Browse the corpus

Arrhythmias l.' I FIGUnE lT.ECGshowingMobitztype2second-degreeatrioventricularblock.Pwavesareblockedintermittently(arows),andthePRinterval isfixed.Although2:1 block can be a manifestation of Mobitz type 1 second-degree atrioventricular block, note the wide QRS complexes, which are more consistent with block below the compact atrioventricular node. FIGURE 18. lnthisECG,thePwaves(shortanowslandtheORScomplexes(longarrows)arenotassociatedwitheachother,indicatingthepresenceof completeheart block. 44

I I Arrhythmias Treatment Types of implar.rted cardiac electronic devices, their func In patients with symptomatic ltradl,cardia and hen.rodynamic tions, and their general indications are reviewed in Table 16. distress. atropine should be aciurinistered. Ifatropine is ineflbc Figure 19 shows a leadless pacemaker in the region of the right tive. chronotnrpic drug intusions (e.g.. dopamine or epineph ventricle. I

Treatment Types of implar.rted cardiac electronic devices, their func In patients with symptomatic ltradl,cardia and hen.rodynamic tions, and their general indications are reviewed in Table 16. distress. atropine should be aciurinistered. Ifatropine is ineflbc Figure 19 shows a leadless pacemaker in the region of the right tive. chronotnrpic drug intusions (e.g.. dopamine or epineph ventricle. I rine) can be giver-r until transcutaneous pacing or a temporary rEY POI]ITS pacing wire (pref'erred) can be implemented. 1'emporary pac . Permanent pacing is indicated fbr symptomatic brady ing is indicated fbr transient conditions causing l.remodynami cardia without reversible cause. \ cally unstable bradycardia or lsystole. In henrodynamically stirble patients. reversible and . Patients who have atrioventricular (AV) and infranodal extrinsic causes of bradycardi:r should always be addressed conduction disturbances with a high risk for progress before more invasive measures. such as permanent pacing, ing to complete heart block or asystole, such as alter- are considered. Common indications for permanent pacing nating bundle branch block, high degree AV block, or include: Mobitz type 2 second-degree AV block, should receive a permanent pacemaker. . Symptom:rtic bradycarclia r,r'ithout reversible ciruse . Pernranent AF and symptomatic bradycardia o Alternating bundle branch block (signifies higl.r risk con Approach to the Patient duction disease) With Tachycardia o Complete heart block. high degree AV block. or Mobitz Clinical Presentation and Evaluation I type 2 sccond degree AV block. regardless of symptoms Patients with tachycardia (heart rate >100,'min) may be Patients with stable letl bundle branch block or right asynlptomatic or experience tachypalpitations, a sens:rtion of bundle branch block with or without a prolonged PR interval skipped beats, light l.readedness, clizziness. chest discomfort, do not require permanent pacing because intraventricular dyspnea. exertional intolerance, tatigue, progressive heart fail conductior.r clelays have a low risk for progressing to complete ure, near syncope, or syncope. In :rsymptomatic patients, heart block (1'){, 3'X, per year). tachycardia nray be discovered incidentally.

rine) can be giver-r until transcutaneous pacing or a temporary rEY POI]ITS pacing wire (pref'erred) can be implemented. 1'emporary pac . Permanent pacing is indicated fbr symptomatic brady ing is indicated fbr transient conditions causing l.remodynami cardia without reversible cause. \ cally unstable bradycardia or lsystole. In henrodynamically stirble patients. reversible and . Patients who have atrioventricular (AV) and infranodal extrinsic causes of bradycardi:r should always be addressed conduction disturbances with a high risk for progress before more invasive measures. such as permanent pacing, ing to complete heart block or asystole, such as alter- are considered. Common indications for permanent pacing nating bundle branch block, high degree AV block, or include: Mobitz type 2 second-degree AV block, should receive a permanent pacemaker. . Symptom:rtic bradycarclia r,r'ithout reversible ciruse . Pernranent AF and symptomatic bradycardia o Alternating bundle branch block (signifies higl.r risk con Approach to the Patient duction disease) With Tachycardia o Complete heart block. high degree AV block. or Mobitz Clinical Presentation and Evaluation I type 2 sccond degree AV block. regardless of symptoms Patients with tachycardia (heart rate >100,'min) may be Patients with stable letl bundle branch block or right asynlptomatic or experience tachypalpitations, a sens:rtion of bundle branch block with or without a prolonged PR interval skipped beats, light l.readedness, clizziness. chest discomfort, do not require permanent pacing because intraventricular dyspnea. exertional intolerance, tatigue, progressive heart fail conductior.r clelays have a low risk for progressing to complete ure, near syncope, or syncope. In :rsymptomatic patients, heart block (1'){, 3'X, per year). tachycardia nray be discovered incidentally. \ TABLE 16. Cardiac lmplantable Electronic Devices forTreatment of Cardiac Rhythm Disorders Functions Device Components lndications Pacemaker Antitachycardia Defibrillation Function Pacing Transvenous Pulse generator and Sinus node dysfunction, Yes No No pacemaker intravascular leads (single AV block, nonreversible or dual chamber) symptomatic bradycardia Lea d I ess Pulse generator with tines Atrial fibrrillation with Yes (atrial No No pacemaker implanted directly into bradyca rdia, paroxysma I sensing and (see Figure 19) the cardiac chamber; no bradycardia (e.9., brief ve ntri cu la r leads sinus node dysfunction or paci ng ) AV block)

\ TABLE 16. Cardiac lmplantable Electronic Devices forTreatment of Cardiac Rhythm Disorders Functions Device Components lndications Pacemaker Antitachycardia Defibrillation Function Pacing Transvenous Pulse generator and Sinus node dysfunction, Yes No No pacemaker intravascular leads (single AV block, nonreversible or dual chamber) symptomatic bradycardia Lea d I ess Pulse generator with tines Atrial fibrrillation with Yes (atrial No No pacemaker implanted directly into bradyca rdia, paroxysma I sensing and (see Figure 19) the cardiac chamber; no bradycardia (e.9., brief ve ntri cu la r leads sinus node dysfunction or paci ng ) AV block) lmplantable Defibrillator and Monitoring and treatment Yes Yes Yes cardioverter intravascular leads (single of ventricu lar arrhythmias defibrillator or dual chamber) Su bcutaneous Defibrillator and a single Monitoring and treatment No No Yes implantable lead that are entirely under of ventricular arrhythmias cardioverler- the skin (extravascular); no defibrillator transvenous leads Cardiac Pulse generator and Restoring electrical Yes No No resynch ro n ization intravascular leads, synchrony in select therapy-paci ng including a pacing lead in patients with (cRr-P) the coronary sinus to symptomatic heart failure pace the left ventricle Cardiac Defibrillator and Restoring electrical Yes Yes Yes resynch ronization intravascular leads, synchrony between the thera py-defi bri llator including a pacing lead in ventricles in patients with (CRT D) the coronary sinus to heart failure; monitoring pace the left ventricle and treating ventricular a rrhyth mias

lmplantable Defibrillator and Monitoring and treatment Yes Yes Yes cardioverter intravascular leads (single of ventricu lar arrhythmias defibrillator or dual chamber) Su bcutaneous Defibrillator and a single Monitoring and treatment No No Yes implantable lead that are entirely under of ventricular arrhythmias cardioverler- the skin (extravascular); no defibrillator transvenous leads Cardiac Pulse generator and Restoring electrical Yes No No resynch ro n ization intravascular leads, synchrony in select therapy-paci ng including a pacing lead in patients with (cRr-P) the coronary sinus to symptomatic heart failure pace the left ventricle Cardiac Defibrillator and Restoring electrical Yes Yes Yes resynch ronization intravascular leads, synchrony between the thera py-defi bri llator including a pacing lead in ventricles in patients with (CRT D) the coronary sinus to heart failure; monitoring pace the left ventricle and treating ventricular a rrhyth mias AV = atrioventricular 45

Arrhythmias most forms of ambulatory monitoring in terms of diagnostic value (see Diagnostic Testing in Cardiologr for strategies in selecting an appropriate monitoring device). Based on ECG findings. tachyarrhythmias are traditionalll' categorized as supraventricular or ventricular. Supraventricular arrhythmias involve conduction through the AV node and are characterized by normal appearing QRS complexes unless complicated by an aberrant ventricular condition (e.g.. bundle branch block). Ventricular arrhythmias originate belor,r'the AV node and are characterized by abnormal appearing and widened QRS compleres. In addition to a thorough history'"r'ith medication review and physical examination, thyroid function testing and echocardiography may be considered in select patients $'ith tachycardia.

most forms of ambulatory monitoring in terms of diagnostic value (see Diagnostic Testing in Cardiologr for strategies in selecting an appropriate monitoring device). Based on ECG findings. tachyarrhythmias are traditionalll' categorized as supraventricular or ventricular. Supraventricular arrhythmias involve conduction through the AV node and are characterized by normal appearing QRS complexes unless complicated by an aberrant ventricular condition (e.g.. bundle branch block). Ventricular arrhythmias originate belor,r'the AV node and are characterized by abnormal appearing and widened QRS compleres. In addition to a thorough history'"r'ith medication review and physical examination, thyroid function testing and echocardiography may be considered in select patients $'ith tachycardia. Antiarrhythmic Drugs Antiarrhythmic agents have trerditionally been organized according to primary mechanism of action using the Vaughan Williams classification system (Table 17). although most antiar- FIGU RE 1 9. Chest radiograph (posteroanterior view) showing a leadless rhyhmic drugs exert their effects through several mechanisms. pacemaker in the region of the right ventricle, which could be verified to be Class I and class III agents are the most effectile antiarrhl'thmic retrosternal on a lateral film. Prior sternotomy and signilicant ascending aorlic calcification are also noted. drugs: however, due to their membrane active effects. they carry some paradoxical risk of inducing arrhythmia. Documentation of tachycardia on ECG and correlation Flecainide and propafenone are the most commonly used with symptoms is the key component of the diagnostic evalu class I agents (lC)r they are primarily used to treat atrial ation, and a 12 lead ECG should be obtained in all patients arrhythmias and usually in conjunction with AV nodal block- with stable tachycardia. A 12 lead ECG recorded during symp- ers to prevent 1:1 atrial flutter. Toxicity can manif'est as toms, although often not possible to obtain, is far superior to QRS widening (Figure 2o and Figure 2l). Class tC agents are

Antiarrhythmic Drugs Antiarrhythmic agents have trerditionally been organized according to primary mechanism of action using the Vaughan Williams classification system (Table 17). although most antiar- FIGU RE 1 9. Chest radiograph (posteroanterior view) showing a leadless rhyhmic drugs exert their effects through several mechanisms. pacemaker in the region of the right ventricle, which could be verified to be Class I and class III agents are the most effectile antiarrhl'thmic retrosternal on a lateral film. Prior sternotomy and signilicant ascending aorlic calcification are also noted. drugs: however, due to their membrane active effects. they carry some paradoxical risk of inducing arrhythmia. Documentation of tachycardia on ECG and correlation Flecainide and propafenone are the most commonly used with symptoms is the key component of the diagnostic evalu class I agents (lC)r they are primarily used to treat atrial ation, and a 12 lead ECG should be obtained in all patients arrhythmias and usually in conjunction with AV nodal block- with stable tachycardia. A 12 lead ECG recorded during symp- ers to prevent 1:1 atrial flutter. Toxicity can manif'est as toms, although often not possible to obtain, is far superior to QRS widening (Figure 2o and Figure 2l). Class tC agents are .-'*J{ ^ t.

Antiarrhythmic Drugs Antiarrhythmic agents have trerditionally been organized according to primary mechanism of action using the Vaughan Williams classification system (Table 17). although most antiar- FIGU RE 1 9. Chest radiograph (posteroanterior view) showing a leadless rhyhmic drugs exert their effects through several mechanisms. pacemaker in the region of the right ventricle, which could be verified to be Class I and class III agents are the most effectile antiarrhl'thmic retrosternal on a lateral film. Prior sternotomy and signilicant ascending aorlic calcification are also noted. drugs: however, due to their membrane active effects. they carry some paradoxical risk of inducing arrhythmia. Documentation of tachycardia on ECG and correlation Flecainide and propafenone are the most commonly used with symptoms is the key component of the diagnostic evalu class I agents (lC)r they are primarily used to treat atrial ation, and a 12 lead ECG should be obtained in all patients arrhythmias and usually in conjunction with AV nodal block- with stable tachycardia. A 12 lead ECG recorded during symp- ers to prevent 1:1 atrial flutter. Toxicity can manif'est as toms, although often not possible to obtain, is far superior to QRS widening (Figure 2o and Figure 2l). Class tC agents are .-'*J{ ^ t. :i !r t*.,nt *,..,,^ ., ) I ii i: I

:i !r t*.,nt *,..,,^ ., ) I ii i: I ;--!-^-r..-. ;1r.ir^ .rn,, i* rn,.., ,l j' li.'','.*. A. ... \r''-.-/4'.*.,.r" -r^ '.-^.{4a...,ti'*.'o-r-a.'' l "r.r,t'..r,'*. l ilr'ir\?'\',r \.d 1't i,,**.r..^.--r.-*-r'zL.- /^\,.r r'\-.r.'t,-^' -.*,rl^^. n ,t rt .l .l 1 ',: rltt' t'" | t ", 1 ^! t! r t' -i .. r 'l .J;i1 l, j r. I'li t

,t rt .l .l 1 ',: rltt' t'" | t ", 1 ^! t! r t' -i .. r 'l .J;i1 l, j r. I'li t t/i \!l ! t^/ i : :l I I ll : i , ,' J i: , tIGURE 20. ECGinapatientwithsignificantflecainidetoxicity,manilestingwithseverelyprolonged0RSduration,withbroadandveryunusual morphologyinthesetting of underlying atrial fibrillation orflutter. 46

Arrhythmias TABLE 17. Commonly Used Antiarrhythmic Medications Classification Mechanismof Examples Primary Use Side Effects Contraindications Action Potential ECG Effects

TABLE 17. Commonly Used Antiarrhythmic Medications Classification Mechanismof Examples Primary Use Side Effects Contraindications Action Potential ECG Effects Class lB Sodium channel Lidocaine, ORS widening Ventricular Headache, dizziness, Advanced liver blockade mexiletine arrhythmias or other neurologic disease symptoms (both drugs) Seizures (lidocaine toxicity) Class lC Sodium channel Flecainide, ORS widening Atrial Headache, lschemic or blockade propafenone fibrillation, SW dizziness, or other structural heart neurologic disease, sinus node symptoms dysfunction, second- or third- degree AV block or bundle branch disease without a pacemaker Class ll p-Adrenergic Metoprolol, Decreased Rate control of Fatigue, drowsiness, Severe asthma, blockade propranolol, heart rate, atrial dizziness, hair loss, cardiogenic shock, carvedilol, prolonged PR arrhythmias, cold hands and feet, second- or third- atenolol, interval SW depression, erectile degree AV block, bisoprolol, dysfunaion, preexcitation nadolol bronchospasm Class lll Potassium Sotalol, OT Atrial Headache, dizziness, Renal insufficiency, channel dofetilide prolongation fibrillation, bradycardia, fatigue, OT prolongation, blockade atrialflutter, dyspnea; rarely, bradycardia, orAV ventricu la r torsades de pointes block without a arrhythmias (sotalol) pacemaker L Headache, dizziness, diarrhea; rarely, torsades de pointes (dofetilide) Class lV Calcium Verapamil, Decreased SW, rate Dizziness, Significant sinus channel diltiazem heart rate, control of atrial constipation, node dysfunction, blockade prolonged PR arrhythmias dependent second- orthird- (nondihy- interval edema, nausea degreeAVblock t dropyridines) withouta pacemaker, preexcitation Multichannel Several Amiodarone, Many effects: Atrial Fatigue, dizziness, Advanced liver, lung, blockers mechanisms, dronedarone decreased arrhyth mias nausea, vomiting, orthyroid disease including heart rate; (both drugs), constipation or (amiodarone) potassium, prolonged PR, ventricular diarrhea, tremor, Advanced liver sodium, and ORS, or OT arrhythmias liver and lung (amiodarone) disease, permanent calcium channel interval toxicities (both atrial fibrillation, blockade d rugs) recent Thyroid and eye decompensated or toxicities advanced heart i (amiodarone) failure (NYHA : functional class lll- i lV) (dronedarone) I Adenosine A1-receptor Adenosine Brief AV block Termination of Flushing, dyspnea, Severe asthma (can t receptor agonist SW(intravenous chest pain, worsen) I agonists only) hypotension, t dizziness, nausea

Class lB Sodium channel Lidocaine, ORS widening Ventricular Headache, dizziness, Advanced liver blockade mexiletine arrhythmias or other neurologic disease symptoms (both drugs) Seizures (lidocaine toxicity) Class lC Sodium channel Flecainide, ORS widening Atrial Headache, lschemic or blockade propafenone fibrillation, SW dizziness, or other structural heart neurologic disease, sinus node symptoms dysfunction, second- or third- degree AV block or bundle branch disease without a pacemaker Class ll p-Adrenergic Metoprolol, Decreased Rate control of Fatigue, drowsiness, Severe asthma, blockade propranolol, heart rate, atrial dizziness, hair loss, cardiogenic shock, carvedilol, prolonged PR arrhythmias, cold hands and feet, second- or third- atenolol, interval SW depression, erectile degree AV block, bisoprolol, dysfunaion, preexcitation nadolol bronchospasm Class lll Potassium Sotalol, OT Atrial Headache, dizziness, Renal insufficiency, channel dofetilide prolongation fibrillation, bradycardia, fatigue, OT prolongation, blockade atrialflutter, dyspnea; rarely, bradycardia, orAV ventricu la r torsades de pointes block without a arrhythmias (sotalol) pacemaker L Headache, dizziness, diarrhea; rarely, torsades de pointes (dofetilide) Class lV Calcium Verapamil, Decreased SW, rate Dizziness, Significant sinus channel diltiazem heart rate, control of atrial constipation, node dysfunction, blockade prolonged PR arrhythmias dependent second- orthird- (nondihy- interval edema, nausea degreeAVblock t dropyridines) withouta pacemaker, preexcitation Multichannel Several Amiodarone, Many effects: Atrial Fatigue, dizziness, Advanced liver, lung, blockers mechanisms, dronedarone decreased arrhyth mias nausea, vomiting, orthyroid disease including heart rate; (both drugs), constipation or (amiodarone) potassium, prolonged PR, ventricular diarrhea, tremor, Advanced liver sodium, and ORS, or OT arrhythmias liver and lung (amiodarone) disease, permanent calcium channel interval toxicities (both atrial fibrillation, blockade d rugs) recent Thyroid and eye decompensated or toxicities advanced heart i (amiodarone) failure (NYHA : functional class lll- i lV) (dronedarone) I Adenosine A1-receptor Adenosine Brief AV block Termination of Flushing, dyspnea, Severe asthma (can t receptor agonist SW(intravenous chest pain, worsen) I agonists only) hypotension, t dizziness, nausea ) Cardiac lncreases vagal Digoxin Slows AV Rate control of Nausea, vomiting, Advanced kidney ' glycoside activity node atrialfibrillation dizziness, blurry impairment conduction vision and (requires dose i yellow halos, adjustment) I th rom bocytopen ia, t I

) Cardiac lncreases vagal Digoxin Slows AV Rate control of Nausea, vomiting, Advanced kidney ' glycoside activity node atrialfibrillation dizziness, blurry impairment conduction vision and (requires dose i yellow halos, adjustment) I th rom bocytopen ia, t I PAT with AV block I (toxicity) t I AV = atrioventricular; PAT = paroxysmal atrial tachycardia; NYHA = New York Heart Association; SVT = supraventricular tachycardia. I t L 47 t r

Arrhythmias va I .tt \,!t I ro vt t \,5 tIGURE 21. ECGinapatienttakingunusuallyhighpropafenonedoses,manifestingwithORSprolongationandbroad,relativelyslowwavesof atrial flutter(bestseenin leads ll and lll).

I .tt \,!t I ro vt t \,5 tIGURE 21. ECGinapatienttakingunusuallyhighpropafenonedoses,manifestingwithORSprolongationandbroad,relativelyslowwavesof atrial flutter(bestseenin leads ll and lll). contraindicated in patients with ischemic or structural heart Adenosine is used in the acute treatment of arrhy'thmias to disease because of the risk for promoting ventricular arrhyth interrupt AV conduction and terminate supraventricular tach- mias and death. ycardia (SVT). Administering adenosine can also help in deter- Class ll agents (p-blockers) and class IV agents (nondihy mining the type of arrhythmia. dropyridine calcium channel blockers) are commonly used to inhibit arrhythmia induction and AV conduction (to decrease rate) in patients with supraventricular or atrial arrhythmias. Sinus Tachycardia Class III agents sotalol and dofetilide are used to treat atrial Sinus tachycardia (sinus rhythm with a heart rate >100/min) is and ventricular arrhythmias. Class III antiarrhy,thmic therapy the most common tachycardia and is typically the result of typically is initiated in an inpatient setting, with regular assess- physiologic demand or distress, including exercise, pain, acute ment of the corrected QT interval (QTc) and caution exercised illness, hypovolemia, or anxiety. Diagnostic evaluation and in patients with kidney disease. Dofetilide is particularly noto treatment are guided by the underlying cause. rious for common and dangerous drug drug interactions. lnappropriate sinus tachycardia (lST) is a disorder charac Amiodarone, a class lll multichannel blocker, is frequently terized by an elevated resting heart rate, with exaggerated used to treat patients with recurrent ventricular tachycardia increases in heart rate with light actMgr. The sinus rate typically (W) or AE Amiodarone has a low risk of pro arrhythmia; how- decreases during sleep. IST frequently presents in women in ever, it is associated with thyroid, liver, lung, and eye toxicities their second to fourth decade. Symptoms vary and can include as well as neurologic side effects. Thyroid and liver function palpitations, light headedness, syncope (or near-syncope), should be monitored every 6 months, and pulmonary function dyspnea, and fatigue. Most importantly, the diagnosis of IST is testing and ophthalmologic examination should be performed based on the exclusion ofsecondary causes oftachycardia, such annually. Amiodarone interacts with many drugs, including as hyperthyroidism, anemia, pheochromocltoma, and struc- warfarin, statins, and digoxin. Dronedarone, another class III tural heart disease. First line therapy is removal ofaggravating multichannel blocker, can be used in patients with paroxysmal factors and exercise therapy. In patients with bothersome and AF and no overt heart failure. persistent symptoms, pharmacologic therapy can be consid Digoxin and adenosine are excluded from the Vaughan ered, but the condition frequently improves over time. Williams classification. Digoxin is a positive inotropic agent Postural orthostatic tachycardia syndrome (POTS) is that also increases vagal activity, Ieading to a lower resting another condition that often presents with tachycardia. POTS is heart rate. It can be used for rate control in patients with AF. a form ofdysautonomia characterized by orthostatic intolerance

contraindicated in patients with ischemic or structural heart Adenosine is used in the acute treatment of arrhy'thmias to disease because of the risk for promoting ventricular arrhyth interrupt AV conduction and terminate supraventricular tach- mias and death. ycardia (SVT). Administering adenosine can also help in deter- Class ll agents (p-blockers) and class IV agents (nondihy mining the type of arrhythmia. dropyridine calcium channel blockers) are commonly used to inhibit arrhythmia induction and AV conduction (to decrease rate) in patients with supraventricular or atrial arrhythmias. Sinus Tachycardia Class III agents sotalol and dofetilide are used to treat atrial Sinus tachycardia (sinus rhythm with a heart rate >100/min) is and ventricular arrhythmias. Class III antiarrhy,thmic therapy the most common tachycardia and is typically the result of typically is initiated in an inpatient setting, with regular assess- physiologic demand or distress, including exercise, pain, acute ment of the corrected QT interval (QTc) and caution exercised illness, hypovolemia, or anxiety. Diagnostic evaluation and in patients with kidney disease. Dofetilide is particularly noto treatment are guided by the underlying cause. rious for common and dangerous drug drug interactions. lnappropriate sinus tachycardia (lST) is a disorder charac Amiodarone, a class lll multichannel blocker, is frequently terized by an elevated resting heart rate, with exaggerated used to treat patients with recurrent ventricular tachycardia increases in heart rate with light actMgr. The sinus rate typically (W) or AE Amiodarone has a low risk of pro arrhythmia; how- decreases during sleep. IST frequently presents in women in ever, it is associated with thyroid, liver, lung, and eye toxicities their second to fourth decade. Symptoms vary and can include as well as neurologic side effects. Thyroid and liver function palpitations, light headedness, syncope (or near-syncope), should be monitored every 6 months, and pulmonary function dyspnea, and fatigue. Most importantly, the diagnosis of IST is testing and ophthalmologic examination should be performed based on the exclusion ofsecondary causes oftachycardia, such annually. Amiodarone interacts with many drugs, including as hyperthyroidism, anemia, pheochromocltoma, and struc- warfarin, statins, and digoxin. Dronedarone, another class III tural heart disease. First line therapy is removal ofaggravating multichannel blocker, can be used in patients with paroxysmal factors and exercise therapy. In patients with bothersome and AF and no overt heart failure. persistent symptoms, pharmacologic therapy can be consid Digoxin and adenosine are excluded from the Vaughan ered, but the condition frequently improves over time. Williams classification. Digoxin is a positive inotropic agent Postural orthostatic tachycardia syndrome (POTS) is that also increases vagal activity, Ieading to a lower resting another condition that often presents with tachycardia. POTS is heart rate. It can be used for rate control in patients with AF. a form ofdysautonomia characterized by orthostatic intolerance 48

I I i i Arrhythmias I

I I i i Arrhythmias I and excessive tachycardia, pafiicularly with standing. Diagnostic present in cases of'bunclle branch block, aberrancy, pacing, t criteria for POTS include an increase in heart rate of 30/min or or anterograde accessory pathway conduction (antidromic : more or an increase to greater than 120/min within 10 minutes tachycardia). t I of standing. The diagnosis is often confirmed with tilt table test- Vagal maneuvers, including the Valsalva maneuver or I ing. Behavioral modification, compression stockings, exercise carotid sinus massage, are first line therapy to restore sinus i i training, and increased fluid intake are important components rhythm acutely in patients with SVT. Adenosine can be used to I of therapy. Medical therapy lor POTS is highly variable and may terminate SVT and simultaneously help diagnose its mecha- i t include p blockers, ivabradine (ofT'label use), tludrocorlisone. nism. Tachycardias that terminate with adenosine are typically selective serotonin reuptake inhibitors (off' label use), midodrine, AV node dependent (atrioventricular nodal reentrant tachy and pyridostigmine (oflf label use). cardia [AVNRT] and atrioventricular reciprocating tachycardia r(rY Potl{I tAVRll), whereas contir.rued atrial activity (P waves) during AV block is consistent with atrial flutter or atrial tachvcardia. t o Sinus tachycardia is the most common tachycardia and is typically the result o[physiologic demand or distress, Atrioventricular Nodal Reentrant Tachycardia including exercise, pain, fever, hypovolemia, and anxiety. AVNRT accounts fbr two thirds of ail cases of SVT. not includ ing cases of AF ancl atrial flutter. It is caused by a reentrant Su praventricu la r Tachycard ias circuit 'o,ithin the AV node that uses both the fast and slow Clinical Presentation pathways. AVNRT is characterized by a short RP interval with SVTs are rapid heart rhythms that arise fiom the atrium or a retrograde P wave inscribed very close to the QRS complex. require conduction through the AV node. AI.'and atrial flutter AVNRT may be terminated with vagal manellvers or aden are technically SVTs, although the term is generally reserved for osine. AV nodal blockers (0 btockers or calcium channel a narrow group of arrhythmias described herein. SVTs can blockers) are usecl to prevent recurrent AVNRT. In patients affect all age groups but are frequently seen in younger patients. with recurrent AVNRl'and those who do not tolerate or prefer Prevalence is higher in women than in men. SVTs usually occur to avoid long term medical therapy, catheter ablation should in the absence olstructural heart disease, although echocardi be considered. Catheter ablation ofAVNRT has a high success ography should be perfbrmed to exclude underlying cardiac rate, although it is associated with a 1',,{, risk lor injury to the AV dysfunction or structural defects. Patients often have repeated node necessitating pacemaker in.rplantation. episodes of tachycardia and may report palpitations, a sensation of pounding in the neck, fatigue, light headedness, chest dis Atrioventricular Reciprocating Tachycardia comfort, dyspnea, presyncope, and, less commonly, syncope. AVRT is an accessory pathway mediated tachyc:rrdia that is The ECG typically demonstrates a narrow complex often observed as preexcitation (delta wave) or.r ECG (Figure 22). tachycardia; however, wide QRS complexes (>t20 ms) may be Early ventricular activation over the accessory pathway causes

and excessive tachycardia, pafiicularly with standing. Diagnostic present in cases of'bunclle branch block, aberrancy, pacing, t criteria for POTS include an increase in heart rate of 30/min or or anterograde accessory pathway conduction (antidromic : more or an increase to greater than 120/min within 10 minutes tachycardia). t I of standing. The diagnosis is often confirmed with tilt table test- Vagal maneuvers, including the Valsalva maneuver or I ing. Behavioral modification, compression stockings, exercise carotid sinus massage, are first line therapy to restore sinus i i training, and increased fluid intake are important components rhythm acutely in patients with SVT. Adenosine can be used to I of therapy. Medical therapy lor POTS is highly variable and may terminate SVT and simultaneously help diagnose its mecha- i t include p blockers, ivabradine (ofT'label use), tludrocorlisone. nism. Tachycardias that terminate with adenosine are typically selective serotonin reuptake inhibitors (off' label use), midodrine, AV node dependent (atrioventricular nodal reentrant tachy and pyridostigmine (oflf label use). cardia [AVNRT] and atrioventricular reciprocating tachycardia r(rY Potl{I tAVRll), whereas contir.rued atrial activity (P waves) during AV block is consistent with atrial flutter or atrial tachvcardia. t o Sinus tachycardia is the most common tachycardia and is typically the result o[physiologic demand or distress, Atrioventricular Nodal Reentrant Tachycardia including exercise, pain, fever, hypovolemia, and anxiety. AVNRT accounts fbr two thirds of ail cases of SVT. not includ ing cases of AF ancl atrial flutter. It is caused by a reentrant Su praventricu la r Tachycard ias circuit 'o,ithin the AV node that uses both the fast and slow Clinical Presentation pathways. AVNRT is characterized by a short RP interval with SVTs are rapid heart rhythms that arise fiom the atrium or a retrograde P wave inscribed very close to the QRS complex. require conduction through the AV node. AI.'and atrial flutter AVNRT may be terminated with vagal manellvers or aden are technically SVTs, although the term is generally reserved for osine. AV nodal blockers (0 btockers or calcium channel a narrow group of arrhythmias described herein. SVTs can blockers) are usecl to prevent recurrent AVNRT. In patients affect all age groups but are frequently seen in younger patients. with recurrent AVNRl'and those who do not tolerate or prefer Prevalence is higher in women than in men. SVTs usually occur to avoid long term medical therapy, catheter ablation should in the absence olstructural heart disease, although echocardi be considered. Catheter ablation ofAVNRT has a high success ography should be perfbrmed to exclude underlying cardiac rate, although it is associated with a 1',,{, risk lor injury to the AV dysfunction or structural defects. Patients often have repeated node necessitating pacemaker in.rplantation. episodes of tachycardia and may report palpitations, a sensation of pounding in the neck, fatigue, light headedness, chest dis Atrioventricular Reciprocating Tachycardia comfort, dyspnea, presyncope, and, less commonly, syncope. AVRT is an accessory pathway mediated tachyc:rrdia that is The ECG typically demonstrates a narrow complex often observed as preexcitation (delta wave) or.r ECG (Figure 22). tachycardia; however, wide QRS complexes (>t20 ms) may be Early ventricular activation over the accessory pathway causes 1l .1f ,'.-.1-".- ;, :' lr l, -'*-t*--".7 .11 v--r^^L"---,f,, tl l1 l,lr rl ^J^ l

1l .1f ,'.-.1-".- ;, :' lr l, -'*-t*--".7 .11 v--r^^L"---,f,, tl l1 l,lr rl ^J^ l ila rrlt ,t r, .i ,:1 .: -- !J..=,-. !\?.+i- \---'_-{ i *--i'----- -^-' :-^--*^., --.,-,.. L) :\T \'l 1'6 r,llttll r'.,',-+'.'p. r: -t, -' a t-t'* -.,t 1,.y'r*-1 . .' *.-.,, -,,- ...', l:lrlrlll!ll,r r ,-,'--v,',-'..-",'..2'.--, >'--':1,-l--.\"r-1-.^ y''*---, r-t'.. -*.. -.:u*'.r:y-/-*-j1-/t-:J;lw-'N'r.^r*, -trrl{ tl r.r"r. t --^.,,.- I .-r ) *ll- nlr- *-.r,- l, - 'l-- '- --t- ,1 FIGURE 22.ECGdemonstratingsinusrhythmwithpreexcitationasindicatedbythepresenceof adeltawave(arror,,u).Theslurringofthe0RSupstrokerepresentspremature depolarization of the ventricular tissue adjacent to the accessory pathway. 49

Arrhythmias shortening of the PR interval, and the initial part of the QRS PACs are O,pically treated with B blockers or calcium channel complex is slurred because of premature ventricular depolari blockers. zation in the myocardial tissue adjacent to the accessory path Atrial tachycardia can arise in the presence or absence of way. In AVRT, conduction is anterograde over the AV node structural heart disease. p Blocker or calcium channel blocker (orthodromic, narrow-complex AVRT) in 90'7, to 95'1, of cases: therapy is first line treatment for symptomatic atrial tachy conduction is anterograde over the accessory pathway (anti cardia. Second line treatment is catheter ablation or antiar dromic, wide-complex AVRT) in the remaining cases. rhythmic drug therapy. Ablation success rates are generalll' Wolff-Parkinson-White (WPW) syndrome is defined by lower in patients with atrial tachycardia than in patients $'ith symptomatic AVRT with evidence of preexcitation on resting other SVTs. ECG. AF occurs in up to one third of patients with WPW syn- Multifocal atrial tachycardia is typified by three or more drome. Rapid conduction over an accessory pathway in AF can P-wave morphologies and a heart rate greater than 100,min result in ventricular fibrillation (VF) and sudden cardiac death (Figure 23). It is usually seen in patients with severe pulmo' (SCD), although this occurs in less than 1'1, of cases of WPW nary disease. syndrome. f,EY POIlITS Risk stratification for SCD can be performed with exercise testing, although more frequently, patients are referred for . Vagal maneuvers may restore sinus rhythm in patients electrophysiolog, testing for both risk stratification and cura with supraventricular tachycardia. tive ablation. Catheter ablation is first line therapy for patients . Patients with recurrent supraventricular tachycardia are with WPW syndrome. The success rate for ablation is high treated with atrioventricular nodal blockers (p blockers but is dictated by the location of the accessory pathway. or calcium channel blockers) or catheter ablation. Antiarrhythmic therapy is second line therapy. r First-line therapy for patients with Wolff Parkinson In asymptomatic patients with preexcitation on ECG, White syndrome is catheter ablation; antiarrhythmic management is controversial. Invasive testing is generally not drugs are second-line therapy. required unless the patient has a high risk occupation, such as a commercial airline pilot. Atrial Fibrillation Premature Atrial Contractions and AF is characterized by disorganized atrial activity with an Atrial Tachycardia irregularly irregular ventricular response on ECG (Figure 24). Premature atrial contractions (PACs) are early isolated beats It is the most common sustained arrhythmia. t.ifetime risk fbr that arise from the atria. They are exceedingly common, and AF is 25'l. in patients older than 40 years. lncidence is strongly their frequency increases with age. During ambulatory ECG associated r,r'ith and increases with age. with 10'7, of persons monitoring, only 1'7, of persons have no PACs. High PAC bur- older than B0 years affected. AF is associated with an increased den is associated with increased risk for AF. Symptomatic risk for adverse cardiac events. including a fivefold increased

shortening of the PR interval, and the initial part of the QRS PACs are O,pically treated with B blockers or calcium channel complex is slurred because of premature ventricular depolari blockers. zation in the myocardial tissue adjacent to the accessory path Atrial tachycardia can arise in the presence or absence of way. In AVRT, conduction is anterograde over the AV node structural heart disease. p Blocker or calcium channel blocker (orthodromic, narrow-complex AVRT) in 90'7, to 95'1, of cases: therapy is first line treatment for symptomatic atrial tachy conduction is anterograde over the accessory pathway (anti cardia. Second line treatment is catheter ablation or antiar dromic, wide-complex AVRT) in the remaining cases. rhythmic drug therapy. Ablation success rates are generalll' Wolff-Parkinson-White (WPW) syndrome is defined by lower in patients with atrial tachycardia than in patients $'ith symptomatic AVRT with evidence of preexcitation on resting other SVTs. ECG. AF occurs in up to one third of patients with WPW syn- Multifocal atrial tachycardia is typified by three or more drome. Rapid conduction over an accessory pathway in AF can P-wave morphologies and a heart rate greater than 100,min result in ventricular fibrillation (VF) and sudden cardiac death (Figure 23). It is usually seen in patients with severe pulmo' (SCD), although this occurs in less than 1'1, of cases of WPW nary disease. syndrome. f,EY POIlITS Risk stratification for SCD can be performed with exercise testing, although more frequently, patients are referred for . Vagal maneuvers may restore sinus rhythm in patients electrophysiolog, testing for both risk stratification and cura with supraventricular tachycardia. tive ablation. Catheter ablation is first line therapy for patients . Patients with recurrent supraventricular tachycardia are with WPW syndrome. The success rate for ablation is high treated with atrioventricular nodal blockers (p blockers but is dictated by the location of the accessory pathway. or calcium channel blockers) or catheter ablation. Antiarrhythmic therapy is second line therapy. r First-line therapy for patients with Wolff Parkinson In asymptomatic patients with preexcitation on ECG, White syndrome is catheter ablation; antiarrhythmic management is controversial. Invasive testing is generally not drugs are second-line therapy. required unless the patient has a high risk occupation, such as a commercial airline pilot. Atrial Fibrillation Premature Atrial Contractions and AF is characterized by disorganized atrial activity with an Atrial Tachycardia irregularly irregular ventricular response on ECG (Figure 24). Premature atrial contractions (PACs) are early isolated beats It is the most common sustained arrhythmia. t.ifetime risk fbr that arise from the atria. They are exceedingly common, and AF is 25'l. in patients older than 40 years. lncidence is strongly their frequency increases with age. During ambulatory ECG associated r,r'ith and increases with age. with 10'7, of persons monitoring, only 1'7, of persons have no PACs. High PAC bur- older than B0 years affected. AF is associated with an increased den is associated with increased risk for AF. Symptomatic risk for adverse cardiac events. including a fivefold increased rVB

shortening of the PR interval, and the initial part of the QRS PACs are O,pically treated with B blockers or calcium channel complex is slurred because of premature ventricular depolari blockers. zation in the myocardial tissue adjacent to the accessory path Atrial tachycardia can arise in the presence or absence of way. In AVRT, conduction is anterograde over the AV node structural heart disease. p Blocker or calcium channel blocker (orthodromic, narrow-complex AVRT) in 90'7, to 95'1, of cases: therapy is first line treatment for symptomatic atrial tachy conduction is anterograde over the accessory pathway (anti cardia. Second line treatment is catheter ablation or antiar dromic, wide-complex AVRT) in the remaining cases. rhythmic drug therapy. Ablation success rates are generalll' Wolff-Parkinson-White (WPW) syndrome is defined by lower in patients with atrial tachycardia than in patients $'ith symptomatic AVRT with evidence of preexcitation on resting other SVTs. ECG. AF occurs in up to one third of patients with WPW syn- Multifocal atrial tachycardia is typified by three or more drome. Rapid conduction over an accessory pathway in AF can P-wave morphologies and a heart rate greater than 100,min result in ventricular fibrillation (VF) and sudden cardiac death (Figure 23). It is usually seen in patients with severe pulmo' (SCD), although this occurs in less than 1'1, of cases of WPW nary disease. syndrome. f,EY POIlITS Risk stratification for SCD can be performed with exercise testing, although more frequently, patients are referred for . Vagal maneuvers may restore sinus rhythm in patients electrophysiolog, testing for both risk stratification and cura with supraventricular tachycardia. tive ablation. Catheter ablation is first line therapy for patients . Patients with recurrent supraventricular tachycardia are with WPW syndrome. The success rate for ablation is high treated with atrioventricular nodal blockers (p blockers but is dictated by the location of the accessory pathway. or calcium channel blockers) or catheter ablation. Antiarrhythmic therapy is second line therapy. r First-line therapy for patients with Wolff Parkinson In asymptomatic patients with preexcitation on ECG, White syndrome is catheter ablation; antiarrhythmic management is controversial. Invasive testing is generally not drugs are second-line therapy. required unless the patient has a high risk occupation, such as a commercial airline pilot. Atrial Fibrillation Premature Atrial Contractions and AF is characterized by disorganized atrial activity with an Atrial Tachycardia irregularly irregular ventricular response on ECG (Figure 24). Premature atrial contractions (PACs) are early isolated beats It is the most common sustained arrhythmia. t.ifetime risk fbr that arise from the atria. They are exceedingly common, and AF is 25'l. in patients older than 40 years. lncidence is strongly their frequency increases with age. During ambulatory ECG associated r,r'ith and increases with age. with 10'7, of persons monitoring, only 1'7, of persons have no PACs. High PAC bur- older than B0 years affected. AF is associated with an increased den is associated with increased risk for AF. Symptomatic risk for adverse cardiac events. including a fivefold increased rVB a!! v2

shortening of the PR interval, and the initial part of the QRS PACs are O,pically treated with B blockers or calcium channel complex is slurred because of premature ventricular depolari blockers. zation in the myocardial tissue adjacent to the accessory path Atrial tachycardia can arise in the presence or absence of way. In AVRT, conduction is anterograde over the AV node structural heart disease. p Blocker or calcium channel blocker (orthodromic, narrow-complex AVRT) in 90'7, to 95'1, of cases: therapy is first line treatment for symptomatic atrial tachy conduction is anterograde over the accessory pathway (anti cardia. Second line treatment is catheter ablation or antiar dromic, wide-complex AVRT) in the remaining cases. rhythmic drug therapy. Ablation success rates are generalll' Wolff-Parkinson-White (WPW) syndrome is defined by lower in patients with atrial tachycardia than in patients $'ith symptomatic AVRT with evidence of preexcitation on resting other SVTs. ECG. AF occurs in up to one third of patients with WPW syn- Multifocal atrial tachycardia is typified by three or more drome. Rapid conduction over an accessory pathway in AF can P-wave morphologies and a heart rate greater than 100,min result in ventricular fibrillation (VF) and sudden cardiac death (Figure 23). It is usually seen in patients with severe pulmo' (SCD), although this occurs in less than 1'1, of cases of WPW nary disease. syndrome. f,EY POIlITS Risk stratification for SCD can be performed with exercise testing, although more frequently, patients are referred for . Vagal maneuvers may restore sinus rhythm in patients electrophysiolog, testing for both risk stratification and cura with supraventricular tachycardia. tive ablation. Catheter ablation is first line therapy for patients . Patients with recurrent supraventricular tachycardia are with WPW syndrome. The success rate for ablation is high treated with atrioventricular nodal blockers (p blockers but is dictated by the location of the accessory pathway. or calcium channel blockers) or catheter ablation. Antiarrhythmic therapy is second line therapy. r First-line therapy for patients with Wolff Parkinson In asymptomatic patients with preexcitation on ECG, White syndrome is catheter ablation; antiarrhythmic management is controversial. Invasive testing is generally not drugs are second-line therapy. required unless the patient has a high risk occupation, such as a commercial airline pilot. Atrial Fibrillation Premature Atrial Contractions and AF is characterized by disorganized atrial activity with an Atrial Tachycardia irregularly irregular ventricular response on ECG (Figure 24). Premature atrial contractions (PACs) are early isolated beats It is the most common sustained arrhythmia. t.ifetime risk fbr that arise from the atria. They are exceedingly common, and AF is 25'l. in patients older than 40 years. lncidence is strongly their frequency increases with age. During ambulatory ECG associated r,r'ith and increases with age. with 10'7, of persons monitoring, only 1'7, of persons have no PACs. High PAC bur- older than B0 years affected. AF is associated with an increased den is associated with increased risk for AF. Symptomatic risk for adverse cardiac events. including a fivefold increased rVB a!! v2 tc o\,,F

shortening of the PR interval, and the initial part of the QRS PACs are O,pically treated with B blockers or calcium channel complex is slurred because of premature ventricular depolari blockers. zation in the myocardial tissue adjacent to the accessory path Atrial tachycardia can arise in the presence or absence of way. In AVRT, conduction is anterograde over the AV node structural heart disease. p Blocker or calcium channel blocker (orthodromic, narrow-complex AVRT) in 90'7, to 95'1, of cases: therapy is first line treatment for symptomatic atrial tachy conduction is anterograde over the accessory pathway (anti cardia. Second line treatment is catheter ablation or antiar dromic, wide-complex AVRT) in the remaining cases. rhythmic drug therapy. Ablation success rates are generalll' Wolff-Parkinson-White (WPW) syndrome is defined by lower in patients with atrial tachycardia than in patients $'ith symptomatic AVRT with evidence of preexcitation on resting other SVTs. ECG. AF occurs in up to one third of patients with WPW syn- Multifocal atrial tachycardia is typified by three or more drome. Rapid conduction over an accessory pathway in AF can P-wave morphologies and a heart rate greater than 100,min result in ventricular fibrillation (VF) and sudden cardiac death (Figure 23). It is usually seen in patients with severe pulmo' (SCD), although this occurs in less than 1'1, of cases of WPW nary disease. syndrome. f,EY POIlITS Risk stratification for SCD can be performed with exercise testing, although more frequently, patients are referred for . Vagal maneuvers may restore sinus rhythm in patients electrophysiolog, testing for both risk stratification and cura with supraventricular tachycardia. tive ablation. Catheter ablation is first line therapy for patients . Patients with recurrent supraventricular tachycardia are with WPW syndrome. The success rate for ablation is high treated with atrioventricular nodal blockers (p blockers but is dictated by the location of the accessory pathway. or calcium channel blockers) or catheter ablation. Antiarrhythmic therapy is second line therapy. r First-line therapy for patients with Wolff Parkinson In asymptomatic patients with preexcitation on ECG, White syndrome is catheter ablation; antiarrhythmic management is controversial. Invasive testing is generally not drugs are second-line therapy. required unless the patient has a high risk occupation, such as a commercial airline pilot. Atrial Fibrillation Premature Atrial Contractions and AF is characterized by disorganized atrial activity with an Atrial Tachycardia irregularly irregular ventricular response on ECG (Figure 24). Premature atrial contractions (PACs) are early isolated beats It is the most common sustained arrhythmia. t.ifetime risk fbr that arise from the atria. They are exceedingly common, and AF is 25'l. in patients older than 40 years. lncidence is strongly their frequency increases with age. During ambulatory ECG associated r,r'ith and increases with age. with 10'7, of persons monitoring, only 1'7, of persons have no PACs. High PAC bur- older than B0 years affected. AF is associated with an increased den is associated with increased risk for AF. Symptomatic risk for adverse cardiac events. including a fivefold increased rVB a!! v2 tc o\,,F I tIGURE 23.ECGshowingmultifocalatrialtachycardiatypiliedbythreeormoreP-wavemorphologies(arows).

shortening of the PR interval, and the initial part of the QRS PACs are O,pically treated with B blockers or calcium channel complex is slurred because of premature ventricular depolari blockers. zation in the myocardial tissue adjacent to the accessory path Atrial tachycardia can arise in the presence or absence of way. In AVRT, conduction is anterograde over the AV node structural heart disease. p Blocker or calcium channel blocker (orthodromic, narrow-complex AVRT) in 90'7, to 95'1, of cases: therapy is first line treatment for symptomatic atrial tachy conduction is anterograde over the accessory pathway (anti cardia. Second line treatment is catheter ablation or antiar dromic, wide-complex AVRT) in the remaining cases. rhythmic drug therapy. Ablation success rates are generalll' Wolff-Parkinson-White (WPW) syndrome is defined by lower in patients with atrial tachycardia than in patients $'ith symptomatic AVRT with evidence of preexcitation on resting other SVTs. ECG. AF occurs in up to one third of patients with WPW syn- Multifocal atrial tachycardia is typified by three or more drome. Rapid conduction over an accessory pathway in AF can P-wave morphologies and a heart rate greater than 100,min result in ventricular fibrillation (VF) and sudden cardiac death (Figure 23). It is usually seen in patients with severe pulmo' (SCD), although this occurs in less than 1'1, of cases of WPW nary disease. syndrome. f,EY POIlITS Risk stratification for SCD can be performed with exercise testing, although more frequently, patients are referred for . Vagal maneuvers may restore sinus rhythm in patients electrophysiolog, testing for both risk stratification and cura with supraventricular tachycardia. tive ablation. Catheter ablation is first line therapy for patients . Patients with recurrent supraventricular tachycardia are with WPW syndrome. The success rate for ablation is high treated with atrioventricular nodal blockers (p blockers but is dictated by the location of the accessory pathway. or calcium channel blockers) or catheter ablation. Antiarrhythmic therapy is second line therapy. r First-line therapy for patients with Wolff Parkinson In asymptomatic patients with preexcitation on ECG, White syndrome is catheter ablation; antiarrhythmic management is controversial. Invasive testing is generally not drugs are second-line therapy. required unless the patient has a high risk occupation, such as a commercial airline pilot. Atrial Fibrillation Premature Atrial Contractions and AF is characterized by disorganized atrial activity with an Atrial Tachycardia irregularly irregular ventricular response on ECG (Figure 24). Premature atrial contractions (PACs) are early isolated beats It is the most common sustained arrhythmia. t.ifetime risk fbr that arise from the atria. They are exceedingly common, and AF is 25'l. in patients older than 40 years. lncidence is strongly their frequency increases with age. During ambulatory ECG associated r,r'ith and increases with age. with 10'7, of persons monitoring, only 1'7, of persons have no PACs. High PAC bur- older than B0 years affected. AF is associated with an increased den is associated with increased risk for AF. Symptomatic risk for adverse cardiac events. including a fivefold increased rVB a!! v2 tc o\,,F I tIGURE 23.ECGshowingmultifocalatrialtachycardiatypiliedbythreeormoreP-wavemorphologies(arows). 50

Arrhythmias I aVl- evF v6 tIGURE 24. ECGdemonstratingatrialfibrillation.NoclearPwavesareseen,andlhevenlricularresponseisirregular risk for stroke. as well as increased risk for heart failure and cardiomyopathy. Patients with AF less commonly present L dementia. Among patients aged 55 years and older with an with tachycardia induced cardiomyopathy, characterized by ischemic neurologic event (i.e., stroke or transient ischemic asymptomatic left ventricular (LV) dysfunction or overt heart attack) of undetermined source. occult intermittent AF is failure. thought to be present in up to 25'1, of cases, and 30 day ambu AF is categorized according to its duration. Paroxysmal AF latory ECG monitoring is indicated for detection. If 30 day stops spontaneously within 7 days of onset, whereas persistent ambulatory monitoring is inconclusive, implantation of a car AF lasts lor 7 days or more. Long standing persistent AF is diac monitor (loop recorder) is reasonable to optimize detec- continuous, with a duration ol more than 1 year. Permanent tion of silent AF. AF refers to cases in which the physician and patient have I AF is usually the result of long standing risk factors, such abandoned attempts to maintain sinus rhythm. as diabetes mellitus, smoking, moderate to heaqr alcohol consumption, obesity, hypertension, coronary artery disease Acute Management (CAD), heart failure, and obstructive sleep apnea. Behavioral Urgent cardioversion (electrical or pharmacologic) is indicated risk factor modification, including increased activity, weight in patients with AF and hypotension, acute myocardial loss, smoking cessation, and abstinence lrom alcohol, is rec- ischemia, or decompensated heart failure. In patients with AF ommended. Bariatric surgery should be considered for appro- or atrial flutter of more than 48 hours' duration or unknown priate candidates. Blood pressure and blood glucose control duration that requires immediate cardioversion, anticoagula- and obstructive sleep apnea management also reduce risk. tion should be initiated as soon as possible and continued for AF is less commonly caused by reversible or acute physi- at least 4 weeks unless contraindicated. The decision about ologic insults, including cardiac surgery pulmonary embo long term anticoagulation should be based on the thrombo lism, critical illness, or hyperthyroidism. When there are no embolic risk profile and bleeding risk profile (see Long Term identified risk factors, a predisposing genetic background is Management). often present. In stable patients, the primary goals ol therapy are to (t) prevent stroke, (2) control heart rate, (3) minimize or eliminate Clinical Presentation symptoms, and (4) modify underlying risk factors. Upon diag- Patients with AF may be asymptomatic or experience palpi- nosis, reversible causes must be ruled out. All patients should tations, light headedness, dizziness, dyspnea, exercise intol undergo thyroid function testing to evaluate for hyperthyroid- erance, chestpain, near syncope, or, rarely, syncope. In some ism. Patients with risk factors for or symptoms suggestive of cases, AF can lead to hemodynamic compromise, especially sleep apnea should undergo testing. Echocardiography is indi in patients with advanced diastolic dysfunction or restrictive cated to evaluate for potential valvular or other structural

risk for stroke. as well as increased risk for heart failure and cardiomyopathy. Patients with AF less commonly present L dementia. Among patients aged 55 years and older with an with tachycardia induced cardiomyopathy, characterized by ischemic neurologic event (i.e., stroke or transient ischemic asymptomatic left ventricular (LV) dysfunction or overt heart attack) of undetermined source. occult intermittent AF is failure. thought to be present in up to 25'1, of cases, and 30 day ambu AF is categorized according to its duration. Paroxysmal AF latory ECG monitoring is indicated for detection. If 30 day stops spontaneously within 7 days of onset, whereas persistent ambulatory monitoring is inconclusive, implantation of a car AF lasts lor 7 days or more. Long standing persistent AF is diac monitor (loop recorder) is reasonable to optimize detec- continuous, with a duration ol more than 1 year. Permanent tion of silent AF. AF refers to cases in which the physician and patient have I AF is usually the result of long standing risk factors, such abandoned attempts to maintain sinus rhythm. as diabetes mellitus, smoking, moderate to heaqr alcohol consumption, obesity, hypertension, coronary artery disease Acute Management (CAD), heart failure, and obstructive sleep apnea. Behavioral Urgent cardioversion (electrical or pharmacologic) is indicated risk factor modification, including increased activity, weight in patients with AF and hypotension, acute myocardial loss, smoking cessation, and abstinence lrom alcohol, is rec- ischemia, or decompensated heart failure. In patients with AF ommended. Bariatric surgery should be considered for appro- or atrial flutter of more than 48 hours' duration or unknown priate candidates. Blood pressure and blood glucose control duration that requires immediate cardioversion, anticoagula- and obstructive sleep apnea management also reduce risk. tion should be initiated as soon as possible and continued for AF is less commonly caused by reversible or acute physi- at least 4 weeks unless contraindicated. The decision about ologic insults, including cardiac surgery pulmonary embo long term anticoagulation should be based on the thrombo lism, critical illness, or hyperthyroidism. When there are no embolic risk profile and bleeding risk profile (see Long Term identified risk factors, a predisposing genetic background is Management). often present. In stable patients, the primary goals ol therapy are to (t) prevent stroke, (2) control heart rate, (3) minimize or eliminate Clinical Presentation symptoms, and (4) modify underlying risk factors. Upon diag- Patients with AF may be asymptomatic or experience palpi- nosis, reversible causes must be ruled out. All patients should tations, light headedness, dizziness, dyspnea, exercise intol undergo thyroid function testing to evaluate for hyperthyroid- erance, chestpain, near syncope, or, rarely, syncope. In some ism. Patients with risk factors for or symptoms suggestive of cases, AF can lead to hemodynamic compromise, especially sleep apnea should undergo testing. Echocardiography is indi in patients with advanced diastolic dysfunction or restrictive cated to evaluate for potential valvular or other structural 51

Arrhythmias heart disease. Echocardiography can also be used to assess left TABLE 1 L CHA2DS2-VASc Score, Adjusted Stroke Rates, atrial size, which helps determine the severity of the underly- and Stroke Prevention Therapy Recommendations for ing atrial myocardial dysfunction. Elective cardioversion can Nonvalvular Atrial Fibrillation and Flutter be pursued in patients with significant symptoms who are cHA2D52- lncidence of Stroke Prevention hemodynamically stable. VASc Score' lschemic Stroke/ Therapy'' 100 Patient-Yearsb Acute Anticoagulation Men Women In patients who are not undergoing cardioversion, acute intra- 0 0.2 None N/A venous anticoagulation is usually unnecessary; however, oral 1 0.6 Consider None anticoagulation should be initiated if the patient has sufficient OAC risk factors for stroke. 2 2.2 OAC Consider If cardioversion is planned, the duration of AF guides oAc therapy. AF with a known duration of less than 48 hours 3 3.2 OAC OAC confers a low risk for thrombus formation and subsequent 4 4.8 oAc oAc stroke, and preprocedural anticoagulation can be considered 5 7.2 OAC OAC in patients who are otherwise at low risk for stroke. Preprocedural anticoagulation is reasonable as soon as pos- 6+ 10.3 oAc OAC

heart disease. Echocardiography can also be used to assess left TABLE 1 L CHA2DS2-VASc Score, Adjusted Stroke Rates, atrial size, which helps determine the severity of the underly- and Stroke Prevention Therapy Recommendations for ing atrial myocardial dysfunction. Elective cardioversion can Nonvalvular Atrial Fibrillation and Flutter be pursued in patients with significant symptoms who are cHA2D52- lncidence of Stroke Prevention hemodynamically stable. VASc Score' lschemic Stroke/ Therapy'' 100 Patient-Yearsb Acute Anticoagulation Men Women In patients who are not undergoing cardioversion, acute intra- 0 0.2 None N/A venous anticoagulation is usually unnecessary; however, oral 1 0.6 Consider None anticoagulation should be initiated if the patient has sufficient OAC risk factors for stroke. 2 2.2 OAC Consider If cardioversion is planned, the duration of AF guides oAc therapy. AF with a known duration of less than 48 hours 3 3.2 OAC OAC confers a low risk for thrombus formation and subsequent 4 4.8 oAc oAc stroke, and preprocedural anticoagulation can be considered 5 7.2 OAC OAC in patients who are otherwise at low risk for stroke. Preprocedural anticoagulation is reasonable as soon as pos- 6+ 10.3 oAc OAC sible before cardioversion for men with a CHATDST-VASc N/A = not applicable; OAC = oral anticoagulation.

heart disease. Echocardiography can also be used to assess left TABLE 1 L CHA2DS2-VASc Score, Adjusted Stroke Rates, atrial size, which helps determine the severity of the underly- and Stroke Prevention Therapy Recommendations for ing atrial myocardial dysfunction. Elective cardioversion can Nonvalvular Atrial Fibrillation and Flutter be pursued in patients with significant symptoms who are cHA2D52- lncidence of Stroke Prevention hemodynamically stable. VASc Score' lschemic Stroke/ Therapy'' 100 Patient-Yearsb Acute Anticoagulation Men Women In patients who are not undergoing cardioversion, acute intra- 0 0.2 None N/A venous anticoagulation is usually unnecessary; however, oral 1 0.6 Consider None anticoagulation should be initiated if the patient has sufficient OAC risk factors for stroke. 2 2.2 OAC Consider If cardioversion is planned, the duration of AF guides oAc therapy. AF with a known duration of less than 48 hours 3 3.2 OAC OAC confers a low risk for thrombus formation and subsequent 4 4.8 oAc oAc stroke, and preprocedural anticoagulation can be considered 5 7.2 OAC OAC in patients who are otherwise at low risk for stroke. Preprocedural anticoagulation is reasonable as soon as pos- 6+ 10.3 oAc OAC sible before cardioversion for men with a CHATDST-VASc N/A = not applicable; OAC = oral anticoagulation. score of 2 or greater and for women with a score of 3 or "CHA2DS2-VASc scoring (maximum 9 points): One point each is given for heart failure, hypertension, diabetes mellrtus, vascular disease (prior myocardial greater followed by long-term anticoagulant therapy. In infarction, peripheral artery disease, aortic plaque), Iemale sex, and age 65 to patients in whom the duration of AF is unclear or in whom 74 years. Two points each are given for previous stroke/transient ischemic attack/ thromboembolic disease and age >75 years. AF has lasted longer than 48 hours, anticoagulation therapy bData from Friberg L, Rosenqvist M, Lip GY. Evaluation of risk strati{icatron schemes for 3 weeks is recommended before cardioversion. In patients for ischaemic stroke and bleeding in 182 618 patients with atrial fibilllation: the Swedish Atrial Fibrillation cohort study. Eur Heart J. 20 1 2;33:1 500- l 0. I PMID: who would benefit from cardioversion sooner, transesopha 222464431 doi:1 0.1 093/eurheartj/ehr488 geal echocardiography can be performed to exclude the pres- 'Recommendations from January CT, Wann LS, Calkins H, et al. 201 9 AHA/ACC/ ence of left atrial appendage thrombus and facilitate urgent HRS focused update of the 20 1 4 AHA,IACCIHRS guideline for the management of patients with atrial fibrillation: a repon of the American College of Cardiology/ cardioversion. Regardless ofthe duration or nature ofAE, all American Hean Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol. 20 1 9;74:1 04'1 32. I PMI D: 3070343 1 ] patients who undergo cardioversion must receive anticoagu- doi:1 0.1 01 6/j.jacc.20 1 9.01 .0 1 1 lants for at least 4 weeks following the procedure because of an increased risk lor thromboembolic events after sinus rhythm is restored. Risk Strotilicotion Stroke prevention with oral anticoagulation depends on the Rate Control patient's thromboembolic risk in the absence of obvious con Heart rate control is necessary in patients with rapid ventricu- traindications. Although several risk stratification scores are lar rates to improve cardiac function and alleviate symptoms. available, current guidelines recommend use of the CHA2DS, Acutely, the goal heart rate should be between 60/min and VASc score in patients with nonvalvular AF. Adjusted stroke 110/min. Commonly used medications include AV nodal block- rates and recommendations for antithrombotic therapy based ers, such as metoprolol or diltiazem. Intravenous or oral admin- on the CHA2DST-VASc score are shown in Table 18. The 2019 istration may be appropriate depending on symptoms. In American College of Cardiologr/American Heart Association/ patients with LV dysfunction, calcium channel blockers should Heart Rhythm Society focused update on AF recommends be avoided. Digoxin can be used as adjunctive therapy to anticoagulation to prevent stroke in patients u,ith nonvalvular improve rate control, especially in patients with heart failure. AF who have a CHATDS, VASc score of 2 or greater in men or 3 or greater in women. The American College of Chest Physicians Long-Term Management guideline on antithrombotic therapy for AF recommends anti- Anticoagulation coagulation for patients with one or more non sex CHA2DS2 Arterial thromboembolic events are the most serious compli- VASc stroke risk factors (score of >1 in men or >2 in women). cation of AF and can occur with any form (paroxysmal, persis- Antiplatelet therapy alone is no longer routinely used for tent, or permanent). In patients with nonvalvular AF (AF in stroke prevention in AE the absence of a mechanical prosthetic valve or moderate/ severe mitral stenosis), the absolute risk for stroke is approxi Antico agulant S ele ctio n mately 4"1, per year; however, the presence of comorbidities Oral anticoagulation in patients with AF can be accomplished (e.g., heart failure, hypertension, diabetes, or vascular disease) with a vitamin K antagonist (warfarin) or direct oral antico- can increase the risk 15- to 20 flold. Hypertension is associated agulant (DOAC) (Table f9). Anticoagulation in patients with with an increased risk for both AF and stroke; therefore, blood valvular AF (moderate/severe mitral stenosis or mechanical pressure control is critical in the management of AF. valve prosthesis) should be obtained with warfarin; DOACs

score of 2 or greater and for women with a score of 3 or "CHA2DS2-VASc scoring (maximum 9 points): One point each is given for heart failure, hypertension, diabetes mellrtus, vascular disease (prior myocardial greater followed by long-term anticoagulant therapy. In infarction, peripheral artery disease, aortic plaque), Iemale sex, and age 65 to patients in whom the duration of AF is unclear or in whom 74 years. Two points each are given for previous stroke/transient ischemic attack/ thromboembolic disease and age >75 years. AF has lasted longer than 48 hours, anticoagulation therapy bData from Friberg L, Rosenqvist M, Lip GY. Evaluation of risk strati{icatron schemes for 3 weeks is recommended before cardioversion. In patients for ischaemic stroke and bleeding in 182 618 patients with atrial fibilllation: the Swedish Atrial Fibrillation cohort study. Eur Heart J. 20 1 2;33:1 500- l 0. I PMID: who would benefit from cardioversion sooner, transesopha 222464431 doi:1 0.1 093/eurheartj/ehr488 geal echocardiography can be performed to exclude the pres- 'Recommendations from January CT, Wann LS, Calkins H, et al. 201 9 AHA/ACC/ ence of left atrial appendage thrombus and facilitate urgent HRS focused update of the 20 1 4 AHA,IACCIHRS guideline for the management of patients with atrial fibrillation: a repon of the American College of Cardiology/ cardioversion. Regardless ofthe duration or nature ofAE, all American Hean Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol. 20 1 9;74:1 04'1 32. I PMI D: 3070343 1 ] patients who undergo cardioversion must receive anticoagu- doi:1 0.1 01 6/j.jacc.20 1 9.01 .0 1 1 lants for at least 4 weeks following the procedure because of an increased risk lor thromboembolic events after sinus rhythm is restored. Risk Strotilicotion Stroke prevention with oral anticoagulation depends on the Rate Control patient's thromboembolic risk in the absence of obvious con Heart rate control is necessary in patients with rapid ventricu- traindications. Although several risk stratification scores are lar rates to improve cardiac function and alleviate symptoms. available, current guidelines recommend use of the CHA2DS, Acutely, the goal heart rate should be between 60/min and VASc score in patients with nonvalvular AF. Adjusted stroke 110/min. Commonly used medications include AV nodal block- rates and recommendations for antithrombotic therapy based ers, such as metoprolol or diltiazem. Intravenous or oral admin- on the CHA2DST-VASc score are shown in Table 18. The 2019 istration may be appropriate depending on symptoms. In American College of Cardiologr/American Heart Association/ patients with LV dysfunction, calcium channel blockers should Heart Rhythm Society focused update on AF recommends be avoided. Digoxin can be used as adjunctive therapy to anticoagulation to prevent stroke in patients u,ith nonvalvular improve rate control, especially in patients with heart failure. AF who have a CHATDS, VASc score of 2 or greater in men or 3 or greater in women. The American College of Chest Physicians Long-Term Management guideline on antithrombotic therapy for AF recommends anti- Anticoagulation coagulation for patients with one or more non sex CHA2DS2 Arterial thromboembolic events are the most serious compli- VASc stroke risk factors (score of >1 in men or >2 in women). cation of AF and can occur with any form (paroxysmal, persis- Antiplatelet therapy alone is no longer routinely used for tent, or permanent). In patients with nonvalvular AF (AF in stroke prevention in AE the absence of a mechanical prosthetic valve or moderate/ severe mitral stenosis), the absolute risk for stroke is approxi Antico agulant S ele ctio n mately 4"1, per year; however, the presence of comorbidities Oral anticoagulation in patients with AF can be accomplished (e.g., heart failure, hypertension, diabetes, or vascular disease) with a vitamin K antagonist (warfarin) or direct oral antico- can increase the risk 15- to 20 flold. Hypertension is associated agulant (DOAC) (Table f9). Anticoagulation in patients with with an increased risk for both AF and stroke; therefore, blood valvular AF (moderate/severe mitral stenosis or mechanical pressure control is critical in the management of AF. valve prosthesis) should be obtained with warfarin; DOACs 52

Arrhythmias TABTE 19. Anticoagulants Approved for Stroke Prevention in Atrial Fibrillation Medication Frequency Type ofAF Cautions and Dosing Warfarin (vitamin K Dose adjusted to INR Valvular" or Avoid in pregnancy antagonist) nonvalvular Caution with idiopathic thrombocytopenic purpura, heparin- induced thrombocytopenia, liver disease, protein C or S deficiency Many drug and food interactions Dabigatran (direct Twice daily Nonvalvula r Caution with use of P-glycoprotein inhibitors thrombin inhibitor) Reduce dose with CrCl 15-30 mUmin/1.73 m2 Rivaroxaban (factor Xa Once daily Nonvalvular Avoid with CrCl <30 mUmin/1 .73 m2, moderate liver impairment, inhibitor) use of strong P-glycoprotein inhibitors, or use of strong cytochrome P-450 inducers and inhibitors Reduce dose with CrCl 30-50 mUmin/1 .73 m2 Apixaban (factor Xa Twice daily Nonva lvular Avoid with use of strong P-glycoprotein inhibitors or strong in h ibitor) cytochrome P-450 inducers and inhibitors Reduce dose with two of the following criteria: creatinine level >1.5 mg/dl (133 pmol/L), age >80 y, or weight <60 kg (132 lb) Edoxaban (factor Xa Once daily Nonvalvular Avoid with use of strong cytochrome P-450 inducers and inhibitors inhibitor) Avoid with CrCl >95 mUmin/1 .73 m2 (reduced stroke prevention effectiveness). Reduce dose with CrCl 30-50 mlJmin/1 .73 m2, weight <60 kg (1 32 lb), or concomitant use of verapamil or quinidine (potent P-glycoprotein inhibitors) AF = atrial fibrillation; CrCl = creatlnine ciearance.

TABTE 19. Anticoagulants Approved for Stroke Prevention in Atrial Fibrillation Medication Frequency Type ofAF Cautions and Dosing Warfarin (vitamin K Dose adjusted to INR Valvular" or Avoid in pregnancy antagonist) nonvalvular Caution with idiopathic thrombocytopenic purpura, heparin- induced thrombocytopenia, liver disease, protein C or S deficiency Many drug and food interactions Dabigatran (direct Twice daily Nonvalvula r Caution with use of P-glycoprotein inhibitors thrombin inhibitor) Reduce dose with CrCl 15-30 mUmin/1.73 m2 Rivaroxaban (factor Xa Once daily Nonvalvular Avoid with CrCl <30 mUmin/1 .73 m2, moderate liver impairment, inhibitor) use of strong P-glycoprotein inhibitors, or use of strong cytochrome P-450 inducers and inhibitors Reduce dose with CrCl 30-50 mUmin/1 .73 m2 Apixaban (factor Xa Twice daily Nonva lvular Avoid with use of strong P-glycoprotein inhibitors or strong in h ibitor) cytochrome P-450 inducers and inhibitors Reduce dose with two of the following criteria: creatinine level >1.5 mg/dl (133 pmol/L), age >80 y, or weight <60 kg (132 lb) Edoxaban (factor Xa Once daily Nonvalvular Avoid with use of strong cytochrome P-450 inducers and inhibitors inhibitor) Avoid with CrCl >95 mUmin/1 .73 m2 (reduced stroke prevention effectiveness). Reduce dose with CrCl 30-50 mlJmin/1 .73 m2, weight <60 kg (1 32 lb), or concomitant use of verapamil or quinidine (potent P-glycoprotein inhibitors) AF = atrial fibrillation; CrCl = creatlnine ciearance. "Valvular atrial fib,riliation refers to atrial fibrillation in the presence of moderate to severe mitral stenosis or mechanical valve prosthesis.

TABTE 19. Anticoagulants Approved for Stroke Prevention in Atrial Fibrillation Medication Frequency Type ofAF Cautions and Dosing Warfarin (vitamin K Dose adjusted to INR Valvular" or Avoid in pregnancy antagonist) nonvalvular Caution with idiopathic thrombocytopenic purpura, heparin- induced thrombocytopenia, liver disease, protein C or S deficiency Many drug and food interactions Dabigatran (direct Twice daily Nonvalvula r Caution with use of P-glycoprotein inhibitors thrombin inhibitor) Reduce dose with CrCl 15-30 mUmin/1.73 m2 Rivaroxaban (factor Xa Once daily Nonvalvular Avoid with CrCl <30 mUmin/1 .73 m2, moderate liver impairment, inhibitor) use of strong P-glycoprotein inhibitors, or use of strong cytochrome P-450 inducers and inhibitors Reduce dose with CrCl 30-50 mUmin/1 .73 m2 Apixaban (factor Xa Twice daily Nonva lvular Avoid with use of strong P-glycoprotein inhibitors or strong in h ibitor) cytochrome P-450 inducers and inhibitors Reduce dose with two of the following criteria: creatinine level >1.5 mg/dl (133 pmol/L), age >80 y, or weight <60 kg (132 lb) Edoxaban (factor Xa Once daily Nonvalvular Avoid with use of strong cytochrome P-450 inducers and inhibitors inhibitor) Avoid with CrCl >95 mUmin/1 .73 m2 (reduced stroke prevention effectiveness). Reduce dose with CrCl 30-50 mlJmin/1 .73 m2, weight <60 kg (1 32 lb), or concomitant use of verapamil or quinidine (potent P-glycoprotein inhibitors) AF = atrial fibrillation; CrCl = creatlnine ciearance. "Valvular atrial fib,riliation refers to atrial fibrillation in the presence of moderate to severe mitral stenosis or mechanical valve prosthesis. are not approved for use in valvular AF or those with any factor Xa inhibitor, is superior to warfarin for stroke preven- mechanical heart valve. DOACs are recommended in prefer- tion and confers less risk for major bleeding, including intra ence to warfarin in DOAC eligible patients, including patients cranial and gastrointestinal bleeding. Edoxaban is noninferior with AF and no valvular disease as well as patients with AF to warfarin for stroke prevention and is associated with less and aortic valve disease, mitral regurgitation, tricuspid regur major bleeding. gitation, or mild mitral stenosis in the absence of a mechani DOACs have shorter half lives than warfarin; however, cal prosthesis. there are no quick, readily available serum assays to accurately determine anticoagulant activity. Andexanet alfa or 4-factor \ Warfarin prothrombin complex concentrates are recommended for life- Dose-adjusted warfarin is an effective, low-cost therapy; how- threatening bleeding due to rivaroxaban, apixaban, or edoxa ever, its limitations include the need for frequent monitoring ban. Idarucizumab is a dabigatran reversal agent available for and adjustment and numerous food and drug interactions. emergency invasive or surgical procedures or in cases of The safeg and efficacy of warfarin therapy depend on the uncontrolled or life threatening bleeding. time that the patient is in the therapeutic range (lNR, 2 3). Kidney and liver function should be evaluated before Management of warfarin overdose and warfarin-related bleed- initiation of a DOAC and reevaluated at least annually. See ing is discussed in MKSAP 19 Hematologr. MKSAP 19 Hematology for recommendations regarding DOAC dosing in patients with chronic kidney or Iiver Direct Acting Oral Anticoagulants disease. Four DOACs are approved for the prevention of stroke in AF. Dabigatran, an oral direct thrombin inhibitor, is superior to Specific Populations warfarin for the prevention of ischemic stroke and results in In patients with AF who have undergone percutaneous less intracranial bleeding. Patients taking dabigatran have a coronary intervention for acute coronary syndrome, both higher risk for gastrointestinal bleeding relative to warfarin anticoagulant and antiplatelet therapies are necessary. and may experience dyspepsia. Rivaroxaban, a direct factor Xa Among these patients with a CHA2DS2 VASc score of 2 or inhibitor, is noninferior to warfarin in the prevention of stroke greater, "double therapy" with clopidogrel or ticagrelor plus or systemic embolism and is associated with less intracranial a DOAC is recommended over "triple therapy" with an oral and fatal bleeding. As with dabigatran, patients taking anticoagulant, aspirin, and P2Y12 inhibitor to reduce the rivaroxaban have a higher risk for gastrointestinal bleeding risk for bleeding. In patients taking two or more antithrom compared with those taking warfarin. Apixaban, another oral botic agents, it is recommended that a proton pump

are not approved for use in valvular AF or those with any factor Xa inhibitor, is superior to warfarin for stroke preven- mechanical heart valve. DOACs are recommended in prefer- tion and confers less risk for major bleeding, including intra ence to warfarin in DOAC eligible patients, including patients cranial and gastrointestinal bleeding. Edoxaban is noninferior with AF and no valvular disease as well as patients with AF to warfarin for stroke prevention and is associated with less and aortic valve disease, mitral regurgitation, tricuspid regur major bleeding. gitation, or mild mitral stenosis in the absence of a mechani DOACs have shorter half lives than warfarin; however, cal prosthesis. there are no quick, readily available serum assays to accurately determine anticoagulant activity. Andexanet alfa or 4-factor \ Warfarin prothrombin complex concentrates are recommended for life- Dose-adjusted warfarin is an effective, low-cost therapy; how- threatening bleeding due to rivaroxaban, apixaban, or edoxa ever, its limitations include the need for frequent monitoring ban. Idarucizumab is a dabigatran reversal agent available for and adjustment and numerous food and drug interactions. emergency invasive or surgical procedures or in cases of The safeg and efficacy of warfarin therapy depend on the uncontrolled or life threatening bleeding. time that the patient is in the therapeutic range (lNR, 2 3). Kidney and liver function should be evaluated before Management of warfarin overdose and warfarin-related bleed- initiation of a DOAC and reevaluated at least annually. See ing is discussed in MKSAP 19 Hematologr. MKSAP 19 Hematology for recommendations regarding DOAC dosing in patients with chronic kidney or Iiver Direct Acting Oral Anticoagulants disease. Four DOACs are approved for the prevention of stroke in AF. Dabigatran, an oral direct thrombin inhibitor, is superior to Specific Populations warfarin for the prevention of ischemic stroke and results in In patients with AF who have undergone percutaneous less intracranial bleeding. Patients taking dabigatran have a coronary intervention for acute coronary syndrome, both higher risk for gastrointestinal bleeding relative to warfarin anticoagulant and antiplatelet therapies are necessary. and may experience dyspepsia. Rivaroxaban, a direct factor Xa Among these patients with a CHA2DS2 VASc score of 2 or inhibitor, is noninferior to warfarin in the prevention of stroke greater, "double therapy" with clopidogrel or ticagrelor plus or systemic embolism and is associated with less intracranial a DOAC is recommended over "triple therapy" with an oral and fatal bleeding. As with dabigatran, patients taking anticoagulant, aspirin, and P2Y12 inhibitor to reduce the rivaroxaban have a higher risk for gastrointestinal bleeding risk for bleeding. In patients taking two or more antithrom compared with those taking warfarin. Apixaban, another oral botic agents, it is recommended that a proton pump 53

Arrhythmias inhibitor be initiated and NSAIDs be avoided to reduce the pseudoaneurysm, arteriovenous fi stula, retroperitoneal bleed risk of gastrointestinal bleeding. ing). Longer term complications, such as pulmonary vein ste In patients with AF and stable CAD, treatment with riva- nosis, are uncommon. roxaban alone is noninferior to rivaroxaban plus aspirin in AV node ablation is an option for patients with AF who the prevention of the composite end point of stroke, systemic have continued symptomatic tachycardia despite rate and embolization, myocardial infarction (MI), need for revascu rhyhm control therapy. Therapeutic ablation of the AV node Iarization, or death from any cause. Rivaroxaban monotherapy requires implantation of a permanent pacemaker. These also is associated with significantly less bleeding. patients remain in AF and still require anticoagulation. Approximately lOn/,' to 25"1' of patients with AF have con- Rate-Only Versus Rate Plus Rhythm Control Treatment traindications to oral anticoagulation or discontinue therapy The first priority among patients with AF is to control the ven- for various reasons, including bleeding events. In patients who tricular rate. Rate control with a resting heart rate goal ofless are at moderate to high risk for stroke (CHA,,DS, VASc score than 80/min is reasonable for symptomatic management of >3), left atrial appendage occlusion to prevent stroke and sys AF. A lenient rate-control strates/ (resting heart rate <110/min) temic thromboembolism can be considered. Occlusion of the may be reasonable for asymptomatic patients without LV dys- left atrial appendage can be achieved percutaneously rt'ith an function. p Blockers, calcium channel blockers, and, less implanted self expanding device or r.tith surgical closure. often, digoxin are used to control the ventricular rate, although However, appropriate patient selection remains a challenge, combination therapy may be necessary. Aside from resting and most patients undergoing percutaneous left atrial append- heart rate assessment. evaluation of the heart rate with activ age occlusion require at least short term oral anticoagulation ity, such as with a 6 minute walk test, stress test, or 24 hour while the device endothelializes. These patients also remain on ambulatory ECG monitoring, may be performed. long term antiplatelet therapy. Although historical trials have not proved a mortality benefit to maintaining sinus rhythm, numerous studies Management in Patients With Heart Failure have demonstrated superior symptom treatment with rate AF complicates nearly 40"/,, of cases of heart failure, and the plus rhythm control compared with rate control alone. combination of AF and heart failure dramatically worsens Furthermore, because the long term effects of rate only con- outcomes. Several clinical trials have demonstrated that trol are unknown, rhythm control is often pursued in younger aggressive efforts to achieve rhythm control in patients with patients (aged <50 years) and may improve long term clinical AF and concomitant heart failure decrease morbidity and outcomes. A strategz of early rhythm control (within 1 year of mortality. In patients with heart failure with reduced ejection diagnosis) among patients at high risk for adverse cardiovas fraction, recent clinical trials have shown that catheter abla- cular events was tested in the randomized EAST AFNET 4 trial. tion of AF is associated with a favorable effect on morbidity High risk was defined as age older than 75 years or a previous and mortality compared with medical therapy. Patient selec transient ischemic aftack or stroke, or meeting two of the tion for catheter ablation remains important. and many of the following criteria: age older than 65 years, female sex, heart trials enrolled selected patients. failure, hypertension, diabetes, severe CAD, chronic kidney disease, and LV hypertrophy. Early rhythm control (drugs or Subclinical Atrial Fibrillation ablation) reduced the primary composite end point of cardio- The entity of subclinical AF is being increasingly recognized vascular death, stroke, or hospitalization for heart failure or because of the growing prevalence of implantable cardiac acute coronary syndrome, compared with usual care. Rhythm devices and widespread availability of ambulatory ECG moni control may require cardioversion in addition to antiarrhyth tors (e.g., mobile continuous telemetry) and consumer devices mic therapy, which is guided by the patient's comorbid condi- (e.g., personal ECG monitors, smartwatches). Subclinical AF tions and safet5z considerations. However, catheter ablation most commonly refers to AF that is asymptomatic and brief has been shown to be more effective than antiarrhy,thmic (definitions range from 20 seconds to <24 hours). Although drugs, with an acceptable safety profile. definitive studies to guide management are lacking, there are several important considerations. First, episodes are frequently Nonpharmacologic Approaches to Atrial Fibrillation asymptomatic and short lived; thus, symptom management Catheter ablation with pulmonary vein isolation is an effective and rate control are rarely required. Second, subclinical AF is rhy.thm control therapy in patients with recurrent sympto associated with progression to AF; therefore, it is reasonable to matic AF despite antiarrhy.thmic drug therapy. Catheter abla consider traditional AF risk factor modification. Lastly. stroke tion is most effective in patients without significant left risk in these patients is unclear. Studies have varied in their atrial enlargement and multiple comorbid conditions. One definition ofsubclinical AF and its associated stroke risk. and year after the procedure ,7O"/,, to 90'7, of patients with paroxys there is no consensus on the net clinical benefit of anticoagu mal AF are symptom-free; however, success rates vary. Iation for subclinical AF. One notable exception is the detec- Complications include thromboembolism (0.5'2, 1'l,, risk), tam- tion of AF lasting more than 30 seconds among patients with ponade, and vascular complications (e.g., insertion hematoma, embolic stroke of undetermined source (cryptogenic stroke);

inhibitor be initiated and NSAIDs be avoided to reduce the pseudoaneurysm, arteriovenous fi stula, retroperitoneal bleed risk of gastrointestinal bleeding. ing). Longer term complications, such as pulmonary vein ste In patients with AF and stable CAD, treatment with riva- nosis, are uncommon. roxaban alone is noninferior to rivaroxaban plus aspirin in AV node ablation is an option for patients with AF who the prevention of the composite end point of stroke, systemic have continued symptomatic tachycardia despite rate and embolization, myocardial infarction (MI), need for revascu rhyhm control therapy. Therapeutic ablation of the AV node Iarization, or death from any cause. Rivaroxaban monotherapy requires implantation of a permanent pacemaker. These also is associated with significantly less bleeding. patients remain in AF and still require anticoagulation. Approximately lOn/,' to 25"1' of patients with AF have con- Rate-Only Versus Rate Plus Rhythm Control Treatment traindications to oral anticoagulation or discontinue therapy The first priority among patients with AF is to control the ven- for various reasons, including bleeding events. In patients who tricular rate. Rate control with a resting heart rate goal ofless are at moderate to high risk for stroke (CHA,,DS, VASc score than 80/min is reasonable for symptomatic management of >3), left atrial appendage occlusion to prevent stroke and sys AF. A lenient rate-control strates/ (resting heart rate <110/min) temic thromboembolism can be considered. Occlusion of the may be reasonable for asymptomatic patients without LV dys- left atrial appendage can be achieved percutaneously rt'ith an function. p Blockers, calcium channel blockers, and, less implanted self expanding device or r.tith surgical closure. often, digoxin are used to control the ventricular rate, although However, appropriate patient selection remains a challenge, combination therapy may be necessary. Aside from resting and most patients undergoing percutaneous left atrial append- heart rate assessment. evaluation of the heart rate with activ age occlusion require at least short term oral anticoagulation ity, such as with a 6 minute walk test, stress test, or 24 hour while the device endothelializes. These patients also remain on ambulatory ECG monitoring, may be performed. long term antiplatelet therapy. Although historical trials have not proved a mortality benefit to maintaining sinus rhythm, numerous studies Management in Patients With Heart Failure have demonstrated superior symptom treatment with rate AF complicates nearly 40"/,, of cases of heart failure, and the plus rhythm control compared with rate control alone. combination of AF and heart failure dramatically worsens Furthermore, because the long term effects of rate only con- outcomes. Several clinical trials have demonstrated that trol are unknown, rhythm control is often pursued in younger aggressive efforts to achieve rhythm control in patients with patients (aged <50 years) and may improve long term clinical AF and concomitant heart failure decrease morbidity and outcomes. A strategz of early rhythm control (within 1 year of mortality. In patients with heart failure with reduced ejection diagnosis) among patients at high risk for adverse cardiovas fraction, recent clinical trials have shown that catheter abla- cular events was tested in the randomized EAST AFNET 4 trial. tion of AF is associated with a favorable effect on morbidity High risk was defined as age older than 75 years or a previous and mortality compared with medical therapy. Patient selec transient ischemic aftack or stroke, or meeting two of the tion for catheter ablation remains important. and many of the following criteria: age older than 65 years, female sex, heart trials enrolled selected patients. failure, hypertension, diabetes, severe CAD, chronic kidney disease, and LV hypertrophy. Early rhythm control (drugs or Subclinical Atrial Fibrillation ablation) reduced the primary composite end point of cardio- The entity of subclinical AF is being increasingly recognized vascular death, stroke, or hospitalization for heart failure or because of the growing prevalence of implantable cardiac acute coronary syndrome, compared with usual care. Rhythm devices and widespread availability of ambulatory ECG moni control may require cardioversion in addition to antiarrhyth tors (e.g., mobile continuous telemetry) and consumer devices mic therapy, which is guided by the patient's comorbid condi- (e.g., personal ECG monitors, smartwatches). Subclinical AF tions and safet5z considerations. However, catheter ablation most commonly refers to AF that is asymptomatic and brief has been shown to be more effective than antiarrhy,thmic (definitions range from 20 seconds to <24 hours). Although drugs, with an acceptable safety profile. definitive studies to guide management are lacking, there are several important considerations. First, episodes are frequently Nonpharmacologic Approaches to Atrial Fibrillation asymptomatic and short lived; thus, symptom management Catheter ablation with pulmonary vein isolation is an effective and rate control are rarely required. Second, subclinical AF is rhy.thm control therapy in patients with recurrent sympto associated with progression to AF; therefore, it is reasonable to matic AF despite antiarrhy.thmic drug therapy. Catheter abla consider traditional AF risk factor modification. Lastly. stroke tion is most effective in patients without significant left risk in these patients is unclear. Studies have varied in their atrial enlargement and multiple comorbid conditions. One definition ofsubclinical AF and its associated stroke risk. and year after the procedure ,7O"/,, to 90'7, of patients with paroxys there is no consensus on the net clinical benefit of anticoagu mal AF are symptom-free; however, success rates vary. Iation for subclinical AF. One notable exception is the detec- Complications include thromboembolism (0.5'2, 1'l,, risk), tam- tion of AF lasting more than 30 seconds among patients with ponade, and vascular complications (e.g., insertion hematoma, embolic stroke of undetermined source (cryptogenic stroke); 54

Arrhythmias anticoagulation is routinely indicated in these patients. electrocardiographically by a sawtooth pattern with inverted Implantable loop recorders to detect subclinical AF may be flutter waves in leads II, II], and aVF and positive flutter waves in indicated in selected patients with embolic stroke of undeter lead V, (Figure 25). Typical atrial flutter, the dominant form in mined source. patients without prior cardiac disease, is the result of counter- clockwise reentry around the tricuspid annulus. Atypical flutter is primarily seen among patients with prior ablation for AF or . Urgent cardioversion to sinus rhythm is indicated in prior cardiac surgery In atypical flutter, the circuit is usually in patients with atrial fibrillation who have hypotension, other locations in the right and left atria. acute myocardial ischemia, or decompensated heart Management of anticoagulation in the setting of chronic failure, regardless of atrial fibrillation duration. atrial flutter is similar to that for AF; however, a rhythm con- . Current guidelines recommend calculation of the trol stratery is favored in atrial flutter because rate control may CHA2DS2-VASc score for stroke risk stratification in be difficult and often requires high doses of more than one AV patients with nonvalvular atrial fibrillation; patients nodal blocker. Catheter ablation is the definitive treatment for with a CHATDST-VASc score of 2 or greater in men or 3 typical atrial flutter because of a very high success rate (>95%) or greater in women should be treated with oral antico- and low complication rate. Oral anticoagulation in patients agulation to prevent stroke. with atrial flutter without ablation is approached in the same o Direct-acting oral anticoagulants are recommended in manner as in patients with AE preference to warfarin in patients with atrial fibrillation, excluding those with moderate to severe mitral stenosis or a mechanical valve prosthesis. r Catheter ablation is the definitive treatment for typical atrial flutter, with a high success rate (>957.) and low o In patients with atrial fibrillation, rate plus rhythm con- risk for complications. trol offers superior symptom management compared with rate control alone. Ventricular Arrhythmias Premature Ventricular Contractions Atrial Flufter Premature ventricular contractions (PVCs) occur in up to 75% Atrial flutter is an organized macro-reentrant tachycardia with of healthy persons. Symptoms include palpitations or the per- discrete regular atrial activity on ECG, usually with an atrial rate cepflon ofskipped beats. Forceful beats are caused by increased of 250/min to 300/min. Tlpical atrial flutter is characterized cardiac filling during the pause following the PVC. PVCs are

anticoagulation is routinely indicated in these patients. electrocardiographically by a sawtooth pattern with inverted Implantable loop recorders to detect subclinical AF may be flutter waves in leads II, II], and aVF and positive flutter waves in indicated in selected patients with embolic stroke of undeter lead V, (Figure 25). Typical atrial flutter, the dominant form in mined source. patients without prior cardiac disease, is the result of counter- clockwise reentry around the tricuspid annulus. Atypical flutter is primarily seen among patients with prior ablation for AF or . Urgent cardioversion to sinus rhythm is indicated in prior cardiac surgery In atypical flutter, the circuit is usually in patients with atrial fibrillation who have hypotension, other locations in the right and left atria. acute myocardial ischemia, or decompensated heart Management of anticoagulation in the setting of chronic failure, regardless of atrial fibrillation duration. atrial flutter is similar to that for AF; however, a rhythm con- . Current guidelines recommend calculation of the trol stratery is favored in atrial flutter because rate control may CHA2DS2-VASc score for stroke risk stratification in be difficult and often requires high doses of more than one AV patients with nonvalvular atrial fibrillation; patients nodal blocker. Catheter ablation is the definitive treatment for with a CHATDST-VASc score of 2 or greater in men or 3 typical atrial flutter because of a very high success rate (>95%) or greater in women should be treated with oral antico- and low complication rate. Oral anticoagulation in patients agulation to prevent stroke. with atrial flutter without ablation is approached in the same o Direct-acting oral anticoagulants are recommended in manner as in patients with AE preference to warfarin in patients with atrial fibrillation, excluding those with moderate to severe mitral stenosis or a mechanical valve prosthesis. r Catheter ablation is the definitive treatment for typical atrial flutter, with a high success rate (>957.) and low o In patients with atrial fibrillation, rate plus rhythm con- risk for complications. trol offers superior symptom management compared with rate control alone. Ventricular Arrhythmias Premature Ventricular Contractions Atrial Flufter Premature ventricular contractions (PVCs) occur in up to 75% Atrial flutter is an organized macro-reentrant tachycardia with of healthy persons. Symptoms include palpitations or the per- discrete regular atrial activity on ECG, usually with an atrial rate cepflon ofskipped beats. Forceful beats are caused by increased of 250/min to 300/min. Tlpical atrial flutter is characterized cardiac filling during the pause following the PVC. PVCs are t I G U R E 2 5 . ln this ECG demonstrating typical atrial flutter, negatively directed sawtooth waves are seen in the inferior leads (ll, lll, and aVF), and positive waves a re seen in lead V1. ln the bottom rhythm strip,2:1 and 4:1 conduction patterns aIe most easily seen.

anticoagulation is routinely indicated in these patients. electrocardiographically by a sawtooth pattern with inverted Implantable loop recorders to detect subclinical AF may be flutter waves in leads II, II], and aVF and positive flutter waves in indicated in selected patients with embolic stroke of undeter lead V, (Figure 25). Typical atrial flutter, the dominant form in mined source. patients without prior cardiac disease, is the result of counter- clockwise reentry around the tricuspid annulus. Atypical flutter is primarily seen among patients with prior ablation for AF or . Urgent cardioversion to sinus rhythm is indicated in prior cardiac surgery In atypical flutter, the circuit is usually in patients with atrial fibrillation who have hypotension, other locations in the right and left atria. acute myocardial ischemia, or decompensated heart Management of anticoagulation in the setting of chronic failure, regardless of atrial fibrillation duration. atrial flutter is similar to that for AF; however, a rhythm con- . Current guidelines recommend calculation of the trol stratery is favored in atrial flutter because rate control may CHA2DS2-VASc score for stroke risk stratification in be difficult and often requires high doses of more than one AV patients with nonvalvular atrial fibrillation; patients nodal blocker. Catheter ablation is the definitive treatment for with a CHATDST-VASc score of 2 or greater in men or 3 typical atrial flutter because of a very high success rate (>95%) or greater in women should be treated with oral antico- and low complication rate. Oral anticoagulation in patients agulation to prevent stroke. with atrial flutter without ablation is approached in the same o Direct-acting oral anticoagulants are recommended in manner as in patients with AE preference to warfarin in patients with atrial fibrillation, excluding those with moderate to severe mitral stenosis or a mechanical valve prosthesis. r Catheter ablation is the definitive treatment for typical atrial flutter, with a high success rate (>957.) and low o In patients with atrial fibrillation, rate plus rhythm con- risk for complications. trol offers superior symptom management compared with rate control alone. Ventricular Arrhythmias Premature Ventricular Contractions Atrial Flufter Premature ventricular contractions (PVCs) occur in up to 75% Atrial flutter is an organized macro-reentrant tachycardia with of healthy persons. Symptoms include palpitations or the per- discrete regular atrial activity on ECG, usually with an atrial rate cepflon ofskipped beats. Forceful beats are caused by increased of 250/min to 300/min. Tlpical atrial flutter is characterized cardiac filling during the pause following the PVC. PVCs are t I G U R E 2 5 . ln this ECG demonstrating typical atrial flutter, negatively directed sawtooth waves are seen in the inferior leads (ll, lll, and aVF), and positive waves a re seen in lead V1. ln the bottom rhythm strip,2:1 and 4:1 conduction patterns aIe most easily seen. 55

Arrhythmias more common in patients with hypertension, LV hypertrophy, In adult patients with known structural heart disease, 95'7, of previous MI, and other forms of structural heart disease, such wide-complex tachycardias are VT, and additional ECG or as nonischemic cardiomyopathy. clinical criteria are often unnecessary. However, in patients In the absence of high risk features (syncope, family his without known structural heart disease, several important tory ofpremature SCD, structural heart disease), reassurance clinical and ECG features can distinguish VT from other condi is often appropriate, and medical therapy is unnecessary. tions. Key features of VT on ECG include AV dissociation, However, PVCs require treatment when symptoms are bother- fusion beats. and capture beats (Figure 26). When the origin some or frequent (>to% ofall beats or 10,000 PVCs per day). of a wide complex tachycardia is in question, VT should be PVC-induced cardiomyopathy may result from frequent PVCs assumed. (generally >10'2,-15% of beats), although it occurs only in a Ventricular arrhythmias most commonly occur in minority of patients (see Heart Failure). patients with structural heart disease, including both ischemic First line treatment for PVC suppression is p blocker or and nonischemic cardiomyopathy, in whom the presence of calcium channel blocker therapy. p-Blockers are preferred in abnormal conduction and/or myocardial scar tissue facilitates patients with ventricular dysfunction. Alternative antiarrhyth the development of VT. In these patients, sustained VT mic therapy may be used if PVCs persist despite p-blockade or (>30 seconds) can lead to hypotension, syncope, VF, and car calcium channel blockade. The selection of an antiarrhlthmic diac arrest; however, on occasion, VT can be well tolerated. medication for PVC suppression depends on many factors, Thus, the absence of hemodynamic compromise does not including age, kidney function, cardiac structure, and comor exclude VT as a diagnosis. bid conditions. Catheter ablation should be considered in VT in the absence of structural heart disease (idiopathic patients with continued frequent PVCs despite medical ther VT) typically arises from the ventricular outflow tracts, fasci apy, patients who cannot tolerate medical therapy, and patients cles, and papillary muscles. Patients with idiopathic VT usu- who develop PVC induced cardiomyopathy. ally present with palpitations in the third to fifth decades of life. Episodes of syncope are uncommon. Arrhythmic events Ventricular Tachycardia are often triggered by stress, emotion, or sleeplessness. Clinical Presentation VT is awide-complex tachycardia (QRS complex >120 ms). The Evaluation and Management differential diagnoses for wide-complex tachycardia include Patients with VT and hemodlmamic instability should undergo SW with aberrancy, preexcited tachycardia (antidromic tachy immediate direct current cardioversion (see Sudden Cardiac cardia), ventricular paced rhythms, and most commonly, VL Arrest for a discussion of advanced cardiac life support).

more common in patients with hypertension, LV hypertrophy, In adult patients with known structural heart disease, 95'7, of previous MI, and other forms of structural heart disease, such wide-complex tachycardias are VT, and additional ECG or as nonischemic cardiomyopathy. clinical criteria are often unnecessary. However, in patients In the absence of high risk features (syncope, family his without known structural heart disease, several important tory ofpremature SCD, structural heart disease), reassurance clinical and ECG features can distinguish VT from other condi is often appropriate, and medical therapy is unnecessary. tions. Key features of VT on ECG include AV dissociation, However, PVCs require treatment when symptoms are bother- fusion beats. and capture beats (Figure 26). When the origin some or frequent (>to% ofall beats or 10,000 PVCs per day). of a wide complex tachycardia is in question, VT should be PVC-induced cardiomyopathy may result from frequent PVCs assumed. (generally >10'2,-15% of beats), although it occurs only in a Ventricular arrhythmias most commonly occur in minority of patients (see Heart Failure). patients with structural heart disease, including both ischemic First line treatment for PVC suppression is p blocker or and nonischemic cardiomyopathy, in whom the presence of calcium channel blocker therapy. p-Blockers are preferred in abnormal conduction and/or myocardial scar tissue facilitates patients with ventricular dysfunction. Alternative antiarrhyth the development of VT. In these patients, sustained VT mic therapy may be used if PVCs persist despite p-blockade or (>30 seconds) can lead to hypotension, syncope, VF, and car calcium channel blockade. The selection of an antiarrhlthmic diac arrest; however, on occasion, VT can be well tolerated. medication for PVC suppression depends on many factors, Thus, the absence of hemodynamic compromise does not including age, kidney function, cardiac structure, and comor exclude VT as a diagnosis. bid conditions. Catheter ablation should be considered in VT in the absence of structural heart disease (idiopathic patients with continued frequent PVCs despite medical ther VT) typically arises from the ventricular outflow tracts, fasci apy, patients who cannot tolerate medical therapy, and patients cles, and papillary muscles. Patients with idiopathic VT usu- who develop PVC induced cardiomyopathy. ally present with palpitations in the third to fifth decades of life. Episodes of syncope are uncommon. Arrhythmic events Ventricular Tachycardia are often triggered by stress, emotion, or sleeplessness. Clinical Presentation VT is awide-complex tachycardia (QRS complex >120 ms). The Evaluation and Management differential diagnoses for wide-complex tachycardia include Patients with VT and hemodlmamic instability should undergo SW with aberrancy, preexcited tachycardia (antidromic tachy immediate direct current cardioversion (see Sudden Cardiac cardia), ventricular paced rhythms, and most commonly, VL Arrest for a discussion of advanced cardiac life support). I va

more common in patients with hypertension, LV hypertrophy, In adult patients with known structural heart disease, 95'7, of previous MI, and other forms of structural heart disease, such wide-complex tachycardias are VT, and additional ECG or as nonischemic cardiomyopathy. clinical criteria are often unnecessary. However, in patients In the absence of high risk features (syncope, family his without known structural heart disease, several important tory ofpremature SCD, structural heart disease), reassurance clinical and ECG features can distinguish VT from other condi is often appropriate, and medical therapy is unnecessary. tions. Key features of VT on ECG include AV dissociation, However, PVCs require treatment when symptoms are bother- fusion beats. and capture beats (Figure 26). When the origin some or frequent (>to% ofall beats or 10,000 PVCs per day). of a wide complex tachycardia is in question, VT should be PVC-induced cardiomyopathy may result from frequent PVCs assumed. (generally >10'2,-15% of beats), although it occurs only in a Ventricular arrhythmias most commonly occur in minority of patients (see Heart Failure). patients with structural heart disease, including both ischemic First line treatment for PVC suppression is p blocker or and nonischemic cardiomyopathy, in whom the presence of calcium channel blocker therapy. p-Blockers are preferred in abnormal conduction and/or myocardial scar tissue facilitates patients with ventricular dysfunction. Alternative antiarrhyth the development of VT. In these patients, sustained VT mic therapy may be used if PVCs persist despite p-blockade or (>30 seconds) can lead to hypotension, syncope, VF, and car calcium channel blockade. The selection of an antiarrhlthmic diac arrest; however, on occasion, VT can be well tolerated. medication for PVC suppression depends on many factors, Thus, the absence of hemodynamic compromise does not including age, kidney function, cardiac structure, and comor exclude VT as a diagnosis. bid conditions. Catheter ablation should be considered in VT in the absence of structural heart disease (idiopathic patients with continued frequent PVCs despite medical ther VT) typically arises from the ventricular outflow tracts, fasci apy, patients who cannot tolerate medical therapy, and patients cles, and papillary muscles. Patients with idiopathic VT usu- who develop PVC induced cardiomyopathy. ally present with palpitations in the third to fifth decades of life. Episodes of syncope are uncommon. Arrhythmic events Ventricular Tachycardia are often triggered by stress, emotion, or sleeplessness. Clinical Presentation VT is awide-complex tachycardia (QRS complex >120 ms). The Evaluation and Management differential diagnoses for wide-complex tachycardia include Patients with VT and hemodlmamic instability should undergo SW with aberrancy, preexcited tachycardia (antidromic tachy immediate direct current cardioversion (see Sudden Cardiac cardia), ventricular paced rhythms, and most commonly, VL Arrest for a discussion of advanced cardiac life support). I va li ..1- _.... r .vL v2 y6

I va li ..1- _.... r .vL v2 y6 I I .vF u8' \\ \\\ I FIGURE 26. ECGdemonstratingaregularmonomorphicwide.complextachycardiainaleftbundlebranchblockpattern.Thepresenceof atrioventriculardissociation : confirms the diagnosis of ventricular tachycardia. The arrows identify nonconducting p waves. 56 1 ) t

Arrhythmias Intravenous amiodarone should be administered if the VT per- I n herited Synd romes Cha racterized sists or recurs after cardioversion. Patients with VT or VF with ST elevation MI should undergo emergency revascularization. by Sudden Cardiac Death In patients with hemodynamically stable VT not in the setting Patients younger than 40 years without ischemic or structural of an acute MI, intravenous procainamide can be useful for VT heart disease who have unexplained cardiac arrest, unex termination, or intravenous amiodarone or sotalol may be plained near drowning, or recurrent high risk syncope should considered. be evaluated for inherited arrhythmia and/or cardiomyopathy Evaluation with resting ECG, exercise treadmill testing (to syndromes. Unexplained premature death (age <35 years) or provoke arrhl,thmias), and cardiac imaging (to identiS/ struc sudden death (age <40 years) in a first-degree family member tural heart disease) is indicated in patients with VI, Cardiac also should raise suspicion for an inherited arrhythmia syn- magnetic resonance (CMR) imaging generally allows for tissue drome and prompt referral to a cardiovascular specialist, with characterization, making it an important modality in the evalu- genetic counseling and testing as indicated by clinical find ation of myocardial diseases that may manifest as VI, including ings. The diagnosis of inherited arrhythmia syndromes can be arrhlthmogenic right ventricular cardiomyopathy, myocardial complex because of variable penetrance and expressivity of fibrosis/scarring, cardiac sarcoidosis, and other infiltrative car these disorders. Characteristic findings and treatments for diomyopathies (e.g., amyloidosis). CMR imaging can also clariSr some common syndromes are reviewed in Table 20. the extent and pattern of myocardial scarring. Genetic long QT syndrome is among the most common Patients with ischemic cardiomyopathy who present with inherited arrhythmias, affecting between 1 in 1000 and 1 in VT should be considered for angiography and revasculariza- 5000 persons (Figure 27). However, the presence of a pro tion, if appropriate, primarily to reduce ischemic burden longed QTc (>440 ms in men, >460 ms in women) alone is rather than to treat the arrhythmia. Patients with cardiomy- insufficient to diagnose long QT syndrome. QT prolongation opathy and heart failure should receive guideline directed can have many causes, most of which are acquired, such as medical therapy to minimize risk for ventricular arrhythmia. medication use, structural heart disease, and electrolyte In patients with recurrent VT despite B-blocker therapy, anti- abnormalities. Drugs that have been implicated in QT prolon- arrhythmic drug therapy or catheter ablation may be consid gation include antiarrhythmic agents, antibiotics (including ered. Contemporary evidence suggests ablation to be more some macrolides and fluoroquinolones), antipsychotic drugs, effective than medical therapy. Implantable cardioverter- and antidepressants. Given great variability in QTc across pop defibrillator (lCD) placement is indicated for secondary pre- ulations as well as variable penetrance ofand subtypes oflong vention of SCD in patients with structural heart disease or QT slmdrome, diagnosis is complex and should be referred to a cardiomyopathy who have sustained VT/VF, provided that specialist. A list of drugs categorizcd by their potential to cause QT clearly reversible causes have been excluded (e.g., acute coro- prolongation is available at https: //crediblemeds.org. Treatment nary ischemia, cocaine ingestion). includes B blockers (first line); avoidance of QT-prolonging In patients with idiopathic VT. calcium channel blockers, drugs; and, for selected patients, ICD implantation, surgical sym- especially verapamil, and p blockers are flrst-line therapy. pathectomy, and exercise restriction. Catheter ablation can be considered if symptoms continue Brugada syndrome is distinguished by right precordial despite these therapies. ICD placement is generally unneces ECG abnormalities, including ST segment coving (concave or sary in idiopathic VT because ofthe benign prognosis and high linear downsloping ST segment) in leads V, through V., with efficacy of other therapies. or without right bundle branch block, VF, and cardiac arrest (Figure 28). Brugada syndrome has an increased prevalence in l(EY POTnTS men and persons of Asian descent. Arrhythmic events (includ HVC r Premature ventricular contractions (PVCs) without ing SCD) in patients with Brugada syndrome are more com high-risk features (syncope, family history of premature mon at night during sleep. Abnormalities on ECG can be sudden cardiac death, structural heart disease) are intermittent and may be elicited by fever or pharmacologic managed with reassurance; treatment is reserved for challenge with sodium channel blockade, such as procaina bothersome symptoms or frequent PVCs. mide infusion. . Idiopathic ventricular tachycardia occurs in patients Hypertrophic cardiomyopathy and arrhythmogenic right without structural heart disease and is unlikely to cause ventricular cardiomyopathy/dysplasia (ARVC/D) can often slmcope or sudden cardiac death; p-blockers and calcium present as SCD in young persons. Hypertrophic cardiomy channel blockers are first-line therapy, with catheter abla- opathy and arrhythmic risk stratification are discussed in tion reserved for symptoms refractory to drug therapy. Myocardial Disease. ARVC/D usually appears between puberty o Ventricular tachycardia in the setting of structural heart and young adulthood; however, it can also be identified in older age. Patients with ARVC/D typically present with fre disease often requires eggressive rhythm control along quent ventricular ectopy and/or monomorphic Vl although with implantable cardioverter defibrillator implantation in severe cases, patients can present with heart failure. The for secondary prevention. diagnosis is established by ECG abnormalities, family history

Intravenous amiodarone should be administered if the VT per- I n herited Synd romes Cha racterized sists or recurs after cardioversion. Patients with VT or VF with ST elevation MI should undergo emergency revascularization. by Sudden Cardiac Death In patients with hemodynamically stable VT not in the setting Patients younger than 40 years without ischemic or structural of an acute MI, intravenous procainamide can be useful for VT heart disease who have unexplained cardiac arrest, unex termination, or intravenous amiodarone or sotalol may be plained near drowning, or recurrent high risk syncope should considered. be evaluated for inherited arrhythmia and/or cardiomyopathy Evaluation with resting ECG, exercise treadmill testing (to syndromes. Unexplained premature death (age <35 years) or provoke arrhl,thmias), and cardiac imaging (to identiS/ struc sudden death (age <40 years) in a first-degree family member tural heart disease) is indicated in patients with VI, Cardiac also should raise suspicion for an inherited arrhythmia syn- magnetic resonance (CMR) imaging generally allows for tissue drome and prompt referral to a cardiovascular specialist, with characterization, making it an important modality in the evalu- genetic counseling and testing as indicated by clinical find ation of myocardial diseases that may manifest as VI, including ings. The diagnosis of inherited arrhythmia syndromes can be arrhlthmogenic right ventricular cardiomyopathy, myocardial complex because of variable penetrance and expressivity of fibrosis/scarring, cardiac sarcoidosis, and other infiltrative car these disorders. Characteristic findings and treatments for diomyopathies (e.g., amyloidosis). CMR imaging can also clariSr some common syndromes are reviewed in Table 20. the extent and pattern of myocardial scarring. Genetic long QT syndrome is among the most common Patients with ischemic cardiomyopathy who present with inherited arrhythmias, affecting between 1 in 1000 and 1 in VT should be considered for angiography and revasculariza- 5000 persons (Figure 27). However, the presence of a pro tion, if appropriate, primarily to reduce ischemic burden longed QTc (>440 ms in men, >460 ms in women) alone is rather than to treat the arrhythmia. Patients with cardiomy- insufficient to diagnose long QT syndrome. QT prolongation opathy and heart failure should receive guideline directed can have many causes, most of which are acquired, such as medical therapy to minimize risk for ventricular arrhythmia. medication use, structural heart disease, and electrolyte In patients with recurrent VT despite B-blocker therapy, anti- abnormalities. Drugs that have been implicated in QT prolon- arrhythmic drug therapy or catheter ablation may be consid gation include antiarrhythmic agents, antibiotics (including ered. Contemporary evidence suggests ablation to be more some macrolides and fluoroquinolones), antipsychotic drugs, effective than medical therapy. Implantable cardioverter- and antidepressants. Given great variability in QTc across pop defibrillator (lCD) placement is indicated for secondary pre- ulations as well as variable penetrance ofand subtypes oflong vention of SCD in patients with structural heart disease or QT slmdrome, diagnosis is complex and should be referred to a cardiomyopathy who have sustained VT/VF, provided that specialist. A list of drugs categorizcd by their potential to cause QT clearly reversible causes have been excluded (e.g., acute coro- prolongation is available at https: //crediblemeds.org. Treatment nary ischemia, cocaine ingestion). includes B blockers (first line); avoidance of QT-prolonging In patients with idiopathic VT. calcium channel blockers, drugs; and, for selected patients, ICD implantation, surgical sym- especially verapamil, and p blockers are flrst-line therapy. pathectomy, and exercise restriction. Catheter ablation can be considered if symptoms continue Brugada syndrome is distinguished by right precordial despite these therapies. ICD placement is generally unneces ECG abnormalities, including ST segment coving (concave or sary in idiopathic VT because ofthe benign prognosis and high linear downsloping ST segment) in leads V, through V., with efficacy of other therapies. or without right bundle branch block, VF, and cardiac arrest (Figure 28). Brugada syndrome has an increased prevalence in l(EY POTnTS men and persons of Asian descent. Arrhythmic events (includ HVC r Premature ventricular contractions (PVCs) without ing SCD) in patients with Brugada syndrome are more com high-risk features (syncope, family history of premature mon at night during sleep. Abnormalities on ECG can be sudden cardiac death, structural heart disease) are intermittent and may be elicited by fever or pharmacologic managed with reassurance; treatment is reserved for challenge with sodium channel blockade, such as procaina bothersome symptoms or frequent PVCs. mide infusion. . Idiopathic ventricular tachycardia occurs in patients Hypertrophic cardiomyopathy and arrhythmogenic right without structural heart disease and is unlikely to cause ventricular cardiomyopathy/dysplasia (ARVC/D) can often slmcope or sudden cardiac death; p-blockers and calcium present as SCD in young persons. Hypertrophic cardiomy channel blockers are first-line therapy, with catheter abla- opathy and arrhythmic risk stratification are discussed in tion reserved for symptoms refractory to drug therapy. Myocardial Disease. ARVC/D usually appears between puberty o Ventricular tachycardia in the setting of structural heart and young adulthood; however, it can also be identified in older age. Patients with ARVC/D typically present with fre disease often requires eggressive rhythm control along quent ventricular ectopy and/or monomorphic Vl although with implantable cardioverter defibrillator implantation in severe cases, patients can present with heart failure. The for secondary prevention. diagnosis is established by ECG abnormalities, family history 57

Arrhythmias T&*t[ :*. lnherited Syndromes Characterized by Sudden Cardiac Death Disorder Presenting Symptoms and Potential Treatments' Characteristi< Findings Long QTsyndrome Syncope during sleep, auditorytriggers, p-Blockers, avoidance of OT-prolonging drugs; and/or during exercise (depending on selected patients: lCD, sympathectomy, subtype); QTc usually >460 ms; torsades exercise restriction de pointes Brugada syndrome Syncope during sleep, VF, coved lCD, avoidance or man agement of triggers ST-segment elevation in early precordial (drugs, feved, catheter ablation leads (V1 through V3) Catecholaminergic polymorphic VT Syncope, polymorphic or bidireaional W p-Blockers, verapamil, flecainide, lCD, exercise during exercise or emotional distress abstinence (uniform) ARVC/D Syncope, palpitations, T-wave inversions in lCD, B-blockers, antiarrhythmic medications, leads V1 through at least V3, monomorphic catheter ablation, exercise abstinence VT, frequent PVCs, and abnormal right (uniform) ventricular size and function on echocardiography or CMR imaging Hypertrophic cardiomyopathy Syncope, VF during exercise, increased lCD, p-blockers, disopyramide, catheter QRS voltage with or without repolarization ablation, surgical myectomy abnormalities on ECG ARVC/D = arh)'thmogenic right ventricular cardiomyopathy/dysplasia; CMR = cardiac magnetic resonance; ICD = implantable cardioverter defibrillator; PVC = premature ventricular contraction; OTc = corrected OT interual; VF = ventricular fibrillation; VT = ventricular tachycardaa.

T&*t[ :*. lnherited Syndromes Characterized by Sudden Cardiac Death Disorder Presenting Symptoms and Potential Treatments' Characteristi< Findings Long QTsyndrome Syncope during sleep, auditorytriggers, p-Blockers, avoidance of OT-prolonging drugs; and/or during exercise (depending on selected patients: lCD, sympathectomy, subtype); QTc usually >460 ms; torsades exercise restriction de pointes Brugada syndrome Syncope during sleep, VF, coved lCD, avoidance or man agement of triggers ST-segment elevation in early precordial (drugs, feved, catheter ablation leads (V1 through V3) Catecholaminergic polymorphic VT Syncope, polymorphic or bidireaional W p-Blockers, verapamil, flecainide, lCD, exercise during exercise or emotional distress abstinence (uniform) ARVC/D Syncope, palpitations, T-wave inversions in lCD, B-blockers, antiarrhythmic medications, leads V1 through at least V3, monomorphic catheter ablation, exercise abstinence VT, frequent PVCs, and abnormal right (uniform) ventricular size and function on echocardiography or CMR imaging Hypertrophic cardiomyopathy Syncope, VF during exercise, increased lCD, p-blockers, disopyramide, catheter QRS voltage with or without repolarization ablation, surgical myectomy abnormalities on ECG ARVC/D = arh)'thmogenic right ventricular cardiomyopathy/dysplasia; CMR = cardiac magnetic resonance; ICD = implantable cardioverter defibrillator; PVC = premature ventricular contraction; OTc = corrected OT interual; VF = ventricular fibrillation; VT = ventricular tachycardaa. antiarrhythmic drugs are often required for recurrent ventricular arrhythmias.

T&*t[ :*. lnherited Syndromes Characterized by Sudden Cardiac Death Disorder Presenting Symptoms and Potential Treatments' Characteristi< Findings Long QTsyndrome Syncope during sleep, auditorytriggers, p-Blockers, avoidance of OT-prolonging drugs; and/or during exercise (depending on selected patients: lCD, sympathectomy, subtype); QTc usually >460 ms; torsades exercise restriction de pointes Brugada syndrome Syncope during sleep, VF, coved lCD, avoidance or man agement of triggers ST-segment elevation in early precordial (drugs, feved, catheter ablation leads (V1 through V3) Catecholaminergic polymorphic VT Syncope, polymorphic or bidireaional W p-Blockers, verapamil, flecainide, lCD, exercise during exercise or emotional distress abstinence (uniform) ARVC/D Syncope, palpitations, T-wave inversions in lCD, B-blockers, antiarrhythmic medications, leads V1 through at least V3, monomorphic catheter ablation, exercise abstinence VT, frequent PVCs, and abnormal right (uniform) ventricular size and function on echocardiography or CMR imaging Hypertrophic cardiomyopathy Syncope, VF during exercise, increased lCD, p-blockers, disopyramide, catheter QRS voltage with or without repolarization ablation, surgical myectomy abnormalities on ECG ARVC/D = arh)'thmogenic right ventricular cardiomyopathy/dysplasia; CMR = cardiac magnetic resonance; ICD = implantable cardioverter defibrillator; PVC = premature ventricular contraction; OTc = corrected OT interual; VF = ventricular fibrillation; VT = ventricular tachycardaa. antiarrhythmic drugs are often required for recurrent ventricular arrhythmias. alrR vl va

T&*t[ :*. lnherited Syndromes Characterized by Sudden Cardiac Death Disorder Presenting Symptoms and Potential Treatments' Characteristi< Findings Long QTsyndrome Syncope during sleep, auditorytriggers, p-Blockers, avoidance of OT-prolonging drugs; and/or during exercise (depending on selected patients: lCD, sympathectomy, subtype); QTc usually >460 ms; torsades exercise restriction de pointes Brugada syndrome Syncope during sleep, VF, coved lCD, avoidance or man agement of triggers ST-segment elevation in early precordial (drugs, feved, catheter ablation leads (V1 through V3) Catecholaminergic polymorphic VT Syncope, polymorphic or bidireaional W p-Blockers, verapamil, flecainide, lCD, exercise during exercise or emotional distress abstinence (uniform) ARVC/D Syncope, palpitations, T-wave inversions in lCD, B-blockers, antiarrhythmic medications, leads V1 through at least V3, monomorphic catheter ablation, exercise abstinence VT, frequent PVCs, and abnormal right (uniform) ventricular size and function on echocardiography or CMR imaging Hypertrophic cardiomyopathy Syncope, VF during exercise, increased lCD, p-blockers, disopyramide, catheter QRS voltage with or without repolarization ablation, surgical myectomy abnormalities on ECG ARVC/D = arh)'thmogenic right ventricular cardiomyopathy/dysplasia; CMR = cardiac magnetic resonance; ICD = implantable cardioverter defibrillator; PVC = premature ventricular contraction; OTc = corrected OT interual; VF = ventricular fibrillation; VT = ventricular tachycardaa. antiarrhythmic drugs are often required for recurrent ventricular arrhythmias. alrR vl va t a\rt vil vt

T&*t[ :*. lnherited Syndromes Characterized by Sudden Cardiac Death Disorder Presenting Symptoms and Potential Treatments' Characteristi< Findings Long QTsyndrome Syncope during sleep, auditorytriggers, p-Blockers, avoidance of OT-prolonging drugs; and/or during exercise (depending on selected patients: lCD, sympathectomy, subtype); QTc usually >460 ms; torsades exercise restriction de pointes Brugada syndrome Syncope during sleep, VF, coved lCD, avoidance or man agement of triggers ST-segment elevation in early precordial (drugs, feved, catheter ablation leads (V1 through V3) Catecholaminergic polymorphic VT Syncope, polymorphic or bidireaional W p-Blockers, verapamil, flecainide, lCD, exercise during exercise or emotional distress abstinence (uniform) ARVC/D Syncope, palpitations, T-wave inversions in lCD, B-blockers, antiarrhythmic medications, leads V1 through at least V3, monomorphic catheter ablation, exercise abstinence VT, frequent PVCs, and abnormal right (uniform) ventricular size and function on echocardiography or CMR imaging Hypertrophic cardiomyopathy Syncope, VF during exercise, increased lCD, p-blockers, disopyramide, catheter QRS voltage with or without repolarization ablation, surgical myectomy abnormalities on ECG ARVC/D = arh)'thmogenic right ventricular cardiomyopathy/dysplasia; CMR = cardiac magnetic resonance; ICD = implantable cardioverter defibrillator; PVC = premature ventricular contraction; OTc = corrected OT interual; VF = ventricular fibrillation; VT = ventricular tachycardaa. antiarrhythmic drugs are often required for recurrent ventricular arrhythmias. alrR vl va t a\rt vil vt ,tG \a \6

antiarrhythmic drugs are often required for recurrent ventricular arrhythmias. alrR vl va t a\rt vil vt ,tG \a \6 t/!t FIGURE 2l .ECGdemonstratingsignificantprolongationofthe0Iinterval aswell asabnormal morphology,whichisbestseenintheearlyprecordial leads.0f note, when the heart rate is less than 60/min, the absolute 0T interval is routinely used instead of the conected 0T interval (0Tc) for heart rate. A 0T or OTc greater than 500 ms is a risk factor for adverse events. 58

Arrhythmias I aVL lI aVF v3 t I G U R E 2 8 . ECG demonstrating a type 1 Brugada pattern, >2 m m J-point elevation, ST,segment coving (concave or linea r downsloping 5T seg ment) (arorvs), a nd T,wave inversions in leads V, through V3. arrhythmias, and structural abnormalities of the right ventri In the United States, more than 350,000 episodes of SCD cle. CMR imaging can demonstrate enlargement (segments of occur each year. The annual risk for SCD is 1:1000 in the general poorly contracting heart muscle), focal aneurysms, and wall population. The highest incidence occurs in patients with pre- motion abnormalities in the right ventricle (hypokinesis). existing structural heart disease, although LV function is normal ARVC/D is usually progressive, and patients should abstain in most patients who experience SCD. fusk factors include heart from vigorous exercise. Patients with ARVC/D and cardiac failure, diminished LV function, previous MI, unexplained syn- arrest or risk factors (nonsustained VT, inducible VT) should cope, LV hypertrophy, nonsustained ventricular arrhythmia, be offered an ICD. B Blockers are first line therapy for ven chronic kidney disease, and sleep apnea. It is important to dis tricular arrhythmias, although antiarrhythmic therapy with tinguish between MI precipitating death and nonischemic SCD sotalol or amiodarone or catheter ablation is often required for when a family history of cardiac disease is obtained. recurrent VT.

arrhythmias, and structural abnormalities of the right ventri In the United States, more than 350,000 episodes of SCD cle. CMR imaging can demonstrate enlargement (segments of occur each year. The annual risk for SCD is 1:1000 in the general poorly contracting heart muscle), focal aneurysms, and wall population. The highest incidence occurs in patients with pre- motion abnormalities in the right ventricle (hypokinesis). existing structural heart disease, although LV function is normal ARVC/D is usually progressive, and patients should abstain in most patients who experience SCD. fusk factors include heart from vigorous exercise. Patients with ARVC/D and cardiac failure, diminished LV function, previous MI, unexplained syn- arrest or risk factors (nonsustained VT, inducible VT) should cope, LV hypertrophy, nonsustained ventricular arrhythmia, be offered an ICD. B Blockers are first line therapy for ven chronic kidney disease, and sleep apnea. It is important to dis tricular arrhythmias, although antiarrhythmic therapy with tinguish between MI precipitating death and nonischemic SCD sotalol or amiodarone or catheter ablation is often required for when a family history of cardiac disease is obtained. recurrent VT. IEY POTXI Acute Management . Unexplained premature death or sudden death in a Cardiac arrest necessitates immediate cardiopulmonary resus first degree family member should raise suspicion for citation (CPR) and advanced cardiac life support (Figure 29). an inherited arrhythmia syndrome and prompt referral Interruptions in chest compressions should be minimized, and to a cardiovascular specialist. defibrillation should occur as soon as possible in patients with a shockable rhy'thm because time to defibrillation is an impor- tant determinant of likelihood of survival to hospital discharge. Sudden Cardiac Arrest The presence or absence ol a shockable rhythm guides Epidemiology and Risk Factors management after CPR initiation. In patients with out-of- SCD is defined as a fatal event or collapse within t hour of hospital arrest, early cardiac catheterization has value in (1) symptom onset in a person without recent acute illness. In providing early diagnosis of the etiologr of arrest, (2) facilitat patients in whom death was unwitnessed, SCD is considered ing early intervention when applicable, and (3) providing to have occurred if the patient was known to be alive and well opportunities for advanced hemodynamic support (e.g., extra- within the last 24 hours. VT and VF are the most common corporeal membrane oxygenation). Any reversible causes, causes of SCD. such as tamponade, should be identified and treated.

IEY POTXI Acute Management . Unexplained premature death or sudden death in a Cardiac arrest necessitates immediate cardiopulmonary resus first degree family member should raise suspicion for citation (CPR) and advanced cardiac life support (Figure 29). an inherited arrhythmia syndrome and prompt referral Interruptions in chest compressions should be minimized, and to a cardiovascular specialist. defibrillation should occur as soon as possible in patients with a shockable rhy'thm because time to defibrillation is an impor- tant determinant of likelihood of survival to hospital discharge. Sudden Cardiac Arrest The presence or absence ol a shockable rhythm guides Epidemiology and Risk Factors management after CPR initiation. In patients with out-of- SCD is defined as a fatal event or collapse within t hour of hospital arrest, early cardiac catheterization has value in (1) symptom onset in a person without recent acute illness. In providing early diagnosis of the etiologr of arrest, (2) facilitat patients in whom death was unwitnessed, SCD is considered ing early intervention when applicable, and (3) providing to have occurred if the patient was known to be alive and well opportunities for advanced hemodynamic support (e.g., extra- within the last 24 hours. VT and VF are the most common corporeal membrane oxygenation). Any reversible causes, causes of SCD. such as tamponade, should be identified and treated. 59