MBBS IV WCS 004 – Syncope and irregular heart beat

Syncope and irregular heart beat

Case study
 Palpitations: may be seen as anxious state
 +Syncope: more worrying
 During exercise  collapsed  required resuscitation
Use of automatic external defibrillator
 If identify ventricular fibrillation  shock

Causes of palpitations (symptom – can be tachycardic, bradycardic, normal HR)

 Tachycardia
o Atrium (upper chamber): ST, AT, AF, A flutter
o Junction: conduction system (junctional tachycardia, AVNRT/AVRT)
o Ventricle: VT, VF
o SVT (all atrial tachycardia excluding AF)
 Bradycardia
o Conduction system disease: SAN, AVN
 Ectopic
o Atrium, ventricle (all cells in the heart has pacemaker potential – is not
confined to the SA node, can be present in the AV node of the heart) 
depends on which one fires first (e.g. SA node fires first, other cells will be
suppressed; if those cells fires first  sinus would be suppressed)
o More activity than usual

Causes of arrhythmia
 Primary: occurring de novo
o Idiopathic: may not have reason of development
o Genetic predisposition to certain conditions (environmental changes causing
emergence of the symptoms)
o Part of ageing
 Secondary: underlying structural heart disease/arrhythmic syndromes
o 1. Coronary artery disease (CAD) and MI
o 2. VHD
o 3. Cardiomyopathies: HOCM, DCM, ARVC (Arrhythmogenic right ventricular
cardiomyopathy)P, Lamin CMP (cardiomyopathy)
o 4. Wolff-Parkinson-White (WPW) (extra electrical pathway in heart)
o 5. Inherited channelopathy (e.g. LQTs, Brugada syndrome)
 Systemic causes of arrhythmia: risk factors (environmental changes) and inherent
o 1. Metabolic: alcohol (AF), electrolytes: K+, Mg2+, T4
o 2. Medications
 Bradycardias:
 Antihypertensives (BB, CCB, alpha blockers)
 Antiarrhythmic drugs
 Tachycardias:
 Prolong QT (antihistamine, anti-psychotic)
 Psychological aspects of palpitations (different from syncope)
o Anxiety  sinus tachycardia  palpitation
o Arrhythmia  anxiety
o Menopausal symptom
o Psychosomatic symptom
o Stigmatization and sick role
MBBS IV WCS 004 – Syncope and irregular heart beat

Aim of all history/PE/investigation

 1. Diagnosis: e.g. atrial fibrillation
o Syncope/palpitation are NOT diagnosis
 2. Severity
o Too fast? Too low? Hemodynamic compromise? Heart failure?
 3. Etiology (e.g. thyrotoxicosis)
o Need to correct etiology to control the condition
 4. Management
o Planning pregnancy? (e.g. carbimazole contraindicated in pregnancy)

History taking: palpitations

 1. Evaluate for pathological rhythm
o Onset, termination (abrupt vs gradual)
o Regularity and rate (PSVT1, ectopics, AF)
 First time experience palpitations symptoms?
 Irregular or regular (can count the rate) – know the heart rate
o Symptomatology:
 Functional ischemia  chest pain
 Hemodynamic change  dizziness, syncope, rapid rate, dyspnea
 SVT  increase ANP  polyuria after attack
o Precipitating and relieving factors
o Frequency and duration
 2. Functional status and cardiac symptoms in between attacks
o Compare before and after development of symptoms (mobility?)
o Timeline and progression
o  Suggest the underlying cause of condition
 3. Social and occupation history
o Alcohol, driving, recreation
 4. Family history
 5. Previous history of heart disease especially MI

Physical examination: palpitations – not only cardiovascular system, look for underlying cause
 1. General
o Thyroid dysfunction
o Injury
 2. Evidence of structural heart disease
o Prior MI/DCM: increase JVP, cardiomegaly, CHF
o Valvular HD: AS
o Hypertrophic obstructive cardiomyopathy

1
Paroxysmal supraventricular tachycardia (PSVT) is episodes of rapid heart rate that start in a part of
the heart above the ventricles. "Paroxysmal" means from time to time.
MBBS IV WCS 004 – Syncope and irregular heart beat

Mechanism of arrhythmias (tachycardia, bradycardia)

 2 types: initial when read ECG  judge if bradycardia or tachycardia
 1. Bradycardia
o Impulse formation (disease of sinus node)
 Sinus bradycardia
 Sinus arrest
 Sinoatrial block
o Impulse propagation (conduction system: AV node, bundle/fascicular branches)
 1st degree AVB: PR prolongation
 2nd degree AVB
 Type I: gradual failure (Wenckebach phenomenon)
 Type II: intermittent failure (Mobitz Type II)
 3rd degree AVB: total failure (complete AV dissociation)
 Bundle branch and fascicular block (in case both bundle branch and
AVB are blocked – bradycardia)
 Bradycardia does not occur
 Pacemaker activity is everywhere

 2. Tachycardia
o Re-entry: most common mechanism (loop)
 Causes of structural re-entry:
 Dissociated pathways
 Inhomogeneous conduction properties: inexcitable,
unidirectional block, slow conduction tone zone
 Trigger, critical mass
 Mechanism of structural/”macro” re-entry2 - impulse arrive premature3
 2 adjacent pathways which have different electrophysiological
properties connected proximally and distally
 One of the pathways have short refractory periods (slow conduction),
the other pathway has long refractory period (fast conduction)
 Impulse conducted by fast pathway reach distal connection more
quickly than slow pathway  thus spread to distal slow pathway
 When impulse encounter each other, tissue on both sides are in
refractory period  no impulse or circulating loop (messed up)

2
Intra-mural “micro” re-entry is a different concept (relating to gradient of ion)
3
Premature impulse: tissue of fast pathway still in refractory period, not excited. Spread via the slow
pathway  onto the fast pathway  re-entry loop  AV re-entrant tachycardia, atrial flutter, VT
MBBS IV WCS 004 – Syncope and irregular heart beat

o Triggered activity (repolarization current problem)

  Early afterdepolarization: e.g. LQTS

 Phase 2 (Ca2+ channels) – opened, may trigger Na channel open
 Phase 3 (Na+ channel) – too early allowed to enter
  Delayed afterpolarization: e.g. CPVT (catecholaminergic
polymorphic ventricular tachycardia)
 Phase 4 (Ca2+ channel) – may trigger Na channel open
o Abnormal automaticity

Classification of arrhythmia (tachycardia, bradycardia)

 Bradycardia
 Classification of bradycardia

 Tachycardia:
 Classification of tachycardia
o  Classification of tachycardia by origin of depolarization
 Supraventricular tachycardia
 SA node
 AV node
 Atrium
 Ventricular tachycardia
 MBBS IV WCS 004 – Syncope and irregular heart beat

o  Classification of tachycardia by QRS complex

 Narrow complex tachycardia (rhythm originate from node or above)

 Examples
o 1. Supraventricular tachycardia
o 2. Atrial fibrillation/atrial flutter
 Mechanism: normal QRS duration (<120ms)
o Depolarization of ventricles through normal
conduction system
o Simultaneous activation of both ventricles
o Pathology prior or at very proximal part of conduction
system
Example: AVNRT (AV nodal re-entry tachycardia) AVRT (AV re-entry tachycardia)
 Re-entry circuit in the AV node  slow pathway  Normal: All impulse to AV node  to ventricle
and fast pathway to form a loop  Accessory pathway  usually do not have
 Some impulse will pass to the ventricle propagation to the AV node (not connected to
 Goes back  some impulse pass to the atrium conduction system)  go to ventricle itself
 Thus, atrium and ventricle activated together –  Pathology: impulse to AV node  pathway  form
similar timing re-entry circuit (take time to go to from ventricle to
 P wave cannot be seen (or very small notch) atrium)  sequential p wave and t wave (close to
QRS)
 Wide complex tachycardia4 (rhythm originate from ventricle or
bundle branch5)
 1. Ventricular tachycardia (most common)
 Example: Wolff-Parkinson-White syndrome
o Ventricular flutter
o Impulses originate at SA node and
preexcite peripheral conduction system o Ventricular fibrillation
and ventricular muscle via bundle of  2. Accessory pathway
Kent WITHOUT delay at AV node o Additional pathway connecting atrium to ventricle
o After normal delay at AV node, impulses
o Does not pass through AV node
also arrive at ventricles via normal route
to continue depolarization o Ventricle depolarize slowly, resulting in wide complex
o P wave is immediately followed by short during sinus rhythm (still have wide complex during
delta wave  producing slurred upstroke tachycardia)
on wide-QRS with short or no PR
 3. Aberrancy
interval
 *Note: Exceptions for wide complex tachycardia
o i. BBB (wide complex normally anyways)
o ii. Electrolyte imbalance
o iii. Anti-arrhythmics
4
The normal QRS complex during sinus rhythm is “narrow” (<120 ms) because of rapid,
nearly simultaneous spread of the depolarizing wave front to virtually all parts of the ventricular
endocardium, and then radial spread from endocardium to epicardium.
5
A “wide QRS complex” refers to a QRS complex duration ≥120 ms. Widening of the QRS
complex is related to slower spread of ventricular depolarization, either due to disease of the His-
Purkinje network and/or reliance on slower, muscle-to-muscle spread of depolarization.
MBBS IV WCS 004 – Syncope and irregular heart beat

Management of arrhythmia (overall principles)

 Management of bradycardia
 Short term
o Always examine hemodynamic stability (unstable = always PACE)
 1. Intravenous atropine or isoproterenol (originate from AV node – escape
rhythm near AV node, if not a complete heart block – anything AV node or above can try)
 2. Temporary pacing (deliver electric current) – transcutaneous or
transvenous (catheter through vein) (if have complete heart block, or
type 2 second degree heart block (wide QRS escape) – cannot try atropine)
 3. Exclude reversible causes (hypothyroidism, drugs)
 Long term management: permanent pacemaker implantation
 Management of tachycardia
o Acute treatment
 1. Hemodynamic stable  pharmacological
 2. Hemodynamic unstable  electrical (shock via defibrillation or
direct current cardioversion6)
 3. Administer ATP anyways (unless contraindicated – e.g. asthma)
 Short half-life <10s
 Block AV node  transient AV nodal conduction block
o Hyperpolarization of ATP sensitive K channel in AVN
o Thus, useful in supraventricular tachycardia
 Administration: due to short half life, should be start close to
heart - IV drip (higher dose), central line (lower dose)
o Increase dose in patients on theophylline (prevent
binding to ATP sites)
o Decrease dose in congestive HF, MI, CKD/CLD
o Long term treatment
 Pharmacological
 1. Digoxin, BB, CCB
 2. Quinidine, flecainide, propafenone, mexilletine (class IA, B, C)
 3. Amiodarone, sotalol, dronedarone (class III)
 4. Ranolazine
 5. Adenosine/ATP
 6. Warfarin
 7. NOAC (non-vitamin K antagonist anti-coagulants)
 Non-pharmacological
 Vagal maneuvers: targeting the autonomic nervous system
o Increase vagal tone to slow AV nodal conduction and
terminate SVT (both diagnostic and therapeutic)
o  Carotid sinus massage
o  Valsalva maneuver
o  Gagging
o  Drinking ice water
o  Cold water immersion (face/arm)
 Radiofrequency catheter ablation: PSVT, AT, AFlu, AF, VT
o Ablade pathway of re-entry (not node)
 Electrical cardioversion (CV): AFlu, AF
 Implantable cardioverter defibrillator (ICD): VT, VF
 Surgery: AF, VT

6
Defibrillation: non-synchronised delivery of shock randomly during cardiac cycle (for cardiac arrest)
Electrical cardioversion: delivery of energy synchronized to QRS complex (for persistent tachyarrhythmias)
MBBS IV WCS 004 – Syncope and irregular heart beat

Management of specific arrhythmias

 Supraventricular tachycardia
Acute treatment Long term
Pharmacological -IV adenosine/ATP -Oral AVN blockers:
-IV AVN blockers: beta blockers, Ca channel
verapamil, diltiazem, esmolol blockers, digoxin
-Class I AAD
-Class III AAD
Non- -Vagal maneuvers -RF catheter ablation
pharmacological

 Atrial fibrillation
o Features
 1. Irregular ventricular wave
 2. Baseline p waves
o Treatment overview
 Nodal blockers to control rate
 Anti-arrhythmics to control rhythm
 Direct current cardioconversion  convert to sinus rhythm (low success)
 Long term: Ablation (70% success rate)
Acute treatment Long term
Rate control - IV AVN blocker: -Oral AVN blockers:
diltiazem, esmolol beta blockers, diltiazem
-IV digoxin -Oral digoxin
Rhythm control -IV class I AAD -Class I AAD
-IV amiodarone -Class III AAD
Non- -DC cardioversion -Catheter ablation
pharmacological -Pacing
-Surgery
Anti- Prophylaxis of thromboembolism: by identifying patients at risk
coagulation of stroke (>=2 in “CHA2DS2 – VASc” Score)
(complication 1st line  Warfarin, NOAC
management – 2nd line  left atrial appendage occlude (most clots form in left
e.g HF, stroke) atrial appendage, thus blockage reduces risk of clot forming;
though not 100% since clots can form in other locations)

 Ventricular tachycardia/ventricular fibrillation

o *Always correct reversible factors if present
Acute treatment Long term
Pharmacological -IV lignocaine -Class I AAD
-IV procainamide -Sotalol
-IV amiodarone -Amiodarone
-Overdrive pacing
Non- -CV/defibrillation -ICD implantation
pharmacological -RFA (if de novo arrhythmia)
-Surgery (depends)
MBBS IV WCS 004 – Syncope and irregular heart beat

Syncope (can be a result of arrhythmias)

 Definition of syncope
o 1. Transient loss of consciousness due to global cerebral hypoperfusion
 Perfusion depend on blood pressure (low blood pressure)  syncope
 Blockade to bloodflow  syncope (e.g. subclavian steal syndrome –
when move arm (dynamic)  develop syncope)
o 2. Rapid onset, brevity, spontaneous recovery
o E.g. Different from a seizure
 Cardiovascular causes of syncope
o 1. Cardiac arrhythmia
 Bradycardia (heart rate too slow)
 Tachycardia (shortened diastolic filling time)
  Decrease cardiac output (= stroke volume x heart rate)
o 2. Mechanical/structural
 LV obstruction
 Low cardiac output (e.g. AS, HOCM)
 HOCM: obstruction is dynamic – little blood flow  results in
syncope
o 3. Neurocardiogenic (most common)
 Vasovagal7 (most common in young)
 Carotid hypersensitivity
o 4. Orthostatic (change in posture: normal autonomic tone would increase
when stand up  make sure blood goes to heart  but if not, vasodilated 
blood goes to lower limbs  not enough in the heart)
 Drug induced
 Elderly patients
 Common causes of syncope: relate to age
o Young (<35 years)
 Vasovagal
 Psychiatric
 (Long QT syndrome)
 (WPW and other SVT)
 (Hypertrophic cardiomyopathy)
o Middle aged (35-65 years)
 Vasovagal
 Cardiac: arrhythmic, mechanical/obstructive
o Elderly (>65 years) – more broad
 Multifactorial (may not always identify one cause
 Cardiac
 Mechanical/obstructive
 Arrhythmic
 Orthostatic hypotension (multiple medications)
 Drug induced
 Vasovagal (less common)
 Carotid hypersensitivity

7
Underlying mechanism involves the nervous system slowing the heart rate and dilating blood vessels
resulting in low blood pressure and therefore not enough blood flow to the brain.
MBBS IV WCS 004 – Syncope and irregular heart beat

 History for syncope (should not trust the patient, most important)
o Duration
 Not often usual to be able to tell duration (if brief blackout – may be
able to)
 Use “ambulance” time to get there as a reference – wake up
before it arrives?
 Witnesses as reference?
o Cyanosis and pallor
o Weakness
o Injuries assessment: uncommon to be very long (>30 minutes)
 Serious hypoxic brain damage (10-20 minutes  irreversible)
o Prodrome: symptoms BEFORE the onset of symptoms
 Very important in syncope
 Most of the conditions are associated with prodrome (e.g. 15% of
patients with acute coronary syndrome with syncope  experience
chest pain before passing out; experience palpitations before pass out)
 Especially for vasovagal syncope (prodrome: 2 minutes)
 Autonomic disorder: autonomic imbalance
 Symptoms related to autonomic system – e.g. profuse sweating,
abdominal colic, vomit, nausea, dizziness (activates autonomic
system  innervate different parts of the body = activated)
 Vasovagal syncope diagnosed by symptoms
 May indicate underlying heart disease
o Differentiate from seizure
 More characteristic of seizure
 Convulsion
 Incontinence
 Tongue biting
 Post-ictal drowsiness
 Hypoxia  can lead to seizure (seizure activity itself is not diagnostic of
epilepsy = secondary to hypoxic brain)
 True seizure: have post-ictal drowsiness (do not remember what
happened, lasting for 10-30 minutes)
 Syncope: short, able to remember what is happening (hypoxic brain
seizure due to syncope – should be short, no post-ictal drowsiness)
 Physical examination for syncope
o 1. Cardiovascular examination: underlying causes
o 2. Neurological examination: differentiate from seizure or syncope
o 3. GI examination: can be anaemia (blood loss  cause)  orthostatic (blood
pressure reduces when standing up due to GI bleed – pallor, melena)
 Orthostatic vital signs (taken supine and then standing – identify
orthostatic hypotension)
 Orthostatic hypotension: systolic BP falls >20mmHg, diastolic
BP falls >10mmHg, pulse rise >20bpm within 3 min of standing
o 4. Examination for carotid/subclavian artery disease
 Carotid bruit
o 5. Carotid sinus massage
 Carotid sinus hypersensitivity – hyperactive sinus activity
 Press on carotid pulse  patients can have prolonged pause (>3s)
MBBS IV WCS 004 – Syncope and irregular heart beat

 Basic evaluation (investigations should be driven by symptoms)8

o 1. History and physical examination
o 2. ECG (MUST)
o 3. Echocardiogram (depends on patient – e.g. vasovagal – not needed  but
can evaluate underlying structural HD)
o 4. Blood tests (depends on patient symptoms – CBP, K+, Mg2+, T4)
 Symptom-rhythm correlation  choose the investigations when considering diagnosis
o 1. 24 hour ECG (Holter)
 More frequent symptoms would be useful
o 2. 7 day monitor
o 3. Rhythm patch
o 4. Event recorder
 Press on recorder when have symptoms (e.g. iwatch, iphone)
 Usually only useful for palpitations
o 5. Exercise testing
o 6. Implantable cardiac monitor (ICM) – useful for syncope
 Can monitor burden arrhythmias such as AF to guide therapy
 Continuously record the rhythm (to record ECG) – can set criteria to
when it is recorded (e.g. tachycardia  record, >3s stop in heart rate 
record, patient activate  record, retrospectively record AFTER
passout)  can help exclude e.g. arrhythmia as a cause
o 7. Electrophysiological study (EPS)
 Femoral veins to the heart  check conduction
 Indication: ablation can be done
o 8. Tilt table test
 Put patient on flat surface, table tilt to 70 degrees
 Check for reproducible symptoms of vasovagal syncope (together with
drop in blood pressure and heart rate)

8
Few diagnosis made during investigations