Atrial fibrillation Flashcards
What is the prevalence of AF in the age groups 70-75 and 80-85?
70-75: 5%
80-85: 10%
What are 3 problems to tackle in AF, from most to least important?
- Reducing increased risk of stroke
- Inefficient cardiac function
- Symptomatic palpitations
What are 4 types of atrial fibrillation classification?
- First detected episode
- Paroxysmal
- Persistent
- Permanent
What is paroxysmal AF?
Recurrent AF i.e. 2 or more episodes, but episodes terminate spontaneously
Episodes last less than 7 days, typically <24 hours
What is persistent AF?
2 or more episodes of AF that are not self-terminating
Usually episodes last greater than 7 days
What is permanent AF?
Continuous AF which cannot be cardioverted or if attempts to do so are deemed inappropriate
What are the 2 treatment goals in permanent AF?
Rate control and anticoagulation if appropriate
What are 4 symptoms and signs of AF?
- Palpitations
- Dyspnoea
- Chest pain
- Irregularly irregular pulse
What is the key investigation to diagnose atrial fibrillation?
ECG - will help distinguish from ventricular ectopics or sinus arrhythmia
What are the 2 elements of management of patients with atrial fibrillation?
- Rate/ rhythm control
- Reducing stroke risk
What are the 2 main strategies that can be employed in dealing with the arrhythmia element of AF? What are the aims of each?
- Rate control: accept pace will be irregular but slow rate down to avoid negative effects on cardiac function
- Rhythm control: try to get patient back into, and maintain, normal sinus rhythm - this is termed cardioversion. Drugs (pharmacological cardioversion) and synchornised DC electrical shocks (electrical cardioversion) may be used
What are the 2 types of cardioversion (used for rhythm control of AF)?
- Drugs - pharmacological cardioversion
- DC electrical shocks - electrical cardioversion
What type of control are most patients with AF managed with?
Rate control - rather than trying to maintain sinus rhythm
(except in certain situations - coexistent heart failure, first onset AF or obvious reversible cause)
What is the RATE treatment approach for AF?
Beta blocker or rate limiting CCB e.g. diltiazem used first line. If one drug doesn’t control, combo therapy with any 2 of:
- Betablocker
- Rate limiting calcium channel blocker e.g diltazem
- Digoxin
If doesn’t work/ pt doesn’t want medication - CATHETER ABLATE
What is the key risk of rhythm control in AF?
The moment a patient switches from AF to sinus rhythm presents the highest risk for embolism leading to stroke
Of what 2 condtions must ONE be met prior to attempting cardioversion (i.e. rhythm control) in AF?
- Short duration of symptoms <48hrs
- Anticoagulated for a period of time prior
What stratifying tool can be used to determine the most appropriate anticoagulation strategy in AF?
CHA2DS2-VASc
What does the CHA2DS2VASc score comprise of?
- C: congestive heart failure 1
- H: hypertension (or treated hypertension) 1
- A2: age >= 75: 2 65-74: 1
- D: diabetes 1
- S2: prior stroke or TIA 2
- V: vascular disease (IHD and peripheral arterial disease) 1
- S: sex category (female) 1
What is the suggested anticoagulation strategy in AF based on the CHADSVASc score?
- 0: no treatment
- 1: males: consider anticoagulation
- females: no treatment (because this score is only due to gender)
- 2 or more: offer anticoagulation
Why is digoxin usually not considered first line as rate control for AF any more and when IS digoxin the preferred choice?
Less effective at controlling heart rate during exercise
Preferred choice if coexistent heart failure
What are 3 drugs which are commonly used to maintain sinus rhythm with a history of atrial fibrillation?
- Sotalol
- Amiodarone
- Flecainide
What are 2 factors that favour rate control over rhythm control?
- Older than 65 years
- history of ischaemic heart disease
What are 5 factors that favour rhythm control over rate control in AF?
- Younger than 65 years
- Symptomatic
- First presentation
- Lone AF or AF secondary to a corrected precipitant e.g. alcohol
- Congestive heart failure
When is catheter ablation recommended in AF for rate control?
recommended for those who have not responded, or whish to avoid, antiarrhythmic medication for rate control
What is the aim of catheter ablation and how is it achieved?
Aim is to ablate the faulty electrical pathways that are resulting in AF - typically due to aberrant electrical activity between pulmonary veins and left atrium
Performed percutaneously, typically via groin
Where does the pathway causing AF usually exist in the heart?
Typically aberrant electrical activity between the pulmonary veins and left atrium
What are 2 things that can be used to ablate tissue in catheter ablation for AF?
- Radiofrequency - heat generated from medium frequency alternating current
- Cryotherapy
What must be performed prior to catheter ablation for AF and for how long?
Anticoagulation - 4 weeks
When should anticoagulation be used for catheter ablation in AF?
4 weeks prior AND during; ablation controls rhythm but not stroke risk, even if patients remain in sinus rhythm so still require anticoagulation as per CHADSVASc
How long should anticoagulation be given following catheter ablation in AF?
CHADSVASc
If score 0: 2 months anticoagulation
If score >1: longterm anticoagulation recommended
What are 3 notable complications of catheter ablation in AF?
- Cardiac tamponade
- Stroke
- Pulmonary valve stenosis
What is the success rate of catheter ablation to treat AF?
- around 50% of patients have early recurrence within 3 months, often resolves spontaneously
- longer term, after 3 years, 55% who have had a single procedure remain in sinus rhythm.
- of patients who’ve undergone multiple procedures, around 80% are in sinus rhythm
What are the 2 broad scenarios when cardioversion may be used in atrial fibrillation?
- Electrical cardioversion as an emergency if patient is haemodynamically unstable
- Electrical or pharmacological cardioversion as an elective procedure where a rhythm control strategy is preferred
How should TIME FRAME determine whether to offer a patient rate or rhythm control?
- if onset definitely <48 hours: rate OR rhythm control
- if onset >48 hours or uncertain: rate control
What are the steps to take if a patient has AF that has definitely started within the past 48 hours?
- Patient should be heparinised
- Lifelong oral anticoagulation if risk factors for ischaemic stroke
- Otherwise: electrical or pharmacological cardioversion
What is the pharmacological form of cardioversion?
Amiodarone if structural heart disease, flecainide or amiodarone in those without structural heart disease
If AF onset is <48h should you anticoagulate following electrical cardioversion?
No, further anticoagulation is unnecessary
If you are going to cardiovert someone with AF onset >48h what must be done before? Give the 2 options
Give anticoagulation for at least 3 weeks prior
OR
perform transoeseophageal echo (TOE) to exclude a left atrial appendage (LAA) thrombus. If excluded, patients may be heparinised and cardioverted immediately
If you decide to cardiovert in AF >48h onset, should you choose pharmacological or electrical cardioversion?
Electrical
What are 2 factors that pose a high risk of cardioversion failure?
Previous failure or AF recurrence
What is recommended prior to electrical cardioversion if there’s a high risk of cardioversion failure, in AF >48h onset?
At least 4 weeks of amiodarone or sotalol prior to electrical cardioversion
If AF onset is >48h should anticoagulation follow electrical cardioversion?
yes for at least 4 weeks; after this, further anticoagulation decisions should be on an individual basis depending on risk of recurrence
When is the only time flecainide can be used for atrial fibrillation cardioversion?
if no structural heart disease
What are 5 drugs that can also be used for pharmacological cardioversion in the UK that are less effective than amiodarone and flecainide?
- Beta blockers including sotalol
- Calcium channel blockers
- Digoxin
- Disopyramide
- Procainamide
What are the 2 scoring systems used to guide anticoagulation in AF?
- CHADSVASc: score can be used to determine anticoagulation strategy
- HASBLED to determine risk of bleeds
What does the HASBLED score comprise of?
- H: Hypertension, uncontrolled, systolic BP>160) 1
- A: Abnormal Liver function (cirrhosis, bilirubin>2x normal, ALT/AST/ALP >3x normal) and renal (dialysis or creatinine >200) 1 for liver 1 for renal
- S: Stroke - hisory of 1
- B: Bleeding - history of bleeding or tendency to bleed 1
- L: Labile INR (unstable/high, time in therapeutic range <60%) 1
- E: Ederly (>65) 1
- D: Drugs predisposing to bleeding - antiplatelet agents, NSAIDs or Alcohol Use (>8 drinks/week) 1 for drugs 1 for alcohol
What should be done if CHADSVASc suggests no need for anticoagulation? Why?
Important to ensure transthoracic echocardiogram to exclude valvular heart disease, which in combo with AF is an absolute indiction for anticoagulation
What are the options for anticoagulants to reduce risk of stroke in AF?
Warfarin or DOACs (dabigatran, apixaban, rivaroxaban, edoxaban)
Discuss advantages and disadvantages of each with patient
What are 4 things that might steer us away from using warfarin as an anticoagulant in AF?
- Falls
- Old age
- Alcohol excess
- History of previous bleeding
How does HASBLED inform decisions in AF?
No formal rules but score of 3 ormore indicates high risk of bleeding, defined as intracranial haemorrhage, hospitalisation, haemoglobin decrease >2g/L, and/or transfusion
What are 4 possible outcomes due to the high risk of bleeding indicated by a HASBLED score of 3 or more?
- intracranial haemorrhage
- hospitalisation
- haemoglobin decrease >2g/L
- transfusion
What should be the management of stroke or TIA in a patient with AF? 3 options
- Warfarin or a direct thrombin or factor Xa inhibitor should be given as the anticoagulant of choice
- Antiplatelets should only be given if needed for the treatment of other comorbidities
- In acute stroke patients, in absence of haemorrhage, anticoagulation therapy should be commenced after 2 weeks
- if imaging shows very large cerebral infarction then initiation of anticoagulation should be delayed
After how long should anticoagulation therapy be commenced in acute stroke patients (in absence of haemorrhage)?
after 2 weeks
What should be done if a patient is on an anticoagulant for AF and an antiplatelet for established CVD?
Anticoagulant monotherapy should be given without addition of antiplatelets if secondary prevention of stable cardiovascular disease
Should be done if a patient is on an anticoagulant for AF then develops acute coronary syndrome/ undergoes PCI?
Stronger indication for antiplatlet therapy than CVD; generally triple therapy for 4 weeks - 6 months (2 antiplatelets + 1 anticoagulant) and dual therapy (1 platelet + 1 anticoagulant) to complete 12 months. Variation from patient to patient
What is the advice regarding antiplatelet and anticoagulant therapy in the case of VTE?
If patient on antiplatelets (e.g. for CVD) develops VTE they’re likely to be prescribed anticoagulants for 3-6 months. HASBLED should be calculated, if low risk may continue antiplatelets. If intermediate-high, consider stopping antiplatelets to give the anticoagulants for VTE
What class of drug is digoxin?
Cardiac glycoside with positive inotropic properties
What is the mechanism of action of digoxin to treat AF with concurrent heart failure (not great for active patients)?
- decreases conduction through the AV node which slows ventricular rate in AF and flutter
- Increases force of cardiac muscle contraction due to inhibition of Na+/K+/ATPase pump. Also stimulates vagus nerve
Is digoxin monitored routinely?
No - except in suspected toxicity (has narrow therapeutic index)
How should digoxin be measured in suspected toxicity?
Measure concentration within 8-12 hours of the last dose
What determines whether a patient has developed digoxin toxicity?
Plasma concentration alone doesn’t determine whether patient has it; may occur even when concentration is within therapeutic range.
BNF advises likelihood of toxicity increases progresively from 1.5 to 3 mcg/l
What are 8 features of digoxin toxicity?
- Generally unwell
- Lethargy
- Nausea and vomiting
- Anorexia
- Confusion
- Yellow-green vision
- Arrhythmias e.g. aV block, bradycardia
- Gynaecomastia
What is the classical precipitating factor of digoxin toxicity? What is the mechanism of this?
hypokalaemia: digoxin normally binds to ATPase pump on same site as potassium. Digoxin therefore binds more easily if low potassium, increases inhibitory effects on heart etc.
What are 9 factors that can precipitate digoxin toxicity?
- hypokalaemia
- increasing age
- renal failure
- myocardial ischaemia
- hypomagnesaemia, hypercalcaemia, hypernatraemia, acidosis
- hypoalbuminaemia
- hypothermia
- hypothyroidism
- drugs: amioarone, quinidine, verapamil, diltiazem, spironolactone (competes for secretion in distal convoluted tubule therefore reduced excretion), ciclosporin. also drugs which cause hypokalaemia e.g. thiazides and loop diuretics
What are 3 elements of the management of digoxin toxicity?
- Digibind
- Correct arrhythmias
- Monitor potassium
What are 8 indications for the use of beta blockers?
- Angina
- Post-myocardial infarction
- Heart failure: for symptoms and mortality
- Arrhythmias: AF
- HTN - role diminished in recent years
- Thyrotoxicosis
- Migraine prophylaxis
- Anxiety
What are 5 side effects of beta blockers?
- Bronchospasm
- Cold peripheries
- Fatigue
- Sleep disturbances, including nightmares
- Erectile dysfunction
What are 4 contraindications for beta blockers?
- Uncontrolled heart failure
- Asthma
- Sick sinus syndrome
- Concurrent verapamil use: may precipitate severe bradycardia
What is the mechanism of action of flecainide?
Vaughan Wiliams class 1c antiarrhythmic; slows conduction of action potential by acting as potent sodium channel blocker; widens QRS complex and prolongs PR interval
What are 2 indications of flecainide?
- Atrial fibrillation
- SVT associated with accessory apthway e.g. Wolff-Parkinson-White syndrome
What are 4 contraindications for flecainide?
- Post myocardial infarction
- Structural heart disease e.g. heart failure
- Sinus node dysfunction; second degree or greater AV block
- Atrial flutter
What are 5 adverse effects of flecainide?
- Negatively inotropic
- Bradycardia
- Proarrhythmic
- Oral paraesthesia
- Visual disturbaneces
