Narrow Complex Tachycardias

Narrow complex tachycardias are also called SVTs or supra-ventricular tachycardia. All narrow complex tachycardias are SVT, but not all SVTs are narrow.

1. Atrial Tachycardias
This is a rare paroxysmal tachycardia with abnormal p waves, having a rate of 130 to 140 beats a minute. It has an abrupt onset and termination, and it can be initiated with programmed electrical stimulation during an electrophysiology study. Normally benign and short lived condition of the elderly.

Atrial tachycardias may cause a dilated cardiomyopathy and heart failure if they are not treated.

Treat with a DC shock.




2. Junctional Tachycardia
These arise from the "junction" in between the atria and the ventricles. Conduction to the ventricles is still normal, but there are more conduction pathways than there should be. P waves are often buried in the QRS.


Atrioventricular nodal re-entry tachyarrhythmias
These are more common in women and are responsible for approximately 60% of narrow complex tachycardias. This arrhythmia occurs when there are two atrial conduction paths into the AV node which triggers a perpetual circuit.
In nodal re-entry tachycardias, atrial (retrograde) and ventricular depolarisation is simultaneous so the p waves are buried in the QRS and hard to identify – look for inverted p waves in inferior leads II, III, AVF, sometimes causing a ‘pseudo’ S wave.

There are normally two paths in the AV node causing this. One of these transmits things quickly (retrograde) and one transmits things slowly (usually antegrade). Atrial and ventricular depolarisation is simultaneous.

 
AV reentry tachycardia
In re-entry tachycardias there is an extra connection between the atria and the ventricles - not more than one pathway in the node. Wolff-Parkinson White syndrome is the best known cause of this, and the accessory pathway is the bundle of Kent.

Wolff-Parkinson White
In sinus rhythm, the ventricles are normally excited by the accessory pathway. This leads to the clinical features of WPW - short PR and slurred upstroke of QRS (delta wave).

Patients may present with syncope, rather than palpitations, when atrial arrhythmias are conducted rapidly over the accessory pathway to the ventricles, bypassing the AV node and resulting in haemodynamic collapse.
For those patients with evidence of ventricular pre-excitation and a delta wave on their ECG, you can use the ECG to find the approximate location of the accessory pathway. Theoretically. you can localise it to the left or right side of the heart by assessing the polarity of the delta wave in lead V1, although how this helps you acutely I'm not sure:

    A left sided pathway may give rise to a positive delta wave in V1 and may cause right bundle branch morphology
    A right sided pathway may give rise to a negative delta wave in V1 and may cause left bundle branch morphology. This is because septal activation is initiated from the right side of the septum.

Conduction may be orthodromic or antidromic

    Orthodromic - anterograde conduction - premature atrial impulse is transmitted via the AV antegradely to the ventricles, then retrogradely back up the accessory pathway, depolarising the atria then passing back via the AV node and down the Bundle of His again antegradely, establishing a re-entry circuit.

P waves are present, but inverted and will follow the QRS, and the delta wave disappears.


    Antidromic - anterograde ventricular activation occurs via the accessory pathway and retrograde atrial activation via the AV node. This causes a regular broad QRS tachycardia but is much less common and occurs in 10% of cases.
Retrograde conduction through the AV node leads to atrial depolarisation and consequently the P waves will be buried in the wide and abnormal shape QRS – this may be indistinguishable from ventricular tachycardia unless a previous ECG is available. One clue is that the re-entry tachycardia will be exactly regular. For more details on this, look at the VT page.

3. Atrial Flutter
This is covered on the AF page. 

Management
If adverse features, go straight to DC cardioversion.
Atrial flutter and regular narrow-complex tachycardia will often be terminated by lower energies: start with 70-120 J biphasic (100 J monophasic).


- Dipyridamole enhances the effect of adenosine.
- May need more adenosine if recently had caffeine.
- In pregnancy adenosine is OK


- Once the arrhythmia has terminated you should start the patient on an AV nodal blocking drug, such as a beta blocker or calcium channel blocker at a low dose. This will need to be continued long term in order to reduce the risk of recurrence of the arrhythmia

- Verapamil is contraindicated in patients receiving beta-blocker therapy.
 Some sources advocate using verapamil first line instead of adenosine, as it is better tolerated.
 Verapamil 5- 10mg IV over 3min.
   
- Troponin isn't so useful in analysing SVT. If you really think there's an ischaemic trigger for the MI, then check a troponin:
    Low risk, prior SVT, feels good after conversion, then NO CARDIAC ENZYMES and outpatient f/u
    Intermediate risk, then DO get CARDIAC ENZYMES; If neg, outpatient follow up but if positive consider admission.
    High risk, older age, or known history of ACS, then DO CARDIAC ENZYMES and admit.

Of note...modified release verapamil has no anti-arrhythmic effects! Check the BNF - MR is only listed in the hypertension section...normal is in anti-arrhythmic too. Don't think you're being too nice by swapping it over!
EnlightenMe
http://www.enlightenme.org/knowledge-bank/cempaedia/supraventricular-tachycardias
http://www.enlightenme.org/emimage/ecg/diagnosis-and-treatment-narrow-complex-tachycardia 
http://www.enlightenme.org/learning-zone/cardioversion-conundrum
http://www.enlightenme.org/learning-zone/tiny-tot%E2%80%99s-ticker-flicker
http://www.enlightenme.org/learning-zone/challenging-case-svt
http://www.enlightenme.org/the-learning-zone/node/6724 


Other
http://ekgumem.tumblr.com/post/17949025577/wpw-orthodromic-and-antidromic-svt-episode

http://pulmccm.org/2012/review-articles/supraventricular-tachycardia-svt-diagnosis-treatment-review-nejm/

http://academiclifeinem.com/svt-are-troponins-necessary/

http://lifeinthefastlane.com/tag/svt/
http://emupdates.com/2009/11/26/calcium-channel-blockers-for-svt/ 
http://www.ems12lead.com/tag/treating-svt-with-adenosine/
http://lifeinthefastlane.com/ecg-library/svt/
http://ekgumem.tumblr.com/post/18378351287/diagnosis-and-treatment-of-svt-episode
http://resus.me/verapamil-vs-adenosine-for-svt/
http://bestbets.org/bets/bet.php?id=1884

http://learning.bmj.com/learning/modules/flow/JIT.html?execution=e2s2&locale=en_GB&action=start&sessionTimeoutInMin=90&moduleId=5003248&status=LIVE&_flowId=JIT&page=1

Atrial Fibrillation

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...

Definition
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.

Investigations
TFTs
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)

Management
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.

CHADS2 and CHA2DS2-VASc have been developed as more sophisticated scoring systems. They are not advised to be used in the UK, although an awareness of them is helpful, and there are useful statistics from their use.

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).


Chronic:

Treat any identifiable precipitants.
Control the rate









Acute

AFFIRM and RACE trials looked at whether rhythm or rate control is better.

<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.




Electrical Cardioversion
- 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).

Pharmacological Cardioversion

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

3. Digoxin
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.

Emergency Treatment
- 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.

Driving
Do not drive if arrhythmia has, or is likely to cause incapacity
Cause needs to be controlled and identified for four weeks

EnlightenMe
http://www.enlightenme.org/the-learning-zone/node/7515
http://www.enlightenme.org/knowledge-bank/cempaedia/atrial-fibrillation
http://www.enlightenme.org/learning-zone/rate-or-rhythm-control

BMJ Learning
http://learning.bmj.com/learning/module-intro/atrial-fibrillation--diagnosis-and-management.html?moduleId=5003354&searchTerm=%E2%80%9Cvaso-vagal%E2%80%9D&page=1&locale=en_GB

Doctors.net
http://www.doctors.net.uk/ecme/wfrmNewIntro.aspx?moduleid=1538

Other  
http://emcrit.org/podcasts/crashing-a-fib/    
http://blog.ercast.org/2012/10/should-we-cardiovert-atrial-fibrillation-in-the-ed/
http://guidance.nice.org.uk/CG36
http://calgaryguide.ucalgary.ca/slide.aspx?slide=Atrial%20Flutter.jpg
http://calgaryguide.ucalgary.ca/slide.aspx?slide=Atrial%20Fibrillation%20-%20Clinical%20Findings.jpg
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1163475/
http://circ.ahajournals.org/content/111/23/3141.full
http://academiclifeinem.com/paucis-verbis-card-anticoagulation-in-atrial-fibrillation/
https://www.gov.uk/current-medical-guidelines-dvla-guidance-for-professionals-conditions-a-to-c#arrhythmia
http://www.resus.org.uk/pages/periarst.pdf

Palpitations

Palpitations are a difficult area to cover as there are so many potential ECG abnormalities, and so much detail you could go into about treating them. Luckily, EnlightenMe again comes to the rescue for the generic areas. We'll cover each common abnormality in a bit more detail eventually!

EnlightenMe:
http://www.enlightenme.org/knowledge-bank/cempaedia/palpitations
http://www.enlightenme.org/learning-zone/cardioversion-conundrum
http://www.enlightenme.org/the-learning-zone/node/10940

GoogleFOAM:
http://academiclifeinem.com/modern-em-case-4-palpitations/

Palpitations have an underlying cardiac cause in 43%, are due to anxiety in 31% and have no specific attributable cause in 16% of patients. Worryingly, they're more likely to have a "proper" cause if they occur at work, whilst sleeping, or in the presence of known cardiac disease!

Focused History:
Establish the presence of symptoms which may indicate an underlying cause:
    Chest pain (in the absence of or preceding palpitations)
    Tremor
    Sweating
    Abdominal pain
    Anxiety
    Heat intolerance
    Weight change
    Productive cough
    Depression
    Weakness
    Fatigue
    History of structural heart disease
    Family history of sudden cardiac death



Investigations
    Electrolyte measurement (potassium, calcium and magnesium)
    Glucose
    TFTs
    FBC
    
Management after rhythm or rate control
Admit if:
   At risk of life threatening arrhythmia e.g. those with a previously recorded episode of VT
   Adverse symptoms or signs during the palpitations.
   Implanted cardiac devices suspected of malfunction.
   Family history of sudden death (eg, Brugada Syndrome).
   Require admission for investigation or treatment of an underlying cause or illness
   No protocols for follow up