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 CONT’D

• VITALS:
• HR 45, REGULAR
• RR 16
• BP 108/75
• 02 SATS 97% ON RA
• AFEBRILE
Granny’s 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. LEV’S 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. LENEGRE’S 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
NON-CONDUCTED 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 (2º)
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
• IFBRADYCARDIA
<40BPM: PACEMAKER IS UNRELIABLE CAUSING PROFOUND
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
1. 3WITH
RD DEGREE AVB AT ANY ANATOMIC LEVEL ASSOCIATED
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 3 RD
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 KIDDING…BUT 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 HAND-
CRAFTED 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

1. 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
PACEMAKER COMPONENTS COMBINE WITH
BODY TISSUE TO FORM A COMPLETE CIRCUIT
• PULSE GENERATOR: POWER
SOURCE OR BATTERY
• LEADS OR WIRES
Lead

• CATHODE (NEGATIVE IPG

ELECTRODE)
• ANODE (POSITIVE Anode

ELECTRODE)
• APEX OF RIGHT VENTRICLE Cathode
THE PULSE GENERATOR:
• SUBMUSCULAR OR
SUBCUTANEOUS
IMPLANTATION LOCATION
• CONTAINS A LITHIUM
BATTERY THAT HAS A 4-10
YEAR LIFESPAN Circuitry

• SLOW, GRADUAL DECREASE

IN POWER OVER TIME Battery

• A SUDDEN POWER FAILURE

IS VERY UNCOMMON
ELECTRONIC CIRCUITRY

• SENSING CIRCUIT
• TIMING CIRCUIT
• OUTPUT CIRCUIT
 LEAD SYSTEM
BIPOLAR UNIPOLAR
• LEAD HAS BOTH NEGATIVE, • NEGATIVE (CATHODE)
ELECTRODE IN CONTACT WITH
(CATHODE) DISTAL AND HEART
POSITIVE, (ANODE)
PROXIMAL ELECTRODES • POSITIVE (ANODE)
ELECTRODE: METAL CASING OF
• SEPARATED BY 1 CM PULSE GENERATOR
• LARGER DIAMETER: MORE • PRONE TO OVERSENSING
PRONE TO FRACTURE • NOT COMPATIBLE WITH ICD
• 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 +
Anode

• LARGER PACING SPIKE:

>20MM -
Cathode
 PACEMAKER CODE
I II III IV V
Chamber Chamber Response Programmable Antitachy
Paced Sensed to Sensing Functions/Rate Function(s)
Modulation

V: Ventricle V: Ventricle T: Triggered P: Simple P: Pace

programmable
M: Multi-
A: Atrium A: Atrium I: Inhibited S: Shock
programmable

D: Dual (A+V) D: Dual (A+V) D: Dual (T+I) C: Communicating D: Dual (P+S)

O: None O: None O: None R: Rate modulating O: None

S: Single S: Single O: None

(A or V) (A or V)
COMMON PACEMAKERS
• VVI
• VENTRICULAR PACING : VENTRICULAR SENSING; INTRINSIC QRS
INHIBITS PACER DISCHARGE
• VVIR
• AS ABOVE + HAS BIOSENSOR TO PROVIDE RATE-RESPONSIVENESS
• 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 Disadvantages

• IMPLANTATION OF A • SINGLE VENTRICULAR LEAD

DOES NOT PROVIDE AV
SINGLE LEAD
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 CHAMBER
PACING

AV V-A AV V-A

• ATRIAL PACE, VENTRICULAR PACE (AP/VP)

AP AP
VP VP

Rate = 60 bpm / 1000 ms

A-A = 1000 ms
 FOUR “FACES” OF DUAL CHAMBER
PACING

AV V-A AV V-A

• ATRIAL PACE, VENTRICULAR SENSE (AP/VS)

AP AP
VS VS
Rate = 60 ppm / 1000 ms
A-A = 1000 ms
 FOUR “FACES” OF DUAL CHAMBER
PACING

AV V-A AV V-A

• ATRIAL SENSE, VENTRICULAR PACE (AS/ VP)

AS AS
VP VP

Rate (sinus driven) = 70 bpm / 857 ms

A-A = 857 ms
 FOUR “FACES” OF DUAL CHAMBER
PACING

AV V-A AV V-A

• ATRIAL SENSE, VENTRICULAR SENSE (AS/VS)

AS AS
VS VS
Rate (sinus driven) = 70 bpm / 857 ms
Spontaneous conduction at 150 ms
A-A = 857 ms
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
PATIENT’S 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 LEAD-
INDUCED THROMBOSIS
 PACEMAKER SYNDROME
• 20% OF PATIENTS PRESENT WITH NEW • SYMPTOMS:
COMPLAINTS OR WORSENING OF • PRE/SYNCOPE
INITIAL SYMPTOMS THAT LED TO • ORTHOSTATIC DIZZINESS
PACEMAKER INSERTION • FATIGUE
• MORE COMMONLY WITH SINGLE • EXERCISE INTOLERANCE
CHAMBER PACER • WEAKNESS
• AV SYNCHRONY IS LOST  • LETHARGY
RETROGRADE VA CONDUCTION  • CHEST FULLNESS OR PAIN
ATRIAL CONTRACTION AGAINST • COUGH
CLOSED MV + TV  JUGULAR VENOUS • UNCOMFORTABLE PULSATIONS N NECK
DISTENTION + ATRIAL DILATION  SX OR ABDOMEN
OF CHF AND REFLEX VASODEPRESSOR • RUQ PAIN
EFFECTS • 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 EXTRA-CARDIAC 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
Scheduled pace
Intrinsic beat delivered
not sensed

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

...though no
Marker channel activity is present
shows intrinsic
activity...

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 PACEMAKER-MEDIATED 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 = PACEMAKER-MEDIATED 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

1. TRANSCUTANEOUS
2. TRANSVENOUS
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 CHEST PAIN • PERICARDIAL RUB
• SHOULDER PAIN • INTERCOSTAL OR
• DIAPHRAGMATIC PACING DIAPHRAGMATIC PACING
• SKELETAL MUSCLE PACING • FAILURE TO PACE OR SENSE
• DYSPNEA • NEW PERICARDIAL
• HYPOTENSION (?TAMPONADE) 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:
• PRNDPROLONGATION
• 2 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:
• CONDUCTION CHANGES CAN OCCUR ACUTELY TO DAYS POST MI
• RCA SUPPLIES THE SA NODE, AV NODE, AND BUNDLE OF HIS
1. SINUS BRADYCARDIA
• UP TO 40% OF PATIENTS WITHIN HOURS OF INFARCT
• DUE TO INCREASED VAGAL TONE
• MAY BE DUE TO TRANSIENT SINUS NODE DYSFUNCTION
2. MOBITZ TYPE I AVB
• 9.8% OF PATIENTS
• MAY BE TRANSIENT (X DAYS)
3. CHB
• FROM AN INFRANODAL LESION
• NARROW QRS ST RD
• DEVELOPS FROM 1 TO 3 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 HIS-PURKINJE 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.