Download Heart Blocks and Pacemakers - Calgary Emergency Medicine

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 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
 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
1.
•
•
•
•
•
•
3rd 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 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 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
1.
2.
3.
4.
Stimulate cardiac depolarization
Sense intrinsic cardiac function
Respond to increased metabolic demand
by providing rate responsive pacing
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
► 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 410 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 Chamber
Pacing
► Atrial
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 Chamber
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 Chamber
Pacing
► Atrial
Sense, Ventricular Pace (AS/ VP)
AV
AS
V-A
VP
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 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 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 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 = 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
1.
2.
Transcutaneous
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
► 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.ht
m
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




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
► Risk
of Progression:
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.
2.
3.
Conduction changes can occur acutely to days post MI
RCA supplies the SA node, AV node, and bundle of His
Sinus bradycardia



Up to 40% of patients within hours of infarct
Due to increased vagal tone
May be due to transient sinus node dysfunction


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
Mobitz type I AVB
CHB
► 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 infraHis 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.