Wednesday, 19 March 2014
There's so many arrhythmias that can cause palpitations that I was struggling to get through them. It's difficult to separate them out completely - but I had to in the end! So...atrial fibrillation...
There are many different types of AF and our terminology is always a little loose:
Paroxysmal AF: Discrete episodes that come and go. Episodes of sinus rhythm between.
Persistent AF: When AF lasts longer than a week or doesn’t stop without treatment
Permanent AF: When AF is more longstanding and resistant to therapy, or when no therapy is attempted
The greatest morbidity and mortality associated with AF arises from the thromboembolic sequelae. Up to 25% of all CVAs are attributable to AF-associated thromboembolism. Men are 1.5 times more likely than women to develop atrial fibrillation.
Atrial Flutter is a similar form of re-entry tachycardia where the circuit is almost always confined to the right atrium: rare left atrial cases have been reported. Type 1 or ‘Typical’ atrial flutter will have a rate of around 300/ min (250-350/min) and most commonly produces a negative sawtooth appearance in inferior leads II, III and AVF. ‘Reverse Typical Flutter’ produces a positive sawtooth in the inferior leads at around the same rate, and is due to the electrical impulses passing round the re-entry circuit in the reverse direction.
Type 2 ‘Atypical’ Atrial Flutter is rare, faster, 350-450/min and arises from a different pathway.
Atrial fibrillation looks irregularly irregular on an ECG, with absent P waves. The faster the rate the more regular AF will look but it is always irregularly irregular. An irregularly irregular rhythm isn't always AF- there could be multi-focal atrial tachycardias and atrial flutter present. AF may co-exist with bundle branch block and look like ventricular tachycardias.
Transthoracic echocardiography if:
important for long-term management, eg for younger patients
rhythm-control strategy that includes cardioversion (electrical or pharmacological) possible
high risk or a suspicion of underlying structural/ functional heart disease (such as heart failure or heart murmur) that will influence their subsequent management (for example, choice of antiarrhythmic drug)
Assess Stroke Risk:
Increase of stroke:
1.5% for patients aged 50-59 years to
23.5% for those between 80 and 89 year
The NICE guidelines score patients according to low risk, medium risk, and high risk and advise anticoagulation accordingly.
The risk of stroke must be balanced against the risk of bleeding. Three main scoring systems for risk of bleeding have been validated in people with atrial fibrillation but I have never seen them used in clinical practice:
HEMORR2HAGES (Hepatic or renal disease, ethanol abuse, malignancy, older (age ≥75 years), Reduced platelet count or function, rebleeding risk, hypertension (uncontrolled), anaemia, genetic factors, excessive fall risk, and stroke)
HAS-BLED (Hypertension, abnormal renal/liver function, stroke, bleeding history or predisposition, labile INR, elderly (eg age >65, frailty, etc), drugs/alcohol concomitantly). This is the score recommended by the ESC.
ATRIA (AnTicoagulation and risk factors in atrial fibrillation).
Control the rate
<48 hours = Rhythm Control aka chemical or electrical cardioversion
- If >48 hours needs anticoagulation for six weeks
- If rhythm control unsuccessful, will need rate control instead
- Success rate 65 - 90%
- Relapse high (25- 50% at one month)
- Continue antiarrhythmic drugs afterwards.
- More likely to be successful with AP paddles (sternum and left subscapular)
- If permanent pacemaker in place, cardiovert but then interrogate device. Paddles should be as far away as possible from the device.
- More likely to be successful if pre-treated with antiarrhythmic drugs
- For a broad-complex tachycardia or atrial fibrillation, start with 120-150 J biphasic shock (200 J monophasic) and increase in increments if this fails. Atrial flutter and regular narrow-complex tachycardia will often be terminated by lower energies: start with 70-120 J biphasic (100 J monophasic).
And this is how it works (from a cardiologist):
DC cardioversion works by stunning the entire myocardium. The tissues with the shortest refractory period (i.e. recover and start normal electrical service) earliest are the SA node followed by AV node. Therefore DCCV simply stuns everything, and hopefully the tissues that recover soonest determine the rhythm.
We sync to shock on the R wave to avoid the ST-T segment when the ventricular myocardium is repolarising and very vulnerable to VF (this is why long QT syndromes are a problem - if the QT is long enough then risk of ectopic beat hitting the ventricle at that time and becoming VT/VF. If you do shock someone on the ST-T then it's not usually a problem, just turn the sync off and re-shock (although clearly this isn't taught).
Most AF is rate controlled with drugs, but we still do cardiovert a fair number for various reasons (symptoms/can't take warfarin/employment/heart failure etc), the big problem is the recurrence rate (40% back in AF at 6 months, 60% at 1 year). Electrophysiology with ablation is either aimed at pulmonary vein isolation (potentially curative 60-70%) or destroying the AV node and inserting a pacemaker (palliative procedure).
Class Ib agents (lidocaine) aren't used any more as other agents are more effective.
Class Ic agents (flecainide and propafenone) are safe in patients who do not have evidence of previous myocardial infarction, acute myocardial ischaemia, or ventricular dysfunction. Their use in the ED is often limited by the poor availability of echo. I can't find any where what happens if you give it and there is a stuctural abnormality, but I guess as it can prolong the QT and cause arrhythmias anyway, you're just more likely to have to sort out a mess. The BNF implies structural problems only cause a problem if they cause haemodynamic compromise.
Class II (metoprolol, propanolol) are used for rate control, not rhythm control.
Class III (sotalol, amiodarone and dronedarone)
- I've never seen sotalol used, possibly because it has dose dependent effects. At low doses, sotalol has only class 2 effects and acts simply as a beta blocker with primarily negative chronotropic effects. It can not be given if there is any sign of heart failure. At high doses, Sotalol exerts class 3 effects and is antidysrhythmic. It can prolong the QT interval.
- Amiodarone is toxic. It has lots of different arrhythmic effects, but is normally put in class III. It is the drug of choice in the presence of heart failure. It can prolong the QT interval.
- The combination of amiodarone and Sotalol is contraindicated as they both prolong the QT interval and can precipitate ventricular dysrhythmias.
Class IV (verapamil, diltiazem)
- Used for rate control
>48hours = Rate Control
There are 3 main options for rate control
1. Beta blockers - metoprolol (IV/PO) or bisoprolol (PO).
The BNF doesn't say, but cardiologists I've worked with say bisoprolol is just as easy as metoprolol, wears off less quickly, and they prefer it. But in the ED we like giving things IV...
2. Calcium channel blockers - diltiazem or verapamil
These should not be used in conjunction with beta blockers
Digoxin is not recommended as a first line drug because it does not control the heart rate in ambulant patients. It is positively inotropic, so can be useful.
- Known poor LV function (adequate LV function is dependent upon the 15% of ventricular filling provided by atrial contraction).
- Heart rates (>150 bpm) causing inadequate time for LV filling.
Do not drive if arrhythmia has, or is likely to cause incapacity
Cause needs to be controlled and identified for four weeks