Heart Blocks and Pacemakers - Calgary Em

Heart Blocks and Pacemakers - Calgary Em

Heart Blocks and Pacemakers Juliette Sacks January 25, 2007 Core Rounds Objectives Review heart blocks, their clinical significance and management Provide an overview of pacemaker components, nomenclature and functions Discuss complications of pacemaker implantation Talk about pacemaker malfunction Touch on ED management and disposition of

pacemaker patients Offer a precis of temporary pacing modalities. ICDs not covered in this talk. Case 85 y.o. F complaining of feeling off and being just so tired Denies CP, SOB Vaguely recalls feeling a bit unsteady on a couple of occasions PMHx: osteoporosis, hypothyroidism and depression Meds: Calcium, Vit D, Celexa, Synthroid Case contd

Vitals: HR 45, regular RR 16 BP 108/75 02 sats 97% on RA Afebrile Grannys EKG: Atrioventricular Blocks

Definition: Delay or interruption in the transmission of an impulse from the atria to the ventricles Conduction may be delayed, intermittent or absent. Duration Transient Permanent Causes may be: Anatomical Functional

Etiology Fibrosis and sclerosis of the conduction system Ischemic heart disease Drugs Increased vasovagal tone Valvular disease Congenital heart disease Other: Cardiomyopathies, myocarditis, hyperkalemia, infiltrating malignancies, miscellaneous Surgery CABG, valve replacement Sclerosis and fibrosis of the conduction system

Account for 50% of AV block 2 idiopathic entities: 1. Levs Disease: sclerosis of left side of the heart Affects older people Associated with calcific aortic and mitral valves that extends into the adjacent conduction system 2. Lenegres Disease:

Progressive fibrotic, sclerodegenerative disease Affects younger people May be hereditary Slow progression to complete heart block Presents with bradycardia and some degree of AVB Ischemic Heart Disease Accounts for 40% of AV block Chronic or acute ischemic changes can disrupt conduction

With AMI: 20% will develop AVB 8% 1st degree AVB 5% 2nd degree AVB 6% 3rd degree AVB Up to 20% increased mortality with bradycardia and/or blocks post AMI Drugs Cardiac medications: Digitalis, CCB

(especially verapamil), B-blockers Class Ia: Quinidine, procainamide, disopyramide Cholinergics: cholinesterase inhibitors Opioids and sedatives Drugs with Class IA type effects: TCAs, carbamazepine, quinine, chloroquine Cocaine Increased Vagal Tone Vasovagal Pain Occulocardiac reflex Diving

reflex Carotid sinus massage Hypersensitive carotid sinus syndrome Stimulation of carotid sinus leads to bradyasystole and then to pre/syncope Cardioinhibitory: >3s of asystole with carotid stimulation Vasodepressor effects Valvular Disease Due to extension of calcification into conduction system Associated with AV and MV repair Repair of VSD: including transcoronary

ablation of septal hypertrophy Infectious AVB with the following usually indicates poor prognosis: Myocarditis: Viral: Cocksackie B Bacterial: Diptheria Protozoal: Chagas disease

Spirochetal: Lyme disease Syphilis, toxoplasmosis Other Congenital heart disease, neonatal SLE syndrome Familial heart disease: cardiac sodium channel SCN5A linked

mutations Cardiomyopathies: HOCM, amyloidosis, sarcoidosis Endocrine causes: Hyperthyroidism hypoadrenalism Hyperparathyroidism Acromegaly Electrolyte abnormalities: Hyperkalemia: >6.3 meq/L Hypercalcemia Hypermagnesemia Infiltrative malignancies: lymphoma, multiple myelomas Neuromuscular degenerative diseases Cardiac tumours First Degree Heart Block SA

node is normal Normal P wave AV node conducts more slowly than normal Prolonged PR interval >0.2s PR interval is constant Rest of conduction is normal Normal QRS

First Degree AVB Conduction delay can occur in: Atrium: 3% of cases May be due to intratrial pathology EKG findings: widening of P wave and decreased P wave voltage AV node: Most common site Common causes: increased vagal tone, CCB, digoxin, BB EKG findings: long PR interval with a narrow or wide P wave

and narrow QRS Bundle of His: Drugs that block sodium channels can impair depolarization and slow conduction (Quinidine, procainamide ) First Degree AVB Clinical significance none Treatment none May progress to 2nd or 3rd degree AVB Second Degree AVB Some atrial impulses fail to reach the

ventricles 2 types: Mobitz Type I (Wenckebach): progressive PR interval lengthening to a nonconducted P wave Mobitz Type II: PR interval constant prior to P wave that does not conduct to the ventricles. SECOND DEGREE A-V BLOCK (MOBITZ I OR WENCKEBACH) Mobitz Type I (Wenckebach) AVB Most often involves AV node Benign

Features: Gradually increasing PR interval Gradually decreasing R-R interval Dropped beat Largest delay occurs in the first beat and then decreases beat to beat until block occurs and cycle is reset Group beating: 3:2,4:3 etc. Second Degree Heart Block (2) Mobitz Type I (Wenkebach)

PR PR PR DROPPED BEAT Mobitz Type I Clinical implications: Often asymptomatic May have some symptoms eg lethargy, confusion

If cardiac output is reduced, patient may experience angina, syncope or heart failure due to bradycardia and resultant hypoperfusion state. Can occur in athletes with high vagal tone Elderly: aging prolongs cycle length Further implications: Underlying IHD: Mobitz type I can be complication of inferior MI as: RCA supplies inferior and posterior walls and AV and SA nodes Associated with increased mortality Treatment:

Removing reversible causes (ischemia, increased vagal tone, medications Pacemaker if symptomatic during day No pacemaker is symptoms at night May progress to 3rd degree AVB MOBITZ TYPE II Mobitz Type II AVB Always occurs below the AV node 20% within Bundle of His

80% in bundle branches Widened QRS PR interval may be normal or slightly prolonged but constant Non-conducted P wave on EKG Clinical implications: Dizziness Presyncope Syncope Mobitz Type II AVB Type II is permanent and may progress

to higher levels of block Treatment: Remove reversible causes Potential candidates for pacemaker insertion Second Degree AVB 2:1 Unable to classify as Mobitz type I or II Ratio of 2 P waves to 1 QRS Clinical significance: Will be associated with symptoms (dizziness, lethargy etc.) May progress to 3rd degree AVB Treatment

- pacemaker THIRD DEGREE A-V BLOCK Third degree (complete) AVB No atrial impulses reach the ventricles due failure of AV node therefore no P wave conduction AV dissociation (Ps marching through) QRS complex: Narrow: block at AV node to level of bundle of His Wide: block below level of bundle of His More

distal the block the slower the escape rhythm If <40bpm: pacemaker is unreliable causing profound bradycardia or asystole Syncope is very common Clinical Significance Clinical

Implications: Dizziness Presyncope Syncope Ventricular tachycardia Ventricular fibrillation Confusion Can worsen angina and CHF Treatment: Pacemaker! Class I Indications for Permanent Pacing in Adults per

AHA/ACC rd 1. 3 degree AVB at any anatomic level associated with any of the following: Symptomatic bradycardia (secondary to AVB) Symptomatic bradycardia (secondary to drugs

required for management of dysrhythmias or other medical conditions) Documented asystole >3s or escape rate of <40 bpm in awake, asymptomatic patient After ablation of AV node Postoperative AVB that is not expected to resolve Neuromuscular disease with AVB (neuromuscular dystrophies) 2. Symptomatic bradycardia from 2nd degree AVB regardless of type or site of block. 3. Chronic bifascicular or trifascicular block with intermittent 3rd degree AV block or type II 2nd degree AVB. 4. After AMI with any of the following: Persistent 2nd degree AVB at the His-Purkinje level with bilateral bundle branch block or 3rd degree AVB

at or below His-Purkinje system Transient 2nd or 3rd degree infranodal AVB and associated BBB Symptomatic, persistent 2nd or 3rd degree AVB 5. Sinus node dysfunction with symptomatic bradycardia or chronotropic incompetence. 6. Recurrent syncope caused by carotid sinus stimulation. Pacemaker indications: Class IIa Complete AVB without symptoms: >40bpm while awake = Class IIa indication UNLESS: Activity

or exercise is limited Heart begins to enlarge LV function is depressed LA enlargement is noted Intra- or infra-Hisian block issuspected with of without QRS widening QT interval prolongation Ventricular arrhythmias Episodic profound bradycardia (during sleep or awake) Pacemaker indications: take home points! Complete AVB with: Associated symptoms

Ventricular pauses >3s Resting HR <40 bpm while awake = pacemaker! Granny Remember Granny? Well, she can be helped by some of the information in the next part of the talk Quiz Here

is a photo of the first pacemaker invented (obviously not an internal device!) Circa 1950 True or false: the inventor was Canadian True! Courtesy of John Hopps - an engineer from the University of Manitoba. He recognized that if a heart stopped

beating it could be started again by artificial stimulation using mechanical or electric means. Current pacemakers provide electrical stimulation to cause cardiac contraction when intrinsic cardiac electrical activity is slow or absent. A Brief History of Pacemakers Just kiddingbut did you know?

The implantable cardiac pacemaker was discovered by mistake! Wilson Greatbatch was building an oscillator to record heart sounds. When he accidentally installed a resistor with the wrong resistance into the unit, it began to give off a steady electrical pulse. Greatbatch realized that the small device could be used to regulate the human heart. After two years of refinements, he had handcrafted the world's first successful implantable pacemaker (patent #3,057,356). Until that time, the apparatus used to regulate heartbeat was the size of a television set, and painful to use.

Greatbatch later went one step further, inventing a corrosion-free lithium battery to power the pacemaker. All told, his pacemakers and batteries. Thus in 1985 the National Society of Professional Engineers named Greatbatch's invention one of the ten greatest engineering contributions to society of the last 50 years. Pacemaker Functions Stimulate cardiac depolarization 2. Sense intrinsic cardiac function 3. Respond to increased metabolic demand by providing rate responsive pacing 4. Provide diagnostic information stored by the pacemaker

1. Pacemaker Components Combine with Body Tissue to Form a Complete Circuit Pulse generator: power source or battery Leads or wires Cathode (negative electrode) Anode (positive electrode) Apex of right ventricle

Lead IPG Anode Cathode The Pulse Generator: Submuscular or subcutaneous implantation location Contains a lithium battery that has a 4-10

year lifespan Slow, gradual decrease in power over time A sudden power failure is very uncommon Circuitry Battery Electronic Circuitry Sensing circuit Timing circuit Output circuit

Lead System Bipolar Lead has both negative, (Cathode) distal and positive, (Anode) proximal electrodes Separated by 1 cm Larger diameter: more prone to fracture Compatible with ICD Unipolar Negative (Cathode) electrode in contact

with heart Positive (Anode) electrode: metal casing of pulse generator Prone to oversensing Not compatible with ICD Difference on an ECG? Bipolar current travels only a short distance between electrodes small pacing spike:

<5mm + Anode - Cathode Difference on an ECG? Unipolar current travels a longer distance between electrodes larger pacing spike:

>20mm + Anode Cathode Pacemaker Code I Chamber Paced II Chamber Sensed

III Response to Sensing IV Programmable Functions/Rate Modulation V: Ventricle V: Ventricle T: Triggered P: Simple programmable A: Atrium

A: Atrium I: Inhibited M: Multiprogrammable D: Dual (A+V) D: Dual (A+V) D: Dual (T+I) C: Communicating O: None O: None S: Single S: Single (A or V)

(A or V) O: None V Antitachy Function(s) P: Pace S: Shock D: Dual (P+S) R: Rate modulating O: None O: None Common Pacemakers

VVI Ventricular Pacing : Ventricular sensing; intrinsic QRS Inhibits pacer discharge VVIR As above + has biosensor to provide Rateresponsiveness DDD Paces + Senses both atrium + ventricle, intrinsic cardiac activity inhibits pacer d/c, no activity: trigger d/c

DDDR As above but adds rate responsiveness to allow for exercise Rate Responsive Pacing When the need for oxygenated blood increases, the pacemaker ensures that the heart rate increases to provide additional cardiac output Adjusting Heart Rate to Activity Normal Heart Rate Rate Responsive Pacing Fixed-Rate Pacing Daily Activities

Rate Response Rate responsive (also called rate modulated) pacemakers provide patients with the ability to vary heart rate when the sinus node cannot provide the appropriate rate Rate responsive pacing is indicated for: Patients who are chronotropically incompetent (heart rate cannot reach appropriate levels during exercise or to meet other metabolic demands) Patients in chronic atrial fibrillation with slow ventricular response

Single Chamber VVI - lead lies in right ventricle Independent of atrial activity Use in AV conduction disease Paced Rhythm Recognition AAI / 60 Paced Rhythm Recognition VVI /

60 Advantages and Disadvantages of Single-Chamber Pacing Systems Advantages Implantation single lead Disadvantages of a Single ventricular lead does not provide AV synchrony

Single atrial lead does not provide ventricular backup if A-to-V conduction is lost Dual Chamber Typically in pts with nonfibrillating atria and intact AV conduction

Native P, paced P, native QRS, paced QRS ECG may be interpreted as malfunction when none is present May have fusion beats Four Faces of Dual Chambe Atrial Pacing Pace, Ventricular Pace (AP/VP) AV AP

V-A VP Rate = 60 bpm / 1000 ms A-A = 1000 ms AV AP VP V-A Four Faces of Dual Chambe

Pacing Atrial Pace, Ventricular Sense (AP/VS) AV AP V-A VS Rate = 60 ppm / 1000 ms A-A = 1000 ms

AV AP VS V-A Four Faces of Dual Chambe Pacing Atrial Sense, Ventricular Pace (AS/ VP) AV AS

VP V-A V-A AV AS Rate (sinus driven) = 70 bpm / 857 ms A-A = 857 ms VP Four Faces of Dual Chamber Pacing

Atrial Sense, Ventricular Sense (AS/VS) AV AS V-A VS Rate (sinus driven) = 70 bpm / 857 ms Spontaneous conduction at 150 ms A-A = 857 ms AV

AS V-A VS Paced Rhythm Recognition DDD / 60 / 120 Paced Rhythm Recognition DDD / 60 / 120 Pacemaker Interventions Magnet

application No universal function of magnet Does not inhibit or turn off pacemaker Model-specific magnet that activate a reed switch that coverts unit to asynchronous pacing at a pre-set rate that is no longer inhibited by patients intrinsic electrical activity. Interrogation / Programming

Model-specific pacemaker programmer can non-invasively obtain data on function and reset parameters Magnet Application Complications of Pacemaker Implantation Infection Venous obstruction Pacemaker Syndrome Infection

2% for wound and pocket infection 1% for bacteremia with sepsis NB pacemaker = foreign body! Patient may have symptoms of pain, local inflammation, hematoma Blood cultures should be drawn Culprits are S. aureus (60%) and S. epidermidis (70%)

Vancomycin should be started pending cultures Pacemaker and leads are removed if bacteremic Temporised with transvenous pacing iv antibiotics for 4-6 weeks with new components implanted. Venous Obstruction Incidence 30-50% Can involve axillary, innominate, subclavian veins and SVC 1/3 have chronic complete venous obstruction but are asymptomatic due to collateralization 0.5-3.5% develop symptoms which include: edema, pain, venous engorgement of the ipsilateral arm to insertion US, venography, CT to diagnose acute thrombosis Heparin, lifetime warfarin; early thrombolytic

therapy is most effective Venous Access Issues Pneumo / hemothorax Air embolism CONTROVERSIAL: association of PE with pacemaker RARE: SVC syndrome from pacemaker leadinduced thrombosis Pacemaker Syndrome

20% of patients present with new complaints or worsening of initial symptoms that led to pacemaker insertion More commonly with single chamber pacer AV synchrony is lost retrograde VA conduction atrial contraction against closed MV + TV jugular venous distention + atrial dilation sx of CHF and reflex vasodepressor effects

Symptoms: Pre/syncope Orthostatic dizziness Fatigue Exercise intolerance Weakness Lethargy Chest fullness or pain Cough Uncomfortable pulsations n neck or abdomen RUQ pain Other

Pacemaker Syndrome 1/3 of patients can adapt and these symptoms resolve 1/3 require that a dual chamber pacer replace the single chamber pacer If symptoms occur with dual chamber pacer then optimizing timing of ventricular pacing is key

Beware: symptoms of pacemaker syndrome and pacemaker malfunction are the same! Pacemaker Malfunction Four categories: Failure to Capture Inappropriate sensing: under or over Inappropriate pacemaker rate The good news! Rarely immediately life threatening

Occurs in <5% of patients bold indicates most common malfunctions Failure to Capture Absence of pacemaker spikes despite indication to pace Caused by: Battery depletion - rare Fracture of pacemaker lead most common problem Disconnection of lead from pulse generator unit Lead displacement due to change cardiac Exit block failure of an adequate stimulus to depolarize the paced chamber Seen

in changes in endocardium in contact with pacing system i.e. infarction, ischemia, hyperkalemia, class III antiarrhythmics (amiodarone, bertylium) No Capture Pacemaker artifacts do not appear on the ECG; rate is less than the lower rate Pacing output delivered; no evidence of pacing spike is seen A: failure to capture atria in DDD

Sensing Sensing is the ability of the pacemaker to see when a natural (intrinsic) depolarization is occurring Pacemakers sense cardiac depolarization by measuring changes in electrical potential of myocardial cells between the anode and cathode Accurate Sensing... Ensures that undersensing will not occur the pacemaker will not miss P or R waves that should have been sensed

Ensures that oversensing will not occur the pacemaker will not mistake extracardiac activity for intrinsic cardiac events Provides for proper timing of the pacing pulse an appropriately sensed event resets the timing sequence of the pacemaker Inappropriate sensing: Undersensing Pacemaker incorrectly misses an intrinsic depolarization paces despite intrinsic activity Appearance of pacemaker spikes occurring earlier than the programmed rate: overpacing May or may not be followed by paced complex:

depends on timing with respect to refractory period Causes: AMI, progressive fibrosis, lead displacement, fracture, poor contact with endocardium Undersensing Pacemaker does not see the intrinsic beat, and therefore does not respond appropriately Intrinsic beat not sensed Scheduled pace

delivered VVI / 60 Undersensing An intrinsic depolarization that is present, yet not seen or sensed by the pacemaker P-wave not sensed Atrial Undersensing Inappropriate sensing:

Oversensing Detection of electrical activity not of cardiac origin intermittent, irregular pacing or inhibition of pacing activity State of underpacing Accurate Sensing Requires That Extraneous Signals Be Filtered Out Sensing amplifiers use filters that allow appropriate sensing of P waves and R waves and reject inappropriate signals

Unwanted signals most commonly sensed are: T waves Far-field events (R waves sensed by the atrial channel) Skeletal myopotentials (e.g., pectoral muscle myopotentials) Oversensing Marker channel shows intrinsic activity... ...though no activity is present

VVI / 60 An electrical signal other than the intended P or R wave is detected Environmental Factors Interfering with Sensing Electrocautery: causes temporary pacemaker inhibition MRI: alters pacemaker circuitry and results in fixed-rate or asynchronous pacing Cellular phone: pacemaker inhibition, asynchronous pacing

Arc welding Lithotripsy Microwaves Mypotentials from muscle Inappropriate Pacemaker Rate Rare reentrant tachycardia seen with dual chamber pacers Premature atrial or ventricular contraction sensed by atrial lead triggers ventricular contraction retrograde VA conduction sensed by atrial lead triggers ventricular contraction etc etc etc Tx: Magnet application: fixed rate,

terminates tachyarrthymia, Reprogram to decrease atrial sensing Causes of Pacemaker Malfunction Circuitry or power source of pulse generator Pacemaker leads Interface between pacing electrode and myocardium Environmental factors interfering with normal function Pulse Generator Loose

connections Similar to lead fracture Intermittent failure to sense or pace Migration Dissects along pectoral fascial plane Failure to pace Twiddlers syndrome Manipulation lead dislodgement Leads Dislodgement

or fracture (anytime) Incidence 2-3% Occurs if pacemaker is placed medially Failure to sense or pace Dx with CXR, lead impedance Insulation breaks Current leaks failure to capture

Dx with measuring lead impedance (low) Case continued Granny has had a pacemaker implanted 8d ago. She went home feeling just fabulous! She is in the ED with sharp, stabbing retrosternal chest pain that started after tea this morning. The pain is pleuritic. When pressed, she says she was quite winded getting up the stairs from the cellar yesterday. Diagnosis? Cardiac Perforation

Can happen early or late (days to weeks) post implantation Need high index of suspicion because: Often well tolerated due to small puncture size

May auto-tamponade May be asymptomatic May have hiccups May have pleuritic retrosternal chest pain, SOB May have increased pacing threshold Px: may hear pericardial friction rub CXR, FAST helpful Echo mandatory to rule out Pacemaker Mediated Tachycardia (PMT) PMT is a paced rhythm, usually rapid, which is sustained by ventricular events conducted retrogradely (i.e., backwards) to the atria

PMT can occur with loss of AV synchrony caused by: PVC Atrial non-capture Atrial undersensing Atrial oversensing Built in solution: PMT Intervention Designed to interrupt a PacemakerMediated Tachycardia DDD / 60 / 120

Pseudomalfunction: Hysteresis Allows a lower rate between sensed events to occur; paced rate is higher Lower Rate 70 ppm Hysteresis Rate 50 ppm Management: History Most complications and malfunctions occur within first few weeks or months

Pacemaker identification card: should tell you what you need to know about the device Syncope, near syncope, orthostatic dizziness, lightheaded, dyspnea, palpitations Pacemaker syndrome: diagnosis of exclusion Management: Physical Exam Look

for : Fever: think pacemaker infection Cannon a waves: AV asynchrony Bibasilar crackles if CHF Pericardial friction rub if perforation of RV Management: adjuncts CXR: Determine tip position Determine number of leads and position EKG

May reveal failure to sense or pace Low pacing rate Abnormally rapid rhythm = pacemakermediated tachycardia Management: ACLS Drugs and defibrillation as per ACLS guidelines Recommended to keep paddles >10cm from pulse generator May transcutaneously pace

Transvenous pacing may be inhibited by venous thrombosis: may need fluoroscopic guidance AMI + Pacers Difficult diagnosis Most sensitive indicator is ST-T wave changes on serial ECG If clinical presentation strongly suggestive then should treat as AMI Coarse VF may inhibit pacer (oversensing) Successful resuscitation may lead to failure to capture (catecholamines, ischemia)

Disposition Admit Pacemaker infections /unexplained fever or WBC Myocardial perforation Lead # or dislodgement Wound dehiscence / extrusion or erosion Failure to pace, sense, or capture

Ipsilateral venous thrombosis Unexplained syncope Twiddlers syndrome Disposition Potentially fixable in ED w/ help Pacemaker syndrome Pacemaker-mediated tachycardia

Oversensing Diaphragmatic pacing Myopotential inhibitors Temporary Pacing Modalities Transcutaneous 2. Transvenous 1. Emergency Pacing Hemodynamically compromising bradycardia Bradycardia with escape rhythms Overdrive pacing of refractory tachycardia

Bradyasystolic cardiac arrest (within 5 minutes) Bradycardia dependent ventricular tachyarrhythmia (Torsade-de-Pointes) Indications for temporary pacing With AMI with: Symptomatic sinus node dysfunction Mobitz type II 2nd degree AVB 3rd degree AVB New left, right or alternating BBB or bi-fascicular block Before electrical cardioversion of a patient with sick

sinus syndrome or with a high level of dependency to a permanent pacemaker Prior to permanent pacemaker implantation Prior to PA cath insertion if underlying LBBB Transcutaneous Pacing Pitfalls: Capture is obtained between 40-80 mA regardless of age, body weight and BSA May see INCREASED pacing threshold with:

Suboptimal lead position Poor skin-electrode contact Post surgical chestwall disruption Emphysema Pericardial effusion PPV Hypoxia/ischemia/shock/acidosis/hyperkalemia After electrical cardioversion/defibrillation

After prolonged resuscitation/arrest Transcutaneous Pacing Initiation of pacing: Use maximal current output and asynch setting Adjust current to ~10mA above threshold Confirm capture by: Pulse palpation Doppler Arterial line tracing

Pitfalls/Complications Failure to recognise underlying VF Failure to recognise that pacemaker is NOT capturing Complications: Painful Induction of arrhythmias Tissue damage Transvenous Pacing Most

consistent and reliable means of temporary pacing Can permit atrial and/or ventricular pacing Stable Well tolerated Significant potential complications Transvenous Pacing 4 letter coding system: 1st letter: indicates paced chamber (V,A,D) 2nd letter: indicates sensed chamber (V,A,D) 3rd letter: mode of response when an event is

sensed I = inhibited T = triggered D = inhibited or triggered 0 = neither inhibited, nor triggered 4th letter: R indicates rate responsiveness (only in permanent device) Can be uni or bipolar

Unipolar System Simple Less sophisticated electrode Dipole is between tip of electrode and generator Higher risk of oversensing Larger spike on EKG

Bipolar System More complex electrode Larger electrode Dipole is at tip of electrode Lower risk of oversensing Small spike on EKG Higher risk of electrode failure Contraindications to

transvenous pacing Tricuspid valve mechanical prosthesis Existing endocarditis Infected endocardial pacemaker lead Sepsis/bacteremia Ventricular arrhythmias Capture Depends on: Stable catheter position Viability of paced myocardial tissue Electrical integrity of pacing system

Most common cause of lost capture is lead dislodgement/perforation Other causes include: Poor endocardial contact Local myocardial necrosis/fibrosis/inflammation/ edema Hypoxia/acidosis/electrolyte abnormalities/drug effects

Lead fracture Generator malfunction/battery failure Unstable electrical connections Sensing problems Undersensing Lead dislodgement/ perforation Local tissue

necrosis/fibrosis Lead fracture Electrocautery Generator malfunction Unstable electrical connections Oversensing P wave sensing T wave sensing Myopotential sensing Electromagnetic interference Poor electrical contacts, connections

Lead fracture Complications Arrhythmias Thromboembolic events - ? Need to anticoagulate Clinical infection/phlebitis Bacteremia Perforation Knotting of catheter Tricuspid valve damage Induction of RBBB Phrenic nerve or diaphragmatic pacing

without myocardial perforation Myocardial Perforation Symptoms Signs Pericardial Pericardial chest pain Shoulder pain Diaphragmatic pacing Skeletal muscle pacing Dyspnea

Hypotension (? tamponade) rub Intercostal or diaphragmatic pacing Failure to pace or sense New pericardial effusion or tamponade Investigations EKG:

Change in QRS morphology +/- axis Failure to pace or sense Pericarditis pattern CXR: Change in lead position Extra-cardiac location of lead tip Thanks! References

Thanks to Karen Hillier, Pacemaker Nurse Clinician Rosens: Chapter 28 Barold, S. Serge. Cardiac pacemakers step by step : an illustrated guide. Blackwell, 2004. Haim M et al. Frequency and prognostic significance of high degree

atrioventricular block in patients with first non-Q wave acute myocardial infarction. Am J Cardiol. 1997;79:674. Lamas G et al. Ventricular Pacing or Dual Chamber Pacing for Sinus Node Dysfunction. NEJM. 2002;346(24):1854-61. Lamas G et al. A simplified approach to predicting the occurrence of complete heart block during acute myocardial infarction. Am J Cardiol. 1986;57:1213. Mangrum JM, DiMarco JP. The evaluation and Management of bradycardia. NEJM. 2000;342(10):703-9. www.uptodate.com for heart blocks and pacemaker information ACC/AHA Guidelines for Pacemaker implantation: http://www.acc.org/ qualityandscience/clinical/guidelines/april98/jac5507gtc.htm CHB and AMI Incidence of new CHB 5.4%

Occurring 2.6 days post MI Developed in: >60 y.o. Comorbid CHF Associated with increased risk of developing cardiogenic shock MILIS Trial: Predictors of CHB 1

point for each of the following: PR prolongation 2nd degree AVB LAFB or LPFB LBBB RBBB Risk

of Progression: 1.2-6.8% with score of zero 7.8-10% with score of 1 25-30% with score of 2 36% with a score of 3 or more CHB and NSTEMI SPRINT Study Group: 610 patients with first NSTEMI: 2nd or 3rd degree AVB in 7% (45/610) These patients had:

Increased rate of cardiac arrest Increased rate of CHF Increased rate of elevated cardiac markers Higher in hospital mortality Larger and more complicated infarctions No difference in mortality outcomes at 5 years CHB post AMI and the Elderly Incidence

4.7% New AVB in 3.2% More commonly associated with inferior MI compared to anterior MI (7.3 vs 3.0%) Associated with increased in hospital mortality but no change in long term mortality outcomes Infarct location and conduction disturbances Inferior MIs: 1.

Conduction changes can occur acutely to days post MI RCA supplies the SA node, AV node, and bundle of His Sinus bradycardia 2. Mobitz type I AVB 3. Up to 40% of patients within hours of infarct

Due to increased vagal tone May be due to transient sinus node dysfunction CHB 9.8% of patients May be transient (x days) From an infranodal lesion Narrow QRS Develops from 1st to 3rd degree AVB Asymptomatic bradycardia Resolves within 5-7d

Anterior MI: 1st degree AVB below AV node with widened QRS 2nd degree type II with unpredictable clinical course with block progression CHB occurs in first 24h: Abrupt onset Wide and unstable escape ryhthm High mortality: arrhythmias and pump failure Due to extensive necrosis of bundle branches

Permanent Pacing 3rd degree AVB within or below the HisPurkinje system Persistent 2nd degree AVB Transient advanced infranodal AVB with bundle branch blocks due too infarction Symptomatic and persistent 2nd or 3rd degree AVB ACC/AHA/NASPE: indications for permanent pacing in acquired atrioventricular (AV) block in adults Class I

1. Third-degree and advanced second-degree AV block at any anatomic level, associated with any one of the following conditions: a. Bradycardia with symptoms (including heart failure) presumed to be due to AV block. (Level of Evidence: C) b. Arrhythmias and other medical conditions that require drugs that result in symptomatic bradycardia. (Level of Evidence: C) c. Documented periods of asystole 3.0 seconds or any escape rate <40 beats per minute in (bpm) in awake, symptom-free patients. (Levels of Evidence: B, C) d. After catheter ablation of the AV junction. (Levels of Evidence: B, C) There are no trials to assess outcome without pacing, and pacing is virtually always planned in this situation unless the operative procedure is AV junction modification. e. Postoperative AV block that is not expected to resolve after cardiac surgery. (Level of Evidence: C) f. Neuromuscular diseases with AV block, such as myotonic muscular

dystrophy, Kearns-Sayre syndrome, Erbs dystrophy (limb-girdle), and peroneal muscular atrophy, with or without symptoms, because there may be unpredicatable progression of AV conduction disease. (Level of Evidence B:) 2. Second-degree AV block regardless of type or site of block, with associated symptomatic bradycardia. (Level of Evidence: B) Class IIa 1. Asymptomatic third-degree AV block at any anatomic site with average awake ventricular rates of 40 beats per minute or faster especially if cardiomegaly or left ventricular (LV) dysfunction is present. (Levels of Evidence: B, C) 2. Asymptomatic type II second-degree AV block with a narrow QRS. When type II second-degree AV block occurs

with a wide QRS, pacing becomes a Class I recommendation. (Level of Evidence: B) 3. Asymptomatic type I second-degree AV block at intra- or infra-His levels found at electrophysiological study performed for other indications. (Level of Evidence: B) 4. First- or second-degree AV block with symptoms suggestive of pacemaker syndrome. (Level of Evidence: B) Adapted from Gregoratos, G, Abrams, J, Epstein, AE, et al. Circulation 2002; 106:2145.

Recently Viewed Presentations

  • Motor Control Chapter 12, Part 2

    Motor Control Chapter 12, Part 2

    Motor Control: Various Issues Human Learning & Performance Iver Iversen Fall, 2003 Typical Motor Learning Experiment Acquisition: Some form of KR manipulation is applied to a skill (different levels of KR for different groups of subjects) Transfer Test: Determine the...
  • Chapter 14 Kinetics - Deer Valley Unified School District

    Chapter 14 Kinetics - Deer Valley Unified School District

    Reaction Rates A plot of [C 4 H 9 Cl] vs. time for this reaction yields a curve like this. The slope of a line tangent to the curve at any point is the instantaneous rate at that time.
  • SETO Systems Integration Program Updates

    SETO Systems Integration Program Updates

    A Pathway To 3 Cents per kWh for Utility PV. 100 MW (DC) One-Axis Tracking Systems With 1,860 kWh (AC) /kW (DC) First-Year Performance.. Includes 5 Year MACRS. Horizontal Lines Indicate Low, Median, and High U.S. Solar Resources. Improve efficiency...
  • Chapter 1

    Chapter 1

    MKTG Lamb, Hair, McDaniel 2008-2009 15 CHAPTER Advertising and Public Relations Designed by Amy McGuire, B-books, Ltd. Prepared by Deborah Baker, Texas Christian University
  • Theory 101 - University of Minnesota Duluth

    Theory 101 - University of Minnesota Duluth

    By the early 1900s, most dismissed this as a valid theory of criminal behavior. Changes in legal system didn't lower crime rates "Armchair theorizing" questioned. Humans as "determined" rather than "rational" From early 1900s until the 1970s, the positive school...
  • 1-MVA-4A-GrowOffice-CloudIntro


    250k customers. $1.5. billion. 2. 00. million licenses. Microsoft Cloud Growth FY14. We've come a long way with our cloud business coupled with incredible growth with Windows 8 fueling what is just the beginning of our pathway toward leadership with...
  • Give Me Liberty! Ch21

    Give Me Liberty! Ch21

    Roosevelt was a master of political communication and used his fireside chats to great effect . FDR gave the term "liberalism" its modern meaning . The Liberty League . FDR's opponents organized the American Liberty League . As the 1930s...
  • univ.ency-education.com


    pour spécifier le facteur d'échelle en puissance de 10. Les nombres complexes utilise les caractères 'i' et 'j' (indifféremment) pour designer la partie imaginaire. Le tableau suivant donne un résumé :