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Narrow Complex Tachycardias Moritz Haager PGY-5. Objectives Develop an approach Develop an approach Review treatment options Review treatment options.

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Presentation on theme: "Narrow Complex Tachycardias Moritz Haager PGY-5. Objectives Develop an approach Develop an approach Review treatment options Review treatment options."— Presentation transcript:

1 Narrow Complex Tachycardias Moritz Haager PGY-5

2 Objectives Develop an approach Develop an approach Review treatment options Review treatment options Dispositon decisions Dispositon decisions

3 Perspective SVT SVT –Broad umbrella term for any tachycardia originating above the ventricles –Variable underlying mechanisms but basically one Tx approach –Ranges from physiological pathological, and benign dangerous –Occurs in all age groups –Clinical presentation from asymptomatic shock / CHF When presented with an undifferentiated presentation with a broad DDx and variability in outcome you need an APPROACH

4 Why should we care? Morbidity & Mortality Morbidity & Mortality –Patient discomfort & anxiety –Syncopal events (falls) ~15% –Risk of sudden cardiac death w/ accessory pathway driven arrhythmias –Tachycardia-mediated cardiomyopathy LV dilatation w/ impaired LV function LV dilatation w/ impaired LV function

5 Approach to Tachycardia Stable or unstable? Stable or unstable? –Assess ABCs, O 2, IV, monitors, crash cart to bedside –In general if unstable, givem juice Narrow or wide QRS? Narrow or wide QRS? Regular or irregular? Regular or irregular? Look at the P waves Look at the P waves –Relationship to QRS –P wave axis / rate –P wave morphology(ies) What is the trigger / underlying cause? What is the trigger / underlying cause?

6 Step 1: Stable or Unstable? Not always black & white Not always black & white –Continuum from stable compensated decompensated shock arrest –Stability determined by big picture: Symptoms, signs, & vitals Symptoms, signs, & vitals Cardio-respiratory reserve Cardio-respiratory reserve Age Age Co-morbidities Co-morbidities Be prepared Be prepared –Any dysrhythmia could potentially deteriorate –All therapies are potentially pro-arrhythmic

7 Step 2: Narrow or wide? Measure widest QRS on ECG Measure widest QRS on ECG –Adults: wide = >0.12 sec (3 small boxes) –Kids 0.08 sec (2 boxes)

8 Step 3: Regular or Irregular? Use calipers or paper Use calipers or paper –Irregularity can be subtle, esp at fast rates Generally Generally –Irregular rhythms originate ABOVE the AV node –VT is almost never irregular

9 Step 4: Look at the P waves P waves present? P waves present? Is there a P before every QRS? Is there a P before every QRS? What is the relationship b/w the P and the QRS? What is the relationship b/w the P and the QRS? –What is the P wave rate? Ventricular rate? Is the P wave coming from the SA? Is the P wave coming from the SA? –N axis: upright in II, negative in aVR Is there >1 distinct P wave morhology? Is there >1 distinct P wave morhology?

10 Diagnostic Trick: 50 mm/s ECG Tracings Comparsion study of 8 EPs Comparsion study of 8 EPs –Given 45 ECGs of NCTs printed at 25 mm/s & asked to give Dx & Tx plan –2 wks later given same ECGs printed at 25 & 50 mm/s & asked to give Dx & Tx Results Results –50 mm/s increased diagnostic accuracy from 63 to 71%, P=0.002 J Emerg Med 2002; 22: 123–126 J Emerg Med 2002; 22: 123–126

11 Final Categorization Narrow Complex Tachycardias Narrow Complex Tachycardias –Regular w/ Ps = sinus, a. flutter w/ constant block, Focal atrial tachycardia, AVNRT, junctional tachycardia = sinus, a. flutter w/ constant block, Focal atrial tachycardia, AVNRT, junctional tachycardia –Irregular w/ Ps = MAT, a. flutter variable block = MAT, a. flutter variable block –Regular, no Ps = AVRT, AVNRT = AVRT, AVNRT –Irregular, no Ps = a. fib = a. fib Wide Complex Tachycardias Wide Complex Tachycardias Tx w/ AV nodal blockers Rate control +/- rhythm control

12 Step 5: Underlying Causes HIS DEBTS HIS DEBTS –H – Hypoxia –I – Ischemia / infarction –S – Sympathetic excess Hyperthyroid, CHF, pheochromocytoma, excercise Hyperthyroid, CHF, pheochromocytoma, excercise –D – Drugs Anti-arrhythmics, cocaine, amphetamines, caffeine, etc Anti-arrhythmics, cocaine, amphetamines, caffeine, etc –E – Electrolytes K +, Ca 2+, Mg 2+ K +, Ca 2+, Mg 2+ –B – Bradycardias Eg. Sick sinus syndrome Eg. Sick sinus syndrome –T – Thyroid disease –S – Stretch Hypertrophy / dilation of atria & ventricles (CHF, valvular Dz) Hypertrophy / dilation of atria & ventricles (CHF, valvular Dz) Preciptants vary w/ age, sex, co-morbidities, etc

13 Clinical Presentations Typical Sx Typical Sx –Palpitations96% –Dizziness75% –Dyspnea47% –Fatigue23% –Chest pain35% –Diaphoresis17% –Nausea13% –Neck pounding said to be pathogonomonic

14 Case 27 yo M w/ palpitations & dyspnea 27 yo M w/ palpitations & dyspnea NCT at 160 on ECG c/w PSVT NCT at 160 on ECG c/w PSVT Also tells you he has been pissin like a racehorse Also tells you he has been pissin like a racehorse Does he have diabetes? Does he have diabetes?

15 Polyuria in PSVT Loss of AV synchronization Loss of AV synchronization Atrial contraction against closed AV valves Atrial contraction against closed AV valves Elevated atrial pressure & atrial stretch Elevated atrial pressure & atrial stretch Release of atrial natriuretic peptide polyuria Release of atrial natriuretic peptide polyuria NB: This is trivia – absence of polyuria does NOT exclude Dx of PSVT and you should still check at least a urine for glucose

16 Case 3 mo F w/ dyspnea & wheeze 3 mo F w/ dyspnea & wheeze T 40.5 o C, P 190, RR 60, SpO 2 88% T 40.5 o C, P 190, RR 60, SpO 2 88% Mod resp distress on exam w/ wheezes & crackles bilaterally Mod resp distress on exam w/ wheezes & crackles bilaterally Is this just sinus tachycardia from her fever? Is this just sinus tachycardia from her fever?

17 Tachycardia & Fever Prospective observational study of 490 infants <1 yo Prospective observational study of 490 infants <1 yo –Measured HR & rectal temp in calm, quiet kids w/o evidence of serious illness –Analyzed relationship b/w HR & temp w/ multivariate linear regression Results Results –HR increased ~10 bpm for every 1 o C rise in infants b/w mo Ann Emerg Med. 2004;43: Ann Emerg Med. 2004;43:

18 Tachycardias: Mechanism 1. Reentry 50-80% of NCTs 50-80% of NCTs Abrupt on-/off-set Abrupt on-/off-set Do well w/ electricity Do well w/ electricity 2. Enhanced automaticity Typically catecholamines, drugs, lytes, ischemia Typically catecholamines, drugs, lytes, ischemia Gradual on-/off-set Gradual on-/off-set Not likely to respond to electricity; Tx underlying cause Not likely to respond to electricity; Tx underlying cause 3. Triggered dysthythmias Interruption of repolarization by afterdepolarizations Interruption of repolarization by afterdepolarizations Ischemia, drugs, lytes, catecholamines Ischemia, drugs, lytes, catecholamines Not likely to respond to electricity; Tx underlying cause E.g. Torsades IV magnesium Not likely to respond to electricity; Tx underlying cause E.g. Torsades IV magnesium

19 Case 2 80 yo F w/ sepsis: Is this sinus tachy?

20 Maximal sinus tach 220 – age = maximum HR 220 – age = maximum HR – = 140 –Unlikey this is just sinus tach

21 Regular NCT: DDx P waves present: P waves present: –Sinus tachycardia –Atrial Flutter –AVNRT –AVRT –Focal Atrial Tachycardia No P-waves No P-waves –AVRT –AVNRT –Junctional Tachycardia Consider under PSVT as can be impossible to differentiate on ECG; Tx generally the same

22 AVNRT vs. AVRT AV nodal reentrant tachycardia AV nodal reentrant tachycardia –Most common PSVT (>60%) –Dual AV nodal physiology 2 separate conduction paths in AV node 2 separate conduction paths in AV node –Fast pathway –Slow pathway Allow for re-entry circuit w/in AV node Allow for re-entry circuit w/in AV node Atrioventricular reentrant tachycardia Atrioventricular reentrant tachycardia –accessory pathway(s) (AP) = Tracks of conducting tissue outside of AV node, connecting atria & ventricles Re-entry circuit formed by –AP & AV node (WPW) –2 or more separate APs (bypass AV node completely)

23 AVNRT Typical AVNRT – = 90-95% Anterograde conduction down slow pathwayAnterograde conduction down slow pathway Retrograde conduction up fast pathwayRetrograde conduction up fast pathway If P waves seen RP < PR intervalIf P waves seen RP < PR interval Atypical AVNRT is the reverse of what is pictured here VENTRICLES ATRIA

24 AVRT 2 types of AP 2 types of AP –concealed = capable of retrograde conduction only –manifest = allow anterograde +/- retrograde conduction See pre-excitation on ECG See pre-excitation on ECG

25

26 Preexcitation Syndromes WPW (Wolf- Parkinson-White) WPW (Wolf- Parkinson-White) –PR <120 msec –QRS >100 msec –Delta waves in some leads LGL (Lown-Ganong- Levine) LGL (Lown-Ganong- Levine) –PR <120 msec

27 WPW & SVT Orthodromic SVT Orthodromic SVT –Anterograde via AV & returns via accessory tract –Uses normal conduction system therefore get narrow complex tachycardia Orthodromic makes up 90-95% of WPW SVTs

28 WPW & SVT Antidromic SVT Antidromic SVT –Anterograde conduction from atria to ventricles via accessory path & retrograde flow through AV node –Wide complex tachycardia –Avoid AV nodal blockers Use procainamide or cardiovert Use procainamide or cardiovert (5-10% of WPW SVT)

29 WPW & A Fib Irregular Wide complex tachycardia Irregular Wide complex tachycardia –May see capture & fusion beats Common (~30% of WPW pts) & potentially life-threatening Common (~30% of WPW pts) & potentially life-threatening –AP w/ short refractory period & anterograde conduction near 1:1 conduction VF –0.15 – 0.39% incidence of sudden cardiac death Do NOT block AV node Do NOT block AV node –Channels all impulses down AP & increases risk of VF –Use Procainamide or cardioversion

30 Predictors of Sudden Cardiac Death in WPW Shortest pre-excited R-R interval during atrial fib <250 ms Shortest pre-excited R-R interval during atrial fib <250 ms Hx of symptomatic tachycardia Hx of symptomatic tachycardia Multiple accessory pathways Multiple accessory pathways Ebsteins anomaly* Ebsteins anomaly* Blomström-Lundqvist et al. ACC/AHA/ESC Guidelines for Management of SVA ACC 2003; 42:1493–531 *= abnormal tricuspid valve regurgitation & RA enlargement

31 AVNRT vs. AVRT: Can you tell them apart Helpful ECG findings Helpful ECG findings –Pseudo R in V1 –Pseudo S in II, III, aVF specific (but not sensitive) for AVNRT specific (but not sensitive) for AVNRT –ST elevation in aVR –RP >100 ms –ST depression 2mm Suggest (not highly specific or sensitive) AVRT Suggest (not highly specific or sensitive) AVRT Bottom line = 12-lead lacks 100% accuracy but important to look because AVRT more serious Dx See Adam Osters talk July 22, 2004 for more detailed explanation

32 PSVT: Acute Treatment Summary Unstable Unstable –DC cardioversion Stable Stable –1) Vagal maneuvers (Class I/ level A) –2) Adenosine (Class I/ level A) –3) CCBs (Class I/ level A) –4) BBs (Class IIb/ level C) –5) Amiodarone (Class IIb/ level C) –6) Digoxin (Class IIb/ level C) Blomström-Lundqvist et al. ACC/AHA/ESC Guidelines for Management of SVA JACC 2003; 42:1493–531

33 Cardioversion Sedation Sedation –?1 mg midaz mcg fentanyl Energy Levels Energy Levels –PSVT:- 50 Joules –Atrial fibrillation: 200 Joules –Atrial flutter: Joules –Orthodromic WPW: 50 Joules –Narrow Complex VT: Joules

34 Adenosine Actions Actions –Coronary vasodilator –Transient SA & AV nodal blockade Outward K + current hyperpolarizes cells Outward K + current hyperpolarizes cells –Reflex catecholamine release & sympathetic discharge T 1/2 <10 sec; T 1/2 <10 sec; Duration of action sec Duration of action sec

35 Adenosine: Adverse Effects Hot flash / flushing~25% Hot flash / flushing~25% Dizziness~20-50% Dizziness~20-50% Chest pain / pressure~20-40% Chest pain / pressure~20-40% Dyspnea~10-25% Dyspnea~10-25% Feeling of impending doom~10% Feeling of impending doom~10% Pro-arrhythmia/ blocks~10% Pro-arrhythmia/ blocks~10% >75% of pts will experience side effects w/ adenosine

36 Adenosine: Pro-arrhythmic Effects Significant literature reports Significant literature reports –A fib, VF, Transient sinus arrest / asystole, Torsades de pointes Prospective observational ED study Prospective observational ED study –160 consecutive pts given adenosine Overall 21 (13%) pts had pro-arrhythmic s/e Overall 21 (13%) pts had pro-arrhythmic s/e –Prolonged AV block (>4sec)11 (7%) –Atrial Fib2 (1%) –Non-sustained VT8 (5%) All resolved spontaneously; no serious outcomes All resolved spontaneously; no serious outcomes Euro J Emerg Med 2001; 8:

37 Pearls Adenosine CAN convert some VT, Adenosine CAN convert some VT, – giving it to diagnose SVT w/ aberrancy is misguided Wide & irregular – think WPW + A fib Wide & irregular – think WPW + A fib –NO AV nodal blockers –Amiodarone may not be ideal –Procainamide is the drug of choice

38 Adenosine: Drug Interactions Theophylline Theophylline –s dose requirement Dipyridamole Dipyridamole – s dose requirement Carbamazepine Carbamazepine –potentiates adenosine-induced heart block CCBs / BBs CCBs / BBs –Potentiate hypotension & bradycardia

39 Adenosine Dosing DBRCT of 201 pts w/ PSVT: DBRCT of 201 pts w/ PSVT: –Adenosine DoseConversion Rate –3 mg35.2% –6 mg62.3% –9 mg80.2% –12 mg91.4% P<0.001 for all doses c/w placebo P<0.001 for all doses c/w placebo All administered through PIV All administered through PIV DiMarco et al. Ann Intern Med 1990; 113:

40 Practical Pearl Adenosine administration Adenosine administration –Want to get it in as fast as possible –Use 2 syringes w/ 18g needles one w/ adenosine one w/ adenosine Other w/ 10 cc NS Other w/ 10 cc NS –Put both needles into IV access port Push the adenosine w/ one hand and… Push the adenosine w/ one hand and… …chase immediately w/ the NS w/ the other …chase immediately w/ the NS w/ the other –NB: want an IV in the AC if at all possible

41 Adenosine via Central Line Appears to have increased success rate Appears to have increased success rate –Observational study of 200 pts w/ PSVT induced in EP lab found 99% success rate w/ 12 mg via femoral line found 99% success rate w/ 12 mg via femoral line –Strickberger et al. Ann Intern Med 1997; 127: –Randomized Cross-over study of 30 pts given adenosine via PIV or central line success rate w/ 3 mg was 77% when given via central line vs. 37% via PIV success rate w/ 3 mg was 77% when given via central line vs. 37% via PIV –McIntosh-Yellin et al. JACC 1993; 22:741–5 –Case reports of more severe S/E via central line (felt to be dose-related)

42 Case 4 31 yo F w/ PSVT 31 yo F w/ PSVT –Vagal maneuvers fail –6 mg adenosine IV no response –12 mg adenosine IV slows down briefly What now? Would you give her 18 mg of adenosine? What now? Would you give her 18 mg of adenosine?

43 High Dose Adenosine Background Background –ACLS: 6 mg, then 12 mg x2 if unsuccessful –FDA approves use up to 12 mg –Literature reports of uses up to 25 mg What about higher doses? What about higher doses? –Randomized cross-over comparison of of 31 pts w/ AVNRT/AVRT in EP lab given 12 & 18 mg adenosine via PIV Non-significant increase in efficacy w/ 18 mg Non-significant increase in efficacy w/ 18 mg –25/31 (81%) vs. 29/31 (94%); P = 0.103) No significant increase in adverse effects No significant increase in adverse effects –may have been underpowered to find difference Weismueller et al. Deutsche Med Wochenschrift :

44 Calcium Channel Blockers 2 nd line agents in PSVT 2 nd line agents in PSVT –Verapamil 1 st dose: 2.5 – 5 mg IV over 2 min 1 st dose: 2.5 – 5 mg IV over 2 min 2 nd dose (30 min later): 2.5 – 10 mg IV over 2 min (to max of 20 mg) 2 nd dose (30 min later): 2.5 – 10 mg IV over 2 min (to max of 20 mg) NB: CONTRAINDICATED in <1yo (risk of EMD), wide QRS, or hypotensive pts, CHF, or WPW NB: CONTRAINDICATED in <1yo (risk of EMD), wide QRS, or hypotensive pts, CHF, or WPW –Diltiazem 1 st dose: 0.25 mg/kg IV over 2 min 1 st dose: 0.25 mg/kg IV over 2 min 2 nd dose (15 min later): 0.35 mg/kg IV over 2 min followed by gtt of 5-15 mg/h 2 nd dose (15 min later): 0.35 mg/kg IV over 2 min followed by gtt of 5-15 mg/h Generally felt to be safer than Verapamil but same cautions apply Generally felt to be safer than Verapamil but same cautions apply

45 What about Verapamil? RCT of 122 pts w/ PSVT treated w/ either adenosine or Verapamil RCT of 122 pts w/ PSVT treated w/ either adenosine or Verapamil –NS difference in conversion to NSR 86.0% (52/60) vs. 87.1% (54/62), p=NS 86.0% (52/60) vs. 87.1% (54/62), p=NS –Adenosine worked much faster / sec vs / sec, P < / sec vs / sec, P < Cheng KA Zhonghua Nei Ke Za Zhi 2003; 42(11): Cheng KA Zhonghua Nei Ke Za Zhi 2003; 42(11): 773-6

46 Adenosine vs Verapamil DiMarco et al. Ann Intern Med 1990; 113: DBRCT of 70 pts w/ PSVT

47 Adenosine vs. Verapamil Retrospective study of 106 pts w/ PSVT treated w/ adenosine or verapamil Retrospective study of 106 pts w/ PSVT treated w/ adenosine or verapamil –No sig difference in overall efficacy –Logistic regression found Adenosine worked better w/ faster HR Verapamil had better success w/ slower HR Adenosine worked better w/ faster HR Verapamil had better success w/ slower HR Interesting study, but hypothesis-generating at most; needs prospective, randomized investigation Euro Heart J 2004; 25: 1310–1317

48 Case 78 yo F presents w/ NCT 78 yo F presents w/ NCT Hx of PSVT – ECG looks identical Hx of PSVT – ECG looks identical Had severe side effects w/ adenosine previously & refuses repeat Had severe side effects w/ adenosine previously & refuses repeat Does not want to be shocked either Does not want to be shocked either When you ask for Verapamil the nurse points out her pressure is only 88/65 When you ask for Verapamil the nurse points out her pressure is only 88/65 What can you do? What can you do?

49 Calcium pre-Tx to prevent CCB-induced hypotension Verapamil = vasodilator + myocardial depressant Verapamil = vasodilator + myocardial depressant –Get some decrease in BP (5-40 mm Hg) in up to 75% pts when given via IV route No RCTs looking at Ca 2+ pre-Tx No RCTs looking at Ca 2+ pre-Tx 6 trials totalling 322 pts suggest pre-Tx blunts Verapamil-induced decrease in BP 6 trials totalling 322 pts suggest pre-Tx blunts Verapamil-induced decrease in BP Ca gluconate 1g IV over 5 min appears to be a reasonable choice Ca gluconate 1g IV over 5 min appears to be a reasonable choice –Ann Pharmacother 2000; 34: NB: No studies exist on Ca 2+ pre-Tx for IV Diltiazem

50 PSVT: Chronic Tx Pts w/ frequent episodes / severe Sx Pts w/ frequent episodes / severe Sx –Drugs CCBs CCBs B-blockers B-blockers Digoxin Digoxin Other antirhythmics Other antirhythmics Pill-in-pocket approach Pill-in-pocket approach –Dilitiazem 120 mg PO + propranolol 80 mg PO appears to work best Rarely get hypotension or bradycardia Rarely get hypotension or bradycardia Decreases ED visits Decreases ED visits –Catheter ablation techniques in EP lab Curative in >90% of pts – becoming 1 st line Curative in >90% of pts – becoming 1 st line May be reasonable to start in ED, but need reliable F/U Better left to cardiology or EP

51 Pediatric PSVT Sx may go unnoticed higher risk of M & M Sx may go unnoticed higher risk of M & M Higher rate of structural heart Dz Higher rate of structural heart Dz –Should all have cardiac w/u Tx options are more age & lesion- dependant Tx options are more age & lesion- dependant

52 Pediatric Sx Suggestive of SVT in Infants Symptoms Symptoms –Abrupt onset of Sx –Poor feeding / Vomiting –Irritability –Diaphoresis –Pallor –May present in CHF w/ prolonged (12- 24h) Hx of tachycardia Signs Signs –HR >220 –Minimal beat-beat variability –Signs of CHF Pulmonary edema Cardiomegaly Hepatomegaly

53 Acute Tx of Peds PSVT Unstable Unstable –Ketamine 1-2 mg/kg IV for sedation, then DC cardioversion w/ 1-2 J/kg Stable Stable –1) Vagal maneuvers Dive reflex – ice to face Dive reflex – ice to face –Avoid carotid massage –2) Adenosine 0.1 mg/kg IVP; repeat mg/kg 0.1 mg/kg IVP; repeat mg/kg –3) Verapamil mg/kg IV over 2 min mg/kg IV over 2 min Contraindicated in <1yo (risk of EMD) Contraindicated in <1yo (risk of EMD) –4) Amiodarone, propfenone, sotalol Paediatr Drugs 2000; 2 (3):

54 Chronic Tx of Peds PSVT Refer to cardiology for w/u Refer to cardiology for w/u –Order echo & holter –Very young may need admission Drug Tx Drug Tx –Esp young kids where recurrence may go unnoticed –Drug choice depends on age, underlying rhythym, physician preference Digoxn, BBs, sotalol, propafenone, flecainide etc Digoxn, BBs, sotalol, propafenone, flecainide etc Invasive EP Tx Invasive EP Tx –Catheter ablation is safe and highly effective (>90%) –Becoming Tx of choice in older kids Paediatr Drugs 2000; 2 (3):

55 Disposition of NCT pts Peds Peds –Young, or hemodynamically compromised NCTs admit for monitoring, w/u, & Tx –Older, stable cardiology referral, echo, holter Adults Adults –ALL WPW pts (not previously w/u) –Pts w/ severe Sx or instability –Pts failing drug Tx for NCT –Pts wanting drug-free lifestyle

56 Key Take Home Points PSVT is a heterogenous grouping of arrhythmias PSVT is a heterogenous grouping of arrhythmias Unstable pts get cardioverted Unstable pts get cardioverted Adenosine is the Tx of choice for stable PSVT Adenosine is the Tx of choice for stable PSVT Avoid AV blockers in any WCT or irregular rhythym Avoid AV blockers in any WCT or irregular rhythym WPW has a small but definite risk of sudden cardiac death WPW has a small but definite risk of sudden cardiac death Ablation techniques are curative in >90% of pts w/ severe, or recurrent arrythmias Ablation techniques are curative in >90% of pts w/ severe, or recurrent arrythmias

57 Appendix A: Levels of Evidence Level A Level A –(highest): derived from multiple randomized clinical trials Level B Level B –(intermediate): data are on the basis of a limited number of randomized trials, nonrandomized studies, or observational registries; Level C Level C –(lowest): primary basis for the recommendation is expert consensus.

58 Appendix B: Classes of Recommendations Class I: Class I: –Conditions for which there is evidence for and/or general agreement that the procedure or treatment is useful and effective. Class II: Class II: –Conditions for which there is conflicting evidence and/or a divergence of opinion about the usefulness/efficacy of a procedure or treatment. Class IIa: The weight of evidence or opinion is in favor of the procedure or treatment. Class IIa: The weight of evidence or opinion is in favor of the procedure or treatment. Class IIb: Usefulness/efficacy is less well established by evidence or opinion. Class IIb: Usefulness/efficacy is less well established by evidence or opinion. Class III: Class III: –Conditions for which there is evidence and/or general agreement that the procedure or treatment is not useful/effective and in some cases may be harmful.


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