Pathophysiology of dysrhythmias 2 Flashcards
Discuss bradcardias
• Sinus Bradycardia – Drugs -• Beta Blockers, Diltazem – Vagal activity – Hypothyroidism – Sinus Node disease – Electrolyte abnormalities
• AV Block
– Vagal activity
– Myocardial infarction
– Electrolyte abnormalities
Discuss AV bock
• 1st Degree
– Lengthening of the PR interval
• 2nd Degree
– Mobitz Type 1 (Wenckebach block).
• Progressive lengthening of PR interval until P wave blocked and then PR short again
– Mobitz Type 2
• Block after 2 or 3 conducted beats in regular pattern
• 3rd Degree AV block
– Complete AV dissociation
What are treatments for bradcardias
• Pacemakers – Temporary – Permanent
• Only if needed
– Symptoms of syncope dizziness – Prophylactic at time of operations – Post AMI
Discuss tachycardias
- Narrow Complex / Supraventricular Tachycardias
* Broad Complex Tachycardias
Discuss narrow complex/supraventricular tachycardias
• Narrow Complex / Supraventricular Tachycardias – Atrial Tachycardias – Junctional Tachycardias – AVNRT + AVRT – Atrial Flutter – Atrial Fibrillation
Discuss broad complex tachycardia
– Ventricular Tachycardia
• Monomorphic and polymorphic VT
• Fascicular (RBBB and LAD and not very wide)
• RVOT (LBBB and RAD)
– SVT with aberration (= acquired, rate- dependent bundle branch block)
– SVT with a pre-existing BBB morphology on
ECG
– SVT of antedromic tachycardia in WPW
What are the basic mechanisms of tachycardias
- Ectopic Focus – i.e. tissue with rapid pacemaker function
- Re-entry / circus movement
- Fibrillation – independent wavelets of activity
Discuss tachycardias involving the AV node
• Narrow complex, usually no P waves, usually very fast, and no history of cardiac disease
• AVNRT = AV nodal re-entrant tachycardia
– Tachycardia where re-entry circuit is through juxtanodal material
• AVRT = AV re-entrant tachycardia
– Tachycardia where re-entry is through an accessory pathway
• Revealed accessory pathway means WPW 12 lead ECG
• Concealed accessory pathway means normal non- tachycardia 12 lead ECG (i.e. the accessory pathway only conducts in a retrograde manner)
• All are terminated by i.v. adenosine
What is Wolff-Parkinson-White syndrome
• Pre-excitation (of the ventricles)
• Anatomical atrio-ventricular bypass tract with non-decremental conducting properties
• Results in
– Shortened PR interval <0.12sec
– Slurred upstroke of QRS and widened QRS complex >0.12sec
What is the adenosine test in narrow complex/supraventricular tachycardias?
- i.v. bolus of adenosine (3mg, then 6 mg then 12mg)
- Half life 4.5 secs
- Causes transient and complete AV block
Adenosine will stop any tachycardia with re- entry over the AV node i.e. AVNRT and AVRT
• Responses:
– No effect. = Wrong diagnosis. Sinus Tachy in case of narrow complex or VT in case of broad complex
– Transient slowing with (=atrial flutter or atrial tachycardia) or without revealed P waves (= AF)
– Restoration of sinus rhythm AVNRT or AVRT
(Adenosine lady - remember the eyes - side effect)
Discuss atrial fibrillation
• Very common
• Irregular narrow complex tachycardia with no P waves
• Symptoms
– Fast ventricular response rate – SOB, hypotension – Slow conduction – dizziness and syncope
– Embolism of left atrial thrombus (CVA)
Atrial Fibrillation IRREGULAR no visible P wave activity and usually narrow complex
What are the causes of atrial fibrillation
– Ischaemic Heart Disease – Hypertensive heart disease – Mitral Valve disease – Thyrotoxicosis – Cardiomyopathy – Alcohol – Post bypass – Myocarditis – Accessory pathways – Lone (no cause)
What are the mechanisms fro atrial fibrillation
- Size of left atrium
• Uncommon in children, much more common in large mammals
• >5 independent wavelets of activity
• Foci of wavelet generation around the insertion of the pulmonary veins
Discuss management of atrial fibrillation
• Rate control or rhythm control ?
• Prevention of thrombo-embolism (esp. CVA)
• Who gets which?
– Rate control unless
• Symptomatic with high ventricular response rates refractory to treatment
• Acute presentation with clear precipitating cause
– Rate control
• Drugs to slow AV conduction
– Diltiazem, Verapamil, Beta blockers, (Digoxin)
• AV node ablation and permanent pacemaker
• Cardioversion
– Electrical DC cardioversion
– Chemical – Flecainide, Propafanone, Amiodarone
• Maintainance of Sinus Rhythm – Class 3 Sotalol, Amiodarone
– Class 1c Flecainide
– Radiofrequency/cryo ablation
» Pulmonary Vein ablation with or without atrial lines
Prevention of thrombi-embolism
– High incidence of CVA (embolic stoke) in AF
• First noticed in mitral stenosis
– Warfarin/NOACs therapy became standard
• Non-rheumatic AF
– Less than MS but still very significant
– Warfarin/NOACs causes a 66-70% reduction in stroke risk attributable to AF
– Aspirin (300mg a day) has a weak/no beneficial effect
– Who gets Warfarin/NOACs in non-rheumatic AF? Risk based
• Appreciable risk of stoke other than AF – Age (>65yr)
– Hypertension
– Previous stroke – CHA2DS2-VASc
• No contraindiactions to anticoagulation
– Peptic ulcer disease, Contact sports, alcoholism etc
Discuss ventricular tachycardia
• Serious
– Often fast
– Can degenerate into VF (and death)
• Inherently Unstable rhythm
• Often provokes ischaemia as associated with CAD
• Usually associated with previous LV damage
– MI, hypertensive heart disease, cardiomyopathy, previous heart surgery etc
