Atrial Fibrillation Flashcards
What is atrial fibrillation (AF)?
Most common sustained arrhythmia
Chaotic and disorganised atrial activity resulting in an IRREGULAR heartbeat
Majority with AF?
Incidence increases with age
Types of AF?
Can be:
Paroxysmal
Persistent
Permanent/sustained (chronic) - sustained AF is facilitated by increased parasympathetic tone; atrial refractory periods are decreased, shortening wave length and making it easier for AF to sustain itself (duration of AF is prolonged after AF has been maintained for progressively longer periods of time)
What is paroxysmal AF?
Intermittent, often recurrent and often lasting less than 48 hours
What is persistent AF?
Episode of AF lasting longer than 48 hours, which can still be cardioverted to normal sinus rhythm; it is unlikely to spontaneously revert to normal sinus rhythm
What is permanent AF?
Inability of pharmacologic/non-pharmacologic methods to restore normal sinus rhythm
Associated diseases/causes of AF?
Most often occurs in the presence of cardiac disease: Hypertension Congestive Heart Failure Sick sinus syndrome (slow HR) CHD Valvular heart disease Congenital heart disease Cardiac surgery
Others:
Alcohol can be a trigger, part. in younger patients
Thyroid disease
Familial
COPD, pneumonia, septicaemia, pericarditis, tumours
Obesity is a predisposing factor to AF
Vagal causes
What is lone (idiopathic) AF?
AF in the absence of any heart disease and no evidence of ventricular dysfunction; it is a diagnosis of exclusion
Genetic suspicion
Risks with AF?
Greatest risk is thromboembolism causing stroke
Symptoms of AF?
Palipitations Pre-syncope (dizziness) Syncope Chest pain Dyspnea Sweatiness Fatigue
Symptoms are often worse at the onset of AF
Mechanism by which AF occurs?
RE-ENTRY of multiple wavelets prevents atria from being organised; there is an ectopic focus around the pulmonary veins (a lot of AF arises in this region)
Methods of terminating AF?
Pharmacologic cardioversion with anti-arrhythmic drugs (30% effective), e.g: flecanide, sotalol, amiodarone
Electrical cardioversion (90% effective)
Spontaneous reversion to sinus rhythm
ECG findings in AF?
Atrial rate > 300 bpm
Rhythm - irregularly irregular
Ventricular rate is variable
Recognition - absence of P waves and presence of ‘f’ waves (wavy deflections replace the entire isoelectric line between QRS complexes)
What is the ventricular rate in AF dependent upon?
AV node conduction properties
Sympathetic (facilitates AV node conduction) and parasympathetic tone (inhibits AV node conduction)
Presence of drugs which act on the AV node, e.g: β-blockers and CCBs are effective at slowing conduction and prolonging refractoriness in the AV node
Treatment of AF with a slow ventricular rate?
May co-exist with periods of fast ventricular rate; a pacemaker may be required to allow for pharmacologic control of fast ventricular rate
Ventricular rates
HR in AF?
400 bpm or more; atria quiver instead of contracting
What is pseudo-regularisation?
AF with a fast ventricular response - so fast that the ECG appears regular
What is atrial kick?
Atrial contraction immediately before ventricular systole acts to increase the efficiency of ventricular ejection, due to acutely increased preload
How can AF result in congestive heart failure?
Lost “atrial kick” and decreased filling times (reduced diastole) result in decreased CO
Can result in CHF, esp. in the presence of diastolic dysfunction
Patients with AF and pre-excitation?
WPW syndrome + AF can result in ventricular fibrillation and sudden cardiac death - pre-excitation of the ventricles broadens the QRS via an accessory pathway
Management of AF?
Rhythm control - objective is to maintain sinus rhythm predominantly
Rate control - objective is to control ventricular rate (but AF is accepted)
Anti-coagulation for both approaches IF there is a high risk of thromboembolism (majority of cases)
Treatment options for rate control of AF?
Digoxin
β-blockers
Verapamil, diltiazem
These can be used alone or in combination
Treatment options for rhythm control in AF?
Restoration of normal sinus rhythm:
Pharmacological cardioversion, i.e: anti-arrhythmic drugs like amiodarone
Direct Current Cardioversion (DCCV)
Maintenance of normal sinus rhythm:
Anti-arrhythmic drugs
Catheter ablation of atrial focus/pulmonary veins, i.e: rid of origin
Surgery (maze procedure)
Aim of electrical cardioversion?
Immediate restoration of sinus rhythm by delivery of a dose of electrical current to the heart at a specific moment in the cardiac cycle
Require sedation/general anaesthesia
Mechanism of action of anti-arrhythmic drugs?
Block ionic currents across cell membranes
Classification of anti-arrhythmics?
Class I (A, B, C) - Na+, act on phase 0 of the AP and are mainly used for rhythm control in AF; reduce the Na+ channel current and prolonged of teh QR interval
Class II - β-blockers, act on phase 4 of the AP and are mainly used for rate control in AF; QT interval prolonged
Class III - K+, act on phase 3 of the AP and are mainly used for rhythm control in AF; action potential prolongation; QT interval prolonged
Class IV - Ca2+, act on phase 2 of the AP and are mainly used for rate control in AF
Examples of different class of drugs?
Class I- lignocaine, quinidine, flecainide
Class II - propranolol
Class III - amiodarone, sotalol, dronedarone
Class IV - verapamil
What is Torsades de Pointes (TdP)?
Rapid, distinct ventricular tachycardia with a twisting configuration of the QRS morphology, assoc. with prolonged repolarisation
May be acquired of congenital but is a very deadly form of VT
Recognising TdP?
Heart rate - 200-250 bpm
Rhythm - irregular
Recognition - long QT interval, wide QRS and continuously changing QRS morphology
Mechanisms of TdP development?
Hypokalaemia
Prolongation of the AP duration (can be drug-induced)
Renal impairment (increased drug levels)
Patients that have a high risk of thromboembolism and in whom anti-coagulation is required?
Valvular AF in mitral valve disease, e.g: mitral stenosis and mitral regurgitation
Non-valvular AF if: Age >75 (esp. females have higher incidence) Hypertension Heart failure Previous thromboembolism/stroke CAD or diabetes and >60 years old Thyrotoxicosis
Describe the CHA2DS2-VASc score
Congestive heart failure/LV dysfunction - 1
Hypertension - 1
Age > or equal to 75 years - 2
Diabetes mellitus - 1
Stroke (TIA/TE) - 2
Vascular disease,e e.g: previous MI, PAD, aortic plaque) - 1
Age 65-74 years - 1
Sex (female) - 1
Score of 2 and above is considered high
Describe the bleeding risk assessment
Hypertension - 1 Abnormal renal or liver function - 1/2 Stroke - 1 Bleeding - 1 Iabile INRs - 1 Elderly (age > 65 yrs) - 1 Drugs/alcohol - 1/2
Score >= 3 is considered high risk
Why is radiofrequency ablation used in AF?
To maintain sinus rhythm by ablating AF focus (usually in the pulmonary veins) - creates non-conducting scar tissue
For rate control - ablation of the AV node to stop fast conduction to the ventricles
What is atrial flutter (A-Flutter)?
Rapid and regular form of atrial tachycardia that is usually paroxysmal; episodes can lost seconds/years
Mechanism of A-Flutter generation?
MACRO-REENTRANT circuit that is confined to the right atrial myocardium is sustained by a critical isthmus
End result of A-Flutter?
Usually progressed to AF
May result in thrombo-embolism
Differences in A-Flutter in peoples?
Patients with paroxysms of A-Flutter often have normal hearts
Patients with chronic A-Flutter usually have underlying heart disease
ECG characteristics of A-Flutter?
Atrial rate approx 300 bpm and ventricular rate approx 150 bpm
SAW-TOOTH ‘F’ WAVE
QRS is normal
Conduction is normal but there is physiological 2:1
Rhythm is regular but may be variable
A-Flutter treatment options?
RF ablation has a high long-term success rate
Pharmacological therapy to:
Slow ventricular rate
Restore sinus rhythm
Maintain sinus rhythm once converted
Cardioversion
Warfarin for prevention of thrombo-embolism; can also use NOACs but not in patients with prosthetic heart valves
Goals in A-Flutter treatment?
- Terminate the flutter and prevent recurrence
2. Control ventricular response during the arrhythmia
