Cardiology - Arryhthmias Flashcards
Definition of AF
SVT
Uncoordinated atrial contraction
Irregular and frequently fast ventricular rate
Epidemiology of AF
Commonest cardiac arrhythmia - 1.2%
Prevalence increases with age - 10% > 70yrs, 23% > 80 yrs
ECG appearance in AF
No distinct P wave
Irregularly irregular
Classification of AF
First-diagnosed AF Paroxysmal AF Persistent AF Long standing persistent AF Permanent AF
First-diagnosed AF
AF that hasn’t been diagnosed before
Paroxysmal AF
Self-terminating, usually in 48 hrs
Persistent AF
AF lasting longer >7 days
Long-standing persistent AF
Continuous AF lasting >1 yr when its decided to adopt a rhythm control strategy
Permanent AF
AF accepted by pt and Dr
Rhythm control interventions aren’t pursued
AF symptoms
Palpitations Dyspnoea Chest tightness Fatigue/ lethargy Sleeping disturbances Psychological effects
Modified EHRA symptoms scale
1 - 4
No symptoms to disabling symptoms
Aetiological factors of AF
Aging (structural remodelling) Heart failure HTN and DM Valvular heart disease (esp mitral) CAD Alcohol excess Hyperthyroidism (trigger) Obesity and sleep apnoea Autonomic activation
Autonomic activation of AF
Sympathetic - increased ectopic activity
Vagal - reduced APD and increased spatial heterogeneity
Target BP for AF pts
130/80 mmHg
Mx of wt in AF pts
10% reduction in body wt (BMI < 25)
Increased physical activity
Diet (low-calorie food)
Mx of lipids in AF pts
Lifestyle measures if LDL >100mg/dL after 2/12 started on statins
Glycaemic control in AF pts
HbA1c > 6.5% after 2/12 - metformin
Mx of OSA in AF pts
Sleep study
Nocturnal CPAP
OSA
Obstructive Sleep Apnoea
Diagnostic workup for AF
12 lead ECG BP Bloods Echo Holter monitoring
Bloods for AF
FBC U&Es LFT TFT Coagulation
Why do we measure U&Es for AF
Abnormal K can ppt AF
Holter monitoring
Symptoms/ rhythm correlation
AF burden
Ventricular rate control
Potential consequences of AF
Morbidity associated w/ symptoms
AF +/- tachycardia mediated CM
Stroke
Increased mortality
Rship between AF and stroke
Blood pools in atria –> blood clot forms –> whole/ part of blood clot breaks off –> travels to brain occluding cerebral artery
Mechanisms of AF
Ectopic activity (trigger + AF driver) Re-entry - can be single or multiple circuit
Ectopic activity in AF
Enhances automaticity
Early or delayed after depolarisations
What tissue properties are required before re-entry can cause AF
Shortened & heterogenous ARPs
Areas of slow conduction - fibrosis
Conduction barriers - anatomical vs iatrogenic (scars from catheter ablation/ surgery)
AF induced remodelling
Electrical remodelling
Contractile remodelling
Structural remodelling - irreversible
Mx for AF
- Rhythm control
- Rate control
- Anti-coag
- L atrial ablation and/or ICD placed
Rhythm control for AF
Flecanide is 1st line (Class Ic)
Amiodarone (class III) w/ structural heart disease
Ablation (once drugs have failed)
Rate control for AF
BB - LVEF <40%
Rate-limiting Ca channel blockers (Class IV) - LVEF > 40%
Digoxin (used in combination w/ another drugs as 3rd line)
Cardioversion
What must be considered before anticoagulating an AF pt
CHADVASC (2 for women and 1 for men)
HASBLED/ORBIT
Main anticoagulants given in AF
Apixiban
Dabigatran
CHADVASC score
Congestive heart failure HTN Age >75yrs - 2 points DM Stroke/ TIA - 2 points Vascular disease (MI. PVD, aortic plaque) Age (65-74 yrs) Sc - sec category (female)
HASBLED Score
HTN Abnormal renal/liver function - 1/2 points Stroke Bleeding tendency Labile INR Age > 65 Drugs - 1/2 points
High score is 3/3+
Features of L Bundle of His
Large, diffuse structure
Rare to be damaged unless underlying heart disease
Features of R Bundle of His
Smaller, discrete structure
More commonly damaged without sig underlying heart disease
What part of the cardiac conduction system is supplied by sympathetic nerves
All of it - so drugs that stimulate SNS can increase HR even in heart block
What part of the conduction system is supplied by parasympathetic nerves
SAN
AVN
Hierarchy of pacemakers
Cardiac cells that polarise fastest will drive HR (60 - 100bpm)
SAN is usually fastest then AVN (40-60bpm) then Purkinje network in ventricles (20-40 bpm)
Bradycardia definition
HR <60 bpm
Physiological causes of bradycardia
High vagal tone (sleep, athletes)
Pathogical causes of bradycardia
Fibrosis - occurs in aging
IHD - a/c (MI) and c/c
Drugs - BB, CCB, digoxin, antiarrhytmics
Electrolyte/ metabolic disturbance - esp K
Post cardiac surgery (esp aortic valve surgery)
Infection e.g. IE
What symptoms do pts with bradycardia present with
Dizziness Fatigue Difficulty concentrating Exercise intolerance Falls Syncope Breathlessness
Where is the SAN found
Under epicardium at junction of SVC and RA
What are SA nodal cells set in
Dense, fibrous tissue
Why is the SAN easily damaged in cardiac surgery
Its superficial location
What can go wrong at the sinus node
It can fail to generate an impulse or conduct an impulse at the atrium
Sinus bradycardia
Fewer impulses generated than usual
Pts are usually asymptomatic
Sinus arrest
No impulse is generated at SAN
Sinus arrest on ECG
Period with no wave
Escape rhythm from AVN
Types of escape rhythms
Junctional - normal QRS
Ventricular - broad QRS
Both have no p waves present
Sinoatrial block
Impulse generated but not conducted out of SAN to atrium
Pause is longer than P-P interval
Tachycardia- bradycardia syndrome
Sick sinus syndorme
Alternating bradycardia and tachycardia
Usually seen in AF and another bradycardia
How many types of AV block are there
3
1st to 3rd degree
1st degree AV block
PR interval is prolonged, but all impulses are conducted to the ventricle
2nd degree AV block
Some (but not all) impulses are conducted to the ventricles
Two types - Mobitz type I, Mobitz type II
3rd degree AV block
No impulses are conducted to ventricles
AV dissociation
1st degree heart block on ECG
Prolonged PR interval
Rship between every P wave and QRS complex
3rd degree heart block on ECG
Rship between QRS complexes
Rship between P waves
NO rship between p waves and QRS
AV dissociation
Any situation in which atria and ventricles beat independently
Can be caused by complete heart block
Mobitz type I heart block on ECG
PR interval gets more and more prolonged until one P wave isn’t followed by QRS complex
What is Mobitz type I caused by
Block in AVN
Mx for Mobitz type I
No mx required
Mobitz Type II heart block on ECG
Sudden loss of AV conduction - one P wave isn’t followed by a QRS but PR interval doesn’t get progressively more prolonged
What is Mobitz type II caused by
Block in His-Purkinje system
Can lead to complete heart block
Mx of Mobitz Type II heart block
Mx with pacemaker required even if asymptomatic
Symptoms of Mobitz Type I
Lightheadedness/ dizziness
Syncope
Symptoms of Mobitz Type II
Chest pain
SOB
Postural hypotension
Symptoms of 3rd degree heart block
Feeling faint
SOB
Extreme tiredness, sometimes w/ confusion
Chest pain
2: 1 AV block
Type of 2nd degree AV block
Every other P wave is conducted
Treatment of 2:1 AV block
Pacemaker
Advanced AV block
AV conduction ratio of 3:1 or higher
Always needs a pacemaker
Emergency treatment of bradycardia
ABCDE approach
Atropine 500 mcg IV
If not responding to atropine, give drugs that stimulate SNS
If haemodynamically instable, pace pt
Which bradycardia condns have a risk of asystole
Mobitz II AV block
Complete heart block w/ broad QRS
What does atropine do
Blocks effect of vagus nerve on heart - increases HR in sinus bradycardia and AVN disease caused by block within AVN
What is atropine not effective for
AVN disease caused by block in His-Purkinje
Drugs that stimulate SNS
Adrenaline
Isoprenaline
Types of temp pacing
Central vein - internal jugular, subclavian, femoral
Transcutaneous
Performing transcutaneous pacing w/ defibrillator
Attach pads and connect defibrillator lead
Set defibrillator to pacer
Set pacer rate and output
Conform electrical capture
Confirm mechanical capture - feel femoral (R brachial) pulse
Cardiac devices
Devices implanted for dx or treatment of cardiac arrhythmias or unexplained syncope
Example of a diagnostic cardiac device
Loop recorder
Cardiac devices that treat and dx
Pacemaker (low heart rhythm)
Defib (treat fast and slow heart rhythm)
Cardiac resynchronisation therapy (treat heart failure - either pacemaker or defibrillator)
Pacemaker
Electronic device implanted in body that regulates the heartbeat
Roles of pacemaker
Detect pts own intrinsic impulses (withhold pacing pulse) - capture
Depolarise the heart if there aren’t any impulses - capture
Limitations of traditional pacemakers
Device can become infected
Leads can fail over time
Leadless pacemakers
Only pace RV
Indicated mainly in pts with AF and slow HR
ICD
Implantable Cardioverter Defib
Specialised pacemaker that treats life threatening ventricular arrhythmias
Who needs an ICD - primary prevention
Severe LV impairment
Inherited cardiac condns
Who needs an ICD - secondary prevention
Survivors of a VF/VT cardiac arrest
Sustained VT with haemodynamic compromise
Sustained VT and severe LV impairment
ICD vs anti arrhythmic drugs in SCD
ICD is superior to drugs in preventing Sudden Cardiac Death
Anti-arrhythmics are still important to reduce need for ICD therapies
How does an ICD recognise arrhythmias
ICD looks at HR
If above certain threshold, delivers shock
What do ICDs do in ventricles
Anti-tachycardia pacing
Cardioversion
Defib
Limitations of conventional ICDs
Leads can become damaged and may not be straightforward to remove
What can ICDs NOT do
Treat bradycardia
Provide anti-tachycardia pacing
Prevent death from progressive heart failure
Where are conventional ICDS implanted
Venous system
CRT
Treatment for pts with severe systolic heart failure and a broad QRS who remain symptomatic despite medical therapy
Also used in CRT
Improves symptoms and survival
Indications for pacemaker
Either symptomatic bradycardia or high risk e.g. advanced/ complete heart block (but asymptomatic) bradycardia
Indications for ICD
Ventricular arrhythmias e.g. VT/ VF
High risk of ventricular arrhythmias e.g. severe LV impairment
Indication for CRT
Severe heart failure w/ broad QRS (>120 ms) continuing symptoms despite meds
Mx of sick sinus syndrome (tachycardia-bradycardia)
Treat w/ pacemaker for Brady
Rate lowering drug (BB) for tachycardia
Anticoagulants
Types of cardiac cells
Pacemaker cells - conducting cells (SAN)
Non-pacemaker cells - contracting cells
What does the resting membrane potential of cardiac cells depend on
K ions as the membrane is semi permeable to K
Atrial vs ventricular action potential
Channels in atria are slower and Ca2+ drives depolarisation
Channels in ventricles are faster and Na+ drives depolarisation
Ventricular ap has plateau phase
How many stages does the ventricular ap have
5
0 - 4
Starting membrane potential of atria
-70 mV
Starting membrane potential of ventricles
-85/90 mV
Stage 0 of ventricular ap
K+ outflux (-ve cell) triggers: Rapid influx Na+ Slow influx of Ca+ Via VG ion channels Causes depolarisation to +20mV
Stage 1 of ventricular ap
VG Na+ channels close quickly
VG K+ channels open for K+ outflux
Causes repolarisation
Stage 2 of ventricular ap
Ca+ continues influx
K+ outflux
Membrane potential remains steady = plateau
Stage 3 of ventricular ap
VG Ca2+ ion channel closes
K+ outflux continues
Membrane potential repolarises
Stage 4 of ventricular ap
VG K+ channel closes however a steady flux of K+ remains
Resting membrane potential is restored
Main methods of pharmacological intervention for arrhythmias
Interfere with ap by blocking certain ion channels
Block sympathetic effects of ANS on heart
ERP
Effective Refractive Period
Time within which a new ap cannot be released by same cells (stages 0 - 3)
Acts as protective mechanism
ERP as a protective mechanism
Keeps HR in check
Prevents arrhythmias
Coordinates muscle contraction
Classification of anti arrhythmic agents
Class Ia/ Ib/ Ic - Na channel blockers Class II - BB Class III - K blockers Class IV - Ca blockers Class V - misc
Anti-arrhythmic drugs have cross-class activity
What do Class I anti arrhythmic do
Bind to and block Na channels responsible for depolarisation
- Slower depolarisation
- Increased ERP
- Reduced AV conduction
- Reduced automaticity
Example of Class Ia anti-arrhythmic
Disopyramide
Effects of Class Ia anti-arrhythmic
Prolongs ERP
Reduced cardiac excitability
Increases AP duration
Prolonged repolarisation can increase risk of arrhythmia - torsades de pointes
Indications for Class Ia anti-arrhythmic
Maintain sinus rhythm after MI
Prevent and treat ventricular and SV arrhythmias
Example of Class Ib anti-arrhythmic
Lidocaine
Indication for Class Ib anti-arrhythmic
Cardiopulmonary resuscitation
SE of Class Ib anti-arrhythmic
Bradycardia
Convulsion
What are Class Ib anti-arrhythmics contraindicated in
AV block
Effects of Class Ib anti-arrhythmic
Reduced ERP
Decreases AP duration
Example of Class Ic anti-arrhythmic
Flecanide - most potent Na+ channel blocker
Effects of Class Ic anti-arrhythmic
Normal ERP
Normal AP duration
Reduced contractibility
Indication of Class Ic anti-arrhythmics
Tachycardia
Paroxysmal AF
Ventricular tachycardia resistant to other therapy
Using Flecanide and amiodarone together
Flecanide dose needs to be halved
Examples of Class II anti-arrhythmics
Sotalol
Propanolol
Atenolol
What do Class II anti-arrhythmics do
Block effects of norephedrine and epipharine (SNS) action on SAN