Transcript By Sasha Darwazeh FY1

Arrhythmias
By Sasha Darwazeh FY1
Types of arrhythmias
Site of abnormality:
Supraventricular
●Ventricular
●
Abnormalities of heart rate:
Tachyarrhythmias
●Bradyarrhythmias
●
Tachyarrhythmias
Supraventricular Tachycardias:
Atrial Fibrillation
0.4% of population
2.4-4% >60 year olds, 4% >80 years olds.
50% of paroxysmal & 15-20% of chronic AF are idiopathic.
2º AF caused by dilatation, ↑ muscle mass, inflammation, infiltration &
fibrosis.
Generally associated with LA hypertrophy.
Ineffective contractions = blood stasis in atria → thrombus formation.
If from LA, can cause CVA; in RA can cause PE's.
3 types of AF:
Acute AF - associated with systemic disease, precipated by
electrolyte disturbance or hypoxia, resolves with treatment of
underlying pathology
Paroxysmal AF - recurrent episodes of AF lasting <48 hours which
can progress to:
Risk factors
HTN
Heart disease
Lung disease
Binge drinking
Hyperthyroidism
Carbon monoxide poisoning
Clinical Features
Early signs vague - fatigue & dyspnoea.
Chronic phase- Irregular pulse (some impulses from atrial
walls reach the ventricle, throwing it out of sinus rhythm).
Force of contraction irregular
Deteriorates with exercise
Absent 'a' waves in JVP
Thromboembolic events - CVA & PE.
Investigations
ECG
Chronic AF- ECG
Paroxsysmal- 24h ECG.
Bloods
FBC
U+Es
TFTs
Imaging
CXR
Echo - size of LA, LV function.
Transoesophageal echo for assessment of thrombus formation
.
Management
Aim: return to SR.
If not possible, control ventricular rate & thromboembolism risk
Conservative
Avoid alcohol & caffeine.
Correct underlying pathologies - electrolyte disturbance, hypoxia.
Medical
Acute onset:
If haemodynamicaly unstable → emergency cardioversion if lifethreatening. IV amiodarone if not.
Paroxysmal - treat only if symptomatic:
Beta-blockers 1st-line BISOPROLOL
Class Ic antiarrhythmics 2nd-line FLECAINIDE or SOTALOL
Chronic
Rate-control
<65; symptomatic; presenting 1st time; lone AF; or congestive heart
failure.
Digoxin + rate-limiting calcium-channel blocker i.e verapamil/diltiazem
or digoxin + beta blocker.
If fails pacemaker + ablation.
Rhythm-control
>65; coronary heart disease; contraindications to antiarrhythmics or
elctrical cardioversion; no congestive heart failure.
1st line chemical cardioversion- amiodarone.
2nd-line: flecainide/sotalol, amiodarone in structural heart disease.
Thromboprophylaxis- CHADS-VASc.
Warfarin - ↓ incidence of stroke by 70%. INR 2-3.
Surgery
Percutaneous radiofrequency ablation: catheter up femoral vein to
heart with radiological guidance. Ablate abnormal tissue.
Never use verapamil & beta blocker together as
can cause heart block & asystole
Popular question in pharm exams!
Atrial flutter
Atrial contraction rate >250-300 bpm.
Re-entrant circuit of excitation- it goes straight back into the atria
instead of impulses only travelling to ventricles.
Causes: IHD, hyperthyroidism, cardiomyopathy & rheumatic
heart, idiopathic.
Clinical Features:
Palpitations
Chest pain
SOB
O/E:
Regular, fast pulse
'A' waves in JVP exceeds pulse rate
Carotid compression may slow rate
Signs of heart failure
Investigations
ECG:
3:1 block (3 atrial contractions: 1 ventricular contraction) → saw-tooth
2:1 block, P waves difficult to see.
Carotid sinus pressure can uncouple atria & ventricles, revealing P waves.
Consider in patients with a regular rate of 150 bpm.
Blood:
U+Es
TFTs
Imaging:
Echo
Management
Drugs- antiarrhythmics:
Class Ia - Disopyramide
Class Ic - Flecanide, Propafenone
Class III - Sotalol
DC Cardioversion
Pacing
Re entry SVT's
Caused by 2nd connection between atria & ventricles, in addition to
normal conduction system.
2 types:
nd
●AVRNT (Atrio-Ventricular Node Re-entry Tachycardia) - 2
connection closely related to AV node.
nd connection not
●AVRT (Atrio-Ventricular Re-entry Tachycardia) - 2
related to AV node.
Clinical Features:
Palpitations
Syncope/presyncope
Chest pain & polyuria (release of ANP due to ↑ atrial pressures from
contraction of atria against closed AV valve.)
Symptoms often associated with exertion
Investigation:
ECG
Rate 130-250. Narrow QRS complex
P waves are inverted & one P wave per QRS complex.
- masked by QRS complex (AVNRT)
- or occur halfway between complexes (AVRT)
Management
Vagal - carotid sinus massage, valsalva manoeuvre, apply ice to
face
Drugs- adenosine/verapamil.(Or flecanide, sotalol)
Electrical - pacing & cardioversion
Ablation - burn away extra conduction pathway.
WPW aka pre-excitation syndrome
Abnormal accessory pathway between atrium & ventricle.
Rare → 0.1-0.3% of the population. Males> females, young people
Predisposition to sudden death.
Clinical Features:
Mostly asymptomatic. Occasionally, palpitations/sudden death, general
cardiac symptoms (SoB, dizziness or syncope)
Investigations
ECG: Delta wave
PR interval <0.12s
Management
Ablation 1st line in symptomatics
If unstable - cardioversion
Amiodarone/procainamide
Ventricular Tachyarrhythmias
Ventricular Fibrillation
Ventricular muscle fibres contract randomly causing complete failure of
ventricular function.
Occurs in those with pre-existing disease i.e CHD.
Risk Factors:
CAD & MI
VT which often precedes to VF
Antiarrhythmic drug adminsitration
Hypoxia
Ischaemia
AF
Rapid rates in pre-excitation syndromes (e.g. WPW)
Shock during cardioversion
Electric shock
Pacing to terminate VT
Clinical Features
MI → Chest pain, fatigue, palpitations
Investigations
ECG: VF and If survive look for evidence of MI, WPW etc.
Bloods
●Cardiac enzymes: troponin-T 12 hours after onset of symptoms
●U+Es: metabolic acidosis, hypokalaemia, hyperkalaemia,
hypocalcaemia, hypomagnasaemia
●Drug levels of any antiarrhythmic, particularly digoxin
●Toxicology: cocaine can induce vasospasm
●TSH: hyperthyroidism
CXR: signs of left heart failure, pulmonary hypertension
Echo: check for structural deficiencies
Angiography
Management of VF
Shockable rhythm
Check for response
Check for pulse/ breathing for up to 10 seconds
2222
Head tilt/chin lift
Get help
Chest compressions 30:2
Attach monitor
Assess rhythm
Stand back & shock
Continue compressions for 2 mins
Adrenaline IV every 2-3 mins
VT
Broad-complex tachycardia (QRS >120ms/3 small squares).
Risk Factors:
Structural heart disease/CHD
Electrolyte disturbances: hypokalaemia, hypocalcaemia & hyponatraemia
Clinical Features:
Features of ischaemic heart disease or haemodynamic compromise. Chest
pain, palpitations, dyspnoea, dizziness, syncope & symptoms of heart failure.
Investigations
ECG
Bloods: U+Es: particularly calcium, potassium & magnesium.
Levels of therapeutic drugs like digoxin
Trop T for MI
CXR -? heart failure
Management of VT
Pulseless VT: treat using ALS
●
Unstable VT: synchronised cardioversion- can result in VF!
Amiodarone 1st -line for haemodynamically unstable VT. Treat
electrolyte disturbances.
●
Stable VT: treat with IV lidocaine & cardioversion if lidocaine ineffective
●
Refractory VT: amiodarone.
●
Torsades de pointes (polymorphic VT) ●Acute(acquired) – Stop QT prolonging drugs ?examples
●IV magnesium, then beta 1-adrenergic agonist (isoprenaline),
temporary pacing
●Long-term - beta-blockers (congenital), pacing
●
Bradycardias
Heart Block
1st degree heart block - PR interval > 0.2s; no dropped QRS
complex
2nd -degree heart block
Type 1 (Mobitz I/Wenkebach) - PR interval ↑ with each beat until
you get a dropped QRS complex
Type 2 (Mobitz II) - intermittent failure of P waves to conduct, not
preceded by P wave elongation
2:1 & 3:1 type - regularly dropped QRS complexes with a 2:1 or
3:1 ratio
3rd -degree heart block (complete heart block) - P waves never
conduct & are unrelated on ECG
Causes: usually CAD, inferior or anterior wall MI.
Management
1st degree - no treatment
2nd degree – pacemaker if consciousness is affected.
3rd -degree – pacemaker
Atropine can be used if symptomatic
If patient has heart block, they need to avoid:
●Anti-arrhythmics - amiodarone, flecainide.
●Beta blockers - such as atenolol, bisoprolol, propanolol.
●Calcium channel blockers - such as verapamil, diltiazem.
Bundle branch block
Delay of electrical conduction down either the left of right bundle
branch.
LBBB: aortic stenosis, dilated cardiomyopathy, MI, CAD.
RBBB: atrial septal defect, PE, MI
ECG Changes
WiLLiaM & MaRRoW
Wide QRS complexes.
LBBB: there is a W shape in V1 and an M shape in V6.
RBBB: there is an M shape in V1 and a W shape in V6
Management
Generally nothing but if bundle branch block is severe, needs
pacemaker