Cardiology JC004: Syncope And Irregular Heart Beat: Cardiac Arrhythmia, Heart Blocks, Bradycardia Flashcards
Automated External Defibrillator
Detect:
- Ventricular tachyarrhythmia (e.g. TdP)
- Delivery shock to terminate arrhythmia
***Causes of Palpitations
Feeling of heartbeat (can be felt during tachycardia, bradycardia, irregular, even normal HR)
1. Tachycardia
- Atrium: ***ST, AT, AF, AFlu
- Ventricle: VT, ?VF (not felt usually)
- Junction (structure connecting Atrium and Ventricle): Junctional tachycardia, AVNRT, AVRT
- Supraventricular tachycardia (SVT): AT, Junctional tachycardia, AVNRT, AVRT
- Bradycardia (can be ∵ dysfunction of any parts of conduction system)
- SA node
- AV node
- His-Purkinje system - Ectopic beats (Irregular HR)
- Atrium
- Ventricle
—> sudden + strong heartbeat / missed beat
***Causes of Arrhythmia
Underlying structural heart disease:
1. CAD
2. MI
3. Valvular heart disease
4. Cardiomyopathies
- HOCM
- DCM
- ARVC
- Lamin CMP
Arrhythmic syndromes:
1. WPW
2. Inherited channelopathy
- e.g. Long QT syndrome
- Brugada syndrome
Systemic causes:
1. Metabolic
- Thyrotoxicosis
- Electrolyte imbalance
2. Medications
- Bradycardia: Anti-hypertensive (BB, CCB, Alpha MD), Anti-arrhythmic drugs
- Tachycardia: Prolong QT (Antihistamine, Antipsychotic)
3. Alcohol + illicit drugs (e.g. Amphetamine)
De novo causes:
1. Idiopathic
2. Genetic
3. Part of ageing
Aim of History / P/E / Investigations
- Diagnosis
- Syncope / Palpitations are NOT diagnosis! —> AF - Severity
- Too fast / too slow
- Haemodynamic compromised due to AF - Etiology
- e.g. Thyrotoxicosis causing AF - Management
- Pregnancy —> avoid Carbimazole
History taking of Palpitations
- ***Evaluate for arrhythmia diagnosis + its severity
- Onset / Termination (abrupt / gradual) (e.g. ST usually gradual onset, SVT usually abrupt onset i.e. paroxysmal)
- Regularity, Rate (PSVT, ectopics (presents as isolated irregular heart beat), AF (sustained irregular fast palpitation))
- Precipitating / relieving factors (ST usually precipitated by anxiety / exertion, terminated by rest, SVT usually terminated by vagal maneuver e.g. straining, drinking ice water)
- Associated symptoms
—> Functional ischaemia: chest pain
—> Haemodynamic change: dizziness, syncope
—> Rapid rate: dyspnea
—> SVT: ↑ ANP —> polyuria after attack - Frequency + Duration of attacks
- Functional status + cardiac symptoms in-between attacks
- e.g. deteriorating functional status may suggest underlying structural heart diseases - Previous history of heart disease esp. MI
- Family history
- Social + occupational history
- alcohol, driving, recreation
P/E of Palpitations
- General
- Thyroid dysfunction
- Injury - Evidence of structural heart disease
- Prior MI / DCM: ↑ JVP, Cardiomegaly, CHF
- Valvular HD: AS
- HOCM
Syncope
**Transient loss of consciousness (TLOC)
- ∵ **Global cerebral hypoperfusion —> exclude other causes which not cause global hypoperfusion e.g. CVA, seizures, psychogenic causes
Characteristics:
1. **Rapid onset
2. **Brevity
3. ***Spontaneous recovery
***Prolonged LOC with spontaneous recovery —> not possible ∵ will inevitably have neurological damage —> cannot be called syncope
***Causes of TLOC
Non-traumatic
1. **Syncope
- Neurally-mediated syncope (Reflex syncope)
- Orthostatic hypotension
- **Cardiac arrhythmia
- ***Structural heart / vascular diseases
- Epileptic seizures
- Generalised: Tonic, Clonic, Tonic-clonic, Atonic - Psychogenic
- Psychogenic pseudosyncope (PPS)
- Psychogenic non-epileptic seizures (PNES) (aka Pseudoseizure) - Rare causes
- Vertebrobasilar TIA
- SAH
- Cyanotic breath holding spell
Traumatic (due to head trauma)
***Causes of Syncope
- Neurally-mediated syncope (Reflex syncope) (60%)
- Vasovagal syncope
- Carotid sinus syndrome
- Situational: Cough, Post-micturition - Orthostatic hypotension (15%)
- Drug-induced
- ANS failure: Primary / Secondary - Cardiac arrhythmia (10%)
- Tachycardia (insufficient diastolic filling —> inefficient systolic contraction)
—> VT, SVT
—> LQTS, Brugada
- Bradycardia (transient cessation of CO)
—> Sinus pause / arrest
—> AV block - Structural heart / vascular diseases (5%) (usually ∵ ***outflow obstruction)
- AS
- Hypertrophic cardiomyopathy
- Pulmonary hypertension
- PE
- Aortic dissection (∵ cardiac tamponade, contained aortic rupture, transient cerebral / coronary vessel obstruction by intimal flap, activation of cerebral baroreceptors) - Unexplained causes (10%)
Epidemiology of Syncope
Frequency of causes of syncope depend on age
- >60: cardiogenic causes 25-30%
- <40: cardiogenic causes very small %
Syncope and Mortality risk
Vasovagal syncope
- low mortality risk
- recurrences may be frequent
- not worse prognosis than healthy individuals
Cardiac syncope
- high mortality risk
- mortality determined by severity of heart disease
Evaluation of Syncope
2 important questions
1. Differentiate ***true syncope from non-syncopal TLOC (e.g. epileptic seizures, psychogenic causes)
2. Differentiate between CVS vs Non-CVS syncope
History taking: main factor in diagnosis
***History taking of Syncope
- Patient + witness interview
- Scenario
- ***Prodrome / associated symptoms
- Prodromes of seizures: abnormal sounds, mood disturbance, confusion -
**Precipitating factors
- Reflex syncope often precipitated by **autonomic symptoms (e.g. abdominal discomfort, nausea)
- Syncope during supine position almost never ∵ Reflex syncope
- Exertion / palpitation —> CVS syncope until proven otherwise - Features of seizures: Duration, Convulsion, Incontinence, Tongue biting, Cyanosis, Pallor
—> NOT exclude syncope ∵ severe global cerebral hypoperfusion can lead to hypoxic seizure - Post-ictal drowsiness, Post-syncopal symptoms, Retrograde amnesia
—> Exclude syncope (recovery from syncope always quick + full) - Injuries assessment
- Underlying heart disease
- Past medical + drug history
- Social aspect: Home environment, occupation, hobbies
***P/E for Syncope
- CVS exam
- Neurological exam
- Orthostatic vital signs
- Carotid / Subclavian artery diseases exam
- Carotid sinus massage (performed in selected patients)
***Diagnosis of Cardiac arrhythmia
Basic evaluation
1. History + P/E
2. **ECG
3. Echocardiogram (exclude underlying structural HD)
4. **Blood tests: CBP, K, Mg, T4 (exclude metabolic disturbances)
Symptom-rhythm correlation (i.e. investigations driven by symptoms nature, duration, frequency):
1. **24 hour ECG (Holter) (useful for patients having palpitation everyday)
2. **7 day cardiac monitor
3. Event recorder (useful for prolonged palpitations but not syncope)
4. Mobile devices
5. Exercise testing
6. Implantable cardiac monitor
7. **Tilt table test (young patient with recurrence syncope but no evidence of cardiac diseases —> used to support diagnosis of Reflex syncope + information to guide treatment)
8. **Electrophysiological study (for patients with suspected PSVT)
***Classification + Mechanisms of Arrhythmia (超級重要)
Bradycardia:
1. Defective electrical impulse formation (e.g. Sinus node dysfunction)
- Sinus node disease (SAN disease)
—> Sinus bradycardia
—> Sinus arrest
—> SA block
- Defective electrical impulse propagation (e.g. AV block)
- AV conduction disease
—> 1o AVB: PR prolongation
—> 2o AVB:
——> Type 1: Gradual failure (Mobitz type 1 / Wenckebach phenomenon) (progressive prolongation of PR interval then finally non-conductive P wave (i.e. QRS fails))
——> Type 2: Intermittent failure of P wave conduction (Mobitz type 2)
—> 3o AVB: Total failure (Complete AV dissociation) (P wave and QRS complex at their own pace but no constant relationship with each other)
NB: Bundle branch, Fascicular block do NOT cause bradycardia
Tachycardia (classified according to QRS width than pathology location):
1. Narrow complex (usually ***above junction (AV node + BoH) —> concomitant depolarisation of all ventricular muscle)
- Sinus tachycardia
- SVT (AT, AVRT, AVNRT)
- AF, AFlut
- Wide complex (occurs ***below junction —> slower spread of ventricular depolarisation / disease of His-Purkinje network —> conduction across a portion of ventricular muscle inevitable)
- Ventricular arrhythmia
—> VT (Monomorphic / Pleomorphic / Polymorphic)
—> VFlut
—> VF
- Supraventricular
—> Accessory pathway (∵ starts ventricular depolarisation earlier than expected)
—> Aberrancy (Bundle branch block) —> only occurs in tachycardia, may not be obvious during sinus rhythm
Mechanism of Tachycardia:
1. Abnormal automaticity
2. Triggered activity (majority)
3. Reentry (majority, most common)
Triggered activity
Action potential of Cardiomyocyte
Phase 0: Influx of Na —> Depolarisation
Phase 1: Efflux of K —> Repolarisation
Phase 2: Influx of Ca / Ca release from SR prolong action potential
Phase 3: Efflux of K
Phase 4: Equilibrium maintained by Na-K pump
Triggered activity:
- Spikes of depolarisation in repolarisation phase of an action potential
—> aka Afterdepolarisation
Early afterdepolarisation:
- Phase 2: Excessive Ca influx due to L-type Ca channel
- Phase 3: Multiple mechanisms
—> Ikr blockade (suppression of K efflux)
—> excessive cytosolic Ca —> activate Na/Ca exchanger in forward mode (drives Na influx)
- e.g. Long QT syndrome (LQTS)
Delayed afterdepolarisation:
- Phase 4: ↑ Cytosolic Ca —> activate Na/Ca exchanger in forward mode (drives Na influx)
- e.g. CPVT (Catecholaminergic polymorphic ventricular tachycardia)
Reentry
Most common mechanism of ***Tachyarrhythmia
Prerequisites:
1. Dissociated pathways (a circuit for reentry)
- size of circuit depends on conduction velocity
—> fast conduction —> need big circuit to avoid collision —> able to initiate reentry
- 1 pathway: **Fast conduction, Long refractory period
- another pathway: **Slow conduction, Short refractory period
- Inhomogeneous conduction properties
- Inexcitable tissue
- Unidirectional block (only allow current to flow in 1 direction)
- Slow conduction tone zone (head of wavefront does not collide on its tail) - Trigger, critical mass
- Atrial / Ventricular ectopic required to induce functional unidirectional block —> initiate reentry
Sinus rhythm
PR interval:
- Atrial depolarisation (P wave) + AV node delay
Sinus tachycardia / Atrial tachycardia:
- P wave followed by QRS
Normal P wave:
- +ve in lead 2, 3, aVF
- -ve in lead aVR
AVNRT, AVRT
AVNRT:
Reentry circuit formed between AV node and small amount of atrial tissue around it
—> exiting to both **Atrium + **His-Purkinje system
—> Atrial + Ventricular tissue depolarise **simultaneously
—> **Overlapping of P + QRS, sometimes a ***notched P occur after QRS
Orthodromic AVRT:
- Anterograde: Normal conduction system (Atrium —> AV node —> Ventricle)
- Retrograde (Reentry circuit): Accessory pathway (Ventricle —> Atrium —> AV node)
- Sequential depolarisation of Ventricle followed by Atrium
—> Long delay between QRS and P (∵ passes AV node)
—> ***more obvious P compared to AVNRT
Accessory pathway
Abnormal connection between Atrium + Ventricle
- usually independent of normal conduction system
- can be anterograde only / retrograde only (allow AVRT) / ***bidirectional conduction (allow AVRT)
Anterograde conduction:
- some Atrial depolarisation impulse conducted to Ventricles via Accessory pathway
—> but Accessory pathway do NOT delay impulse transmission
—> Pre-excitation
—> ***short PR interval
Accessory pathway usually connected to myocardium
—> depolarisation from ventricular end of Accessory pathway
—> muscle-to-muscle conduction
—> slow + ineffective
—> ***slurred upstroke in initial portion of QRS (Delta wave)
After delay at AV node completed
—> Rest of Atrial depolarisation at AV node
—> Conducted to ventricles by normal conduction system
—> fast + effective
—> ***sharp upstroke + termination in later portion of QRS
Example of Accessory pathway:
1. WPW
2. Orthodromic AVRT
Atrial flutter
Also a reentry tachycardia
~ to Sinus / Atrial tachycardia:
- Conduction system is a bystander
Reentry circuit formed by Atrium tissue
—> **Continuous depolarisation of Right Atrium
—> **Flutter waves (continuous with / without isoelectric segments in between)
Rate: 250-350 bpm
AV node limits impulse to ventricles
—> only half of flutter waves conducted to ventricles
—> ***2:1 block in most cases
Vagal maneuvers
Increase of vagal tone to slow AV nodal conduction
—> Terminate conduction that uses AV node (e.g. AVRT, AVNRT)
—> Termination of SVT
—> Useful for both diagnosis + treatment
If AV node is bystander (e.g. AT),
- Slowing of AV node conduction
—> cessation of ventricular depolarisation
—> help reveal underlying P waves (atrial depolarisation continues at high rate)
—> tachycardia not resolved
—> indicate mechanism of tachycardia is independent of AV node
- ***Carotid sinus massage
- ***Valsalva maneuver
- Gagging
- ***Drinking ice water
- Cold water immersion (face / arm)
Adenosine / ATP
- If Vagal maneuvers not effective / feasible
Treatment of choice:
- ∵ Short t1/2 <10 seconds
MOA: Interfere with AV nodal conduction
- Hyperpolarisation of ATP-sensitive K channel in AV node
—> Transient AV nodal conduction block
CI:
- Asthma / Bronchospasm