Approach to syncope, Brady

arrhythmia's and pacing

Presenter: Eshetu Bedada

Moderator: Dr Bekele Alemayehu
Consultant internist, cardiologist

1 7/11/2015
 Outline
Approach to syncope
Bradyarrhythmias
Pacemakers

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 Syncope
transient loss of consciousness (TLOC) attributable to
global cerebral hypoperfusion
 rapid onset, short duration and spontaneous recovery
Prognosis is generally favorable: benign for vasovagal to
poor for VAs

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 Epidemiology
Common problem
affects all age groups
men=women
lifetime incidence: 40%;
increases with age
bimodal with peaks at
20 and 80 years

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 Etiologies of TLOC
Unknown: 50%

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 Reflex or Neurally Mediated Syncope
 Settings:  Premonitory Signs:
 nausea, blurred vision
young patients, no SHD
 warmth, diaphoresis
Frightening/stressful  pallor, yawning

situation  Syncopal Event:

 white, pale
hunger, fatigue,
 no injury
dehydration, hot room  aborted by becoming supine
standing position,  Recovery:
sitting occasional  nausea, diaphoresis,
 fatigue

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 Increased sympathetic tone … vigorous contraction of
LV …mechanoreceptors in LV trigger increased vagal
tone (hyperactive Bezold- jarisch reflex)….. Decrease
HR (Cardioinhibitory) and/or BP(Vasodepressor)
Cough, deglutition, defecation, micturition … increase
vagal tone and thus can be precipitants

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 Orthostatic hypotension
insufficient peripheral vasoconstriction in response to
orthostatic stress
may also trigger reflex mediated syncope

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 Cardiac syncope
 Arrhythmia (15%): • Mechanical (5%)
 Sudden, lack warning • Endocardial: AS, MS, PS,
Brady-arrhythmia prosthetic valve thrombosis,
myxoma
Tachyarrhythmia:
 may trigger vasovagal
• Myocardial: MI ,HCMP(usually
syncope VT)
• Percardial: tamponade
• Vascular:
• PE, PHT, Aortic dissection,
ruptured AAA, subclavian
steal syndrome

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 Prognosis and recurrence
Prognosis :
underlying etiology
presence and severity of cardiac disease
reflex mediated: favorable prognosis
Recurrence:20%
Cardiac syncope: highest risk
vasovagal syncope: risk predicted by the frequency of
events

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 Initial assessment
History, physical examination including orthostatic BP,
ECG
An account by a witness: HELPFUL

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 Key historical features

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 Diagnostic Methods & Yield
Test/Procedure Yield
based on mean time to diagnosis of 5.1
months7
History and Physical (including carotid sinus 49-85% 1, 2
massage)
ECG 2-11% 2
Electrophysiology Study without SHD* 11% 3
Electrophysiology Study with SHD 49% 3
Tilt Table Test (without SHD) 11-87% 4, 5
Ambulatory ECG Monitors:
- Holter(worn for 1-3 days) 2% 7
- External Loop Recorder (2-3 weeks duration) 20% 7
-Insertable Loop Recorder (up to 18 months 65-88% 6, 7
duration)
Neurological † (Head CT Scan, Carotid Doppler) 0-4% 4,5,8,9,10

1
Kapoor, et al N Eng J Med, 1983. 6
Krahn, Circulation, 1995
2
Kapoor, Am J Med, 1991. 7
Krahn, Cardiology Clinics, 1997.
3
Linzer, et al. Ann Int. Med, 1997. 8
Eagle K,, et al. The Yale J Biol and Medicine. 1983; 56: 1-8. * Structural Heart Disease
19 4
Kapoor, Medicine, 1990. 9
Day S, et al. Am J Med. 1982; 73: 15-23. †
MRI not studied 7/11/2015
5
Kapoor, JAMA, 1992 10 Stetson P, et al. PACE. 1999; 22 (part II): 782.
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 CHESS BRACES

Congestive cardiac failure B: BNP 300; Brady 50

Hematocrit <30% R: rectal exam: FOB
ECG: abnormal A: Anemia Hgb: 9
Shortness of breath C: chest pain
22 E: ECG: Q waves 7/11/2015
Systolic BP <90 mm Hg)
S: SaO2:94%
 physical examination
Heart rate (<50bpm)
Differential BP
Orthostatic hypotension
Heart failure
Valvular heart disease: murmur
Focal neurological deficits
Carotid sinus massage

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 Carotid sinus massage
>40 year with syncope of Continuous ECG and beat-to-
unknown etiology beat BP monitoring
Contraindications : Positive: suggesting carotid
MI/ Stroke within 3 mo sinus hypersensitivity
presence of carotid bruits asystolic pause of ≥3 seconds
 fall in systolic BP of ≥50 mm
supine position: Gentle
Hg
massage the right followed
Negative: repeat test in the 60 to
by left carotid body for 5–
70° head up tilt position.
10 seconds
reproduction of symptoms:
carotid sinus syndrome
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 Diagnosis of TLOC of Unknown Etiology
initial evaluation: diagnostic in 50% of cases
ECG Monitoring
Echocardiogram: clinical suspicion of structural heart
disease
exercise stress test
Provocative strategy: HUTT
EPS
Psychiatric and neurologic evaluation

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 Head Up Tilt Test
without SHD
vasovagal syncope
positive test: hypotension,
bradycardia or asystole
cardoinhibitory,
vasodepressor, or mixed
response
accelerated with provocative
agents: IV isoproterenol or
sublingual nitroglycerine

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 Treatment
Goals:
Determine for increased risk of death: underlying heart
disease, MI, WPW, life-threatening genetic
disease(LQTS, Brugada)
reduce mortality, injury, and recurrences.
correction of the underlying cause
 ICD: syncope + VA detected or suspected
preventive measures: reflex mediated syncope or
orthostatic hypotension

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 Pharmacological Treatment Device therapy

?Beta Blockers: age ≥42 yrs.

• carotid sinus syndrome(class
+ HTN IIA)
?Fludrocortisone • Severe, frequent neurally-
?Alpha Agonists/Midodrine: mediated syncope,
 age >40
OH
 spontaneous symptomatic
?SSRI: Paroxetine asystolic pauses of >3 seconds
or
 asymptomatic pauses >6
seconds

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 Bradyarrhythmia
arbitrarily defined as a heart below 60bpm
Numerous causes
Physiologic or pathologic
Persistent or intermittent
Failure of impulse formation or conduction

SAN dysfunction and AV block: most common causes

of pathologic bradycardia

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 BradyarrhythmiaClassification
Classifications
Based on Disorder

Impulse Formation • Sinus Arrest

Disorders • Sinus Bradycardia
• Brady/Tachy Syndrome

Impulse Conduction • Exit Block

Disorders • 1st Degree AV Block

• 2nd Degree AV Block

• 3rd Degree AV Block

• Bundle Branch Block

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 Diagnosis
asymptomatic or symptomatic
Easy fatigability, reduced exercise capacity and sxs of
HF:
esp. persistent
Subtle: irritability, lassitude, inability to concentrate,
apathy, forgetfulness and dizziness

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 symptom-arrhythmia correlation
attempt to obtain ECG documentation during syncope
Persistent: ECG
intermittent: standard or prolonged ECG recordings
Exercise testing: syncope during or shortly a/r exertion
bradycardia suspected but not documented:
Provocative testing or EPS

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 SA Node disease
DDx: physiologic sinus bradycardia: young
Higher frequency: 5th and 6th decades
Intrinsic or Extrinsic
Failure of impulse generation or conduction

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 Extrinsic dysfunction Intrinsic sinus node dysfunction

Reversible SSS - degenerative: fibrous

drugs: BB, CCB, digoxin, replacement

 CAD: transient in MI
adenosine
autonomic nervous system Inflammatory processes:
influences replacement fibrosis
Pericarditis, myocarditis, and
hypothyroidism,
rheumatic heart disease
sleep apnea, and
Carditis : SLE, RA, MCTDs
 critically ill: hypothermia,
Senile amyloidosis
hypoxia, increased ICP ,
 iatrogenic : surgery, radiation
and endotracheal suctioning
via activation of the vagus heritable forms: SSS
nerve neuromuscular diseases

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 Clinical Features of SA Node Disease
clinical or ECG diagnosis Asymptomatic WITH ECG
longer-term recording and anomaly
symptom correlation Symptoms
generally are required  from concomitant

Exercise testing: cardiovascular disease

Minority: ssx of heart failure
chronotropic incompetence
tachycardia-bradycardia
ANS testing: carotid sinus
syndrome
hypersensitivity  palpitations, angina pectoris,
EPS: abnormal SNRT, and heart failure
 hypotension, syncope,
abnormal SACT, low IHR:- presyncope, fatigue, and
intrinsic SA node disease weakness

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 Natural History
varying, progression over long periods
 mortality not compromised in the absence of
comorbid conditions
1/3rd-1/2: SVT- Af /AFL :-Associated with Sx
improvement
increased risk of cardiovascular events:
Thromboembolism
1/4th: concurrent AV conduction disease

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 ECG of SAN Disease
sinus bradycardia
sinus pauses
sinus arrest
sinus exit block
tachycardia (in SSS) : AT, AFL, Af
chronotropic incompetence

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 Sinus bradycardia
“inappropriate”/ pathologic:
Symptomatic
 failure to appropriately increase heart rate during activity or
vigorous exercise.

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Sinus arrest/pause
Sinus Bradycardia
• Failure of sinus node discharge
• ECG: a pause without P waves
• no relationship between the pause and the basic cycle
length.

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 Brady/Tachy Syndrome
occurs when the SA node has alternating periods of
firing too slowly (< 60 BPM) and too fast (>100 BPM)
ECG: Paroxysmal AT, flutter, or fibrillation
 Cessation of the tachycardia is often followed by long
pauses from the SA node…. presyncope or syncope

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 Sino-atrial Exit Block
Transient block of impulses from the SA node
Identified by P-P interval relationship: because SAN
continues to fire regularly
ECG: a pause without P waves
Second-degree SA block : intermittent absence of P waves
 Type I second-degree SA block: progressive prolongation of SA node
conduction with intermittent failure of the impulses originating in the
sinus node to conduct to the surrounding atrial tissue.
 type II second-degree SA block: no change in SAN conduction before
the pause.
Complete/ third-degree SA block: no P waves

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 Treatment: SAN Dysfunction
Aim: alleviation of symptoms
Exclusion of extrinsic causes: D/C BB, CCB, AAD class
I and III
no specific treatment /temporary rate support: inferior MI
? pharmacologic therapy: digitalis (shorten SNRT),
Isoproterenol, atropine(Incr. sinus rate),
Theophylline(A,C)
Pacemaker implantation: symptomatic
Dual chamber pacing is preferred: increased incidence of
Af, AVB

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 Atrioventricular Conduction Disease
Prognosis: the underlying myocardial process
AV node: a normal delay occurs
Etiologies :
Functional/reversible : Drugs, K/Mg, CSS, sleep
infectious diseases
autoimmune and infiltrative diseases
Aging: degenerative changes
neuromuscular diseases
Congenital
Iatrogenic
CAD :transient(10–25%) or persistent AV block

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 AV nodal block Infranodal block

• Second and higher-grade AV • block in the distal AV nodal

complex, His bundle, or bundle
block
branches
prolongation of the P-R sudden block without
interval before block prolongation of the P-R
• stable escape rate: 40 – 60 interval
bpm unstable escape rhythms: often
QRS narrow ventricular (heart rate, 40
bpm)
Inferior AMI
QRS duration wide
anterior AMI:
worse prognosis with high
mortality rates
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 First-degree AV block
each atrial impulse is successfully conducted to the
ventricle (1:1) but with a delay
• PR interval >200 ms is diagnostic
• predominantly within the AV node or above…. narrow
QRS
• wide QRS: delay in the distal conduction system

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 second-degree AV block
intermittent failure of electrical impulse conduction
from atrium to ventricle
some P waves are not followed by a QRS complex

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 2nd Degree AV Block–Mobitz Type I (Wenckebach)
progressive prolongation of the P-R interval with shortening of the R-R
intervals before the blocked cycle.
• a pause that is less than two times the immediately preceding
RR interval
associated shortening of the P-R interval in the first conducted cycle after the
block
block in the AV node: narrow QRS
Progressive prolongation of the PR interval until there is failure to
conduct and a ventricular beat is dropped

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 2nd Degree AV Block–Mobitz Type II
• more serious
block occurs without prolongation in the preceding P-R
intervals
no change in the first conducted P-R interval after the
blocked P wave .
block is usually infranodal: very dangerous
 associated with intraventricular conduction delays (e.g.,
BBB)
more likely to proceed to higher grades of AV block
AV block= 2:1…. difficult to distinguish type I from type II

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 2:1 AV Block
every other P wave is followed by a QRS
 impossible to tell if PR prolongs before the non-
conducted P waves
QRS duration

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 Third-Degree AV Block =
complete heart block

no atrial impulses are conducted to the ventricles:

complete AV dissociation
level of block: AV node or infranodal
acquired causes: infranodal, life-threatening
acute inferior MI
Digitalis toxicity: reversible AV block
 PR interval = variable

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 Bundle Branch Block
Bifascicular block:
RBBB + left anterior hemiblock -prolonged QRS
RBBB + left posterior hemiblock
Complete LBBB (both left anterior and posterior)

Left bundle branch block

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Right bundle branch block
 Diagnostic Testing
determining the level of conduction block: AV node
and infranodal
EPS:
His bundle electrogram: intraatrial, AV nodal, and
infranodal conduction times
Tilt table

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 Brady-arrhythmias Associated with Acute
Myocardial Infarction
Bradycardia: 4% to 5% -- SAN Dysfunction or AV block
Inferior MI
Sinus node dysfunction
 Mechanism:
 direct
affect on the SAN blood supply or
 Bezold-Jarisch reflex
AV block
 Mechanism: primarily disruption of blood supply to the AV nodal artery
 transient and asymptomatic

anterior MI
AV block: infranodal - dependent on blood supply from the LAD.
symptomatic and irreversible
Prognosis and management depend on the location of the MI, degree
of AV block, and hemodynamic stability.

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 Management of AV Conduction Block
exclusion of reversible causes
Adjunctive treatment: atropine, isoproterenol, theophylline
temporary pacing: transcutaneous/ transvenous
permanent pacemakers -in the absence of prompt resolution

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 Indication for pacing in patients with persistent bradycardia
Recommendation Class Level
Sinus node disease. I B
Pacing is indicated when symptoms can clearly be attributed to
bradycardia.
Sinus node disease. IIB C
Pacing may be indicated when symptoms are likely to be due
to bradycardia, even if the evidence is not conclusive.
Sinus node disease. III C
Pacing is not indicated in patients with SB which is asymptomatic or
due to reversible causes.
Acquired AV block. I C
Pacing is indicated in patients with third- or second-degree
type 2 AV block irrespective of symptoms.
Acquired AV block. IIA C
Pacing should be considered in patients with second-degree
type 1 AV block which causes symptoms or is found to be
located at intra- or infra-His levels at EPS.
Acquired AV block. III C
Pacing is not indicated in patients with AV block which is due to
reversible causes.
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 Choice of pacing mode
Recommendations Class Level
Sinus node disease. I A
A)Dual-chamber PM with preservation of (Vs VVI)
spontaneous AV conduction is indicated for reducing
the risk of AF and stroke, avoiding PM syndrome and B
improving quality of life. (Vs AAI)

B)Rate response features should be adopted for IIA C

patients with chronotropic incompetence, especially
if
young and physically active
Acquired AV block. IIA A
In patients with sinus rhythm, dual-chamber PM
should be preferred to single chamber ventricular
pacing for avoiding PM syndrome and improving
quality of life
Permanent AF and AV block I C
Ventricular pacing with rate-response function is
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 Outcome of RCTs of dual-chamber vs ventricular pacing
Outcome Dual chamber benefit Notes
over ventricular pacing

All cause deaths No benefit

Stroke, embolism Benefit(in meta-analysis; HR 0.80. Benefit higher in SSS.
not in single trial )

Atrial fibrillation Benefit HR 0.8112and 0.76. Benefit higher

in SSS.

HF, hospitalization for HF No benefit

Exercise capacity Benefit Overall improvement of 35%
Pacemaker syndrome Benefit 25% of VVI patients. Not significant
compared to VVIR

Functional status No benefit

Quality of life Variable Consistent effect on QOL
Complications More complications with Higher rate of lead dislodgment
dual-chamber (4.25 vs. 1.4%) and inadequate
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 Optimal pacing mode in sinus node disease
and AV block

• minimum rate of 70 bpm: to compensate

for loss of active atrial filling
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– 120 bpm:
avoid ‘overpacing’
 Intermittent bradycardia
In intermittent bradycardia, pacing may be required only for
short periods of time.
Patients should not be subjected to permanent ventricular
stimulation: choices
manual adaptation of AV interval (up to 250 ms)
AV hysteresis :
 allow spontaneous sinus rate to emerge
 restrict pacing to the period of time in which bradycardia occurs

 dual-chamber: to decrease the risk of PM syndrome

pacing is indicated in pts with intrinsic intermittent AV
block, even in the absence of documentation of symptom –
ECG correlation
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Indication for pacing in intermittent documented bradycardia

Recommendation Class Level

1) Sinus node disease (including brady-tachy form). I B
Pacing is indicated in patients affected by sinus node disease who have the
documentation of symptomatic bradycardia due to sinus arrest or sinus-
atrial block.

2) Intermittent/paroxysmal AV block (including AF with slow ventricular I C

conduction).
Pacing is indicated in patients with intermittent/paroxysmal intrinsic third-
or second-degree AV block

3) Reflex asystolic -syncope. IIA B

Pacing should be considered in patients ≥40 years with recurrent,
unpredictable reflex syncopes and documented symptomatic pause/s due to
sinus arrest or AV block or the combination of the two

4) Asymptomatic pauses (sinus arrest or AV block). IIA C

Pacing should be considered in patients with history of syncope and
documentation of asymptomatic pauses >6 s due to sinus arrest, sinus-
atrial block or AV block.
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5) Pacing is not indicated in reversible causes of bradycardia III C
 Recommendation class Level
6) Intermittent documented bradycardia. I B
Preservation of spontaneous AV conduction is recommended.
7) Reflex asystolic syncope. I C
Dual-chamber pacing with rate hysteresis is the preferred
mode of pacing in order to preserve spontaneous sinus
Rhythm

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 Indication for cardiac pacing in patients with
BBB
Recommendation Class Level
1) BBB, unexplained syncope and abnormal EPS. I B
Pacing is indicated in patients with syncope, BBB
and positive EPS defined as HV interval of ≥70 ms,
or second- or third-degree His-Purkinje block
demonstrated during
incremental atrial pacing or with pharmacological
challenge.
2) Alternating BBB. I C
Pacing is indicated in patients with alternating BBB
with or without symptoms.
3) BBB, unexplained syncope non diagnostic IIB B
investigations. Pacing may be considered in selected
patients with unexplained syncope and BBB
4) Asymptomatic BBB. III B
Pacing is not indicated for BBB in asymptomatic
patients
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 Pacemakers
primary indication: symptomatic bradycardia
Temporary pacemakers:
 ER: bridge to permanent pacing
transient dysrhythmia

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 Transcutaneous pacing
stimulation through electrodes placed on the chest wall
Limitations:
pain with impulse delivery
skeletal muscle stimulation
decreased ability to capture the ventricle.
Role: ACLS- cardiac arrest attributable to bradycardia
or asystole

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 Transvenous Pacing
current method of choice for temporary pacing
pacing catheter: directly stimulate the RV
myocardium
Advantages: patient comfort and relative ease, speed,
and safety of insertion
• CI: prosthetic tricuspid valve
Complications:4% to 20% - prolonged use
pneumothorax, myocardial perforation, infection,
bleeding, ventricular ectopy/nonsustained VT, or (rarely)
thromboembolism

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 Permanent Pacemakers
Miniaturized, increased longevity of pulse generators,
multiprogrammable, versatile, rate responsive
placed transvenously via left subclavian or cephalic
vein.
In sinus node dysfunction, dual-chamber or atrial
pacing is preferred over ventricular pacing.

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 Permanent Pacemakers
most common: VVIR , DDDR
modes and function are named using a five-letter code

Position I II III IV V V`
Category Rate antitachyc
Chamber( Chamber( Response Multisite
modulatio ardia
s) paced s) sensed to sensing pacing
n functions
0 = None 0 = None 0 = None 0 = None 0 = None O, none;
A= A= T= R = Rate A= P,
Atrium Atrium Triggered modulatio Atrium antitachyc
V= V= I= n V= ardia
Ventricle Ventricle Inhibited Ventricle pacing;
D = Dual D = Dual D = Dual D = Dual S, shock;
(A+V) (A+V) (T+I) (A+V) D, pace +
shock
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 Features

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 Pacing modes
Single chamber pacing
VVI, VVIR
AAI, AAIR
Dual chamber pacing
DDD, DDDR
DDI, DDIR
Less common modes: VDD, DVI
Asynchronous pacing: AOO, VOO,
DOO

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 Pacemaker malfunction
Loss of capture
pacing spike with no P wave or QRS complex
lead dislodgement or malposition
 inflammation or fibrosis at the lead/tissue interface,
 low pacemaker output, lead failure, or battery depletion
Failure of sensing
Undersensing: pacemaker does not see native cardiac activity
and paces inappropriately in the middle of or after a P wave or
QRS complex, or has no relationship to the native cardiac
signal.
Oversensing: pacemaker sees non-physiology activity and
inhibits pacing. No pacing spikes are seen at the expected times.

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 Complications related to implantation and
electronic function
Acute: rare- infection, hematoma, pneumothorax,
cardiac perforation, diaphragmatic/phrenic nerve
stimulation, and lead dislodgment
Chronic: infection, erosion, lead failure, and
abnormalities resulting from inappropriate
programming or interaction with the patient's native
electrical cardiac function.
"twiddler's syndrome" - now rare

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 Complications from chronic cardiac pacing
AV dyssynchrony LV mechanical synchrony
pacemaker syndrome Right ventricular apical
neck pulsation, fatigue, pacing:
palpitations, cough, LV systolic dysfunction
confusion, exertional mitral valve
dyspnea, dizziness, regurgitation
syncope congestive heart failure.
 elevation in JVP, canon A
Rx: Proper Selection of
waves, edema, rales,S3
Rx: Maintenance of AV pacing modes or
synchrony biventricular pacing
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 Patient information
Need for follow-up: earlier if redness and discharge PM site
Avoid tight clothing or rubbing over your pacemaker site.
Avoid lifting greater than 10 pounds, vacuuming, moving
furniture for six weeks
Avoid lifting your arms over your head for 2 weeks
Avoid strong magnetic fields: power plants, large running
engines and MRI
Use cellular and portable phones on the opposite side of your
pacemaker site.
DO NOT walk through the metal detector at airport
Consult before any procedure: ESWL, Electrocautery, defib,
central venous catheter, radiation….

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 References
Kaushik et al. Bradyarrhythmias, temporary and
permanent pacing. Crit care med 2000
2013 ESC Guidelines on cardiac pacing and CRT
Syncope, ESC 2009
Syncope, circulation 2013
Harrisons principles of internal medicine, 18th ed.
Up-to-date
Syncope, circulation 2013
The only EKG book you will ever need, 4th ed.

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 Thank you

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