolic; LLSB None Elevated central venous Low-pitched frequency ste nosl s low-pitched, pressure with prominent may be difficultto decrescendo; a wave, signs of venous auscultate, especially at increased congestion (hepato- higher heart rate intensity during megaly, ascites, edema) inspiration Pulmonary valve Systolic; LUSB Left clavicle Pulmonic ejection click lncreased intensity of stenosls crescendo- after Sr (diminishes with murmur with late peaking decrescendo inspiration) Pulmonary valve Diastolic, LLSB None Loud P2 if pulmonary Murmur may be minimal or regu rgitation decrescendo hypertension present absent if severe because of minimal difference in pulmonary artery and right ventricular diastolic pressures

STUDY TABLE: Valvular and Other Cardiac Lesions and TheirAssociated Examination Findings (Continued) Cardiac Characteristic Location Radiation Associated Findings Severity and Pitfalls Condition Murmur Tricuspid Holosystolic LLSB LUSB Merged and prominent c Right ventricular impulse regurgitation and v waves in jugular below sternum venous pulse; murmur Pulsatile, enlarged liver increases during with possible ascites inspiration Murmur may be high- pitched if associated with severe pulmonary hypertension Tricuspid Diastolic; LLSB None Elevated central venous Low-pitched frequency ste nosl s low-pitched, pressure with prominent may be difficultto decrescendo; a wave, signs of venous auscultate, especially at increased congestion (hepato- higher heart rate intensity during megaly, ascites, edema) inspiration Pulmonary valve Systolic; LUSB Left clavicle Pulmonic ejection click lncreased intensity of stenosls crescendo- after Sr (diminishes with murmur with late peaking decrescendo inspiration) Pulmonary valve Diastolic, LLSB None Loud P2 if pulmonary Murmur may be minimal or regu rgitation decrescendo hypertension present absent if severe because of minimal difference in pulmonary artery and right ventricular diastolic pressures Benign Midsystolic, RUSB None Normal intensity of ,A2, May be present in (innocent)flow grade 1/6 or normal splitting of 52, no conditions with increased murmur 2/6 in intensity radiation flow (e.g., pregnancy, fever, anemia, hyperthyroidism) Hypertrophic Systolic, LLSB None Enlarged, hyperdynamic Murmur may not be obstructive crescendo- apical impulse; bifid present in nonobstructive cardiomyopathy decrescendo carotid impulse with delay; hypertrophic increased intensity during cardiomyopathy Valsalva maneuver or with squatting to standing Atrial septal Systolic, RUSB None Fixed split 52; right May be associated with defect crescendo- ventricular heave; rarely, pulmonary hypertension decrescendo tricuspid inflow murmur with increased intensity of P2, pulmonary valve regurgitation Ventricularseptal Holosystolic LLSB None Palpable thrill; murmur Murmur intensity and defect increases with handgrip duration decrease as maneuver pulmonary hypertension develops (Eisenmenger syndrome) Cyanosis if Eisenmenger syndrome develops

Benign Midsystolic, RUSB None Normal intensity of ,A2, May be present in (innocent)flow grade 1/6 or normal splitting of 52, no conditions with increased murmur 2/6 in intensity radiation flow (e.g., pregnancy, fever, anemia, hyperthyroidism) Hypertrophic Systolic, LLSB None Enlarged, hyperdynamic Murmur may not be obstructive crescendo- apical impulse; bifid present in nonobstructive cardiomyopathy decrescendo carotid impulse with delay; hypertrophic increased intensity during cardiomyopathy Valsalva maneuver or with squatting to standing Atrial septal Systolic, RUSB None Fixed split 52; right May be associated with defect crescendo- ventricular heave; rarely, pulmonary hypertension decrescendo tricuspid inflow murmur with increased intensity of P2, pulmonary valve regurgitation Ventricularseptal Holosystolic LLSB None Palpable thrill; murmur Murmur intensity and defect increases with handgrip duration decrease as maneuver pulmonary hypertension develops (Eisenmenger syndrome) Cyanosis if Eisenmenger syndrome develops upper sternal border.

Benign Midsystolic, RUSB None Normal intensity of ,A2, May be present in (innocent)flow grade 1/6 or normal splitting of 52, no conditions with increased murmur 2/6 in intensity radiation flow (e.g., pregnancy, fever, anemia, hyperthyroidism) Hypertrophic Systolic, LLSB None Enlarged, hyperdynamic Murmur may not be obstructive crescendo- apical impulse; bifid present in nonobstructive cardiomyopathy decrescendo carotid impulse with delay; hypertrophic increased intensity during cardiomyopathy Valsalva maneuver or with squatting to standing Atrial septal Systolic, RUSB None Fixed split 52; right May be associated with defect crescendo- ventricular heave; rarely, pulmonary hypertension decrescendo tricuspid inflow murmur with increased intensity of P2, pulmonary valve regurgitation Ventricularseptal Holosystolic LLSB None Palpable thrill; murmur Murmur intensity and defect increases with handgrip duration decrease as maneuver pulmonary hypertension develops (Eisenmenger syndrome) Cyanosis if Eisenmenger syndrome develops upper sternal border. Aortic Stenosis Diagnosis T'he most common cause of AS is progressive degenerative disease of a normal trileaflet valve that is usually diagnosed in patients aged >60 years. Patients with a congenital bicuspid aortic valve usually present at a younger age (+0 60 years).

Benign Midsystolic, RUSB None Normal intensity of ,A2, May be present in (innocent)flow grade 1/6 or normal splitting of 52, no conditions with increased murmur 2/6 in intensity radiation flow (e.g., pregnancy, fever, anemia, hyperthyroidism) Hypertrophic Systolic, LLSB None Enlarged, hyperdynamic Murmur may not be obstructive crescendo- apical impulse; bifid present in nonobstructive cardiomyopathy decrescendo carotid impulse with delay; hypertrophic increased intensity during cardiomyopathy Valsalva maneuver or with squatting to standing Atrial septal Systolic, RUSB None Fixed split 52; right May be associated with defect crescendo- ventricular heave; rarely, pulmonary hypertension decrescendo tricuspid inflow murmur with increased intensity of P2, pulmonary valve regurgitation Ventricularseptal Holosystolic LLSB None Palpable thrill; murmur Murmur intensity and defect increases with handgrip duration decrease as maneuver pulmonary hypertension develops (Eisenmenger syndrome) Cyanosis if Eisenmenger syndrome develops upper sternal border. Aortic Stenosis Diagnosis T'he most common cause of AS is progressive degenerative disease of a normal trileaflet valve that is usually diagnosed in patients aged >60 years. Patients with a congenital bicuspid aortic valve usually present at a younger age (+0 60 years). Cardinal symptoms of'AS are dyspnea, angina, and syncope.

Aortic Stenosis Diagnosis T'he most common cause of AS is progressive degenerative disease of a normal trileaflet valve that is usually diagnosed in patients aged >60 years. Patients with a congenital bicuspid aortic valve usually present at a younger age (+0 60 years). Cardinal symptoms of'AS are dyspnea, angina, and syncope. 32

Cardiovascular Medicine The primary diagnostic modality is TTE, which may show: r echocardiogram showing left atrial enlargement and LVH . calcified aortic valve leaflets with restricted motion DOil'T BE TRICKED o Echocardiography may significantly underestimate the transvalvular gradient in patients with severe LV dysfunction. o Do not select exercise stress testing for symptomatic patients with AS. Treatment The indications for aortic valve replacement in severe AS are: . symptoms of dyspnea, angina, presyncope, syncope, or HF . ejection fraction <50% in an asymptomatic patient . a concomitant cardiac surgical procedure for other indications For symptomatic patients aged 65 to B0 years, either SAVR or TAVI is appropriate following shared decision making. TAVI is preferred to SAVR for symptomatic patients with severe AS: . aged >80 years . younger patients with <10 years' life expectancy o any age with a high or prohibitive surgical risk Medical therapy does not stall the progression of disease but is indicated for patients with symptoms and lV dysfunction or hypertension who are awaiting valve repair or replacement. Treat these patients with guideline directed medical therapy. DON'T BE TRICKED . Do not select balloon valvuloplasty as a definitive treatment for AS in adults. o Medical therapy with statins does not alter the natural history of AS. Follow-up Recommended follow up involves obtaining a history and physical examination, focusing on findings consistent with AS indi cating the need for surgery and serial echocardiography (TTE), with intervals determined by AS severity (mild, moderate, or severe). TEST YOURSEIF A 71-year-old man has dyspnea with exertion. An echocardiogram shows severe tricuspid aortic stenosis without regurgitation. ANSWER: Choose TAVI over SAVR. Bicuspid Aortic Valve Diagnosis Bicuspid aortic valve disease is the most common congenital heart abnormality. A bicuspid aortic valve may occur with other cardiovascular and systemic abnormalities, including aortic coarctation, aneurysm of the sinuses of Valsalva, PDA, and aortic 33

Cardiovascular Medicine aneurysm and dissection. In patients with a bicuspid aortic valve, the ascending aorta and aortic arch should be examined for aortopathy with TTE. First-degree relatives of patients with a bicuspid aortic valve and aortopathy should be screened with echocardiography. Treatment Surgical aortic valve replacement is first-line therapy for a stenotic bicuspid aortic valve. Recommendations regarding when to intervene are the same as for tricuspid aortic valves. For a regurgitant bicuspid aortic valve, valve replacement is the treatment of choice when regurgitation is clinically significant, manifesting as symptomatic HF or asymptomatic LVEF <50%. Aortic root repair indications: . severe AS or regurgitation requiring replacement and aortic diameter >4.5 cm o aortic root diameter >5 cm with an additional risk factor for dissection o aortic root diameter >5.5 cm without risk factors Follow-up The ascending aortic diameter should be assessed at least annually by echocardiography ifthe aortic root or ascending aorta dimension is >4.5 cm. Aortic Regurgitation Diagnosis AR is classified as chronic or acute. Acute severe AR usually is caused by IE or aortic dissection. Chronic severe AR is most com- monly associated with dilated ascending aorta from hypertension or primary aortic disease, calcific AS, bicuspid aortic valve, or rheumatic disease. Findings in chronic severe AR include: . angina, orthopnea, and exertional dyspnea o widened pulse pressure . left axis deviation and LVH on ECG . cardiomegaly and aortic root dilatation and calcification on chest x-ray Acute AR is associated with a short, soft, and sometimes inaudible diastolic murnur and normal heart size and pulse pressure. Treatment Schedule immediate aortic valve replacement for patients with acute AR. Bridging medical therapy includes sodium nitro- prusside and IV diuretics. Indications for open surgical valve replacement: . symptoms (dyspnea, angina) . Ieft ventricular EF <55% . undergoing other cardiac surgery TAVI is effective in select symptomatic patients who are not surgical candidates. ACE inhibitors or ARBs and nifedipine may be used in patients with chronic AR and hypertension. 34

Cardiovascular Medicine DON'T BE TRICKED . Do not select p-blockers or intra-aortic balloon pumps for patients with acute AR, because both may worsen the AR. . Therapy with ACE inhibitors or calcium channel blockers does not delay the need for surgery in asymptomatic patients with chronic AR. Follow-up Recommended follow up involves obtaining history and physical examination, focusing on findings consistent with HF, and performing serial echocardiography (TTE), with intervals determined by AR severity (mild, moderate, or severe). TEST YOURSEIF A 36 year old man with aortic valve endocarditis is transferred to the ICU because of the abrupt onset of hypotension and hypox emia. Physical examination findings include a BP of 80/30 mm Hg, HR of 120/min, bilateral crackles, and a gallop. No murmurs are heard. ANSWER: For diagnosis, choose acute AR. For management, select echocardiography, IV sodium nitroprusside, and dobutamine as a bridge to urgent surgery. Mitral Stenosis Diagnosis Mitral stenosis usually presents 20 to 40 years after an episode of RF. The most common symptoms are fatigue, orthopnea, and paroxysmal nocturnal dyspnea. Patients may have a history of AF or systemic thromboembolism. Chest x ray shows an enlarged pulmonary artery left atrium, right ventricle, and right atrium. The ECG shows RV hypertrophy and a notched P wave duration >0.12 s in lead II (P mitrale). TTE is used to assess disease severity of mitral stenosis by measuring valve area and transvalvular gradient. TEE provides better visualization for the presence of left atrial appendage thrombus. Treatment Percutaneous balloon mitral commissurotomy is first line therapy for symptomatic patients and for asymptomatic patients with severe mitral stenosis or moderate mitral stenosis associated with PH. Medical therapy lor mitral stenosis consists of diuretics or long-acting nitrates, which may help improve symptoms such as dyspnea. In addition, p-blockers or nondihydropyridine calcium channel blockers can lower HR and improve LV diastolic filling time.

Treatment Percutaneous balloon mitral commissurotomy is first line therapy for symptomatic patients and for asymptomatic patients with severe mitral stenosis or moderate mitral stenosis associated with PH. Medical therapy lor mitral stenosis consists of diuretics or long-acting nitrates, which may help improve symptoms such as dyspnea. In addition, p-blockers or nondihydropyridine calcium channel blockers can lower HR and improve LV diastolic filling time. TESTYOURSETF A 28-year-old woman who is 29 weeks pregnant has progressive dyspnea. Physical examination shows tachycardia, JVD, a paraster- nal impulse, an opening snap, and a grade 2/6 diastolic rumble with presystolic accentuation. ANSWER: This is the classic presentation for mitral stenosis with associated increased intravascular volume in a pregnant patient. For management, select metoprolol to allow greater time for LV diastolic filling and relief of PH. DO]I'T BE TRICKED o Treat all patients with mitral stenosis and AF, regardless of CHATDS2-VASc score, with warfarin 35

Cardiovascular Medicine Adult Congenital Heart Disease Lesion Exam, ECG, and CXR Findings Late Complications and Repair Patent foramen ovale Normal Paradoxical embolism Repair: Percutaneous closure plus aspirin to prevent recurrent stroke of un known source Ostium secundum ASD splittins 52, pulmonary midsystolic Right heart enlargement, AF };frJi""O Repair: device closure for right heart enlargement, ECG: incomplete RBBB, RA enlargement, RAD large right-to-left shunt, symptoms. CXR: right heart enlargement, prominent After repair: residual shunt (rare) pulmona ry artery, i ncreased pu monary vascularity I

Lesion Exam, ECG, and CXR Findings Late Complications and Repair Patent foramen ovale Normal Paradoxical embolism Repair: Percutaneous closure plus aspirin to prevent recurrent stroke of un known source Ostium secundum ASD splittins 52, pulmonary midsystolic Right heart enlargement, AF };frJi""O Repair: device closure for right heart enlargement, ECG: incomplete RBBB, RA enlargement, RAD large right-to-left shunt, symptoms. CXR: right heart enlargement, prominent After repair: residual shunt (rare) pulmona ry artery, i ncreased pu monary vascularity I Ostium primum ASD splittins 52, pulmonary midsystolic Right heart enlargement, AE MR (from mitralvalve fffrJI"O cleft), PH (rare) ECG: LAD, first-degree AV block Repair: surgical closure CXR: right heart enlargement, prominent After repair: residual shunt (rare), MR (from mitral pulmonary artery increased pulmonary vascularity valve cleft), LV outflow tract obstruction Large VSD Exam: loud holosystolic murmur obliterating 52 PH with associated RA and RV enlargement, RV hypertrophy, Eisenmenger synd rome ECG: RV or RV/LV hypertrophy Repair: volume overload CXR: RA and RV enlargement, increased pulmonary vascular markings; with PH: prominent After repair: residualVSD, residual shunt (rare) centra I pu I monary arteries, reduced peripheral pulmonary vascular markings Large PDA Exam: continuous "machinery" murmur beneath Endocarditis, RVfailure, PH, Eisenmenger left clavicle syndrome ECG: LA enlargement, LV hypertrophy; with PH: RV Repair: closure hypertrophy After repair: residual shunt (rare) CXR: cardiomegaly, increased pulmonary vascular markings; with PH: prominent central pulmonary arteries, reduced peripheral pulmonaryvascular markings Pulmonary valve stenosis Exam: RV hypertrophy, prominent jugulara wave, Repair: pulmonary balloon valvuloplasty palpable right ventricular lift Afte r re pai r: seve re pu mo na ry va lve re g u rg itation I

Ostium primum ASD splittins 52, pulmonary midsystolic Right heart enlargement, AE MR (from mitralvalve fffrJI"O cleft), PH (rare) ECG: LAD, first-degree AV block Repair: surgical closure CXR: right heart enlargement, prominent After repair: residual shunt (rare), MR (from mitral pulmonary artery increased pulmonary vascularity valve cleft), LV outflow tract obstruction Large VSD Exam: loud holosystolic murmur obliterating 52 PH with associated RA and RV enlargement, RV hypertrophy, Eisenmenger synd rome ECG: RV or RV/LV hypertrophy Repair: volume overload CXR: RA and RV enlargement, increased pulmonary vascular markings; with PH: prominent After repair: residualVSD, residual shunt (rare) centra I pu I monary arteries, reduced peripheral pulmonary vascular markings Large PDA Exam: continuous "machinery" murmur beneath Endocarditis, RVfailure, PH, Eisenmenger left clavicle syndrome ECG: LA enlargement, LV hypertrophy; with PH: RV Repair: closure hypertrophy After repair: residual shunt (rare) CXR: cardiomegaly, increased pulmonary vascular markings; with PH: prominent central pulmonary arteries, reduced peripheral pulmonaryvascular markings Pulmonary valve stenosis Exam: RV hypertrophy, prominent jugulara wave, Repair: pulmonary balloon valvuloplasty palpable right ventricular lift Afte r re pai r: seve re pu mo na ry va lve re g u rg itation I ECG: if RV systolic pressure >60 mm Hg: RA after pulmonary valvotomy or valvuloplasty enlargement, RAD, RV hypertrophy CXR: Pulmonary artery dilatation, RA enlargement may be noted Aortic coarctation Exam: diminished femoral pulses, radial-femoral Hypertension (75% of cases), bicuspid aortic valve pulse delay, continuous murmur over back (>50% of cases), increased risk for aortic aneurysm and intracranial aneurysm ECG: LV hypertrophy Repair: balloon dilation for hypertension CXR: "figure 3 sign" beneath aortic arch, rib notching from collateral vessels Aft er re pa i r: Recoa rctation, hyperte nsion, aortic aneurysm CXR = chest radiography; LA = left atriai; LAD: left axis deviation; RA: right atrial; RAD: right axis deviation.

ECG: if RV systolic pressure >60 mm Hg: RA after pulmonary valvotomy or valvuloplasty enlargement, RAD, RV hypertrophy CXR: Pulmonary artery dilatation, RA enlargement may be noted Aortic coarctation Exam: diminished femoral pulses, radial-femoral Hypertension (75% of cases), bicuspid aortic valve pulse delay, continuous murmur over back (>50% of cases), increased risk for aortic aneurysm and intracranial aneurysm ECG: LV hypertrophy Repair: balloon dilation for hypertension CXR: "figure 3 sign" beneath aortic arch, rib notching from collateral vessels Aft er re pa i r: Recoa rctation, hyperte nsion, aortic aneurysm CXR = chest radiography; LA = left atriai; LAD: left axis deviation; RA: right atrial; RAD: right axis deviation. DOil'T BETRICKED . Closure ofan ASD is contraindicated ifshunt reversal (right to left) is present. . A small ASD with no associated symptoms or right heart enlargement can be followed clinically TESTYOURSELF An asymptomatic 26-year old woman who is 30 weeks pregnant has a recently discovered heart murmur. physical examination shows a right parastema.l lift, a normal S,, fixed splitting of Sr, and a grade 2/6 early systolic murmur at the upper left sternal border. 38

Cardiovascular Medicine ANSWER: Fbr diagnosis, choose ASD.'l'he murmllr is often first discoverccl during pregnancy as a result of increased intravascular volume. I II ti: i Ostium Secundum Atrial Septal Defect: The ECG shows right axis deviation, partial RBBB, and evidence of RV hypertrophy characteristic of o:,tium secun' dum ASD. DOIII,T BE TRICKED . Obtain BP in the legs in young people presenting with unexplained hypertension. TEST YOURSELF A :15 year old woman reports colcl teet and leg cramping when walking long clistances. LIP is 160/90 mm Hg. Cardiac examina tion shows a sustained apical impulse, an early systolic ejection sound, and an early systolic murntllr at the upper right sternal border. ANSWER: Fbr diagnosis, choose coarctation of'the aorta with an associated bicuspid aortic valve. Aortic Coarctation: A chest x-ray sh ows i nfe ri or ri b n otch i ng and the cl assic "fig u re I nfective Endocarditis 3 sign" (an indented aortic wall at the site of the coarctation with dil,rtation above and below the coarctation). Prevention I'rovide prophylaxis for II'. only in patients with the highest risk' including those with: o prosthetic cardiac virlve . history of'lE . unrepaired cyanotic congenital heart disease 39

Cardiovascular Medicine . repaired congenital heart defect with prosthesis or shunt ((6 months postprocedure) or residual defect . valvulopathy following cardiac transplantation o prosthetic material used for cardiac valve repair (annuloplasty rings and chords) Antibiotic prophylaxis is reasonable in patients at high risk for IE before dental procedures that involve mucosal bleeding. Antibiotic prophylaxis is not recommended in patients at high risk for IE undergoing nondental procedures (e.g., TEE, EGD, colonoscopy, or cystoscopy) in the absence ofactive infection. Most patients requiring prophylaxis willbe undergoing dental procedures, and the indicated antibiotic is oral amoxicillin 30 to 60 min utes before the procedure. If the patient is allergic to penicillin, use cephalexin, azithromycin, clarithromycin, or clindamycin. Diagnosis Fever, malaise, and fatigue are sensitive but nonspecific symp- toms associated with IE. Suggestive physical examination find ings include: . new cardiac murmur o new onset HF o conduction abnormalities on ECG (suggests perivalvular abscess) o petechiae, splinter hemorrhages o Osler nodes (violaceous, circumscribed, painful nodules fbund in the pulp ofthe fingers and toes) . Janeway lesions (painless. erythematous, macular lesions found on the soles and palms) o Roth spots (hemorrhagic lesions of the retina) . leukocytosis, anemia, and hematuria o focal neurologic signs (septic emboli) Osler ilodes:0sler nodes are red to purple painful papules, papulopustules, or nodules found in the pulp of fingers or occasionally on hands and feet. . multiple bilateral small nodules on chest x ray (septic emboli) ffi*l;., Janeway lesions: Janeway lesions are macular, erythematous, nontender micro Septic Pulmonary Emboli: Septic pulmonary emboli are characterized by abscesses in the dermis of the palms and soles caused by septic emboli that are multifocal, pakhy, and otherwise ill-defined infiltrates; cavitation may ocrur. considered pathoqnomonir for lE. 40

Cardiovascular Medicine TTE is the initial imaging test in all patients. TEE is recommended in the following situations: . all patients with known or suspected IE and nondiagnostic TTE . when complications have developed or are clinically suspected . when intracardiac device leads are present Diagnose endocarditis in patients with two major Duke criteria, one major and three minor criteria, five minor criteria, or pathologic confirmation. STUDY TAB!"f, I Diagnosing Endocarditis With Modified Dul<e Criteria Major Duke Criteria Minor Duke Criteria Positive blood culture for endocarditis x 2 or single positive Predisposing heart condition or injection drug use blood culture for Coxiella burnetii or antiphase I lgG antibody Fever titer >1 :800 Embolic vascular phenomena Positive echocardiogram New valvular regurgitation lmmunologic phenomena (GN or rheumatoid factor) Positive blood culture not meeting major criteria DOil'T BE TRICKED . Don't give antimicrobial prophylaxis to patients with MVP or other low-risk valvular abnormalities. . Look for colon cancer in patients with Streptococcus bouis or Clostridium septicum endocarditis. Treatment Indications for surgery include: . valvular dysfunction and acute HF o left-sided IE caused by Staphylococcus oureus, fungal infection, or highly resistant organisms o heart block . annular or aortic abscess . recurrent systemic embolization on antibiotic therapy Splinter Hemorrhages: A fingernail with splinter hemonhages, which are non- blanching, linear, reddish-brown lesions found under the nail bed. Reprinted from o prosthetic valve endocarditis with relapsing infection Sparkla/Wikimedia Commons/Public Domain. or dehiscence o S. cureus prosthetic valve endocarditis Patients with suspected IE and good cardiovascular function do not require empiric treatment before culture results. In decompensated patients, start empiric antibiotics immediately after blood cultures are obtained.

. valvular dysfunction and acute HF o left-sided IE caused by Staphylococcus oureus, fungal infection, or highly resistant organisms o heart block . annular or aortic abscess . recurrent systemic embolization on antibiotic therapy Splinter Hemorrhages: A fingernail with splinter hemonhages, which are non- blanching, linear, reddish-brown lesions found under the nail bed. Reprinted from o prosthetic valve endocarditis with relapsing infection Sparkla/Wikimedia Commons/Public Domain. or dehiscence o S. cureus prosthetic valve endocarditis Patients with suspected IE and good cardiovascular function do not require empiric treatment before culture results. In decompensated patients, start empiric antibiotics immediately after blood cultures are obtained. Narrow antibiotic selection after susceptibilities are known. Continue treatment for 4 to 6 weeks except in uncomplicated right-sided native valve endocarditis caused by MSSA, which can be treated for 2 weeks with a combination of nafcillin, oxacillin, or flucloxacillin. DON'T BE TRICKED . Oral antibiotics are not recommended for treatment of IE. 41

Cardiovascular Medicine Follow-up Most AAAs are asymptomatic. Abdominal ultrasonography surveillance intervals are based on aortic diameter: . <4 cm -+ every 2 to 3 years o 4.0-5.5 cm -+ every 6 to 12 months Aortic Atheroemboli Diagnosis Plaque in the thoracic aorta is associated with an increased risk of clinical thromboembolism, including TIA and stroke. Less commonly, cholesterol crystal embolization can occur, resulting in livedo reticularis, gangrene of the digits (blue toe syndrome), transient vision loss (a golden or brightly refractile cholesterol body within a retinal artery [Hollenhorst plaquel is patho- 1 gnomonic), and AKI, typically following recent cardiac or aortic surgery or other intravascular procedures (catheterization). l Testing Aortic atheromas are often detected incidentally on imaging studies. Uuedo Reticularis: Livedo reticularis in the lower extremities caused by choles- Hollenhorst Plaque: A highly refractile yellow body (cholesterol crystals) terol emboli following cardiac catheterization. within a retinal artery. Treatment Aortic atheromatous plaques represent a CAD risk equivalent, and patients should be considered for antiplatelet and statin therapies in addition to other risk factor interventions. Peripheral Artery Disease Screening The USPSTF has concluded that the current evidence is insufficient to recommend routine screening for PAD. Diagnosis PAD most commonly involves the lower extremities and is the result of atherosclerosis involving the aorta and branch vessels. Risk factors are the same as traditional ASCVD risk factors. 44

Cardiovascular Medicine Intermittent claudication is the classic sign of PAD. Most patients with PAD have coexisting coronary artery and cerebrovas- cular disease. Differentiate claudication caused by PAD from claudication caused by spinal stenosis. $IUDY TABLE: Discriminatinq Claudication from Pseudociaudication Characteristic Claudication Pseudoclaudication (Spinal Stenosis) Nature of discomfort Cramping, tightness, aching, fatigue Same as claudication plus tingling, burning, numbness, weakness Location of discomfort Buttock, hip, thigh, calt foot Same as claudication, most often bilateral Exercise induced Yes Variable Walking distance at onset of symptoms Consistent Variable Discomfort occurs with standing still No Yes Action for relief Stand or sit Sit, flexion at the waist Time to relief <5 minutes (30 minutes Testing Resting ABI should be performed on all patients with a history or physical examination suggesting PAD. Exercise treadmill ABI testing should be performed for patients with normal or borderline resting ABI values and unexplained exertional leg symptoms. Noninvasive angiography with duplex ultrasonography, CTA, or MRA is performed for anatomic delineation of PAD in patients requiring surgical or endovascular intervention. Interpret the ABI: o ABI for each side is the ratio of the highest systolic ankle BP for that side to the highest systolic arm BP (regardless of side). o Normal ABI is >0.9 to <1.40. r ABI <0.90 is compatible with PAD. o False normal ABI occurs in patients with diabetes with calcified, noncompressible arteries (ABI >1.40). A toe brachial index is used for diagnosis in patients with an ABI >7.40; a toe-brachial index <0.70 indicates PAD. Recall the "six P's" to diagnose acute limb ischemia:

o ABI for each side is the ratio of the highest systolic ankle BP for that side to the highest systolic arm BP (regardless of side). o Normal ABI is >0.9 to <1.40. r ABI <0.90 is compatible with PAD. o False normal ABI occurs in patients with diabetes with calcified, noncompressible arteries (ABI >1.40). A toe brachial index is used for diagnosis in patients with an ABI >7.40; a toe-brachial index <0.70 indicates PAD. Recall the "six P's" to diagnose acute limb ischemia: . pain o paresthesias . pallor . paralysis r pulselessness r poikilothermia (coolness) Acute ischemia can be caused by in situ thrombosis or remote embolization. Anticoagulation and diagnostic angiographl' should be performed immediately in patients with acute limb ischemia to define the anatomic level of occlusion. I DO]{'T BE TRICKED o When the ABI is >1.40, select a toe-brachial index to provide a better assessment of lower extremity perfusion. Treatment Exercise training is the most effective treatment for improvement in functional status in patients with PAD. 45