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HEART BLOCKS AND CARDIAC PACEMAKERS
Arun Abbi Jason Mitchell Jan 21, 2010
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OUTLINE SINUS NODE DYSFUNCTION ATRIOVENTRICULAR BLOCKS
INTRODUCTION TO CARDIAC PACEMAKERS INSERTION OF TRANSVENOUS CARDIAC PACEMAKER
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HEART BLOCK RELEVENT ANATOMY
Conduction: SA > Atrium > AV Node > His > Purkinje Network AV node highly innervated Responsive to sympathetic and vagal stimuli RCA blood supply His bundle less responsive Dual blood supply
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SINUS NODE DYSFUNCTION
Abnormal sinus impulse formation and propagation AKA Sick Sinus Syndrome Umbrella term for: Sinus bradycardia Sinus arrest Sinoatrial exit block Tachy-brady syndrome
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SINUS NODE DYSFUNCTION
ETIOLOGY Unclear Fibrosis (most common) Structural heart disease Medications Electrolyte imbalances (HypoK, HypoCa) Endocrine (HypoTSH, HypoT)
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SINUS NODE DYSFUNCTION
SINUS ARREST Absent sinus P waves > 2 – 3 seconds Result of absent sinus impulse formation Duration of pause is not a function of the P-P interval
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SINUS NODE DYSFUNCTION
SINOATRIAL EXIT BLOCK Conduction delay between sinus node and atrium Three types
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SINUS NODE DYSFUNCTION
SINOATRIAL EXIT BLOCK First Degree Conduction delay between sinus node and atria Cannot be identified on ECG ?Clinical significance
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SINUS NODE DYSFUNCTION
SINOATRIAL EXIT BLOCK Second Degree Intermittant conduction block Type I (Wenkebach) – Progressive shortening of P-P intervals – Pause duration less than twice the P interval – Grouped P waves
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SINUS NODE DYSFUNCTION
SINOATRIAL EXIT BLOCK Type II – Pause duration that is a multiple of the P-P interval
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SINUS NODE DYSFUNCTION
SINOATRIAL EXIT BLOCK Third Degree Complete conduction block from sinus node to atrium Cannot be distinguished from sinus arrest on ECG Typically results in an escape rhythm
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SINUS NODE DYSFUNCTION
TACHY-BRADY SYNDROME Bradycardia alternating with brief episodes of SVT Usually Afib ???Cause
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ATRIOVENTRICULAR BLOCK
ETIOLOGY Congenital Acquired – Extensive DDX Medications Hyperkalemia (>6.3 mEq/L) Hypoxia Increased vagal tone Ischemia/Infarction (~40%) Fibrosis (~50%) Infection/Inflammation Vascular Disease Idiopathic Usually never identified
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ATRIOVENTRICULAR BLOCK
FIRST DEGREE AV BLOCK Prolongation of PR > 200 ms Location of block AV node, His bundle, His-Purkinje system Correlate with QRS complex Prognosis Framingham: More likely to develop Afib, require permanent pacemaker, and increased all-cause mortality Locate source of block If AV node, generally benign and no further Ix If infranodal, may require His-bundle electrocardiogram No specific intervention required for stable 1st degree block
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ATRIOVENTRICULAR BLOCK
FIRST DEGREE AV BLOCK
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ATRIOVENTRICULAR BLOCK
SECOND DEGREE AV BLOCK Type I (Wenckebach/Mobitz I) - Normal Gradual prolongation of the PR interval followed by dropped QRS Atrial impulses reach AV node while it is partially refractory Location usually the AV node
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ATRIOVENTRICULAR BLOCK
SECOND DEGREE AV BLOCK Type II – Never normal PR interval constant Usually a result of underlying structural disease Location typically His-Purkinje system High Grade Second Degree 2 or more consecutively blocked P waves
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ATRIOVENTRICULAR BLOCK
SECOND DEGREE BLOCK Different sites of involvement/prognoses Type I: Generally involves AV node and is benign Type II: Almost always infranodal and may progress to 3rd degree (slow unreliable escape) Difficult to distinguish type in 2:1 conduction block
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ATRIOVENTRICULAR BLOCK
THIRD DEGREE BLOCK Complete AV node failure to conduct Block may be anywhere in conduction system Constant P-P and R-R intervals but no relationship Variable PR intervals, Atrial HR > Ventricular HR May be hemodynamically unstable Slow heart rate may produce Torsade , especially in women
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HEART BLOCK ECG PRACTICE
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ECG 1
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SSS (Tachy-Brady)
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ECG 2
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Type II Second Degree AV Block
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ECG 3
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Sinus Arrest
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ECG 4
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3rd Degree AV Block
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ECG 5
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Type II Second Degree SA Node Exit Block
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ECG 6
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First Degree AV Block
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ECG 7
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Type 1 Second Degree AV Block
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HEART BLOCK INITIAL ASSESSMENT Hemodynamic Instability
Fatigue, Dizziness, NV, Diaphoresis Hypotension Syncope Dyspnea Chest Pain ACLS Guidelines for Symptomatic Bradycardia Medications Β- Blockers Ca2+ Channel Blockers Digitalis Amiodarone
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HEART BLOCK INITIAL ASSESSMENT Investigations Stabilize first! ECG
Bloodwork Electrolytes Dig level Troponin
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HEART BLOCK MANAGEMENT O2, IV, Monitors Transcutaneous pacing
Transvenous pacing > 30 minutes transcutaneous pacing Unable to obtain capture Consider atropine Consider catecholamines (be cautious)
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HEART BLOCK CARDIOLOGY CONSULTATION Outpatient Inpatient
New, asymptomatic Type I 2nd Degree (while awake) Inpatient Any symptomatic block New, asymptomatic Type II 2nd Degree Asymptomatic 3rd Degree Concomitant MI/Ischemic symptoms High Grade AV Block
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CARDIAC PACING INDICATIONS Temporary Permanent
Any symptomatic AV block Asymptomatic, but associated with Torsade Permanent ACC/AHA/HRS 2008 Guidelines: Divided into Class Based Recommendations
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CARDIAC PACING
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CARDIAC PACING INDICATIONS AV Block Class I 2nd and 3rd Degree
Bradycardia with symptoms (C) Associated arrhythmias and medications that produce symptomatic bradycardia (C) Asymptomatic, but asystole >3 sec or escape < 40 bpm or wide QRS escape or Afib and bradycardia with systole >5 seconds (C) After ablation of AV node or unresolving post-op block (C) Associated with MD, Kearns-Sayre syndrome, Erb dystrophy (B) Associated with exercise w/o MI (B)
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CARDIAC PACING INDICATIONS AV Block Class IIa Class IIb
Asymptomatic persistent 3rd degree with escape > 40 (C) Asymptomatic 2nd degree with intra or infra-Hisian block (B) Symptomatic 1st or 2nd degree block (B) Asymptomatic 2nd degree block with narrow QRS (B) Class IIb 1st or 2nd degree with MD, Erb dystrophy, peroneal muscular atrophy +/- symptoms (B) AV block in setting of drug toxicity when block expected to recur (B)
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CARDIAC PACING INDICATIONS AV Block Class III Also not indicated in:
Not indicated for asymptomatic 1st Degree (B) Not indicated for asymptomatic Mobitz I with block at AV node (C) Not indicated for AV block that is expected to resolve and unlikely to recur (drug toxicity, Lyme disease, transient increased vagal tone) (B) Also not indicated in: PEA Arrest Traumatic cardiac arrest
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Some Things Just Won’t Work
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CARDIAC PACING PACING MODES 5 Position Nomenclature
First 3 Positions most common in pacemaker description Position I: Chamber being paced Atrium (A), Ventricle (V), Both (D), None (O) Position II: Chamber being sensed Position III: Pacemaker’s response to sensing Triggers (T), Inhibits (I), Both (D), None (O)
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CARDIAC PACING PACING MODES
Position IV: Programmability and Rate Control Hierarchical Rate Modulation (R), Communicating (C), Programmable (P), (O) Position V: Antitachydysrrhythmia Function Pacing (P), Shocking (S), Both (D)
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CARDIAC PACING PACING MODES Most pacemakers encountered are:
AAIR – Useful for sinus node dysfunction with intact AV node VVIR – Useful for chronically ineffective atria (AF, AFlutter) DDD – Most common. Preserves AV synchrony Reduces risk of AF, reduces signs/symptoms HF, improves QOL No significant mortality benefit over single-chamber pacing
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CARDIAC PACING ECG MANIFESTATIONS Depends on Pacing Mode Atrial Pacing
Small pacemaker spike prior to P wave with normal morphology Ventricular Pacing LBBB-like and prolonged, inverted QRS (V5/6) and LAD
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CARDIAC PACING
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CARDIAC PACING
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CARDIAC PACING TEMPORARY PACING
Goal: Restore effective myocardial contraction to increase adequate cardiac output Transcutaneous vs. transvenous pacing modalities
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CARDIAC PACING TRANSCUTANEOUS PACING
Temporary stabilization of symptomatic bradycardia Most patients tolerate pacing for < 15 minutes Pain directly related to current and inversely related to pad size
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CARDIAC PACING TRANSCUTANEOUS PACING Technique
Apply pads front/back or left/right Front/back preferred Sedate Set HR to 60-80 Set current to 0 mA Choose mode Synchronous vs. asynchronous Turn pacemaker on Increase current by 10 mA increments until capture obtained Manifested by wide QRS relating to palpable carotid pulse If unconscious, start at 200 mA and decrease to lowest current
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CARDIAC PACING TRANSVENOUS PACING
Placement of electrode into R Ventricle Pacer is VVI mode Allows for asynchronous vs synchronous
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CARDIAC PACING TRANSVENOUS PACING Equipment Introducer Kit
Introducer sheath Pacing catheter External pacing generator Cardiac monitor
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CARDIAC PACING TRANSVENOUS PACING External Pacing Generator
Delivers electrical current (mA) Output Control Dial Regulates current from 0.1 – 20 mA Rate Control Dial Selects pacing rate Sensitivity Control Rate Threshold suppression of pacer based on native R wave Asynchronous pacing when sensitivity control turned down
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CARDIAC PACING TRANSVENOUS PACING Transvenous Pacing Catheter
3 types: Flexible, Semifloating, Rigid/Non-floating Risk of cardiac perforation with rigid catheters Two electrodes attached: + and – Introducer Sheath Facilitates central venous access
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CARDIAC PACING TRANSVENOUS PACING Technique
Seldinger technique for central venous access R IJ or L Subclavian shown to be most successful Secure introducer sheath Introduce pacing electrode Inflate balloon when electrode passed through the 20 cm mark Moot if no pulse Set pacing generator to max current Set rate between 60-80 Asynchronous sensitivity
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CARDIAC PACING TRANSVENOUS PACING
As cath is advanced, monitor will show pacing spikes Pacing spikes followed by wide QRS indicating of RV placement Electrical capture Assess for pulse Mechanical capture Deflate balloon and secure cath in place Set pacing threshold
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CARDIAC PACING TRANSVENOUS PACING Complications
Inherent to central venous access Arterial puncture, PTX, infection Right heart catheterization Failure to capture, failure to sense, dysrrhythmias Cardiac perforation Lead displacement Electrode coiling
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