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
***DDx of Wide complex tachycardia
Ventricular
1. VT (Monomorphic / Pleomorphic / Polymorphic)
2. VFlut
3. VF
Supraventricular tachycardia
Conducted via
1. Accessory pathway
- including **antidromic AVRT / SVT / AF / AFlut with **accessory pathway conduction
2. Aberrancy / Bundle branch block
Differentiate VT and SVT with aberrant conduction
Brugada criteria:
- heavily relies on **QRS morphology to make differentiation
- may not be accurate for patients on anti-arrhythmics / serious electrolyte imbalance
- SVT with aberrant conduction:
—> **Presence of RS complex in all precordial leads
—> R to S interval <100 ms in all precordial leads
—> ***No AV dissociation
—> Morphology criteria for VT in V1-2 and V6 not present
—> Otherwise VT
aVR algorithm:
- Initial depolarisation of ventricle is always from above to below
—> Presence of an initial positive + dominant deflections at aVR (i.e. R wave)
—> suggest depolarisation from ventricle
—> VT
- highly accurate in differentiate VT from SVT
Other useful features of diagnosing **VT:
1. **Capture beat (Return of atrial control over ventricular contraction —> followed by a period of AV dissociation)
2. ***Fusion beat (Supraventricular + Ventricular impulse coincide to produce a hybrid complex —> indicate 2 foci of pacemaker cells firing simultaneously)
—> Both indicate intermittent AV conduction —> suggest sustained tachycardia is of ventricular origin
3. History of structural heart disease
4. PVC (Premature ventricular contractions) (i.e. Ventricular ectopics) of similar morphology
***Management of Bradycardia
Acute:
1. Exclude reversible causes (hypothyroidism, drugs)
2. IV drugs (***Atropine, Isoproterenol) (for patients with haemodynamic compromise)
3. Temporary pacing (transcutaneous, transvenous) (If IV Atropine ineffective)
Long-term:
- Permanent ***pacemaker implantation (Only effective treatment)
***Management of Tachycardia
Acute:
1. Correct reversible causes
2. Haemodynamically **stable —> Pharmacological
3. Haemodynamically **unstable —> Electrical (Direct current cardioversion, Defibrillation)
Long-term (depend on underlying cause, symptom, CVS risk factors):
- Pharmacological / Non-pharmacological
- ***Drugs no longer 1st line for SVT
- Synchronised cardioversion ***mandatory in ALL patients with regular tachycardia / SVT
- Defibrillation only indicated in those with **Polymorphic tachycardia, **Pulseless VT, ***VF
Cardioversion vs Defibrillation:
Cardioversion:
- Synchronised shock
- Low energy shock
- Less damage to myocardium
- Elective procedure
Defibrillation:
- Unsynchronised shock
- High energy shock
- More damage to myocardium
- Life saving procedure
***Management of SVT
Acute:
1. IV **Adenosine / ATP
2. IV **AV node blockers (Verapamil, Diltiazem, Esmolol)
3. Non-pharmacological: Vagal maneuvres
Long-term:
1. Oral AV node blockers (β blockers, CCB, Digoxin)
2. Class 1 AAD
3. Class 3 AAD
4. Non-pharmacological: Radiofrequency catheter ablation (1st line, high effectiveness, low risk, esp. in patients with recurrent SVT)
***Management of AT, AFlut, AF
Acute:
***Rate control:
1. IV AVN blockers (Diltiazem, Esmolol)
2. IV Digoxin
***Rhythm control:
1. IV Class 1c AAD (Flecainide)
2. IV Amiodarone
Non-pharmacological:
- ***DC cardioversion
Long-term:
Rate control:
1. Oral AVN blockers (β blockers, Diltiazem)
2. Oral Digoxin
Rhythm control:
1. Class 1c AAD
2. Class 3 AAD (Amiodarone)
Non-pharmacological:
- **Catheter ablation (less successful for AF), pacing, surgery
- Drugs **no longer 1st line for AT / AFlut
Other drugs:
- ***Anticoagulation may be required for prophylaxis of thromboembolism
Long-term medications for AF
- Rate control / Rhythm control
- Rate control: AVN blocker (β blocker, Digoxin, CCB)
- Rhythm control: Anti-arrhythmic drugs (Class 1c, Class 3) —> judicious use + close monitoring (∵ serious toxicity) - Anticoagulation for CHADS-VASc ***>=2 (same apply to AFlut)
- Warfarin
- NOAC
—> prevent thromboembolism
CHADS-VASc score: ***Stroke risk
C: Congestive heart failure
H: Hypertension
A: Age >75
D: DM
S: Stroke = 2
V: Vascular disease
A: 65-74
Sc: Sex category (female) —> no longer considered a risk factor
Vaughan Williams classification
Class 1: Na blockers
Class 2: β blockers
Class 3: K blockers
Class 4: CCB
Class 5: unknown mechanisms
Other treatment of AF
***Left atrial appendage occluder:
- High risk patients CI for anticoagulation
- Left atrial appendage: source of thrombus in 91% of cases
***Management of VT / VF
Correct reversible factors if present
Acute (drugs only considered when without haemodynamic compromise (rare) / to prevent acute recurrence after Cardioversion / Defibrillation):
1. **IV Lignocaine (good when associated with myocardial ischaemia (SpC Revision))
2. IV Procainamide (negative inotrope (SpC Revision))
3. **IV Amiodarone
4. Overdrive pacing
5. Non-pharmacological: **Cardioversion / **Defibrillation (1st line)
Long-term (avoid long-term use of drug ∵ toxicity):
1. Class 1 AAD
2. Sotalol
3. **Amiodarone
4. Non-pharmacological: **ICD (implantable cardioverter-defibrillator) implantation in high risk patients of sudden cardiac death, Catheter ablation, Surgery
Psychological aspects of Palpitations + Syncope
- Anxiety —> Sinus tachycardia —> Palpitation
- Arrhythmia —> Anxiety
- Menopausal symptom
- Psychosomatic symptom
- Stigmatisation + Sick role
(Atropine in Mobitz type 2 and 3rd degree heart block)
From web:
Atropine increases the firing of the sinoatrial node (atria) and conduction through the atrioventricular node (AV) of the heart by blocking the action of the vagus nerve.
With 3rd-degree block, there is a complete block and disassociation of the electrical activity that is occurring in the atria and ventricles. Since atropine’s effect is primarily on the SA node in the atria, a 3rd-degree block would prevent its effect on the SA node from influencing the rate of ventricular contraction which is needed to improve perfusion.
With Mobitz-II, aka, second-degree AV block type II, the situation is similar. There is a partial block in the electrical impulses from the atria (SA) to the ventricles, and thus the effects of atropine would not significantly change the status of the ventricles. This block can also rapidly progress to 3rd-degree block. If the conduction block is infranodal (eg if the block is Mobitz II), an increase in AV nodal conduction by atropine only worsens the infranodal conduction delay and increases the AV block (more impulse hitting diseased infranodal conduction —> rendering it refractory for longer periods (IG therhythmdoc)).
(From Harrison:
- Atropine improve conduction through AV node and impair infranodal conduction
- Vagal stimulation slow conduction in AV node but have less of an effect on infranodal tissue and may even improve conduction due to reduced rate of activation of distal tissues)
To summarize, atropine may speed the firing rate of the SA node (atria), but the ventricles are not responding to anything the atria (SA node) puts out. Thus, the heart rates will not increase.
There may be some action at the AV-node with atropine, but the effect will be negligible and typically not therapeutic. In most cases, atropine will not hurt the patient with 3rd-degree block unless they are unstable and cardiac pacing is delayed in order to administer atropine.
Caution with Atropine
It is important to note that Mobitz II and complete heart block may be associated with acute myocardial ischemia. If atropine is used when there is ongoing myocardial ischemia this may worsen myocardial ischemia because of an increase in oxygen consumption. The increased heart rate will also reduce the diastolic filling time which may worsen coronary perfusion.
Digoxin (from IASM + CPRS Practicals + Fastlane)
Digoxin
- 2 compartment
- high volume of distribution —> distribute mainly in tissue
- blood concentration correlate with effect after 6-8 hours
- collection time (minimum 8 hours, prefer 12 hours)
- renal excreted
- 0.5-2.0 ng/mL (critical value: 2.5)
- toxicity: arrhythmia, nausea, vomiting
***- hypokalaemia, hypomagnesemia, hypercalcemia, impaired renal function enhance toxicity
- activated charcoal, Digibind (Digoxin-specific antibody), haemodialysis not effective since distribute in tissue
- immunoassays may not be accurate: Interference: Digoxin-like immunoreactive substance (DLIS), Megdigoxin, steroid, Spironolactone
ECG (Fastlane):
- Downsloping ST depression with a characteristic **“reverse tick” or **“Salvador Dali sagging” appearance
- Flattened, inverted, or biphasic T waves
- Shortened QT interval
