Arrhythmias Flashcards
Indications for DOAC use
1) Prevention of stroke, systemic embolism and reduction of vascular mortality in patients with nonvalvular atrial fibrillation with one or more of the following risk factors:
• Previous stroke, transient ischaemic attack, or systemic embolism
• Left ventricular ejection fraction <40%
• Symptomatic heart failure, ≥New York Heart Association Class 2
• Age ≥75 years
• Age ≥65 years associated with one of the following: diabetes mellitus, coronary artery disease or hypertension.
2) Prevention of venous thromboembolic events in patients who have undergone major orthopaedic surgery.
3) Treatment of acute deep vein thrombosis (DVT) and/or pulmonary embolism (PE) and prevention of related death.
4) Prevention of recurrent deep vein thrombosis (DVT) and/or pulmonary embolism (PE) and related
death.
Indications for permanent pacemaker
1) Sinus node dysfunction
2) AV block
- Type III
- Type II Mobitz or Wenchebach w/ symptoms
- Bifascicular or trifascicular block w/ symptoms
3) Persistent AV block post infarct
4) Neurocardiogenic syncope w/ ventricular standstill >3secs
Management of AF
Rate control
- Beta blocker
- non-dihydropyridone Calcium channel blocker
- Digoxin
- Amiodarone
Rhythm control
- DC cardioversion
- Amiodarone, sotalol, flecanide, dronedarone, propafenone
- Maze procedure
- Radiofrequency or cryothermal catheter ablation
Anticoagulation
- Warfarin, DOACs
- Watchman procedure
Classification of AF
Paroxysmal AF - >1 episode of self limiting AF, terminating within 7 days usually within 24hrs
Persistent AF - AF episode continuing for beyond 7 days requiring DC cardioversion. >50% of patients develop permanent AF within 10yrs
Long standing persistent AF - Persistent AF >1 yr
Permanent AF - long standing AF where the persuit of rhythm control is no longer indicated
Recurrence rates of paroxysmal AF after rhythm control
Anti arrhythmic drugs - 25-50% recurrence
Catheter ablation - 20% recurrence
(SEs catheter ablation - pulmonary vein stenosis, phrenic nerve damage, stroke, cardiac tamponade, atrio-oesophageal fistula)
Indications for catheter ablation in AF
Failure or intolerance of AAD in symptomatic paroxymsal, persistent and long standing persistent AF patients
First line in pts <70yrs with structurally normal hearts
Pathophysiology of AF and atrial flutter
AF - Extra-cardiac tissue found in the left atrial pulmonary vein, also vena cava and coronary sinus; triggering aided by sympathetic nervous system; persistence aided by electrical/cellular and structural/fibrotic remodelling
Atrial flutter - the cavotricuspid isthmus adjacent to the the IVC of the tricuspid annulus on the right atrium triggers a macroreentrant circuit
Atypical flutter may arise from infarcted atria in either the left or right atrium
May occur concurrently, rhythm control for AF may induce flutter
AF history
Symptoms intermittent/constant
Prior DC cardioversions
Prior stroke
Alcohol history
Patient’s medication, wafarin and INR
Previous history rheumatic heart disease, valvular disease, cardiac surgery, T2DM and hyperthyroidism
Symptoms of amiodarone toxicity
Causes of secondary AF
Chronic hypertension
Mitral valve disease
Hyperthyroidism
Cardiomyopathy/CCF
Wolff-Parkinson-White syndrome
Rheumatic Heart Disease
Side effects of amiodarone
Hyperthyroidism/hypothyroidism
Hepatotoxicity
Photosensitivity
Pulmonary fibrosis
Skin and corneal deposition
Bradycardia/hypotension
Torsades de pointes
Polyneuropathy
Phlebitis
Diagnosis of Brugada syndrome
ST segment elevation in V1 and/or V2
- Coved ST elevation and T wave inversion (type I)
- Saddleback ST elevation and upright or biphasic T wave (Type II)
- pseudo RBBB
Periarrest, not related to exercise, w/ polyventricular VT
FHx of sudden cardiac death <45
Sleep disordered breathing
Unexplained syncopal episodes
Increased risk of sudden unexpected nocturnal death, syncopal episodes and AF
Drug challenge in the following
- Symptomatic, type I Brugada changes, all of the above changes - not necessary, proceed to AICD
- asymptomatic, type I or II brudaga changes, FHx of brudaga ECG changes or SCD <45yrs - Drug testing
- Brugada trait only, symptomatic or not - no drug testing
Characteristics, diagnosis and management of congenital long QT syndrome
- Long QT - diagnosed on ECG measuring V5 and lead II and using QTc value
- Genes - 35% KCNQ1, 30% KCNH2, 10%SCN5A
- Three phenotypes LQT
- LQT1 - exertional/swimming (KCNQ1), Tx beta blockers
- LQT2 - exertional, Auditory triggers post partum (KCNH2), Tx beta blockers
- LQT3 - Sleep/rest, Tx Mexiline, beta blockers
Catecholaminergic polymorphic VT
Bidirectional polymorphic VT occurring with strenuous exercise or emotional or physical stress.
Normal ECG
*most common genes RyR2 Autosomal dominant 50-60% frequency (Ryanodine receptor)
*KCNJ2 10% Kir2.1 protein
*CASQ2 - calsequestrin 2 1-3%
*Genetic testing for patients suspected, and relatives if a gene is then identified
Arrythmogenic right ventricular cardiomyopathy
- Characterised by progressive fibrofatty plaque formation in RV and subsequent arrhythmias
ECG diagnosis
- inverted T waves in right precordium w/o RBBB (major criterion)
-inverted T waves V4,5,6 or TWI w/ incomplete RBBB (minor criterion)
- TWI V1-4 w/ RBBB (minor criterion), VPB (minor)
- ECG evolution - S wave upstroke >10ms, QRS prolongation >10ms or episilon waves V1
- Ambulatory monitoring
ECG w/ isoproteneol provocation - CMR -> LGE, focal wall thinning, ventricular dilatation, global and regional ventricular dysfunction
4 Clinicopathologies of Wolff-Parkinson-White syndrome
1 Sinus rhythm with Delta wave
2 Orthodromic AVRT, narrow QRS with inverted p waves post QRS
3 Antidromic AVRT with antidromic tachycardia (similar to VT) (10% of patients) -wide QRS from large delta wave, retrograde P waves
4 AF/flutter induced anterograde accessory conduction
