Ability is what you are capable of doing. Motivation determines what you do. Attitude determines how well you do it. - Lou Holtz

Transcription

1 Presented by: Cynthia Webner DNP, RN, ACNPC-AG, CCNS, CCRN-CMC, CHFN Karen Marzlin DNP, RN, ACNPC-AG CCNS, CCRN-CMC, CHFN 1 Ability is what you are capable of doing. Motivation determines what you do. Attitude determines how well you do it. - Lou Holtz 3 CNEA / Key Choice 1

2 Atrial Fibrillation: It s Not So Simple Anymore 4 ECG Recognition of AF Lack of coordinated atrial activity (no consistent P waves) Irregular, chaotic atrial f waves Irregularly irregular ventricular response 5 CNEA / Key Choice 2

3 Atrial fibrillation can be Coarse or Fine 6 Fast or Slow 7 CNEA / Key Choice 3

4 Conduct Aberrantly 8 Not conduct at all 9 CNEA / Key Choice 4

5 Occurs Intermittently 10 Organized Atrial Tachycardias Focal ectopic atrial tachycardia Typical isthmus - dependent flutter Isthmus: Tricuspid valve annulus inferior vena cava Counterclockwise flutter Clockwise flutter Macroreentry non-isthmus dependent flutter Prior atrial surgery or scarring Lateral wall RA Left atrial flutter and 11 CNEA / Key Choice 5

6 The Scope of Atrial Fibrillation The most frequently occurring arrhythmia 2.2 million adults in the US have AF 0.4% - 1% of the general population 70% of cases occur in people years old < 0.1% in people < 55 years old 9% - 10% in people > 80 years old More common in men than women More common in Caucasians 12 Classifications Recurrent Two or more episodes of AF Paroxysmal Terminates spontaneously Persistent When sustained beyond 7 days Long Standing Persistent - Greater than 12 months Permanent Opinion based on the provider and the patient to no longer attempt to restore NSR 13 CNEA / Key Choice 6

7 Mechanisms of AF Requires a trigger and an anatomic substrate capable of initiating and maintaining AF Enhanced automaticity Rapid firing of foci in or near the pulmonary veins in LA (most common site) Other common sites: in posterior wall of LA, RA, SVC, coronary sinus Reentrant circuits One or more reentry circuits within the atria with wavelets that spread in multiple directions 14 Paroxysmal AF Pathological triggers repeatedly initiate AF Triggers often related to autonomic nervous system Patients often younger and without structural heart disease About 25% of patients with paroxysmal AF progress to permanent AF within 5 years Persistent & Permanent AF Involve abnormal atrial substrate that perpetuates AF Multiple reentry circuits Additional trigger sites 15 CNEA / Key Choice 7

8 Trigger Sites Posterior view of atria SVC Left superior pulmonary vein Right superior pulmonary vein Left inferior pulmonary vein Coronary Sinus IVC Right inferior pulmonary vein 16 Reentry Circuits SVC Left superior pulmonary vein Right superior pulmonary vein Left inferior pulmonary vein Right inferior pulmonary vein Coronary Sinus IVC 17 CNEA / Key Choice 8

9 Pathophysiology Atrial fibrosis Triggers of fibrosis include Inflammation C-reactive protein levels higher in persistent AF patients Autoimmune disorders AF itself causes alterations in atrial architecture and function contributing to atrial remodeling Atrial fib begets atrial fib Atrial electrical remodeling Progressive shortening of effective refractory periods 18 Pathophysiology Autonomic nervous system Stimulation of parasympathetic system shortens atrial and PV refractory periods Atrial ischemia Atrial dilation from volume overload Structural changes associated with aging 19 CNEA / Key Choice 9

10 Reversible Acute, temporary causes Alcohol intake Surgery (common in cardiac surgery) Electrocution AMI Pericarditis Myocarditis Pulmonary Embolism Other pulmonary diseases Obstructive sleep apnea Hyperthyroidism A flutter WPW AVNRT Causes Obesity LA size increases as BMI increases Without associated Heart Disease Lone AF Familial arrhythmia 20 Causes: Associated Heart Disease Valvular heart disease Most often mitral valve HF CAD HTN Especially if LVH present Hypertrophic cardiomyopathy Dilated cardiomyopathy Restrictive cardiomyopathy Constrictive pericarditis Cardiac tumors Congenital diseases Atrial septal defects 21 CNEA / Key Choice 10

11 Hemodynamic Consequences Loss of synchronous atrial mechanical activity Loss of atrial contraction Compounded in cases of mitral stenosis, HTN, HCM, restrictive cardiomyopathy Irregular ventricular response Cardiac output falls Rapid heart rate Impaired coronary arterial blood flow Diastolic duration inconsistent and unreliable Increased coronary vascular resistance 22 Stroke: The Most Devastating Complication of AF Atrial fibrillation is an independent risk factor for stroke: increases risk about five-fold. AF is responsible for >15% of all strokes Strokes associated with AF are more severe and TIAs last longer than those due to carotid disease Strokes associated with AF have more disability and higher mortality than strokes that occur in absence of AF 23 CNEA / Key Choice 11

12 Atrial Fibrillation Rate Control Rhythm Control Prevention of Stroke Calcium Channel Blockers Beta Blockers Always first priority Strict versus lenient rate control - Strict is now recommended AV node ablation if pharmacological therapy cannot control rate Electrical or chemical cardioversion - Chemical effective if atrial fib < 7 days - TEE guided or full anticoagulation Class I and Class III antiarrhythmics AFFIRM and RACE trials Registry data supports slowing progression of disease All patients regardless of rate or rhythm control Amount of time in atrial fibrillation is not deciding factor Decision based on stroke risk CHA2DS2VASC C HF or LVEF < 35% H Hypertension A 2 < 65, 65 to 74, and > 75 D Diabetes Mellitus S 2 Stroke, TIA, or Thromboembolism VA Vascular Disease Sc Gender 24 Rate Control First and ALWAYS a priority Anticipate need for rhythm control with atrial flutter Avoid development of tachycardia-induced cardiomyopathy Rate controlled when HR Less than 110 bpm at rest (lenient control RACE II) Less than 80 at rest (strict rate control) Accomplished through medications that slow conduction through the AV node Beta blockers, calcium channel blockers (verapamil, diltiazem) most common Pacemaker may be required if HR becomes too low AV Ablation is an option if pharmacological therapy is unsuccessful in controlling rate Continued anticoagulation required Avoid toxic effects of antiarrhythmics 25 CNEA / Key Choice 12

13 Pharmacological Considerations in Rate Control Calcium channel blockers versus beta blockers Pros and Cons of Digoxin Blood pressure effect Heart rate control at rest versus exercise Pros and Cons of Amiodarone Limiting use of other antiarrhythmics (terminal half-life elimination 40 to 55 days) Use in heart failure Cannot use with accessory pathway Might convert your patient 26 A Closer Look at Calcium Channel Blockers Verapamil Dihydropyridines Diltiazem Heart Rate AV Nodal Conduction Contractility Arterial Vasodilatation 27 CNEA / Key Choice 13

14 Additional Rate Control Information RACE II Strict versus lenient rate control Strict Resting HR < 80 Exercise < 110 Lenient Resting HR < 110 Note: Study population did not include a high percentage of patients with heart failure. No benefit of strict rate control 28 ACCF/AHA/HRS Atrial Fibrillation 2011 Atrial Focused Fibrillation Update Guidelines Class III Recommendation: Treatment to achieve strict rate control of heart rate (<80 bpm at rest or <110 bpm during a 6-minute walk) is not beneficial compared to achieving a resting heart rate <110 bpm in patients with persistent AF who have stable ventricular function (left ventricular ejection fraction >0.40) and no or acceptable symptoms related to the arrhythmia, though uncontrolled tachycardia may over time be associated with a reversible decline in ventricular performance (Level of Evidence: B) 29 CNEA / Key Choice 14

15 New 2014 Guideline Update A randomized trial suggested that a lenient (<110 bpm) rate control strategy was as effective as a strict strategy (<80 bpm) in patients with persistent/permanent AF. However, the writing committee still advocates for the latter (Class IIa), as the results of this single trial were not thought to be definitive. 30 Rhythm Control Prevention of thrombus formation Prevention of atrial myopathy Relief of symptoms Initially mechanical cardioversion without antiarrhythmics Subsequent cardioversions with antiarrhythmics Antiarrhythmics toxic side effects 31 CNEA / Key Choice 15

16 AFFIRM Trial (2002) Compared rate control and rhythm control in patients with AF to determine which approach was associated with better survival outcome Results Mortality rate nearly equal in the two groups More ischemic strokes in rhythm control group (anticoagulation often DC d with NSR) More adverse drug effects in rhythm control group More hospitalizations in rhythm control group 32 AFFIRM Conclusions: Rhythm control offers no survival advantage over rate control Trend toward increased mortality with rhythm control Potential advantages to rate control: fewer adverse drug effects Anticoagulation should be continued in all AF patients at risk for stroke regardless of rate or rhythm control strategies 33 CNEA / Key Choice 16

17 RACE (2002) Compared rate control and rhythm control in patients with recurrent persistent AF End point was composite of CV death, admission for HF, thromboembolic event, severe bleeding, severe side effects from drugs Results: Primary end point occurred in 17.2% of rate control group and 22.6% of rhythm control group (trend in favor of rate control) Thromboembolism more frequent in rhythm control group More adverse drug effects in rhythm control group 34 RACE Conclusions: Rate control is not inferior to rhythm control for prevention of death and morbidity from CV causes in patients with persistent AF Cardiovascular risk (including risk of stroke) is not reduced with rhythm control even when sinus rhythm is maintained Anticoagulation therapy should continue in all AF patients at risk for stroke regardless of rate or rhythm control therapy 35 CNEA / Key Choice 17

18 Rate Vs Rhythm Control Recommendations Data from 7 trials do not support a routine strategy of rhythm control in patients with atrial fibrillation with or without HF Rate control recommended in most patients with AF Rhythm control can be considered based on specific patient considerations Continuing symptoms on rate control Exercise intolerance with rate control drugs Patient preference 36 Registry data showing support for rhythm control in select patients to decrease disease progression. (Registry on Cardiac Rhythm Disorders Assessing the Control of Atrial Fibrillation) HOWEVER! 37 CNEA / Key Choice 18

19 Class Antiarrhythmics in Atrial Fibrillation Specific Medications Purpose of Medication Major Cardiac Side Effects Class I A Class I B Class I C Disopyramide Procainamide Quinidine Not used in atrial fibrillation Flecainide Propofenone Rhythm Control Rhythm Control Rhythm Control Rhythm Control Rhythm Control Class II Beta Blockers Rate Control Torsade de pointes, HF Torsade de pointes Torsade de pointes Ventricular tachycardia, HF, Atrial Flutter Ventricular tachycardia, HF, Atrial Flutter Class III Class IV Amiodarone Dronedarone Dofetilide Ibutilide Sotalol (Also contains beta blocker) Calcium Channel Blockers Rhythm / Rate Control Rhythm Control Rhythm Control Rhythm Control Rhythm Control (also controls rate) Rate Control Torsade de pointes (rare) * Organ toxicity Torsade de pointes Torsade de pointes Torsade de pointes Torsade de pointes, HF, Beta blocker side effects 38 Defined as wall thickness exceeding 1.5 cm. In addition to cardiac criteria; sotolol and dofetilide are renally cleared 39 CNEA / Key Choice 19

20 40 41 CNEA / Key Choice 20

21 Antiarrhythmic Medications Effecting the Action Potential Class II??? 42 Effects of Class 1 Antiarrhythmics All Class 1 antiarrhythmics by definition block the fast sodium channel Different drugs do this to a different degree IC > IA > IB Blocking of the fast sodium channel interferes with rapid depolarization and decreases conduction velocity This will increases the duration of the cardiac action potential Note: This effect is seen in the action potential of the purkinge fibers but not in the action potential of the nodal tissue 43 CNEA / Key Choice 21

22 Benefits of Reducing Rate and Degree of Depolarization Decrease in conduction velocity in non-nodal tissue is called negative dromotropy. This is suppresses reentrant tachycardias because reentrant tachycardias are caused by abnormal conduction. 44 Effects of Class 1 Antiarrhythmics In addition to blocking the fast sodium channel (Phase 0) some class I agents also block the potassium channel (Phase 3) Potassium channel blockade directly affects the duration of the cardiac action potential and the effective refractory period. Benefits and disadvantages of effecting refractory period Beneficial in reentrant tachycardias Can increase risk for Torsades Different drugs do this to a different degree IA (increase refractory period) > IC (no effect) > IB (decrease refractory period) 45 CNEA / Key Choice 22

23 Effects of Class 1 Antiarrhythmics Depression of Automaticity Can suppress abnormal automaticity Not related to sodium channel effect Mechanism not fully understood Anticholinergic Effect Strong inhibitors of vagal activity Offsets some of benefit (i.e. an increase ventricular rate during the treatment of atrial arrhythmias) Can increase SA rate and conduction through the AV node 46 Class I C Antiarrhythmics Action Potential Actions Cautions Uses Drugs Potent inhibition of fast sodium channel; decrease in maximal rate of phase 0 depolarization Slow His-Purkinge conduction and cause QRS widening; QT intervals are also usually prolonged No effect on refractory period Proarrhythmic effects Life threatening ventricular arrhythmias Conversion to SR (Flecainide) Flecainide (Tambocor) Propofenone (Rhythmol) 47 CNEA / Key Choice 23

24 Class I C Antiarrhythmics Flecainide (Tambocor) Propafenone (Rhythmol) Not a first line agent for ventricular arrhythmias Will slow conduction over accessory pathways in WPW tachycardias Used in atrial fibrillation for rhythm control (can be used as pill in the pocket) CAST Trial: propensity for fatal proarrhythmic effects Not used post MI or with depressed LV function Used in atrial fibrillation and life threatening ventricular arrhythmias Also has small beta blocking actions and calcium channel blocking effects that can worsen HF Must be initiated in hospital setting to monitor ECG in structural heart disease. 48 Excess deaths related to arrhythmia and shock. 49 CNEA / Key Choice 24

25 Class III Antiarrhythmics Action Potential Actions Cautions Uses Drugs Inhibits potassium ion fluxes during phase II and III of the action potential Directly on myocardium to delay repolarization (prolongs QT); prolongs effective refractory period in all cardiac tissue; By definition act only on repolarization phase and should not impact conduction Proarrhythmic Effects (amiodarone less) Drug dependent Amiodarone (Pacerone, Cordorone) Dronedarone (Multaq) Ibutilide (Corvert) Dofetilide (Tikosyn) most pure class III Sotalol (Betapace) 50 Class III Antiarrhythmics Amiodarone (ARREST Trial) Survival to hospital admission improved 29% Approved for life threatening refractory ventricular arrhythmias; considered before lidocaine in pulseless VT or V fib; considered ahead of lidocaine for stable VT with impaired cardiac function; expanded to atrial and ventricular arrhythmias, conversion and maintenance of atrial fib Use in atrial fibrillation is off label Slows conduction in accessory pathways Originally marketed as anti-anginal (potent vasodilator) Relaxes smooth and cardiac muscle, reduces afterload and preload (well tolerated in heart failure and cardiomyoapthy) Proarrhythmias less frequent Is also a weak sodium channel blocker, also has effects similar to class II and IV, also has anticholinergic properties 51 CNEA / Key Choice 25

26 Amiodarone Dosing Life-threatening ventricular arrhythmias (with pulse Rapid loading infusion 150 mg administered at a rate of 15 mg/minute (over 10 minutes); initial infusion rate should not exceed 30 mg/minute The slow loading phase is 360 mg at a rate of 1 mg/minute (over 6 hours) First maintenance phase of the infusion is 540 mg at a rate of 0.5 mg/minute (over 18 hours). After the first 24 hours, maintenance infusion rate of 0.5 mg/minute should be continued; the rate of the maintenance infusion may be increased to achieve effective arrhythmia suppression. In the event of breakthrough episodes supplemental infusions of 150 mg administered at a rate of 15 mg/minute (over 10 minutes) may be given. For cardiac arrest secondary to pulseless ventricular tachycardia / ventricular fibrillation Initial adult loading dose is 300 mg (diluted in ml of a compatible IV solution) given as a single dose, rapid IV Peripheral IV concentration not to exceed 2mg/ml Oral administration = GI symptoms 52 More on Amiodarone Advantages Efficacious Works on atrial and ventricular arrhythmias One of few antiarrhythmics tolerated in HF Although prolongs QT least likely to cause torsades IV use short term does not lead to extra cardiac effects Potential Disadvantages Although it slow conduction over accessary pathway may slow it more over AV node and cannot be used in patients with WPW Long ½ life (40 to 55 days)limits the ability to change to another agent until amiodarone is cleared 53 CNEA / Key Choice 26

27 Potential Extra Cardiac Effects Pulmonary toxicity without initial symptoms / Potentially lethal interstitial pneumonitis / Hepatotoxicity Photosensitivity Corneal micro deposits Optic neuropathy / neuritis Thyroid dysfunction Toxic side effects increase with length of use and increased dose 54 WPW and Atrial Fibrillation Mechanism of Action Development of Atrial Fibrillation in WPW 10-32% of patients Refractory period of accessory pathway 55 CNEA / Key Choice 27

28 New 2014 Atrial Fibrillation Guidelines CHANGE IN RECOMMENDATION REGARDING AMIODARONE FOR PATIENTS WITH PRE-EXCITATION 56 Lethal Outcome After Intravenous Administration of Amiodarone in Patient with Atrial Fibrillation and Ventricular Preexcitation MUJOVIĆ NEBOJŠA M.D. 1, SIMIĆ DRAGAN M.D. 1, ANTONIJEVIĆ NEBOJŠA M.D. 1 and ALEMPIJEVIĆ TAMARA M.D. 2 Journal of Cardiovascular Electrophysiology Volume 22, Issue 9, pages , September 2011 Article first published online: 18 FEB 2011 DOI: /j x 57 CNEA / Key Choice 28

29 58 Postoperative CABG AF 20% to 50% of patients Almost always within 5 days Peak time: 2 days Increased risk morbidity Up to 4 x risk for disabling embolic stroke Increased risk mortality Up to 3 x risk for cardiac related mortality Most patients (without pre-existing AF) convert within 6 weeks 59 CNEA / Key Choice 29

30 Postoperative CABG AF Class I Recommendations Unless contraindicated, treatment with an oral beta blocker at least 24 hours before CABG to prevent post-operative AF is recommended for patients undergoing cardiac surgery. Continued post operatively and at hospital discharge Administration of AV nodal blocking agents is recommended to achieve rate control in patients who develop post-operative AF. Class IIa Recommendations Preoperative administration of amiodarone is appropriate prophylactic therapy for patients at high risk for postoperative AF. Digoxin and calcium channel blockers can be used for rate control 60 Newer Antiarrhythmic Dronedarone (Multaq) Rejected by FDA 2006 Approved by FDA 2009 Decreases hospitalizations in atrial fibrillation Not permanent atrial fibrillation Proposed safer alternative to amiodarone in terms of extra cardiac side effects Iodine content 61 CNEA / Key Choice 30

31 Dronedarone Similar to amiodarone without iodine component and less fat soluble Class III antiarrhythmic (K + channel blocker) with effects from all four classes Less effective than amiodarone at maintaining sinus rhythm but also less toxic Elimination half-life hours Has both rate and rhythm control effects but is primarily indicated for rhythm control May reduce incidence of stroke (mechanism uncertain) 62 Dronedarone (ATHENA) Approved for maintenance of sinus rhythm in patients with history of paroxysmal or persistent AF or flutter with EF > 35% who are in sinus rhythm or will be cardioverted Dose: 400 mg PO bid with meals (no grapefruit juice) Contraindicated in patients with NYHA Class IV HF or NYHA Class II-III HF with recent decompensation requiring hospitalization or referral to a specialized HF clinic > twofold increase in mortality in HF patients Side Effects GI, skin disorders Can prolong QTc but low risk of Torsades Increases serum creatinine Interferes with digoxin metabolism Concern: LIVER Dysfunction: 1/ CNEA / Key Choice 31

32 Atrial ACCF/AHA/HRS Fibrillation Atrial 2011 Fibrillation Focused Update Guidelines Class II A Recommendation: Dronedarone is reasonable to decrease the need for hospitalization for cardiovascular events in patients with paroxysmal AF or after conversion of persistent AF. Dronedarone can be initiated during outpatient therapy (Level of Evidence: B) Reduces risk of recurrent atrial fibrillation after cardioversion by 25%. 64 ACCF/AHA/HRS Atrial Fibrillation Guidelines Class III Recommendation: Dronedarone should not be administered to patients with class IV heart failure or patients who have had an episode of decompensated heart failure in the past 4 weeks, especially if they have depressed left ventricular function (left ventricular ejection fraction 35%) (Level of Evidence: B) 65 CNEA / Key Choice 32

33 Evidence to Support the Recommendation 66 More on Dronederone PALLAS Trial Dronederone in permanent atrial fibrillation Stopped early due to adverse outcomes in dronederone arm Adverse outcomes were cardiovascular in nature and not hepatic in nature 67 CNEA / Key Choice 33

34 Class III Antiarrhythmics Ibutilide (Corvert) Indicated for rapid conversion of atrial fib or flutter to sinus rhythm; IV use only over 10 minutes; also facilitated cardioversion (Don t convert atrial fib or flutter of duration without anticoagulation) Rather than blocking outward potassium currents promotes influx of sodium through slow inward sodium channel Dofetilide (Tykosin) Renal dose adjustment Prescribing limited by REMS program More pure class III agent Conversion to and maintenance of SR in A fib and flutter Reserved for very symptomatic patients, monitored 3 days in hospital, not used QTc > 440msec (500msec) Widens the QT; cannot be given with many other drugs (prolong QT or inhibit metabolism or elimination); no negative inotropic effects, neutral effect on mortality from arrhythmias post MI and in in HF, can be used in this population to prevent worsening HF 68 from atrial fib CLINICAL PEARL ALWAYS check potassium level prior to use of ibutilide potassium level should be in high normal range. Hypomagnesaemia should also be corrected. 69 CNEA / Key Choice 34

35 Simultaneous 2-lead ECG (leads II and V1) showing initiation and termination of torsade de pointes in patient in AF after ibutilide infusion. VanderLugt J T et al. Circulation. 1999;100: Copyright American Heart Association, Inc. All rights reserved. Class III Antiarrhythmics Sotalol (Betapace R ) (Betapace AF ) * Renal dose adjustment Used in atrial arrhythmias and life threatening ventricular arrhythmias Indicated for stable monomorphic VT or Polymorphic VT with normal QT in ACLS protocol Non selective beta blocking agent with class III properties Significant class III effects are only seen at doses > 160 mg Proarrhythmic potential (prolonged QT) More effective in preventing reoccurring arrhythmias than several other drugs 71 CNEA / Key Choice 35

36 MED REC EXAMPLE: RHYTHM CONTROL AGENTS 72 Anticoagulation Decision Making Chronic anticoagulation is recommended in all patients at high risk for stroke C HF / LVEF < 35% H Hypertension A Age D Diabetes Mellitus S 2 - Stroke or TIA 73 CNEA / Key Choice 36

37 CHA 2 DS 2 VASc C HF or LVEF < 35% H Hypertension A 2 < 65 (0), 65 to 74 (1), and > 75 (2) D Diabetes Mellitus S 2 Stroke, TIA, or Thromboembolism (2) VA Vascular Disease Sc Gender (Female = 1) 74 Point 1 In assessing risk of stroke in a patient with nonvalvular AF, the writing committee recommends (Class I) the usage of the CHA 2 DS 2 -VASc (C=congestive heart failure; H=hypertension; A 2 =age 75 years [doubled]; D=diabetes mellitus; S 2 =stroke, transient ischemic attack, or thromboembolism (doubled); V=vascular disease; A=age years; Sc=sex category, i.e., female gender) score, as opposed to the CHADS 2 score. 75 CNEA / Key Choice 37

38 Point 2 For nonvalvular AF patients with a history of stroke or transient ischemic attack, or a CHA 2 DS 2 -VASc score 2, oral anticoagulation is recommended (Class I). Options for oral anticoagulation include warfarin, dabigatran, rivaroxaban, and apixaban. 76 Point 3 For patients with nonvalvular AF and a CHA 2 DS 2 -VASc score of 0, it is reasonable to omit antithrombotic therapy (Class IIa). 77 CNEA / Key Choice 38

39 Point 4 The following options may be considered with a patient with nonvalvular AF and a CHA 2 DS 2 -VASc score of 1: no antithrombotic therapy, oral anticoagulation, or aspirin (Class IIb). 78 Point 5 None of the new novel oral anticoagulants (dabigatran, rivaroxaban, or apixaban) are recommended to be used in patients with AF and a mechanical or bioprosthetic heart valve (Class III harm). 79 CNEA / Key Choice 39

40 Point 6 Oral anticoagulation should be prescribed to patients with hypertrophic cardiomyopathy and AF irrespective of the CHA 2 DS 2 -VASc score (Class I). 80 Preventing Thromboembolism Warfarin established as gold standard Eliminates excess rates of ischemic stroke, reduces stroke severity and reduces post stroke mortality Target INR of Superior to ASA and ASA plus clopidogrel Warfarin in atrial fibrillation in stable CAD Warfarin in atrial fibrillation post ACS / PCI 81 CNEA / Key Choice 40

41 Oral anticoagulants with predictable doseresponse relationship: No lab monitoring of coagulation status needed 82 Newer Oral Agents Generic Trade Name Class Dabigatran Pradaxa Direct thrombin inhibitor Dosing for Atrial Fibrillation 150 mg PO BID 75 mg PO BID with Cr. Cl. 15 to 30 ml/minute Rivaroxaban Xarelto Factor Xa inhibitor Dose 20 mg PO daily Abixaban Eliquis Factor Xa inhibitor Dose: 5 mg BID Dose: 2.5 mg BID (if 2 of the following) Creatinine > 1.5 mg/dl Age > 80 years Weight < 60 kg Edoxaban Savaysa Factor Xa inhibitor 60 mg daily for Cr. Cl. > 50 to < mg daily for Cr. Cl. 15 to CNEA / Key Choice 41

42 Newer Oral Agents Generic Peak Plasma Level Elimination Half-life Clearance Dabigatran 1.5 hrs 12 to 18 hr Mostly by kidneys Rivaroxaban 3 hrs 5-9 hours (up 11 to 13 hrs if > 75 years old) Abixaban Edoxaban Rapid absorption Hepatic and renal excretion 8 to 15 hours 25% cleared by the kidneys Concern in patients with normal renal function 84 Drug Afib Study Highlights: Note all studies tested for primary endpoint of stroke (ischemic and hemorrhagic) and systemic embolism Dabigatran Rivaroxaban Abixaban Edoxaban RE-LY trial (Connolly et al, 2009) ROCKET AF (Patel et al., 2011) ARISTOTLE (Granger et al., 2011.) ENGAGE AF-TIMI mg BID superior to warfarin (p< 0.001) (stroke / systemic embolism) Ischemic stroke and hemorrhagic stroke both lower Rate of major bleeding same (potential concern for GI bleeding) Did not test approved 75 mg dose 32 to 33% of patients with CHADS2 score > 2 Non-inferiority of rivaroxaban (P<0.001) (stroke / systemic embolism) No significant difference in the risk of major bleeding, intracranial and fatal bleeding occurred less frequently in the rivaroxaban group 87% to 86.9% had CHADS2 score > 3 Primary objective: Found to be non inferior to warfarin (p = <0.001) Secondary objective: Found to be superior to warfarn (p= 0.01) Major bleeding: Statistically less with apixaban (p<0.001) Interesting: No statistical difference in ischemic stroke. Non-inferior to warfarin (P = < 0.001) for high dose and (P = 0.005) for low dose Significantly lower rates of bleeding & CV death compared to 85 warfarin at both doses (Not less GI bleeding) CNEA / Key Choice 42

43 Hold Times for Newer Oral Agents Surgery with high risk for bleeding (i.e. CABG) Dabigatran 3 to 5 days. For urgent cases until clotting times are normal or until four half-lives has passed Hold times for surgery are dependent on renal function DO NOT USE INR. Can be falsely elevated Rivaroxaban / Apixaban Renal impairment Cr. Cl.: > 50 = 3 days Cr. Cl. < 50 = 4 days Liver impairment Mild: 2 days Mod: At least 4 days Severe: At least 7 days Surgery Low Bleeding Risk Minimum hold time for low risk surgery and normal renal function is > 24 hours Renal impairment Cr. Cl.: > 50 = 1 days Cr. Cl. < 50 = 3 days Liver impairment Mild: 1 day Mod: At least 2 days Severe: At least 5 days Edoxaban Not specifically addressed in product information. Minimum hold time of at least 24 hours 86 Assessment of Bleeding Assessment of Bleeding Risk Dabigatran Bleeding risk can be assessed by an ecarin clotting time if available If not available, a PTT can be assessed to determine clearance of the drug because dabigatran has been shown to prolong aptt (aptt not used for quantitative assessment) > 2 x upper normal limit 12 to 24 hours after drug may be indicative of high risk for bleeding Thrombin time is most sensitive test. Diluted thrombin time (DTT) is a quantitative test (calibrated Hemoclot ) Rivaroxaban Apixaban Edoxaban PT may provide qualitative assessment of presence of factor Xa; not sensitive for quantitative anticoagulation effect Point of care INR should not be used to gauge anticoagulation effects Chromogenic assay can provide quantitative assessment not widely available, not fully studied, not recommended at this time 87 CNEA / Key Choice 43

44 Antidotes Dabigatran 19 October 2015FDA Approves Praxbind (idarucizumab), Specific Reversal Agent for Pradaxa (dabigatran etexilate) Factor Xa Inhibitors andexanet alfa breakthrough therapy desgination by FDA; orphan drug status Should have FDA decision August 16 th CNEA / Key Choice 44

45 Electrical Cardioversion Direct current cardioversion Involves delivery of an electrical shock synchronized with the intrinsic activity of the heart Usually is done by sensing R wave on the EKG. 90 Electrical Cardioversion Often performed electively Need for anesthesia Immediate need for hemodynamically unstable rhythms Anticoagulation prophylaxis (same with pharmacological cardioversion) Full anticoagulation versus TEE / Heparin strategy 3 to 4 weeks before with full anticoagulation 4 weeks post minimum with either strategy Risk for thromboembolism greatest when atrial fibrillation present greater than 48 hours 91 CNEA / Key Choice 45

46 Indications for Emergent DC Cardioversion Active ischemia Symptomatic hypotension Severe heart failure Preexcitation via an accessory pathway Contraindicated in presence of digitalis toxicity or hypokalemia CNEA / Key Choice 46

47 94 Electrical Cardioversion: Technical Issues Need for good R wave and good P wave visualization AP placement preferred (short axis) Initial energy delivered (monophasic) for atrial flutter may be as low as 50 J Higher energy is needed for atrial fibrillation starting at least 200 J Initial higher energy produces more immediate success and may reduce total energy delivered Maximum J is 400 Biphasic waveforms use less energy Time between shocks not less than one minute 95 CNEA / Key Choice 47

48 Treatment: Electrical Cardioversion Factors Predicting Success: Short duration of atrial fibrillation Atrial flutter Young Age Factors Predicting Failure: Left atrial enlargement Underlying heart disease Cardiomegaly Success rates vary from 70% to 90% The relapse rate is high without continuation of antiarrhythmic drug therapy 96 Complications Electrical Cardioversion Embolism (1%-7% without prophylactic anticoagulation) Benign arrhythmias Ventricular arrhythmias with hypokalemia and digitalis toxicity Myocardial damage has not been confirmed Reoccurrence of atrial fibrillation Prophylactic antiarrhythmic drug therapy before cardioversion for patients at risk 97 CNEA / Key Choice 48

49 Pharmacological Cardioversion Works best if AF present for < 7 days Most effective drugs are Ibutilide (Corvert) Flecainide (Tambocor) Dofetilide (Tykosin) Propafenone (Rhythmol) Amiodarone Associated with side effects Bradycardia (8%) QT prolongation (1.5%) Ventricular arrhythmias (1.3%) 98 Pulmonary Vein (Antral) Isolation (PVI; PVAI) Procedures Focus on isolating the triggers in the PVs from the left atrial myocardium Circumferential ablation creates lesions that encircle the ostia of all four pulmonary veins and completely isolates them from atrial myocardium most common procedure 99 CNEA / Key Choice 49

50 Ablation for Atrial Fibrillation Potential energy sources: Radiofrequency (heats tissue) Cryothermy (freezes tissue) balloon delivery 100 CNEA / Key Choice 50

51 Complications of PV Isolation Pulmonary vein stenosis (can lead to pulmonary hypertension) Cardiac tamponade Esophageal injury or atrio-esophageal fistula Phrenic nerve injury Thromboembolism Mitral valve trauma Radiation exposure due to long procedures 103 CNEA / Key Choice 51

52 Guideline Update Catheter ablation is useful in patients with symptomatic, paroxysmal AF who have not responded to or tolerated antiarrhythmic medications (Class I). 104 Guideline Update Catheter ablation is also reasonable in selected patients with symptomatic, paroxysmal AF prior to a trial of medical therapy, provided that it can be performed at an experienced center (Class IIa). 105 CNEA / Key Choice 52

53 Ablation for Persistent and Long Standing Persistent Atrial Fibrillation 106 Ablation Targets for Persistent and Long Standing Persistent AF Rotors Regions in the LA with complex atrial activity Focal Impulse and Rotor Modulation (FIRM) This alone not efficacious; OASIS trial Complex Fractionated Atrial Electrograms Located in LA, detected by mapping systems Ganglionated Plexi Areas of high autonomic innervation in LA CNEA / Key Choice 53

54 CNEA / Key Choice 54

55 AV Node Ablation Creates complete AV block to prevent conduction of AF into ventricles (requires insertion of permanent pacemaker) 111 CNEA / Key Choice 55

56 Cox-Maze III (Cox-Maze, Cox-Maze II) Cut & sew method developed in 1987 Considered the gold standard for surgical treatment of AF Isolates the pulmonary veins Isolate the posterior left atrium Interrupts the macro reentrant circuits responsible for atrial fibrillation and atrial flutter Amputates the left atrial appendage 112 Creates a pathway from sinus node to AV node and allows all of atrium to be activated 113 CNEA / Key Choice 56

57 Technical challenges of procedure limited its use. Posterior View L Anterior View 114 Unipolar Cox-Maze IV Using Ablation Unipolar radiofrequency (RF) (heats tissue) Cryothermia (freezes tissue) Other sources Bipolar Bipolar radiofrequency (RF) Delivered between two electrodes held in place inside a jaw like clamp 115 CNEA / Key Choice 57

58 Cox-Maze IV Using Ablation Must create transmural lesions from epicardial or endocardial surface Unipolar sources don t consistently create transmural lesion Unipolar cryosurgery or radiofrequency ablation can also cause unintended cardiac injury Bipolar RF clamps most widely used device Limitation: Only tissue fitting between clamp can be ablated, particularly limiting when performed on beating heart Right atrial isthmus and left atrial isthmus are not able to be fully ablated 117 CNEA / Key Choice 58

59 Role of the Isthmus Right Atrial Isthmus Left Atrial Isthmus Source: Journal of Cardiovascular Electrophysiology, CNEA / Key Choice 59

60 Performed through median sternotomy or right mini thoracotomy (Mini Maze) Uses combination of unipolar and bipolar RF ablations Left atrial appendage is also amputated Results similar to Cox-Maze III The term Maze procedure implies entire biatrial lesion set of the Cox-Maze procedure (includes ablation of both the right and left atrial isthmuses) 120 Surgical Procedures for Atrial Fibrillation Cox-Maze IV: Cox-Maze III lesion set using ablation technology Pulmonary vein isolation EP Physician may do catheter based combined with external surgical based (Convergent) Pulmonary vein isolation with a left atrial lesion set connecting to the mitral valve annulus Amputation of left atrial appendage usually done in conjunction with all surgical interventions 121 CNEA / Key Choice 60

61 Mini Maze Thorascopic MAZE (5 Box Procedure) Closed chest, beating heart Hybrid Procedures CNEA / Key Choice 61

62 Percutaneous Left Atrial Appendage Occlusion The LAA is a multi-lobed structure of variable anatomy that is attached to the LA More than 90% of clots in patients with nonrheumatic AF form in the LAA Many patients are unable to take coumadin and are at risk for stroke in chronic AF Mechanical occlusion of LAA can prevent thrombus embolization 124 LAA Occlusion Devices Watchman Amplatzer 125 CNEA / Key Choice 62

63 LAA Occlusion Devices: Watchman Protect AF Trial 2009: Non inferior but safety concern: Pericardial effusion May 2013: New long term data (45 month follow up of 800 patients) superior to warfarin with respect to all-cause and CV mortality and hemorrhagic stroke in patients with nonvalvular atrial fibrillation and stroke risk factors Prevail Trial 2013 Did not meet 1 st primary endpoint Non inferiority to warfarin for composite of stroke, systemic embolism, or cardiovascular or unexplained death Met 2 nd primary endpoint Non inferiority to warfarin for prevention of ischemic stroke or systemic embolism CNEA / Key Choice 63

64 Watchman and FDA Approval 2010 FDA denied approval December 2013 advisory board 13 to 1 recommended marketing approval October FDA Panel Voted it was safe Split votes on efficacy and risk / benefit profile March 26 th 2015 FDA approval 128 Indications Are deemed by their physicians to be suitable for warfarin; and Have an appropriate rationale to seek a nonpharmacologic alternative to warfarin, taking into account the safety and effectiveness of the device compared to warfarin WATCHMAN is not intended to be a broad replacement for Oral Anticoagulants (OAC) 129 CNEA / Key Choice 64

65 130 November 2015 The device was approved by the FDA in March of this year for stroke prevention in patients with atrial fibrillation (AF). However, the CMS announced on Tuesday that there's enough evidence to show that use of the LAA-closure device is not "reasonable and necessary" for managing patients who are treatable with warfarin and so should not be covered by Medicare [1]. Instead, the organization recommends that reimbursement should cover only Watchman procedures in patients not receiving warfarin, according to a proposed decision memo In other news, the FDA announced a class 2 recall for the device's implant and delivery system because of blood leakage risks if the Watchman's hemostasis valve is "tightened with the dilator in place," it could lead to cross-threading and inadequate valve sealing. The field correction "reinforces the directions for use and gives further guidance on correct use of the hemostasis valve, minimizing potential for undesired blood leakage," said the agency. 131 CNEA / Key Choice 65

66 LAA Occlusion Devices : Amplatzer AMPLATZER Cardiac Plug FDA approval 2001 for septal occluder European CE Mark Approval The AMPLATZER Cardiac Plug Clinical Trial (ACP Trial) First patient enrolled in March 2013 Seeking to enroll 3,000 patients; 2 plus years follow up Study complete Results not available 132 LARIAT Procedure Performed under general anesthesia, Uses two catheters The first, FDA-approved LARIAT Suture Delivery Device, is inserted under the patient s rib cage The second which guides it into place, is sent to the heart's left atrial appendage (LAA) The LARIAT Suture Delivery Device places and tightens a loop stitch around the base of the LAA, permanently sealing it off from the rest of the heart. Note: FDA approved LARIAT Suture Delivery Device was not for LAA closure Safety concerns regarding pericardial effusion 133 CNEA / Key Choice 66

67 134 Atrial Fibrillation Clinical Considerations: Case Examples 38 year old female with palpitations and light headedness No past medical history Monitor AVNRT (SVT) and infrequent short (seconds) runs atrial fibrillation AVNRT associated with symptoms. Atrial fibrillation incidental finding. 86 year old male presenting with TIA symptoms. Found in atrial fibrillation of unknown origin. History of HTN and debilitating arthritic pain and spinal stenosis. Options? Options? 135 CNEA / Key Choice 67

68 136 I m not telling you it is going to be easy, I m telling you it is going to be worth it. ~ Art Williams 137 CNEA / Key Choice 68

69 Definition Heart Failure is a complex clinical syndrome resulting from any structural or functional cardiac disorder impairing the ability of the ventricle to either fill or eject 138 Clinical Syndrome Resulting Clinical Manifestations Dyspnea and fatigue May limit exercise tolerance Fluid overload AND / OR May lead to pulmonary congestion and peripheral edema Impaired functional capacity and quality of life 139 CNEA / Key Choice 69

70 DEFINITIONS 140 Classification I. Heart Failure with Reduced Ejection Fraction (HFrEF) II. Heart Failure with Preserved Ejection Fraction (HFpEF) Definition of Heart Failure Ejection Description Fraction 40% Also referred to as systolic HF. Randomized clinical trials have mainly enrolled patients with HFrEF and it is only in these patients that efficacious therapies have been demonstrated to date. 50% Also referred to as diastolic HF. Several different criteria have been used to further define HFpEF. The diagnosis of HFpEF is challenging because it is largely one of excluding other potential noncardiac causes of symptoms suggestive of HF. To date, efficacious therapies have not been identified. a. HFpEF, Borderline b. HFpEF Improved 41% - 49% These patients fall into a borderline or intermediate group. Their characteristics, treatment patterns, and outcomes appear similar to those of patient with HFpEF. >40% It has been recognized that a subset of patients with HFpEF previously had HFrEF. These patients with improvement or recovery in EF may be clinically distinct from those with persistently preserved or reduced EF. Further research is needed to better characterize these patients. 141 CNEA / Key Choice 70

71 HFrEF (Systolic Dysfunction) vs HFpEF (DiastolicDysfunction) 142 HFrEF - Systolic Dysfunction Impaired wall motion and ejection Dilated chamber 50% of HF Population Hallmark: Decreased LV Ejection Fraction < 40% Coronary artery disease is cause in 2/3 of patients Remainder other causes of LV dysfunction Cardiomyopathy not synonymous with HF 143 CNEA / Key Choice 71

72 HFpEF - Diastolic Dysfunction Filling impairment Normal chamber size 50% of patients with HF have preserved LV function Normal EF or elevated Caused by Hypertension Restrictive myopathy (C) Ischemic heart disease Ventricular hypertrophy (D) Valve disease Idiopathic Primarily disease of elderly women with HTN 144 HFpEF - Diastolic Dysfunction Diagnosis is made when rate of ventricular filling is slow Elevated left ventricular filling pressures when volume and contractility are normal In practice: the diagnosis is made when a patient has typical signs and symptoms of heart failure and has a normal or elevated ejection fraction with no valve disease. 145 CNEA / Key Choice 72

73 Left versus Right Sided Heart Failure Two sides of the heart form a circuit, neither side can pump significantly more blood than the other for long Signs/symptoms of failure reflect each respective ventricle 146 The Real Culprit: Neurohormonal Response SNS Response Ventricular Remodeling RAAS Response 147 CNEA / Key Choice 73

74 Activation of SNS First Responder Decreased CO BP activates baroreceptors and vasomotor regulatory centers in medulla Increase circulating catecholamines Stimulates alpha and beta receptors Increase HR Peripheral vasoconstriction Contractility Positive effect: CO and BP Negative effect: O2 demand ischemia, arrhythmias, sudden death 148 Chronic Stimulation of SNS Norepinephrine (circulating catecholamine) is Cardiotoxic Decreases heart s ability to respond to sympathetic stimulation Down regulation of B1 receptor sites (less sensitive) Contributes to decreased exercise tolerance Can also lead to ventricular remodeling Be aware of your patient s heart rate response to activity. 149 CNEA / Key Choice 74

75 Activation of RAAS Kidney s response to decreased perfusion due to decreasing CO Concentrations of angiotensin II, and aldosterone rise as end result Potent vasoconstriction Sodium/water absorption increases Result Increased preload and increased afterload Increased myocardial oxygen demand CNEA / Key Choice 75

76 Harmful Result of RAAS Activation Enhanced preload increases end-diastolic volume dilating the LV LV becomes overstretched LV changes size and shape (ventricular remodeling) Contractility decreases Congestive symptoms develop 152 Ventricular Remodeling Process of pathological growth Can occur from prolonged activation of SNS/RAAS Involves Hypertrophy of myocytes Pressure thicken (concentric) Volume elongate (eccentric) Genetically abnormal inefficient contraction Increased ventricular muscle mass, change in ventricular shape Collagen matrix becomes fibrotic 153 CNEA / Key Choice 76

77 Apoptosis (a component of remodeling) Preprogrammed cell death without inflammation/scarring (necrosis) Process is accelerated in HF but in a random pattern Cell slippage Bricks myocytes Morter collagen Degredation (slippage) or Fibrotic 154 Changes in Systolic Dysfunction Ventricular Dilatation Dilated Mitral Valve Annulus Decreased Ventricular Contractility Decreased Ejection of Ventricular Contents Mitral Regurgitation Increased Ventricular Pressure / Volume Increased Atrial Pressure / Volume Atrial Dilatation Activation of Neurohormonal Responses Vasoconstriction / Fluid Retention Atrial Overload Increased Pulmonary Pressure / Volume Fluid Accumulates in Pulmonary Capillary Bed Symptoms 155 CNEA / Key Choice 77

78 156 The Good Guys: Natriuretic Peptides Cardiac hormones secreted by myocytes Atrial natriuretic peptide (ANP) Produced in atria Brain natriuretic peptide (BNP) Produced in ventricles in response to increased ventricular pressure/stretching Stronger release than ANP Promote vasodilatation (preload/afterload reduction) Reduce sodium/water retention (diuretic response) Reduce production/action of vasoconstrictor peptides Plasma concentrations elevated in patients in fluid overload Neseritide (Natrecor) is the synthetic form of BNP 157 CNEA / Key Choice 78

79 Lower levels than NT-pro- BNP Cleared more quickly from the circulation 20 minutes Cleared by natriuretic peptide receptors Higher levels than BNP Cleared more slowly from the circulation- 120 minutes Cleared by various organs Skeletal tissue, liver, kidneys Both equally cleared by kidneys Both equally useful in the diagnosis of acute decompensated heart failure Both may be elevated for reasons other than HF 158 Good to assess in patients with dyspnea being evaluated for Heart Failure Should not be used as the sole tool to diagnose HF Must be used in concert with signs and symptoms Low values have strong negative predictive value Adds to prognostic information marker of risk Predictor of increased risk If levels do not fall after aggressive HF care, risk for death or hospitalization for HF is significant (ACC/AHA 2013) 159 CNEA / Key Choice 79

80 BNP < 100 pg/ml - HF unlikely > 400 pg/ml - HF likely pg/ml - Use clinical judgment NT-proBNP < 300 ng/ml - HF unlikely Age < 50 years, NT-proBNP >450 pg/ml - HF likely Age years, NT-proBNP >900 pg/ml HF likely Age >75 years, NT-proBNP >1800 HF likely Levels increase as age increase Levels increase as renal function decreases Levels decrease as BMI increase HOWEVER: Elevated levels are a marker of risk 160 Cardiac Heart failure, including RV syndromes Acute coronary syndrome Heart muscle disease, including LV Hypertrophy Valvular heart disease Pericardial disease Atrial fibrillation Myocarditis Cardiac surgery Causes of Elevated Naturetic Peptide Levels Non-cardiac Advancing age Anemia Renal failure Pulmonary: obstructive sleep apnea, severe pneumonia, pulmonary hypertension Critical illness Bacterial sepsis Severe burns Toxic-metabolic insults, including cancer, chemotherapy and environmental 161 CNEA / Key Choice 80

81 Heart Failure Symptoms Exercise intolerance (hallmark) Ability to perform ADLs Fatigue Dyspnea Paroxysmal nocturnal dyspnea Frequent night urination with less during the day Peripheral edema/weight change Chest pain GI problems Confusion/altered mental status 162 Heart Failure Symptoms Symptoms in the elderly Many don t experience exertional dyspnea because they are sedentary More common: Daytime oliguria/nocturia Mental disturbances Anorexia GI disturbances 163 CNEA / Key Choice 81

82 Classification of Heart Failure New York Heart Association 164 Physical Exam Findings General Appearance (resting dyspnea, cyanosis, cachexia) Weight gain BP/HR Include orthostatic pressures JVD Hepatojugular reflux Edema Displaced apical impulse S3/S4 Lung sounds 165 CNEA / Key Choice 82

83 Measuring JV Pulsation / Pressure Raise HOB degrees Internal jugular preferred May use external Use tangential light Use centimeter ruler Difficult to assess if HR>100 Normal JV pulsation level is < 3 cm above the sternal angle CNEA / Key Choice 83

84 Jugular Vein No pulsations palpable. Pulsations obliterated by pressure above the clavicle. Level of pulse wave decreased on inspiration; increased on expiration. Usually two pulsations per systole (x and y descents). Prominent descents. Pulsations sometimes more prominent with abdominal pressure. Carotid Artery Palpable pulsations. Pulsations not obliterated by pressure above the clavicle. No effects of respiration on pulse. One pulsation per systole. Descents not prominent. No effect of abdominal pressure on pulsations. Additional assessment tips: Lying flat to verify location of jugular Sitting or standing patient up to see top of column 168 TREATMENT STRATEGIES 169 CNEA / Key Choice 84

85 Heart Failure STAGE C Structural heart disease with prior or current symptoms of HF STAGE D Refractory HF velopment of mptoms of HF e.g., Patients with: Known structural heart disease and HF signs and symptoms Refractory symptoms of HF at rest, despite GDMT e.g., Patients with: Marked HF symptoms at rest Recurrent hospitalizations despite GDMT HFpEF THERAPY Goals Control symptoms Improve HRQOL Prevent hospitalization Prevent mortality Strategies Identification of comorbidities Treatment Diuresis to relieve symptoms of congestion Follow guideline driven indications for comorbidities, e.g., HTN, AF, CAD, DM Revascularization or valvular surgery as appropriate HFrEF THERAPY Goals Control symptoms Patient education Prevent hospitalization Prevent mortality Drugs for routine use Diuretics for fluid retention ACEI or ARB Beta blockers Aldosterone antagonists Drugs for use in selected patients Hydralazine/isosorbide dinitrate ACEI and ARB Digoxin In selected patients CRT ICD Revascularization or valvular surgery as appropriate THERAPY Goals Control symptoms Improve HRQOL Reduce hospital readmissions Establish patient s endof-life goals Options Advanced care measures Heart transplant Chronic inotropes Temporary or permanent MCS Experimental surgery or drugs Palliative care and hospice ICD deactivation 170 HFpEF No evidence based medical therapy ARBs, aldosterone antagonists, and sildenafil have all been tested ARBs and aldosterone antagonists may reduce hospitalizations but not mortality TOPCAT Study Focus on co-morbid conditions: HTN Sleep apnea Atrial Fibrillation Anemia DM Obesity 171 CNEA / Key Choice 85

86 Stages, Phenotypes and Treatment of HF At Risk for Heart Failure Heart Failure STAGE A At high risk for HF but without structural heart disease or symptoms of HF STAGE B Structural heart disease but without signs or symptoms of HF STAGE C Structural heart disease with prior or current symptoms of HF STAGE D Refractory HF e.g., Patients with: HTN Atherosclerotic disease DM Obesity Metabolic syndrome or Patients Using cardiotoxins With family history of cardiomyopathy Structural heart disease e.g., Patients with: Previous MI LV remodeling including LVH and low EF Asymptomatic valvular disease Development of symptoms of HF e.g., Patients with: Known structural heart disease and HF signs and symptoms Refractory symptoms of HF at rest, despite GDMT e.g., Patients with: Marked HF symptoms at rest Recurrent hospitalizations despite GDMT HFpEF HFrEF THERAPY Goals Heart healthy lifestyle Prevent vascular, coronary disease Prevent LV structural abnormalities Drugs ACEI or ARB in appropriate patients for vascular disease or DM Statins as appropriate THERAPY Goals Prevent HF symptoms Prevent further cardiac remodeling Drugs ACEI or ARB as appropriate Beta blockers as appropriate In selected patients ICD Revascularization or valvular surgery as appropriate THERAPY Goals Control symptoms Improve HRQOL Prevent hospitalization Prevent mortality Strategies Identification of comorbidities Treatment Diuresis to relieve symptoms of congestion Follow guideline driven indications for comorbidities, e.g., HTN, AF, CAD, DM Revascularization or valvular surgery as appropriate THERAPY Goals Control symptoms Patient education Prevent hospitalization Prevent mortality Drugs for routine use Diuretics for fluid retention ACEI or ARB Beta blockers Aldosterone antagonists Drugs for use in selected patients Hydralazine/isosorbide dinitrate ACEI and ARB Digoxin In selected patients CRT ICD Revascularization or valvular surgery as appropriate THERAPY Goals Control symptoms Improve HRQOL Reduce hospital readmissions Establish patient s endof-life goals Options Advanced care measures Heart transplant Chronic inotropes Temporary or permanent MCS Experimental surgery or drugs Palliative care and hospice ICD deactivation 172 Diuretics Decrease congestive symptoms No mortality benefit First line: Loop diuretics Thiazide diuretic my be added Potassium and magnesium monitoring Use with moderare NA restriction Fluid restriction criteria Monitor response to therapy Adequate diuresis BNPt goal JVP assessment Orthopnea Over diuresis Hypotension Dizziness Orthostatic BP 173 CNEA / Key Choice 86

87 Diuretic Therapy Outpatient Weight loss goal of 0.5 to 1.0 kg per day Patients can be educated for adjustable diuretic dosing Weight gain Weight loss Change in oral intake or during periods of illness Diuretic Resistance Diuretic resistance Reasons High sodium levels NSAIDs Severe renal impairment Renal hypoperfusion Strategies IV instead of PO Continuous infusion versus intermittent dosing if BP is a concern Change the loop diuretic Addition of thiazide 174 Renal Anatomy: Nephron and Loop Diuretics Work in ascending loop of Henle Loss of H2O, K+, Na+, Cl-, H+ More loss of H2O and less K+ and Na+ than thiazides Promotes venous vasodilatation Rapid onset and short duration Can be effective in presence of renal failure High ceiling diuretic / threshold medications 175 CNEA / Key Choice 87

88 Loop Diuretics Bumetanide (Bumex) Furosemide (Lasix) Torsemide (Demadex) Equivalents Furosemide 40 mg Torsemide 20 mg Bumetanide 1 mg Dosing Recommended max dose 600 mg furosemide 200 mg torsemide 10 mg bumetanide 176 Differences in Loop Diuretics Bumetanide Furosemide Torsemide Lack of randomized control data with comparison to furosemide. Better pharmacokinetic profile (oral bioavailability) than furosemide but turosemide has evidence of more efficacy and more safety. (Wargo &Banta, 2009) BID Dosing when GFR is low 2 randomized trials comparing Torsemide and Furosemide N=471 Torsemide associated with reduction in HF and CV readmission in systolic HF with a trend towards reduction of all cause mortality. (DiNicolantonio, 2012) 177 CNEA / Key Choice 88

89 More on Loop Diuretics DOSE Trial NEJM: Felker et al., 2011 No significant difference in symptoms or renal function between continuous drip versus intermittent dosing Non significant trend toward improvement in symptoms with high dose (IV at 2.5 x PO dose) versus low dose; (IV at same as PO dose) no change in renal function 178 Thiazide Diuretics Inhibit reabsorption of Na+ and Cl- In the distal tubule More sodium loss than loop diuretics Delayed onset but longer duration of action than loop diuretics Give 30 minutes before a loop diuretic Low ceiling diuretics Less potent diuretic than loop diuretics Diminished effectiveness in presence of 179 renal failure CNEA / Key Choice 89

90 Bendrofluazide (Naturetin) Thiazide Diuretics Side effects: Benthiazide (Aquatag, Exna) Chlorothiazide (Diuril) Chlorthalidone (Hygroton) Cyclothiazide (Anhydron) Hydrochlorothiazide (HCTZ) (HydroDiuril, Esidrix) Hydroflumethazide (Saluron, Diucardin) Indapamide (Lozol) Metolazone (Zaroxolyn) Polythiazide (Renese) Trichlormethiazide (Metahydrin, Naqua) Blood Chemistry changes: Hyponatremia ( Na + ) Hypokalemia ( K + ) Hypomagnesemia ( Mg + ) Hyperglycemia ( blood sugar) Hyperuricemia ( uric acid) Hypercalcemia ( Ca ++ ) Decreased glomerular filtration in kidneys ( BUN, creatinine) cholesterol triglycerides HDL cholesterol Other side effects: Impaired glucose tolerance Gout Impotence Ventricular arrhythmias ( K + ) Nausea, dizziness, headache 180 Diuretics and Renal Function Role of venous congestion in worsening renal function Role of volume depletion / hypotension and worsening renal function 181 CNEA / Key Choice 90

91 Cardiorenal Syndrome Moderate to severe renal dysfunction with fluid overload Continue to treat with diuretics In severe fluid overload renal dysfunction my improve with continued treatment May need to hold ACE I secondary to AKI Venous congestion plays a role in worsening renal function (not just hypoperfusion) 182 Details for HF pharmacology were discussed during yesterday s CV pharmacology session. 183 CNEA / Key Choice 91

92 Cardiac Resynchronization Therapy 184 Cardiac Resynchronization Therapy (CRT) Treatment modality for heart failure not just pacing Treatment modality in conjunction with drug therapy Goals: Improve hemodynamics by restoring synchrony of ventricular contraction Improve quality of life Decrease mortality and morbidity 185 CNEA / Key Choice 92

93 Normal Ventricular Depolarization 186 Ventricular Depolarization with LBBB 187 CNEA / Key Choice 93

94 Indications for CRT Therapy Patient with cardiomyopathy on GDMT for >3 mo or on GDMT and >40 d after MI, or with implantation of pacing or defibrillation device for special indications LVEF <35% Evaluate general health status Acceptable noncardiac health Comorbidities and/or frailty limit survival with good functional capacity to <1 y Continue GDMT without implanted device Evaluate NYHA clinical status NYHA class I LVEF 30% QRS 150 ms LBBB pattern Ischemic cardiomyopathy QRS 150 ms Non-LBBB pattern NYHA class II LVEF 35% QRS 150 ms LBBB pattern Sinus rhythm LVEF 35% QRS ms LBBB pattern Sinus rhythm LVEF 35% QRS 150 ms Non-LBBB pattern Sinus rhythm QRS 150 ms Non-LBBB pattern NYHA class III & Ambulatory class IV LVEF 35% QRS 150 ms LBBB pattern Sinus rhythm LVEF 35% QRS ms LBBB pattern Sinus rhythm LVEF 35% QRS 150 ms Non-LBBB pattern Sinus rhythm LVEF 35% QRS ms Non-LBBB pattern Sinus rhythm Special CRT Indications Anticipated to require frequent ventricular pacing (>40%) Atrial fibrillation, if ventricular pacing is required and rate control will result in near 100% ventricular pacing with CRT Colors correspond to the class of recommendations in the ACCF/AHA Table 1. Benefit for NYHA class I and II patients has only been shown in CRT-D trials, and while patients may not experience immediate symptomatic benefit, late remodeling may be avoided along with long-term HF consequences. There are no trials that support CRT-pacing (without ICD) in NYHA class I and II patients. Thus, it is anticipated these patients would receive CRT-D 188 unless clinical reasons or personal wishes make CRT-pacing more appropriate. In patients who are NYHA class III and ambulatory class IV, CRT-D may be chosen but clinical reasons and personal wishes may make CRT-pacing appropriate to improve symptoms and quality of life when an ICD is not expected to produce meaningful benefit in survival. CRT Goal: Force biventricular pacing Goal: Ventricular Pacing 90% of time or greater Causes of Loss of Bi V pacing: Long AV Delays Prolonged PVARP ST with 1 degree AV Block Lead dislodgement 189 CNEA / Key Choice 94

95 Automatic Implantable Cardioverter Defibrillators Functional status / 1 year Turning off CNEA / Key Choice 95

96 ICD Device Pulse Generator Single chamber, dual chamber, or biventricular pacing Back up pacing Antitachycardia pacing Implanted subcutaneously same as pacemaker Defibrillator lead Detects arrhythmias Delivers therapy Defibrillator lead capable of pacing and defibrillating Placed in right ventricle 192 ICD Functions ATP-Anti tachycardia Pacing Tiered Antiarrhythmic Therapies 193 CNEA / Key Choice 96

97 ICD Functions Cardioversion Shock Delivers shocks from 0.1 to 30 joules synchronized on the R wave 194 ICD Functions Defibrillating Shock Delivers high energy (20-34 joules) unsynchronized shock for VF 195 CNEA / Key Choice 97

98 Internal Monitoring with Devices Heart rate variability / Night heart rate Patient activity Impedance / Volume assessment Atria fib burden Ventricular arrhythmias Routine re-evaluation of pacing burden is important in the treatment of HF. 196 Data from ICD 197 CNEA / Key Choice 98

99 CardioMEMs CHAMPOIN Trial (2011) Clinical Trial Indications: Patients 18 years older with NYHA Class III heart failure for at least 3 months, irrespective of left ventricular ejection fraction and a hospitalization for heart failure within the past 3 months. Current manufacturer recommendations (post FDA approval): NYHA Class III HF hospitalized in the past year for heart failure. Randomized to CardioMEMS or standard treatment for heart failure. During the entire follow-up (mean 15 months [SD 7]), the treatment group had a 37% reduction in heart-failure-related hospitalization compared with the control group (158 vs 254, HR 0 63, 95% CI ; p<0.0001). Conclusion: The addition of information regarding pulmonary artery pressure to clinical signs and symptoms improves heart failure management and reduces heart failure readmissions. Quality of life data is also available. Current Practice: Current practice is representative of the control group in this trial which includes monitoring signs and symptoms(reporting of symptoms and daily weights) as in the control group in the CHAMPION Trial. Safety: 98.6% free of device complications CNEA / Key Choice 99

100 ACUTE DECOMPENSATED HEART FAILURE 200 Common Precipitating Factors of ADHF Non adherence with Medications Dietary sodium intake Fluid intake Excessive alcohol or drug use ACS Arrhythmias Persistent hypertension Valvular heart disease Recent addition of negative inotrope Nonsteroidal antiinflammatory drugs Worsening renal function Endocrine abnormality Concurrent infection New anemia Pulmonary embolism 201 CNEA / Key Choice 100

101 Hospitalization Recommended Evidence of severe ADHF, including: Hypotension Worsening renal function Altered mentation Dyspnea at rest Typically reflected by resting tachypnea Less commonly reflected by oxygen saturation <90% Hemodynamically significant arrhythmia - including new onset of rapid atrial fibrillation Acute coronary syndromes 202 Hospitalization Should be Considered Worsened congestion: Even without dyspnea Signs and symptoms of pulmonary or systemic congestion Even in the absence of weight gain Major electrolyte disturbance Associated comorbid conditions Pneumonia Pulmonary embolus Diabetic ketoacidosis Symptoms suggestive of transient ischemic accident or stroke Repeated ICD firings Previously undiagnosed HF with signs and symptoms of systemic or pulmonary congestion 203 CNEA / Key Choice 101

102 Treatment Goals Improve symptoms, especially congestion and low-output symptoms Optimize volume status Identify etiology Identify and address precipitating factors Optimize chronic oral therapy Minimize side effects Identify patients who might benefit from revascularization Identify patients who might benefit from device therapy Identify risk of thromboembolism and need for anticoagulant therapy Educate patients concerning medications and self management of HF Consider and, where possible, initiate a disease management program Clinical Presentations Patient 1: Volume overload (Backwards Failure) Patient 2: Profound depression of cardiac output hypoperfusion (Forwards Failure) Patient 3: Signs and symptoms of both fluid overload and hypoperfusion (cardiogenic shock) 205 CNEA / Key Choice 102

103 Evaluation Guides Treatment Decisions Determine Volume Status Perfusion Status Role of / or presence of precipitating factors and/or comorbidities Ejection fraction HFpEF HFrEF 206 Hypoperfusion vs. Volume Overload Hypoperfusion Narrow pulse pressure Resting tachycardia Cool Skin Altered mentation Decreased urine output Increased BUN/Creatinine Cheyne Stokes Respirations Intravascular Volume Overload Elevated jugular venous pressure Hepatojugular reflex Orthopnea Dyspnea Crackles Weight gain Peripheral edema 207 CNEA / Key Choice 103

104 Forwards Flow: CI, Skin temp (warm or cold) Hemodynamic and Clinical Subsets Normal Hemodynamics (I) No pulmonary congestion: PAOP < 18; Dry lungs No hypoperfusion: CI > 2.2; Warm skin Backwards Failure (II) Pulmonary congestion PAOP > 18; Wet lungs No hypoperfusion CI > 2.2; Warm skin Forwards Failure (III) No pulmonary congestion PAOP < 18; Dry lungs Hypoperfusion CI < 2.2; Cold skin The Shock Box (IV) Pulmonary congestion PAOP > 18; Wet lungs Hypoperfusion CI < 2.2; Cold skin Preload: Pulmonary artery occlusive pressure CNEA / Key Choice 104

105 Forwards Flow: Cardiac Index Skin temp (warm or cold) Treatment for Acute Decompensated Heart Failure Congestion with Adequate Perfusion Subset II Reduce Preload Hypoperfusion with No Congestion Subset III Increase contractility Assure adequate preload Hypoperfusion with Congestion Subset IV Reduce Afterload 210 Preload changes: move patient along the current curve Preload 211 CNEA / Key Choice 105

106 Forwards Flow: CI, Skin temp (warm or cold) Forwards Flow: CI, Skin temp (warm or cold) Changing Contractility: moves patient to a higher curve Preload 212 Changing Afterload:: moves patient up and to the left (improves forwards flow and reduces preload) Preload 213 CNEA / Key Choice 106

107 Acute Decompensated Heart Failure Increase Contractility Positive Inotropes Dobutamine Milronone Dopamine Reduce Preload Diuretics Venous Vasodilators Low dose NTG Neseritide Ultrafiltration Reduce Afterload Arterial vasodilators High dose Nitroglycerin Nitroprusside Neseritide Intra aortic balloon pump 214 Ultrafiltration UNLOAD Trial Veno-venus ultrafiltration (UF) vs standard IV diuretic therapy for hypervolemic HF 200 patients randomized UF with statistical significance for: greater weight loss (48 hours), greater fluid loss (48 hours), less 90-day resource utilization for HF. No statistically significant difference in dyspnea scores or creatinine levels (safety endpoint) CARESS-HF Trial Treatment of ADHF, worsening renal function, persistent congestion with stepped pharmacologic approach vs ultrafiltration 188 patients randomized UF: inferior to pharmacologic therapy and associated with adverse events. 215 CNEA / Key Choice 107

108 ADDITIONAL CARE ISSUES 216 Routine use not recommended When to consider: Refractory to initial therapy Volume status and cardiac filling pressures are unclear Pulmonary and systemic pressures unclear Clinically significant hypotension (SBP < 80 mm Hg) Worsening renal function 217 CNEA / Key Choice 108

109 Foley Catheter Not recommended routinely in heart failure If need to closely monitor hourly urine output Possible outlet obstruction High risk patients include those with BPH and or right sided volume overload 218 Dietary Sodium Restriction Water follows sodium If hyponatremic Serum sodium < 130 meq/l 2 liters per day Serum Sodium < 125 meq/l Stricter fluid restriction may be considered If persistent fluid overload Assure sodium restriction in conjunction with fluid restriction 219 CNEA / Key Choice 109

110 Oxygen therapy is recommended if the patient exhibits hypoxemia If not hypoxemic no need for oxygen therapy Use of non-invasive positive pressure ventilation may be considered for severely dyspneic patients with clinical evidence of pulmonary edema. 220 Criteria for Discharge Exacerbating factors addressed Near optimal volume status achieved Transition from intravenous to oral diuretic successfully completed Patient and family education completed, including clear discharge instruction LVEF documented Smoking cessation counseling initiated Near optimal pharmacologic therapy achieved, including ACE inhibitor and beta-blocker (for patients with reduced LVEF), or intolerance documented Follow-up clinic visit scheduled, usually for 7 to 10 d 221 CNEA / Key Choice 110

111 Criteria for Discharge Advanced HF Patient or recurrent admission Oral medication regimen stable for 24 h No intravenous vasodilator or inotropic agent for 24 h Ambulation before discharge to assess functional capacity after therapy Plans for post discharge management (scale present in home, visiting nurse or telephone follow up generally no longer than 3 d after discharge) Referral for disease management, if available 222 Decision Making ADVANCED HF 223 CNEA / Key Choice 111

112 Indicators for Advanced Heart Failure Severe symptoms of HF with dyspnea and/or fatigue at rest or with minimal exertion (NYHA class IIIb or IV) on optimal medical therapy Repeated episodes of fluid retention (pulmonary and/or systemic congestion, peripheral edema) and/or reduced cardiac output at rest (peripheral hypoperfusion) on optimal medical therapy Objective evidence of severe cardiac dysfunction shown by at least 1 of the following on optimal medical therapy: LVEF <30% Mean PCWP >16 mmhg and/or RAP >12 mmhg by PA catheterization High BNP or NT-proBNP plasma levels in the absence of non-cardiac causes 224 Indicators for Advanced Heart Failure Severe impairment of functional capacity while on optimal medical therapy shown by 1 of the following: Inability to exercise 6-Minute walk distance < 300 m Peak Vo2 <12 to 14 ml/kg/min Repeated ( 2) hospitalizations or ED visits for HF in the past year or > 1 hospitalization for heart failure Progressive deterioration in renal function Progressive decline in serum sodium, usually to <133 meq/l Weight loss without other cause Intolerance to ACE inhibitors due to hypotension and/or worsening renal function Intolerance to beta blockers due to worsening HF or hypotension Frequent systolic blood pressure <90 mm Hg High diuretic requirements to maintain volume status (i.e. furosemide equivalent dose >160 mg/d and/or use of supplemental metolazone therapy) 225 Frequent ICD shocks CNEA / Key Choice 112

113 Prognostic Models Heart Failure Survival Score All cause mortality Seattle Heart Failure Model All cause mortality, urgent transplantation or LVAD implant EVEREST Risk Model Combined endpoint of mortality or persistently poor quality of life over the 6 months after discharge EFFECT 30-day and 1-year mortality ADHERE In-hospital mortality ESCAPE Discharge Score 6 month mortality 226 Risk Factors for Mortality > 2 Referral for Advanced Treatment >2 Prompt Referral for Advanced Rx Hospitalization for HF on oral HF therapy Inability to take ACEI/ARB/BB BUN> 45, Creat>2.5, CrCl< 45 cc/min BNP >4 x s upper limit of normal Na+ < 136 Malnutrition/Cachexia VO2 <55% predicted LVEDD >7.0 cm 227 CNEA / Key Choice 113

114 CNEA / Key Choice 114

115 End of Life Decision Making Palliative Care versus Hospice When should they be involved Making an assessment Having the discussion 230 Components of effective shared decision making include: Establishing trust Identifying patient values, preferences, and goals for care early in the course of treatment Using the framework Ask-Tell-Ask to determine both what patients know and what they want to know Understanding the reasons why there are conflicts regarding decisions of care Using numeric data in a clear and understandable way as a decision aid Respecting that patient s may change their goals as the disease progresses Allen, CNEA / Key Choice 115

116 Bridge to transplant (BBT) for those who are transplant eligible Destination therapy (DT) for those who are not transplant eligible. Bridge to Decision (BTD) Careful consideration for all therapies Some patients may be too ill with multisystem issues to benefit from MCS Some decisions are best made in the hands of the most experienced centers 232 Absolute and Relative Contraindications for Durable MCS Absolute Contraindications Irreversible hepatic disease Irreversible renal disease Irreversible neurological disease Major coagulopathy Right sided heart failure (unless candidate for biventricular support) Medical non-adherence Severe psychosocial limitations Source: Peura et al., 2012; Slaughter et al., * May be a relative contraindication Relative Contraindications * Hypertrophic, infiltrative, or restrictive cardiomyopathy Uncorrectable moderate or greater aortic insufficiency Age _80 y(for destination therapy) Obesity or malnutrition MS disease that impairs rehabilitation Active systemic infection Prolonged intubation Untreated malignancy Severe PVD Active substance abuse Impaired cognitive function Unmanaged psychiatric disorder Lack of social support 233 CNEA / Key Choice 116

117 234 Long Term Therapy Extracorporeal Bridge to Transplant MCS Thoratec pvad II Implantable MCS Heart Mate II HeartWare HVAD Total Artificial Heart CardioWest Abiomed: Abiocor II Destination Heart Mate II Therapy HeartWare HVAD Investigational Devices 235 CNEA / Key Choice 117

118 Heart Mate II 236 HeartWare HVAD 237 CNEA / Key Choice 118

119 Key Strategies in the Treatment of HF EDUCATION EDUCATION EDUCATION 238 I sure hope my wife is getting this? Are we going to be able to afford these medications? No, I think we ve got it. BLAH, BLAH, BLAH, BLAH! ANY QUESTIONS? 239 CNEA / Key Choice 119

120 Discharge Focus 1. Diet and nutrition 2. Discharge medications 3. Activity level 4. Follow up appointments 5. Daily weight 6. Response to symptoms 240 ACC / AHA Guidelines the addition of a 1-hour, nurse educator delivered teaching session at the time of hospital discharge using standardized instructions resulted in improved clinical outcomes, increased self-care measure adherence, and reduced cost of care 241 CNEA / Key Choice 120

121 Education and Counseling Individualized education and counseling to focus on self care Patients literacy, cognitive status, psychological state, culture, and access to social and financial resources should be taken into account Treat depression and anxiety to improve education comprehension Repeat, repeat, repeat Use teach back method Hospital education should be limited to essential education Should be delivered by providers using a team approach in which nurses with expertise in HF management provide the majority of education and counseling (HFSA 2010). 242 Who should be involved? Identify primary care giver / support person and include in ALL education. 243 CNEA / Key Choice 121

122 The Best Treatment Patient Education & Self-Care Maintenance and Self-Care Management Self-care maintenance following the rules and instructions related to the disease process Self-care management decision-making process and critical thinking to make decisions in response to changes in the client s current health status 244 Self-Care Behaviors Daily weight monitoring; avoidance of high sodium foods, taking of all prescribed medication Smoking cessation; avoidance of heavy alcohol intake Avoidance of non-steroidal anti-inflammatory drugs and other over-the-counter herbal therapies and drugs, especially decongestants and sodium-based antacids Monitoring for changes in HF signs and symptoms; Responding to symptoms (first person to call for all issues or when to call which member on the team) Activity and exercise: easy warm up/cool down; getting started; when to stop or slow down 245 CNEA / Key Choice 122

123 Barriers to Self-Care Management Higher acuity Multiple needs Co-morbidities Shorter LOS Noncompliance Transportation issues Financial concerns Depression / anxiety Lack of knowledge Literacy Multiple medications Fear of medication side effects Living alone (lack of social support) Memory problems 246 Education Content 247 CNEA / Key Choice 123

124 The Big Picture What HF is, its causes and symptoms, timeline (chronic), consequences (poor prognosis; premature death; greater risk for hospitalization) and measures to control it (self-care actions and monitoring) Importance of provider follow up and ongoing monitoring Why drugs are used in HF; how they improve survival or reduce symptoms; Understanding reason for uptitration; how to take medications for greatest effectiveness; common adverse effects 248 Medications Don t wait until discharge! Include the person who will assist with medication What is the plan for filling prescriptions? What is the system for medication administration used at home? Need to know trade/generic names Issue of medication reconciliation Use of instruction sheets versus labeled pill bottles Don t use term meds as at home 249 CNEA / Key Choice 124

125 Medications Alternatives for routine schedule Diuretics after errands Flexible diuretic dosing ACE inhibitor at night Discussion regarding medications to avoid Non-steroidals Adherence history Financial concerns Importance of not running out of their medication (refill verifications with pharmacy) Regular follow-up with provider to monitor labs 250 Fluid Volume Status Causes of intravascular volume overload; can occur silently (without symptoms) Role of excess sodium in fluid retention How diuretics work Rationale for BID dosing if CKD Role of additional thiazide diuretic Need to know when NOT to take diuretics 251 CNEA / Key Choice 125

126 Daily Weights Use same scale, same amount of clothing Empty bladder and before breakfast Record!! Report 2 pounds in one day or 3 to 4 pounds in a week Many patients don t call because they feel OK Barriers: Confusion fluid gain from over eating gain Use of device data Do you weight all patients with heart failure daily while hospitalized even when admitted for non cardiac reasons? Special considerations with ECF concern for weight loss 252 Response to Symptoms Focus on changes! Is there a change in their activity tolerance? Impact on their ADL s? Pants are becoming tight? Unable to sleep lying flat? 253 CNEA / Key Choice 126

127 Diet and Nutrition Moderate sodium restriction Exact amount is not known Most have moderate restriction when attempting to diurese May liberalize when nutrition or orthostatic hypotension is a concern Nutritional support for cardiac cachexia Caloric supplementation Limit alcohol 254 Low Sodium Tips Low sodium considered to be <4 grams / day 2-3 grams / day recommended for patient with clinical syndrome of heart failure < 2 grams with moderate to severe heart failure Discuss how sodium impacts fluid retention Salt = sodium Focus on what they can eat High sodium foods Approximately 70% of sodium intake comes from processed and pre-packaged foods. Some never or hardly every foods 255 CNEA / Key Choice 127

128 Low Sodium Tips Dining at restaurants or in another person s home Reading labels Per SERVING Percent sodium (or) mg sodium per serving Salt used in cooking Sodium alternatives Be realistic there must be joy in life AHA: Eat Less Salt resource book Teach people how to do rather than tell them what to do!! 256 Fluid Limitation In the outpatient fluid restrictions reserved for patients with advanced heart failure refractory to high dose oral diuretics Indicated in the hospital setting in the presence of severe hyponatremia Sodium level < 130 meq/l (2L) - Sosium < 125 meq (< 2L) Explain the thirst mechanism 257 CNEA / Key Choice 128

129 Activity Screen for depression Evaluate anxiety levels Exercise training should be considered for all stable outpatients with chronic HF who are able to participate in protocols needed to produce physical conditioning. Get them in Cardiac Rehab if systolic HF or diagnosis of stable angina Consider pulmonary rehab if co-existing COPD 30 minutes moderate activity / exercise 5 days per week Work if at all possible 258 Follow Up Contact within hours from discharge Appointment within on week from discharge Will need to have actual date, time and location included in discharge instructions Enrollment in a HF Clinic Allows for up titration of medications Continues evaluation for progression of disease Need for ICD Need for CRT Referral for advanced therapies End of life planning 259 CNEA / Key Choice 129

130 IS THERE ONE CORRECT ANSWER? 260 Readmission Data Nearly 2 million Medicare patients readmitted within 30 day of discharge Cost of those readmissions = $17.5 BILLION National average for readmission 19% Readmissions a symptom of an overly expensive and uncoordinated healthcare system Limited connection from inpatient to outpatient HF readmissions rate 20-25% at 30 days > 50% at 6 months 35% of 30 day readmissions due to HF 261 CNEA / Key Choice 130

131 What We Know Readmissions are prevalent and costly Adverse events associated with hospital discharge are common And about ¼ of them are readmissions Patients are not taking ideal medication regimens No f/u on meds, tests and workups is common Real room for improving hospital-receiver communication Value of PCP f/u unclear probably ; might not be as powerful as hospitalist f/u Creating the perfect in-house discharge process probably won t make enough difference SES is probably related to readmission risk But the CMS measures do not adjust for it Ideal risk identification strategies are unavailable Clinicians often have a different perspective on what led to the readmission than patients do 262 Multidimensional Nursing Roles Coordinate care with interdisciplinary team members who can target coexisting medical, social, and financial issues Facilitate behavioral strategies that ease patient and caregiver burdens related to adherence to the treatment plan Educate on advance directive planning and community services that meet learning needs Promote continuity of care between home, HF clinic, or palliative care services Foster collaborative relationships Coach collaborators to use evidence-based therapies Ensure open communication Position patients and caregivers to proactively assess and manage signs and symptoms of worsening condition Assess goal progression Recognize and target unresolved HF issues 263 CNEA / Key Choice 131

132 Transitional Care Interventions Feltner, C., Jones, C. D., Cené, C. W., Zheng, Z. J., Middleton, J. C., & Jonas, D. E. (2014). Transitional Care Interventions to Prevent Readmissions for Persons With Heart Failure. Ann Intern Med, 160, Systematic review 47 trails At 30 days a high intensity home-visiting program reduced all cause readmissions At 3-6 months home-visiting programs and multidisciplinary heart failure clinic (MDS-HF) interventions reduced all cause readmissions Structured telephone support (STS) reduced HF specific readmissions but not all cause readmissions Mortality benefit with MDS-HF clinic, home-visiting programs, and STS Based on current evidence, telemonitoring interventions (non structured) and primarily educational interventions are not efficacious for reducing readmissions or mortality 264 Final Thought They may forget your name, but they will never forget how you made them feel. -Maya Angelou 265 CNEA / Key Choice 132

133 BE THE BEST THAT YOU CAN BE EVERY DAY. YOUR PATIENTS ARE COUNTING ON IT! CNEA / Key Choice 133

134 The ECG is a graphic recording of electrical activity spreading through the heart 12 lead ECG provides 12 different views of electrical activity Each bedside monitoring lead provides one view 268 SA Node AV Node Bundle of His AV Junction Right and Left Bundle Branches Anterior and Posterior Fascicles Purkinge Fibers 269 CNEA / Key Choice 134

135 WAVES and COMPLEXES QRS P P wave: atrial depolarization QRS: ventricular depolarization T wave: ventricular repolarization PR interval: AV conduction time QRS width: intraventricular conduction time ST Segment: entire ventricular depolarization QT interval: used to reflect ventricular repolarization time QT Interval T PR Interval QRS ST Segment 270 Lead 1 + Left Arm High Lateral Wall LAD (Diagonal) Axis Quadrant avr + Right Arm P Wave always V1 + 4 th ICS, RSB Septal Wall & RV LAD (Septal) Ectopy VS Aberrancy RBBB LBBB LVT RVT Reciprocal to Posterior V4 + L MCL, 5 th ICS Anterior Wall LAD Lead 2 + Left Leg Inferior Wall RCA L Ant Hemi rs P Wave always + avl + Left Arm High Lateral Wall LAD (Diagonal) Reciprocal to Lead 3 V2 + 4 th ICS, LSB Septal Wall LAD (Septal) Reciprocal to Posterior V5 + L anterior axillary, same level as V 4 Low Lateral Wall Circumflex (Marginal) Lead 3 + Left Leg Inferior Wall RCA L Ant Hemi rs Reciprocal to avl ST Segment Lead RCA avf + Left Leg Inferior Wall RCA L Ant Hemi rs Axis Quadrant V3 + Midway Between V 2 & V 4 Anterior Wall LAD Reciprocal to Posterior ST Segment Lead LAD V6 + L midaxillary line, same level as V 4 Low Lateral Wall Circumflex (Marginal) Ectopy VS Aberrancy RBBB LBBB ST Segment Lead Circ 271 CNEA / Key Choice 135

136 Dual Electrode Leads Single Electrode Leads 272 Dual Electrode Leads One positive electrode One negative electrode Records difference in electrical potential between selected electrodes Leads I, II, and III Single Electrode Leads One positive electrode One negative reference point Zero electrical potential Center of heart Leads avr, avl, avf V1-V6 273 CNEA / Key Choice 136

137 274 Consider the positive pole of each lead as the camera (exploring electrode) RA LA + RV LV 275 CNEA / Key Choice 137

138 276 Note: Nothing travels toward the right leg as a positive electrode. The right leg is the ground used to absorb any excess electrical activity. 277 CNEA / Key Choice 138

139 278 Standard Limb Leads (Dual Electrode Leads) Leads I, II, III RA Left Arm + RA Left leg + _ Lead I + RA LA LA Left leg + + LL CNEA / Key Choice 139

140 Augmented Limb Leads Leads avr, avl, avf 280 Augmented Limb Leads (Single Electrode Leads) avr, avl, avf + RA LA + - Right Arm + LL + Left Arm + Left Leg CNEA / Key Choice 140

141 CNEA / Key Choice 141

142 RA LV V6 RV + 4 th ICS, RSB + L MCL, 5 th ICS V5 + 4 th ICS, LSB + L anterior axillary, same level as V 4 V1 V2 V3 V4 + Midway Between V 2 & V 4 + L midaxillary line, same level as V RA Left Arm + Right Arm th ICS, RSB + L MCL, 5 th ICS RA Left leg + Left Arm th ICS, LSB + L anterior axillary, same level as V 4 LA Left leg + Left Leg + + Midway Between V 2 & V 4 + L midaxillary line, same level as V CNEA / Key Choice 142

143 Posterior wall of the left ventricle and the right ventricle are not captured on the standard 12 lead ECG Septum depolarizes from left to right 2. Both ventricles depolarize from endocardium to epicardium 3. Basal portions of ventricles depolarize last 4. Mean direction of depolarization is downward, leftward, and posterior 287 CNEA / Key Choice 143

144 If positive electrode sees depolarization approaching it, it records an upright complex If positive electrode sees depolarization heading away from it, it records a negative complex. 288 Lead 1 avr V1 V4 + Left Arm High Lateral Wall + Right Arm + 4 th ICS, RSB Septal Wall + L MCL, 5 th ICS Anterior Wall Lead 2 avl V2 V5 + Left Leg Inferior Wall + Left Arm High Lateral Wall + 4 th ICS, LSB Septal Wall + L anterior axillary, same level as V 4 Low Lateral Wall Lead 3 avf V3 V6 + Left Leg Inferior Wall + Left Leg Inferior Wall + Midway Between V 2 & V 4 Anterior Wall + L midaxillary line, same level as V 4 Low Lateral Wall 289 CNEA / Key Choice 144

145 290 In limb leads the ST segment is normally isoelectric but may be slightly elevated or depressed by less than 1mm In precordial leads ST segment elevation is normally not more than 1 to 2 mm (small elevation normal in many people) 291 CNEA / Key Choice 145

146 Point where the QRS complex and the ST segment meet. 292 Represents ventricular repolarization Slightly asymmetrical Usually upright Most likely abnormal If inverted in two contiguous leads Not normally > than 5mm (limb leads) to 10 mm (precordial) high 293 CNEA / Key Choice 146

147 CNEA / Key Choice 147

148 1) Assess for ST segment elevation first ST elevation and need for reperfusion 2) Assess for T wave inversion next Non STEMI or Unstable angina ischemia 3) Assess for ST segment depression thirdly Supply and demand ischemia (often in V5 regardless of vessel occlusion) OR reciprocal changes to ST elevation Clinical application: Supply and demand ischemia is typically not the primary problem in patients at rest 296 New ST elevation at the J point in at least 2 contiguous leads > 2 mm in men and > 1.5 mm in women for leads V 2 and V 3 > 1 mm for other chest leads and limb leads on standard 12 lead > 0.5 mm in leads V 7 -V 9 True Posterior MI No ST segment elevation on ECG. Look for ST segment depression > 2 mm in leads V 1 -V 4 Hyperacute T wave changes May be observed early in a before the J point elevates & the ST segment significantly lifts off baseline. Special criteria exist for interpreting the ECG in the presence of LBBB. Baseline ECG abnormalities such as left ventricular hypertrophy, ventricular paced rhythm, and Brugada syndrome make the interpretation of the ECG challenging 297 CNEA / Key Choice 148

149 CNEA / Key Choice 149

150 CNEA / Key Choice 150

151 CNEA / Key Choice 151

152 T wave should be positive in lead I and II Inversion in lead III, avl and avf may be normal Inversion in V1 is common - always compare to previous ECG CNEA / Key Choice 152

153 Wellen s Warning when seen in chest leads(v2-v3) of undiagnosed patient Represents LAD occlusion that spontaneously reperfused prior to the ECG (lesion at risk for reocclusion) Seen on ECG done during pain free period Can be UA / NSTEMI CNEA / Key Choice 153

154 CNEA / Key Choice 154

155 Can be seen in exercise stress testing with supply and demand ischemia. Often seen with left ventricular hypertrophy. 310 ECG Be suspicious of horizontal ST segment depression in patient at rest. Suspect left main disease (or significant 3 vessel disease) when diffuse depression and ST elevation in lead avr (and V1 to lesser extent) Presentation Assess for reasons for supply and demand ischemia at rest (i.e. low hemoglobin). Rule out medical reason for falls, motor vehicle crashes, and other trauma (i.e. syncope or near syncope due to cardiac cause). 311 CNEA / Key Choice 155

156 CNEA / Key Choice 156

157 T wave inversion is a warning for ACS (either unstable angina or NonSTEMI) unless T wave inversion occurs after a STEMI After a STEMI T wave inversion is expected Terminal T wave inversion is a sign of reperfusion after a STEMI Symmetrical T wave inversion will develop after terminal T inversion CNEA / Key Choice 157

158 CNEA / Key Choice 158

159 18 Hours Post STEMI 36 Hours Post STEMI CNEA / Key Choice 159

160 Primary Change is most important look for: ST Elevation: ACS (STEMI) T Wave Inversion: ACS (Non STEMI or UA) ST Depression (ischemia) Reciprocal Changes ST segment depression in leads reciprocal (opposite) those with ST elevation Reciprocal changes can help confirm primary changes 320 Lead 1 avr V1 V4 Left Arm High Lateral Wall Right Arm 4 th ICS, RSB Septal Wall L MCL, 5 th ICS Anterior Wall Posterior Wall Lead 2 avl V2 V5 Left Leg Inferior Wall Left Arm High Lateral Wall 4 th ICS, LSB Septal Wall L anterior axillary, same level as V 4 Low Lateral Wall Lead 3 avf V3 V6 Left Leg Inferior Wall Left Leg Inferior Wall Midway Between V 2 & V 4 Anterior Wall L midaxillary line, same level as V 4 Low Lateral Wall 321 CNEA / Key Choice 160

161 CNEA / Key Choice 161

162 Assessing the RV 324 VI V4 V2 V5 V3 V6 325 CNEA / Key Choice 162

163 VIR V4R V2R V5R V3R V6R 326 Right Ventricular Leads Posterior Leads 327 CNEA / Key Choice 163

164 These are vulnerable areas of myocardium: Not directly assessed on 12 Lead! 328 Place electrode in V4R Position 5 th ICS Right MCL Attach V monitoring lead (Brown Lead) to electrode Assure monitor lead selector is on V Run strip and clearly mark V4 Right Chest Lead Place electrode in V8 position Under tip of left scapula same level as V6 Attach V monitoring lead (Brown Lead) to electrode Assure monitor lead selector is on V Run strip and clearly mark V8 Posterior Lead 329 CNEA / Key Choice 164

165 Patient post cardiac arrest on hypothermia CNEA / Key Choice 165

166 Same Patient as Previous 12 Lead: Due to hypotension the point of care nurse used the V lead from bedside monitoring to record a V4R lead. This recording confirms RV injury and this knowledge was used to guide treatment. Right Sided Lead ST segment elevation in lead V4R demonstrates high risk for high grade AV node block (Wellen & Conover, 2006) CNEA / Key Choice 166

167 CNEA / Key Choice 167

168 CNEA / Key Choice 168

169 Bundle Branch Blocks Ventricular Ectopy Morphology Challenges: BBB Reentrant VT Idiopathic RVOT Antidromic tachycardia 339 CNEA / Key Choice 169

170 LBBB RBBB LVT RVT V1 and V6 are gold standard for evaluating QRS complexes Bundle branch block patterns and ventricle ectopy can be differentiated by using the morphology of these leads. DON T rely on Lead II!! CNEA / Key Choice 170

171 Standard 6 Lead Placement 342 MCL6 Standard 5 Lead Placement V1 & V6 Modified 5 lead Placement V1 & MCL6 Monitor Settings: V and III 343 CNEA / Key Choice 171

172 Not every QRS complex contains a Q wave, R wave and S wave!! Q always negative (below baseline) R first positive above the baseline R second positive above the baseline S always negative deflection following the R wave or second component to entirely negative [[; /complex 344 Let s Practice QS qr QR Qr qrs R RS rs Rs rsr 346 CNEA / Key Choice 172

173 Conduction System Review Left Bundle Branch Left anterior fascicle Left posterior fascicle Right Bundle Branch Ventricular conduction time increases with increased heart size Measured on ECG by earliest onset to latest off set in all leads 347 Normal Depolarization 2 V 6 1 QRS sec V CNEA / Key Choice 173

174 Bundle Branch Block QRS complex is 0.12 sec or greater (in adults) Fixed or heart rate dependent Causes Structural abnormalities Functional (relative refractory period) 349 Right Bundle Branch Block V 6 = qrs V6 V 1 = rsr V1 QRS =.12 sec or more 350 CNEA / Key Choice 174

175 Right Bundle Branch Block Causes Myocardial infarction Disease of right side of the heart Pulmonary Embolism Myocarditis Congenital heart disease Atrial septal defects Note: Right bundle is more vulnerable than left bundle due to single fascicle. 351 Right Bundle Branch Block V1 Triphasic complex rsr (rsr, rsr ) pattern Or an M shaped R wave with right peak taller Or a qr pattern (In patients with septal infarct) V6 Triphasic complex Large R is maintained qrs with wide S waves Note: Also a wide S wave in lead 1 V1 V1 V6 rsr R qr qrs 352 CNEA / Key Choice 175

176 353 Left Bundle Branch Block V 6 = wide R V 1 = QS V6 V1 QRS =.12 sec or more V1 = rs 354 CNEA / Key Choice 176

177 Left Bundle Branch Block Causes Coronary artery disease Hypertension Left ventricular hypertrophy Cardiomyopathy 355 V1 Left Bundle Branch Block Wide QS or rs complex - negative Slick downstroke Time to nadir <0.06 sec V6 Large R wave is maintained Wide R wave with no initial septal q wave V6 356 CNEA / Key Choice 177

178 Additional diagnostic criteria include: Broad slurred or notched R waves in leads 1,aVL, V5, and V CNEA / Key Choice 178

179 Lead 1 avr V1 V4 + Left Arm High Lateral Wall + Right Arm + 4 th ICS, RSB Septal Wall VT vs Aberrancy + L MCL, 5 th ICS Anterior Wall Lead 2 avl V2 V5 + Left Leg Inferior Wall + Left Arm High Lateral Wall + 4 th ICS, LSB Septal Wall + L anterior axillary, same level as V 4 Low Lateral Wall Lead 3 avf V3 V6 + Left Leg Inferior Wall + Left Leg Inferior Wall + Midway Between V 2 & V 4 Anterior Wall + L midaxillary line, same level as V 4 Low Lateral Wall VT vs Aberrancy 359 Wide complex tachycardia presumed to be VT if diagnosis is unclear Don t assume VT cannot be well tolerated! The rate, size of the heart and presence of additional complications are often more important than the source of the tachycardia Check the patient (need to defib?) Check the blood pressure (need to cardiovert?) Check the ECG (determine the rhythm) 360 CNEA / Key Choice 179

180 Patient history / assessment QRS Width AV Dissociation Concordance Axis Morphology Note: VT is much more common than supraventricular tachycardia with bundle branch aberration. In wide QRS tachycardias VT is the right answer up to 80% of the time. 361 Acute ischemia / injury (Abnormal automaticity) Post myocardial infarction / ischemic cardiomyopathy (Reentrant circuit within myocardium) Non ischemic dilated cardiomyopathy (Bundle branch reentrant VT) The wider the QRS VT is favored However: SVT with LBBB will have a wider QRS than SVT with RBBB QRS will be wider in pre-existing BBB Other causes of SVT with wider than expected QRS: antidromic tachycardia and patients on Class IC or IA antiarrhythmics or amiodarone Not all VT is significantly wide VT originating from septum more narrow than VT from free wall If QRS more narrow than sinus rhythm = VT 362 CNEA / Key Choice 180

181 Independent atrial and ventricular activity (AV dissociation) is diagnostic for ventricular ectopy Ventricular tachycardia may also have retrograde P waves (retrograde P waves do not confirm VT) CNEA / Key Choice 181

182 365 Axis Right Superior (Extreme / Northwest) axis deviation is strong indicator of ventricular ectopy Ventricular tachycardia rarely occurs with normal axis Ventricular tachycardia can occur with right or left axis deviation 366 CNEA / Key Choice 182

183 Use Lead I and avf Left hand represents QRS in Lead I Right hand represents QRS in avf Fingertips will point in the same direction as the QRS complex Handy Method of Axis Calculation developed by J. Cooper, PhD., American College of CV Nursing 367 I avf I avf I avf I avf 368 CNEA / Key Choice 183

184 Lead 1 avr V1 V4 + Left Arm High Lateral Wall + Right Arm + 4 th ICS, RSB Septal Wall VT vs Aberrancy + L MCL, 5 th ICS Anterior Wall AXIS Lead 2 avl V2 V5 + Left Leg Inferior Wall + Left Arm High Lateral Wall + 4 th ICS, LSB Septal Wall + L anterior axillary, same level as V 4 Low Lateral Wall Lead 3 avf V3 V6 + Left Leg Inferior Wall + Left Leg Inferior Wall AXIS + Midway Between V 2 & V 4 Anterior Wall + L midaxillary line, same level as V 4 Low Lateral Wall VT vs Aberrancy 369 Morphology Need to Know! 370 CNEA / Key Choice 184

185 RBBB LBBB Left ventricle first Right ventricle first VT from Left Ventricle VT from Right Ventricle Left ventricle first Right ventricle first 371 Right Bundle Branch shaped R wave with an early left peak (Rr ) R wave with a single peak q wave followed by R wave 372 CNEA / Key Choice 185

186 LBBB shaped Primarily negative wide rs complex delay to the nadir > 0.06 sec r wave broader than 0.03 sec Slurring on the down stroke Note: LBBB shaped VT can come from RV or septum. VT from RV includes: Idiopathic VT, BB Reentrant VT, Arrhythmogenic right ventricular dysplasia, VT from Brugada Syndrome 373 RBBB with Aberration LBBB with Aberration VT from Left Ventricle VT from Right Ventricle 374 CNEA / Key Choice 186

187 RBBB LBBB 375 Left Ventricular Tachycardia Right Ventricular Tachycardia QS complex r wave followed by S wave with R:S ratio < 1 - Any Q Wave - QS wave 376 CNEA / Key Choice 187

188 SVT RBBB SVT LBBB VT VT CNEA / Key Choice 188

189 SVT RBBB SVT LBBB LVT RVT 379 SVT RBBB SVT LBBB LVT RVT 380 CNEA / Key Choice 189

190 SVT RBBB SVT LBBB LVT RVT 381 SVT RBBB SVT LBBB LVT RVT 382 CNEA / Key Choice 190

191 SVT RBBB SVT LBBB LVT RVT 383 SVT RBBB SVT LBBB LVT RVT 384 CNEA / Key Choice 191

192 SVT RBBB SVT LBBB LVT RVT 385 SVT RBBB SVT LBBB LVT RVT 386 CNEA / Key Choice 192

193 SVT RBBB SVT LBBB LVT RVT 387 SVT RBBB SVT LBBB 12 Lead ECG Post Inferior STEMI on Arrival to CCU LVT RVT 388 CNEA / Key Choice 193

194 389 SVT RBBB SVT LBBB LVT RVT 390 CNEA / Key Choice 194

195 SVT RBBB SVT LBBB LVT RVT CNEA / Key Choice 195

196 I avr V1 V4 II avl V2 V5 III avf V3 V6 393 Caution: Hyperkalemia CNEA / Key Choice 196

197 395 The Lewis Lead 396 When P waves are not clearly seen in a rhythm strip (see lead 3 above), the Lewis lead can be very helpful in assessing for the presence of atrial activity. As seen in the Lewis lead above this patient is clearly in an atrial flutter. The atrial flutter is not as obvious in the lead III rhythm strip. CNEA / Key Choice 197

198 397 Telemetry Pack R A Lead 1 L A 398 CNEA / Key Choice 198