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HEART BLOCKS AND CARDIAC PACEMAKERS. Arun Abbi Jason Mitchell Jan 21, 2010. OUTLINE. SINUS NODE DYSFUNCTION ATRIOVENTRICULAR BLOCKS INTRODUCTION TO CARDIAC PACEMAKERS INSERTION OF TRANSVENOUS CARDIAC PACEMAKER. HEART BLOCK. RELEVENT ANATOMY - PowerPoint PPT Presentation
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HEART BLOCKS AND CARDIAC PACEMAKERS
Arun AbbiJason MitchellJan 21, 2010
OUTLINE
SINUS NODE DYSFUNCTION ATRIOVENTRICULAR BLOCKS INTRODUCTION TO CARDIAC PACEMAKERS INSERTION OF TRANSVENOUS CARDIAC
PACEMAKER
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
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
SINUS NODE DYSFUNCTION
ETIOLOGY Unclear Fibrosis (most common) Structural heart disease Medications Electrolyte imbalances (HypoK, HypoCa) Endocrine (HypoTSH, HypoT)
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
SINUS NODE DYSFUNCTION
SINOATRIAL EXIT BLOCK Conduction delay between sinus node and
atrium Three types
SINUS NODE DYSFUNCTION
SINOATRIAL EXIT BLOCK First Degree
Conduction delay between sinus node and atria Cannot be identified on ECG ?Clinical significance
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
SINUS NODE DYSFUNCTION
SINOATRIAL EXIT BLOCK Type II – Pause duration that is a multiple of
the P-P interval
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
SINUS NODE DYSFUNCTION
TACHY-BRADY SYNDROME Bradycardia alternating with brief episodes of
SVT Usually Afib ???Cause
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
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
ATRIOVENTRICULAR BLOCK
FIRST DEGREE AV BLOCK
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
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
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
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
HEART BLOCK
ECG PRACTICE
ECG 1
SSS (Tachy-Brady)
ECG 2
Type II Second Degree AV Block
ECG 3
Sinus Arrest
ECG 4
3rd Degree AV Block
ECG 5
Type II Second Degree SA Node Exit Block
ECG 6
First Degree AV Block
ECG 7
Type 1 Second Degree AV Block
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
HEART BLOCK
INITIAL ASSESSMENT Investigations
Stabilize first! ECG Bloodwork
Electrolytes Dig level Troponin
HEART BLOCK
MANAGEMENT O2, IV, Monitors Transcutaneous pacing Transvenous pacing
> 30 minutes transcutaneous pacing Unable to obtain capture
Consider atropine Consider catecholamines (be cautious)
HEART BLOCK
CARDIOLOGY CONSULTATION Outpatient
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
CARDIAC PACING
INDICATIONS Temporary
Any symptomatic AV block Asymptomatic, but associated with Torsade
Permanent ACC/AHA/HRS 2008 Guidelines:
Divided into Class Based Recommendations
CARDIAC PACING
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)
CARDIAC PACING
INDICATIONS AV Block Class IIa
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)
CARDIAC PACING
INDICATIONS AV Block Class III
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
Some Things Just Won’t Work
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
Atrium (A), Ventricle (V), Both (D), None (O) Position III: Pacemaker’s response to sensing
Triggers (T), Inhibits (I), Both (D), None (O)
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)
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
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
CARDIAC PACING
CARDIAC PACING
CARDIAC PACING
TEMPORARY PACING Goal: Restore effective myocardial contraction
to increase adequate cardiac output Transcutaneous vs. transvenous pacing
modalities
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
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
CARDIAC PACING
TRANSVENOUS PACING Placement of electrode into R Ventricle Pacer is VVI mode Allows for asynchronous vs synchronous
CARDIAC PACING
TRANSVENOUS PACING Equipment
Introducer Kit Introducer sheath Pacing catheter
External pacing generator Cardiac monitor
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
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
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
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
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