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MBBS IV - Junior Clerkship WCS > JC04 (Medicine) - Syncope and Arrhythmia > Flashcards

JC04 (Medicine) - Syncope and Arrhythmia Flashcards

1
Q

Define Syncope

A
  • Sudden transient loss of consciousness (TLOC) specifically caused by global cerebral hypoperfusion
  • Spontaneously self-limited condition with rapid recovery
  • Most most often due to abrupt decrease in systemic BP
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2
Q

Define Palpitation

A

Abnormal awareness of own heart beat

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3
Q

4 major etiologies of palpitations

A

Cardiac - arrhythmia, VHD, Cardiomegaly, Pacing, High output (pregnancy, fever, anemia)
Drug -related- Sympathomimetics, Vasodilators, Anticholinergics, Recreational (Cocaine, amphetamine, nicotine, caffeine)
Metabolic - Thyrotoxicosis, Pheochromocytoma, Hypoxia, Hypoglycemia
Psychiatric - Panic attack, anxiety, depression

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4
Q

4 major categories of cause of TLOC

A
  1. Head trauma/ traumatic TLOC

Non-traumatic TLOC:

  1. Syncope
  2. Epileptic seizures
  3. Psychogenic
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5
Q

4 Main etiologies of syncope

A

Cardiac syncope
Orthostatic hypotension
Neurocardiogenic (Neurally-mediated)
Neurological

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6
Q

Causes of cardiac syncope

A
  1. Arrhythmia
    - Bradyarrhythmia: Sick sinus syndrome, heart block, pacemaker malfunction
    - Tachyarrhythmia: SVT, VT
  2. Structural heart disease
    - Valvular heart disease (AS, MS)
    - MI
    - HOCM/ cardiomyopathies
    - Pericardial effusion/ cardiac tamponade
    - Inherited channelopathy
    - Wolff Parkinson White syndrome
  3. Others:
    - Aortic dissection
    - PE
    - PHT
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7
Q

Causes of orthostatic hypotension

A
  1. Hypovolemia:
     Dehydration (Vomiting/ Diarrhea)
     Bleeding
     Hypopituitarism
  2. Adrenal gland failure (Addison’s disease)
  3. Neuropathy:
    - DM
    - Degenerative
  4. Drugs:
    - Diuretics
    - Nitrates
    - α-blockers (Terazosin), β-blockers (Propranolol), CCB
    - Phosphodiesterase inhibitors (Sildenafil)
    - Anti-depressants and anti-psychotics
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8
Q

Causes of neurocardiogenic syncope

A
  1. Situational: e.g. coughing, defecation, poist-exercise
  2. Vasovagal: Emotional distress, pain
  3. Carotid sinus hypersentivity: Exaggerated vagal response to carotid massage
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9
Q

Causes of neurological syncope

A
  • Vertebrobasilar insufficiency
  • Transient ischemic attack (TIA)/ Cerebrovascular accident (CVA)
  • Subarachnoid hemorrhage
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10
Q

Specific physical exams for palpitations

A
  1. General:
    - syndromes
    - Thyroid
    - Injuries
    - signs of IE
  2. Evidence of structural heart disease:
    - Pulse rate and rhythm
    - Signs of MI/ cardiomyopathy: JVP, apex, signs of HF
    - Valvular heart disease: heart sounds
    - HOCM
  3. Sequelae
    - HF, Stroke signs
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11
Q

Most common causes of syncope in <40, 40-60, and >60 years old pt

A

<40 = neural -mediated syncope/ neurocardiogenic (situational, vasovagal, carotid sinus hypersensitivity)

40-60 = 10% orthostatic hypotension, 10% cardiac syncope, 80% NMS

> 60: 25% cardiac syncope, 25% orthostatic, 50% NMS

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12
Q

Which type of syncope is associated with high mortality

A

Cardiac syncope

Mortality determined by severity of heart disease

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13
Q

Typical precipitating/trigger events to neurocardiogenic syncope

A

Prolong standing

Post-prandial

Being in hot/ crowded places

Head rotation/ pressure on carotid sinus

Long history of recurrent syncope

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14
Q

Typical precipitating/ trigger events to cardiogenic syncope

A

Exertion

Family history of unexplained death at young age

Presence of structural heart disease/ CAD

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15
Q

Typical precipitating/ trigger events to Orthostatic hypotension

A

Prolong standing

Standing after exertion

Post-prandial hypotension (blood pool in splanchnic circulation)

Vasopressin drugs

Autonomic neuropathy/ parkinsons

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16
Q

2 pathophysiological mechanisms to syncope

A
  1. Cardioinhibitory and vasodepressor response

2. Autonomic dysfunction

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17
Q

Explain Cardioinhibitory and vasodepressor response causing syncope

A

 Cardioinhibitory response
• Results from increased parasympathetic activation
• Manifested as sinus bradycardia, prolonged PR interval, advanced AV block or asystole

 Vasodepressor response
• Results from decreased (inhibition of) sympathetic activation
• Manifests as symptomatic hypotension

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18
Q

Explain abnormal autonomic response causing syncope

A

Autonomic dysfunction contributes to vasovagal syncope

  • Baroreceptors in the atria, LV and great veins with pressure or volume changes activates afferent C-fibers to midbrain > activation of vagal afferents and efferents > reflex bradycardia and vasodilation
  • Increase in BP or pressure on carotid sinus increase baroreceptor firing in carotid sinus and aortic arch > activate vagal activity > bradycardia and hypotension
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19
Q

Diagnostic criteria of orthostatic hypotension

A

≥ 20 mmHg fall in systolic pressure
(OR)
≥ 10 mmHg fall in diastolic pressure

within 2 – 5 mins of quiet standing after ≥ 5 mins of supine rest

Syncope resulting from orthostatic hypotension occurs when change from supine to erect posture but several minutes may pass between arising and the collapse

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20
Q

List prodromal symptoms of syncope

A

Light-headedness/ Feeling of warm or cold/ Pallor/ Palpitation/ Sweating/ Nausea/ Blurring of vision/ Diminution of hearing

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21
Q

How to distinguish neurocardiogenic syncope from orthostatic hypotension

A

Tilt table test: tilt table that raises to 70o above supine

Sudden significant fall in BP or HR with loss of consciousness or the inability to maintain posture = Positive for vasovagal syncope

Progressive orthostatic hypotension with or without symptoms = Orthostatic hypotension

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22
Q

Patient with syncope examined and shows difference in BP in each arm

2 Ddx

A

Aortic dissection

Coarctation of aorta

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23
Q

Patient with syncope examined and showed cardiac murmurs

2 Ddx

A

Aortic stenosis/ Mitral stenosis

Hypertrophic cardiomyopathy (HOCM)

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24
Q

1 major iatrogenic cause of carotid sinus syndrome

A

patients > 60 years with prior head and neck surgery or irradiation (e.g. NPC irradiation)

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25
Q

First-line investigations for arrhythmia or cardiac syncope

A
  1. ECG - arrhythmia
  2. Echocardiography - Structural abnormalities
  3. Ambulatory ECG monitoring: Continuous Holter, Event recorder, External loop recorder, Implantable loop recorder
  4. Electrophysiology study: invasive investigation for strongly suspected arrhythmia
26
Q

What are the leading causes of sudden cardiac death in young athletes?

A

 Hypertrophic obstructive cardiomyopathy (HOCM)
 Arrhythmogenic right ventricular dysplasia (ARVD)
 Congenital anomalies of coronary arteries
 Atherosclerotic coronary heart disease (probably homozygous familial hyperlipidemia)

27
Q

Classification of tachyarrhythmia by origin of depolarization

A

Supraventricular:

  • SA node: Sinus tachycardia
  • AV node: AVRT, AVNRT
  • Atrium: A-fib, A-flutter, A-tachycardia, Premature atrial complex

Ventricular:
- V-fib, V-flutter, V-tachycardia, Premature ventricular complex

28
Q

Classification of narrow complex tachycardia

A

Narrow complex tachycardia

a) Regular 
 Sinus tachycardia
 Atrial flutter
 Atrial tachycardia
 AV re-entry tachycardia (AVRT)
 AV nodal re-entry tachycardia (AVNRT)
b) Irregular 
 Atrial fibrillation (AF)
 Atrial flutter with variable AV block
 Atrial tachycardia with variable AV block
 Multi-focal atrial tachycardia (MAT)
29
Q

Classification of wide complex tachycardia

A

Wide complex tachycardia = prolonged QRS duration (> 120 ms):
Most often ventricular in origin: delay in interventricular & intraventricular conduction, depolarization is not through the normal conduction system

Ventricular tachycardia, Ventricular flutter, Ventricular fibrillation

Supraventricular tachycardia with BBB

Accessory pathway (AP): Wolf-Parkinson-White syndrome

Aberrancy: (rate-dependent) bundle branch block

Electrolyte imbalance

Antiarrhythmics

30
Q

Classification of bradyarrhythmia

A

SAN disease:

  • Sinus bradycardia
  • Sinus arrest
  • Sinoatrial block

AV conduction disease:

  • 1st degree AV block
  • 2nd degree AV block, Type I gradual failure
  • 2nd degree AV block, Type II intermittent failure
  • 3rd degree AV block, Type III total failure/ complete dissociation

Bundle branch & fascicular block

31
Q

Describe type 1,2,3 AV block

A

Type I AV block = prolonged PR interval + missed beats

Type II = intermittent loss of beats, normal PR interval

Type III = Atrial and ventricular dissociation, beat on their own (automicity)

32
Q

3 mechanisms of tachyarrhythmia

A
  1. Re-entry, eg. AFL, AVRT/AVNRT, VT, AF, VF
  2. Abnormal automaticity, eg. ST, AT (some), JT, VT (some), ectopic rhythms
  3. Triggered activity, eg. torsades de pointes, digitalis- and LQTS-related arrhythmias, extrasystoles
33
Q

Explain difference between normal and abnormal impulse formation

A

Impulse formation: spontaneous depolarization by cells with automaticity
→ Physiologically by native (SA node) or latent (cells of conducting system) pacemakers
→ Pathologically by atrial/ventricular cardiomyocytes acquiring automaticity

34
Q

2 mechanisms of bradyarrhythmia

A

1) Decrease impulse formation, eg. sinus bradycardia, escape rhythms62
→ Mechanism: changes in phase 4 pacemaker potential waveform

2) Decrease impulse propagation, eg. AV blocks
→ Mechanism: part of conduction pathway becomes electrically inexcitable

35
Q

Explain re-entry mechanism causing tachyarrhythmia

A

dissociated pathways with inhomogeneous conduction properties:

  • Unidirectional block: conduction along a pathway is blocked on one direction but not another
  • Slow conduction zone: decreased conduction speed along re-entry pathway

‘Critical mass’: short pathways cannot result in re-entry because the wavefront will encounter refractory tissues

36
Q

Explain the automaticity mechanism causing tachyarrhythmia

A

1) Increased automaticity in pacemaker cells (ST, JT)
- Cause: ↑SN input, damage → changes in phase 4 pacemaker potential

2) Gained automaticity in non-pacemaker cells (AT, VT, ectopic rhythms)
- Cause: injury → ‘leaky’ membranes → spontaneous depolarization

37
Q

Explain trigger afterdepolarizations that cause tachyarrhythmia

A

→ Early afterdepolarization occurring in phases 2-3
- Cause: ↑AP duration, incl. LQTS, some antiarrhythmics

→ Delayed afterdepolarization occurring in phase 4
- Cause: ↑Ca2+ or ↑catecholamine

38
Q

Systemic causes of arrhythmia

A

Metabolic:

  • alcoholism (AF),
  • Electrolytes: hypo/hyperK, hypo/hyperMg, hypo/hyperCa,
  • thyroid disease

Medications:
- Bradycardias:
 Antihypertensives (beta blockers, calcium channel blockers, alpha methyldopa)
 Antiarrhythmic drugs

  • Tachycardias: prolong QT (antihistamine, antipsychotic)
39
Q

Cardiac causes of arrhythmia

A
  1. Coronary artery disease, myocardial infarction
  2. Valvular heart disease
  3. Cardiomyopathies:
     Hypertrophic obstructive cardiomyopathy (HOCM)
     Dilated cardiomyopathy (DCM)
     Arrhythmogenic right ventricular cardiomyopathy (ARVC)
     Lamin cardiomyopathy
  4. Wolff-Parkinson-White (WPW) (Associated with supraventricular tachycardia (SVT))
  5. Inherited channelopathy, e.g.:
     Long QTs
     Brugada syndrome
40
Q

De novo causes of arrhythmia

A

Idiopathic, due to unknown genetic causes

Age-related degeneration of conduction system

41
Q

Cause of sick sinus syndrome

A

dysfunction of SA node resulting in a variety of disorders in SAN activity

Causes: may be multifactorial in origin, most commonly occur due to age-related degeneration

□ Intrinsic: idiopathic degenerative fibrosis (commonest), ischaemia (SAN a), cardiomyopathy,
infiltrative diseases (eg. sarcoidosis, haemochromatosis), congenital mutations

□ Extrinsic: drugs (eg. digoxin, BB, CCB), autonomic dysfunction, hypothyroidism, hyperkalaemia

42
Q

Outline history taking questions for suspected arrhythmia

A
  1. Evaluate for a pathological rhythm:
     Onset and/or termination (abrupt vs. gradual)
     Regularity and rate
     Precipitating / relieving factors
     Frequency and duration
     Symptomatology: chest pain (functional ischemia), dizziness or syncope (hemodynamic changes), dyspnea, polyuria after attack (SVT)
  2. Functional status and cardiac symptoms in-between attacks
  3. Previous history of heart disease especially MI
  4. Social and occupational history: alcohol, driving, recreation
  5. Family history
43
Q

Causes of syncope in young <35 years old pt

A 
 Vasovagal (most common)
 Psychiatric
 (Long QT syndrome)
 (WPW and other SVT)
 (Hypertrophy cardiomyopathy)
44
Q

Causes of syncope in middle aged pt

A

Vasovagal

Cardiac:
o Arrhythmic
o Mechanical / obstructive

45
Q

Causes of syncope in elderly

A

Multifactorial:
o Cardiac
o Mechanical / obstructive
o Arrhythmic

Orthostatic hypotension

Drug-induced:
o Vasovagal (less common)
o Carotid hypersensitivity

46
Q

Outline history taking questions for syncope

A

Patient and witness interview

Scenario, precipitating / relieving factors

Prodrome e.g.:
 Chest pain or palpitation – acute coronary syndrome
 Sweating, abdominal colic before passing out – vasovagal

Duration

Associated symptoms:
 Convulsion, tongue biting, post-ictal drowsiness of 10-30min and retrograde amnesia - True seizure
 Incontinence
 Cyanosis, pallor

Injuries assessment
 After 10min of hypoxia = brain damage
 After 30min = irreversible brain damage

Past medical and drug history, e.g. underlying heart disease

Social: home environment, occupation and hobbies

47
Q

Outline P/E for syncope

A

 Detailed cardiovascular and neurologic (seizures) examination

 Assessment for injuries

 Orthostatic vital signs

 Examination for carotid / subclavian artery disease (carotid and subclavian bruit): Carotid sinus massage

48
Q

Wolff- Parkinson-White syndrome

Cause
Rhythm abnormality

A

congenital condition involving abnormal conductive cardiac tissue between the atria and the ventricles: provides an accessory pathway for a reentrant tachycardia circuit

1) Impulses originate at SA node and preexcite peripheral conduction system and ventricular muscle via bundle of Kent without normal delay at AV node
2) After normal delay at AV node, impulses also arrive at ventricles via normal route to continue depolarization
3) P wave is immediately followed by short delta wave - slurred upstroke on wide QRS with short or no PR interval

Associated with supraventricular tachycardia (SVT)

49
Q

Outline all investigations for syncope and arrhythmia

A

Symptom-rhythm correlation:

ECG monitor: 24-hour ECG (Holter), 7-day external/ internal implantable loop recorder, Event recorder / cardiac memo

Exercise testing

Electrophysiological study (EPS)

Tilt table test (vasovagal syncope)
~~~

50
Q

Management options for bradyarrhythmia

A

Acute management:
Exclude reversible causes (hypothyroidism, drugs)

Intravenous drug:
Atropine: antimuscarinic
Isoproterenol (beta agonist)

Temporary Transvenous Pacing (for hemodynamic instability, below AV node, 2nd degree or complete heart block):
 Transvenous (usually used)
 Transcutaneous (painful, need sedation)

Long term: permanent pacemaker implantation

51
Q

Diagnostic tests for atrial fibrillation/ atrial flutter

A

Vagal maneuvers to increase vagal tone to slow down AV nodal conduction & terminate supraventricular tachycardia:
 Carotid sinus massage
 Valsalva maneuvre
 Gagging
 Drinking ice water
 Cold water immersion (face/arm)

Adenosine / ATP: Hyperpolarize ATP-sensitive K-channel in AVN causing transient AV nodal conduction block

52
Q

Acute management/ resuscitation options of tachyarrhythmia

A

Acute treatment:

  1. Haemodynamically stable: drugs (IV adenosine, ATP, Esmolol, Diltiazem), Vagal maneuvers
  2. Haemodynamically unstable = Cardiac Defibrillation or Direct Current Cardioversion
53
Q

Acute and long-term treatment of supraventricular tachycardia

A

Acute:
- IV adenosine / ATP
- IV AVN blockers:
 Verapamil, diltiazem (cardiac-selective CCB)
 Esmolol (beta blocker)
- Vagal maneuvers

Long-term:
- Oral AVN blockers:
 B-blockers
 CCBs
 Digoxin
- Antiarrhythmics:
 Class I (Na+)
 Class III (K+)
- Radiofrequency catheter ablation

54
Q

Acute and long-term management of atrial tachycardia, atrial flutter, and atrial fibrillation

A

Rate control:

  • Acute: IV AVN blockers: diltiazem, esmolol; IV digoxin
  • Long-term: Oral AVN blockers: beta blockers, diltiazem; Oral digoxin

Rhythm control:

  • Acute: class I antiarrhythmics (flecainide, rhythmonorm); IV amiodarone (only difference with tachyarrhythmia tx)
  • Long-term: Class I antiarrhythmics, Class III antiarrhythmics (amiodarone, dronedarone)

Non-pharmacological/ surgical:

  • Acute: Direct current cardioversion
  • Long-term: Catheter ablation, Pacing (electrical cardioversion (CV), Surgery
55
Q

Criteria to determine prophylaxis of thromboembolism

A

require anticoagulation for prophylaxis of thromboembolism: warfarin, NOAC

>=2 factors in CHA2DS2- VASc:
 C: congestive heart failure
 H: hypertension
 A2: age >75
 D: DM
 S2: stroke = 2
 V: vascular disease
 A: 65-74
 Sc: sex category (female)
56
Q

Treatment of ventricular tachycardia/ ventricular fibrillation

A

Acute:
Class I: IV procainamide or lignocaine
Class III: IV amiodarone
Direct current Cardioversion/ defibrillation

Chronic:
Class I antiarrhythmics
Class III antiarrhythmics: Sotalol, Amiodarone
Implantable cardioverter defibrillator (ICD) implantation**
Radiofrequency ablation**

57
Q

Digoxin

  • Indications
A

 Acute heart failure
 Atrial fibrillation, atrial flutter
 Supraventricular tachycardia

58
Q

Digoxin

MoA

Side effects

A

Inhibit Na+ -K + ATPase activity&raquo_space; Increase intracellular Na+ level&raquo_space; Reduce Ca2+ expulsion by Na+/Ca2+ exchanger&raquo_space; Accumulate intracellular Ca2+ to increase contractility&raquo_space; trigger reflexive decrease in ventricular filling pressure, causes delayed afterdepolarizations (risk of ectopic beats; pro-arrhythmia)

S/E:
Pro-arrhythmia: exacerbated by HypoK, HyperCa, HypoMg
GI disturbances, e.g. diarrhea, nausea, vomiting (inhibited Na+-K+ ATPase in gastrointestinal tract)
Central nervous system disturbances, e.g. drowsiness, disorientation

59
Q

Beta-blockers

Indications

A

Major use = treat angina, hypertension by reducing cardiac workload and lower BP

Cardiac arrhythmias (supraventricular tachycardia, atrial tachycardia, atrial flutter, atrial fibrillation)

topical treatment of glaucoma (lower aqueous humor production)

hyperthyroidism (suppress sympathetic activity)

Off-label uses: Prophylaxis of migraine, suppression of anxiety and sympathetic overdrive

60
Q

S/E of beta blockers

A

Depression of cardiac performance: Bradycardia, Acute worsening of heart failure

Asthma: Block β2 receptor in airway and cause bronchospasm

Sympathetic overdrive with sudden withdrawal

CNS effects: sedation, sleep disturbance, depression

Worsen glucose control/ hypoglycemia in insulin-dependent diabetics

61
Q

CCB

  • indications
  • MoA
A

Effect: Lowers CO, BP, BP

MoA:

  • Slow down conduction in atria, AV node&raquo_space; Increase conduction block&raquo_space; abolish re- entrant supraventricular arrhythmias / tachycardias
  • Slow down AV conduction&raquo_space; Increase AV block&raquo_space; Decrease impulses from atrium to ventricles and slows ventricular rate&raquo_space; reduce atrial fibrillation and flutter
62
Q

CCB S/E

A

Lower Ca2+ influx in heart, causing cardiac depression:
 Bradycardia (common)
 Cardiac arrest, AV block, heart failure (uncommon: unless overdose)

MBBS IV - Junior Clerkship WCS (131 decks)

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