JC04 (Medicine) - Syncope and Arrhythmia Flashcards
Define Syncope
- 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
Define Palpitation
Abnormal awareness of own heart beat
4 major etiologies of palpitations
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
4 major categories of cause of TLOC
- Head trauma/ traumatic TLOC
Non-traumatic TLOC:
- Syncope
- Epileptic seizures
- Psychogenic
4 Main etiologies of syncope
Cardiac syncope
Orthostatic hypotension
Neurocardiogenic (Neurally-mediated)
Neurological
Causes of cardiac syncope
- Arrhythmia
- Bradyarrhythmia: Sick sinus syndrome, heart block, pacemaker malfunction
- Tachyarrhythmia: SVT, VT - Structural heart disease
- Valvular heart disease (AS, MS)
- MI
- HOCM/ cardiomyopathies
- Pericardial effusion/ cardiac tamponade
- Inherited channelopathy
- Wolff Parkinson White syndrome - Others:
- Aortic dissection
- PE
- PHT
Causes of orthostatic hypotension
- Hypovolemia:
Dehydration (Vomiting/ Diarrhea)
Bleeding
Hypopituitarism - Adrenal gland failure (Addison’s disease)
- Neuropathy:
- DM
- Degenerative - Drugs:
- Diuretics
- Nitrates
- α-blockers (Terazosin), β-blockers (Propranolol), CCB
- Phosphodiesterase inhibitors (Sildenafil)
- Anti-depressants and anti-psychotics
Causes of neurocardiogenic syncope
- Situational: e.g. coughing, defecation, poist-exercise
- Vasovagal: Emotional distress, pain
- Carotid sinus hypersentivity: Exaggerated vagal response to carotid massage
Causes of neurological syncope
- Vertebrobasilar insufficiency
- Transient ischemic attack (TIA)/ Cerebrovascular accident (CVA)
- Subarachnoid hemorrhage
Specific physical exams for palpitations
- General:
- syndromes
- Thyroid
- Injuries
- signs of IE - Evidence of structural heart disease:
- Pulse rate and rhythm
- Signs of MI/ cardiomyopathy: JVP, apex, signs of HF
- Valvular heart disease: heart sounds
- HOCM - Sequelae
- HF, Stroke signs
Most common causes of syncope in <40, 40-60, and >60 years old pt
<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
Which type of syncope is associated with high mortality
Cardiac syncope
Mortality determined by severity of heart disease
Typical precipitating/trigger events to neurocardiogenic syncope
Prolong standing
Post-prandial
Being in hot/ crowded places
Head rotation/ pressure on carotid sinus
Long history of recurrent syncope
Typical precipitating/ trigger events to cardiogenic syncope
Exertion
Family history of unexplained death at young age
Presence of structural heart disease/ CAD
Typical precipitating/ trigger events to Orthostatic hypotension
Prolong standing
Standing after exertion
Post-prandial hypotension (blood pool in splanchnic circulation)
Vasopressin drugs
Autonomic neuropathy/ parkinsons
2 pathophysiological mechanisms to syncope
- Cardioinhibitory and vasodepressor response
2. Autonomic dysfunction
Explain Cardioinhibitory and vasodepressor response causing syncope
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
Explain abnormal autonomic response causing syncope
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
Diagnostic criteria of orthostatic hypotension
≥ 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
List prodromal symptoms of syncope
Light-headedness/ Feeling of warm or cold/ Pallor/ Palpitation/ Sweating/ Nausea/ Blurring of vision/ Diminution of hearing
How to distinguish neurocardiogenic syncope from orthostatic hypotension
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
Patient with syncope examined and shows difference in BP in each arm
2 Ddx
Aortic dissection
Coarctation of aorta
Patient with syncope examined and showed cardiac murmurs
2 Ddx
Aortic stenosis/ Mitral stenosis
Hypertrophic cardiomyopathy (HOCM)
1 major iatrogenic cause of carotid sinus syndrome
patients > 60 years with prior head and neck surgery or irradiation (e.g. NPC irradiation)
First-line investigations for arrhythmia or cardiac syncope
- ECG - arrhythmia
- Echocardiography - Structural abnormalities
- Ambulatory ECG monitoring: Continuous Holter, Event recorder, External loop recorder, Implantable loop recorder
- Electrophysiology study: invasive investigation for strongly suspected arrhythmia
What are the leading causes of sudden cardiac death in young athletes?
Hypertrophic obstructive cardiomyopathy (HOCM)
Arrhythmogenic right ventricular dysplasia (ARVD)
Congenital anomalies of coronary arteries
Atherosclerotic coronary heart disease (probably homozygous familial hyperlipidemia)
Classification of tachyarrhythmia by origin of depolarization
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
Classification of narrow complex tachycardia
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)
Classification of wide complex tachycardia
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
Classification of bradyarrhythmia
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
Describe type 1,2,3 AV block
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)
3 mechanisms of tachyarrhythmia
- Re-entry, eg. AFL, AVRT/AVNRT, VT, AF, VF
- Abnormal automaticity, eg. ST, AT (some), JT, VT (some), ectopic rhythms
- Triggered activity, eg. torsades de pointes, digitalis- and LQTS-related arrhythmias, extrasystoles
Explain difference between normal and abnormal impulse formation
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
2 mechanisms of bradyarrhythmia
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
Explain re-entry mechanism causing tachyarrhythmia
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
Explain the automaticity mechanism causing tachyarrhythmia
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
Explain trigger afterdepolarizations that cause tachyarrhythmia
→ Early afterdepolarization occurring in phases 2-3
- Cause: ↑AP duration, incl. LQTS, some antiarrhythmics
→ Delayed afterdepolarization occurring in phase 4
- Cause: ↑Ca2+ or ↑catecholamine
Systemic causes of arrhythmia
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)
Cardiac causes of arrhythmia
- Coronary artery disease, myocardial infarction
- Valvular heart disease
- Cardiomyopathies:
Hypertrophic obstructive cardiomyopathy (HOCM)
Dilated cardiomyopathy (DCM)
Arrhythmogenic right ventricular cardiomyopathy (ARVC)
Lamin cardiomyopathy - Wolff-Parkinson-White (WPW) (Associated with supraventricular tachycardia (SVT))
- Inherited channelopathy, e.g.:
Long QTs
Brugada syndrome
De novo causes of arrhythmia
Idiopathic, due to unknown genetic causes
Age-related degeneration of conduction system
Cause of sick sinus syndrome
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
Outline history taking questions for suspected arrhythmia
- 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) - Functional status and cardiac symptoms in-between attacks
- Previous history of heart disease especially MI
- Social and occupational history: alcohol, driving, recreation
- Family history
Causes of syncope in young <35 years old pt
Vasovagal (most common) Psychiatric (Long QT syndrome) (WPW and other SVT) (Hypertrophy cardiomyopathy)
Causes of syncope in middle aged pt
Vasovagal
Cardiac:
o Arrhythmic
o Mechanical / obstructive
Causes of syncope in elderly
Multifactorial:
o Cardiac
o Mechanical / obstructive
o Arrhythmic
Orthostatic hypotension
Drug-induced:
o Vasovagal (less common)
o Carotid hypersensitivity
Outline history taking questions for syncope
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
Outline P/E for syncope
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
Wolff- Parkinson-White syndrome
Cause
Rhythm abnormality
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)
Outline all investigations for syncope and arrhythmia
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)
~~~
Management options for bradyarrhythmia
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
Diagnostic tests for atrial fibrillation/ atrial flutter
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
Acute management/ resuscitation options of tachyarrhythmia
Acute treatment:
- Haemodynamically stable: drugs (IV adenosine, ATP, Esmolol, Diltiazem), Vagal maneuvers
- Haemodynamically unstable = Cardiac Defibrillation or Direct Current Cardioversion
Acute and long-term treatment of supraventricular tachycardia
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
Acute and long-term management of atrial tachycardia, atrial flutter, and atrial fibrillation
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
Criteria to determine prophylaxis of thromboembolism
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)
Treatment of ventricular tachycardia/ ventricular fibrillation
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**
Digoxin
- Indications
Acute heart failure
Atrial fibrillation, atrial flutter
Supraventricular tachycardia
Digoxin
MoA
Side effects
Inhibit Na+ -K + ATPase activity»_space; Increase intracellular Na+ level»_space; Reduce Ca2+ expulsion by Na+/Ca2+ exchanger»_space; Accumulate intracellular Ca2+ to increase contractility»_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
Beta-blockers
Indications
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
S/E of beta blockers
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
CCB
- indications
- MoA
Effect: Lowers CO, BP, BP
MoA:
- Slow down conduction in atria, AV node»_space; Increase conduction block»_space; abolish re- entrant supraventricular arrhythmias / tachycardias
- Slow down AV conduction»_space; Increase AV block»_space; Decrease impulses from atrium to ventricles and slows ventricular rate»_space; reduce atrial fibrillation and flutter
CCB S/E
Lower Ca2+ influx in heart, causing cardiac depression:
Bradycardia (common)
Cardiac arrest, AV block, heart failure (uncommon: unless overdose)
