Bradycardia

Bradycardia module: http://www.doctors.net.uk/ecme/wfrmNewIntro.aspx?moduleid=1575

Bradycardia
Bradycardia is defined as a heart rate of < 60 min-1. It may be:
- physiological (e.g., in athletes);
- cardiac in origin (e.g., atrioventricular block, sinus node disease, aortic stenosis);
- non-cardiac in origin (e.g., vasovagal, hypothermia, head injury, hypothyroidism, hyperkalaemia, muscular dystrophies);
- drug-induced (e.g., beta blockade, diltiazem, digoxin, amiodarone).

Adverse Signs
- Shock – hypotension (systolic blood pressure < 90 mmHg), pallor, sweating, cold, clammy extremities, confusion or impaired consciousness.
- Syncope – transient loss of consciousness due to global reduction in blood flow to the brain.
- Myocardial ischaemia – typical ischaemic chest pain and/or evidence of myocardial ischaemia on 12-lead ECG.
- Heart failure – pulmonary oedema and/or raised jugular venous pressure (with or without peripheral oedema and liver enlargement).

ECG Things

1st degree heart block: no worries
2nd degree (Mobitz I, Wenkenback): progressive PR prolongation. Normally a benign rhythm.
2nd degree block (Mobitz II): Regular P waves, but not all conducted.
Complete Heart Block: Maintained by junctional or escape rhythm. Might be caused by drugs or inferior MI.

J waves - sign of hypothermia. Resolve as patient warms up. Size is proportional to degree of bradycardia.
Carotid hypersensitivity - see later
Sick sinus syndrome
Junctional rhythm

Treatment Options
Treat any reversible causes.

1. Electrical (cardioversion for tachyarrhythmia or pacing for bradyarrhythmia)
2. Simple clinical intervention (e.g., vagal manoeuvres, fist pacing)
3. Pharmacological (drug treatment)
4. No treatment needed

Atropine
Give atropine 500 mcg intravenously if adverse signs present.
Repeat every 3-5 min to a total of 3 mg.

Doses of atropine of less than 500 mcg have been reported to cause paradoxical slowing of the heart rate.
Use atropine cautiously in the presence of acute coronary ischaemia or myocardial infarction.
Do NOT give atropine to patients with cardiac transplants. Their hearts are denervated and will not respond to vagal blockade by atropine, which may cause paradoxical sinus arrest or high-grade AV block.
The half life is 2-3hours. May not work on older SA nodes.

Second-line drugs
Seek expert help to select the most appropriate choice. In some clinical settings second-line drugs
may be appropriate before the use of cardiac pacing.
Intravenous glucagon -  beta-blocker or calcium channel blocker
Digibind -  in digoxin toxicity
Theophylline (100-200mg slow IV infusion) - for bradycardia complicating acute inferior wall myocardial infarction, spinal shock
Thyroxine - if myxoedemic crisis suspected

Pacing 
- First pacing can be used.
- Verify electrical capture on the monitor or ECG and check that it is producing a pulse.
- Use analgesia and sedation as necessary to control pain; sedation may compromise respiratory effort so continue to reassess the patient at frequent intervals.
- Consider if there is documented recent asystole (ventricular standstill of more than 3s), Mobitz type II AV
block; complete (third-degree) AV block (especially with broad QRS or initial heart rate <40 beats min-1).
- AP pads. Start at 70mA and increase until capture achieved.
- If no capture at 130mA, re-site pads and repeat.

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
  

Syncope Overview and the ECG in the Athlete

My attempt to cover all of the curriculum in ST4/ST5, ready to revise in ST6 is doomed to failure. I'm going to set myself the target of the compulsory topics by the end of ST4-  that's a bit more achievable. I'll hope to do more than just compulsory. Luckily, HAP5 is one of the ST4 topics!

HAP 5  - revisit CAP32, CAP25, CAP5

BMJ Learning
ECG interpretation in athletes
Abnormal ECG findings in athletes
Normal ECGs in athletes

Other
BMJ
ECGs in Athletes
ECG in a Marathon Runner

Junctional (nodal) rhythm: QRS rate is faster than the resting P wave rate which is slowed in athletes due to increased vagal tone. This is normal in a trained athlete.


Premature Ventricular Contractions: LBBB morphology suggests an origin from the right ventricle. The presence of 2 or more PVCs on a 10 second tracing is abnormal and requires additional testing. 

Left Ventricular Hypertrophy:
Sokolow-Lyon voltage criterion: sum of the S wave in V1 and the R wave in V5 or V6 (using the largest R wave) as >3.5 mV (35 small squares with a standard amplification of the ECG at 10 mm/1 mV).
LVH in athletes is normal but other features in conjunction with it, like left atrial enlargement, left axis deviation, ST segment depression, T wave inversion, or pathologic Q waves, should raise the possibility of pathologic LVH and should prompt further evaluation.

Incomplete Right Bundle Branch Block: rSR’ pattern in V1 with QRS duration <120 ms is commonly present in athletes (12-32%. 
May be easily confused with a Brugada pattern.


Early Repolarisation: 35-91% of trained athletes and is more prevalent in young males and black/Afro-Caribbean individuals. Late QRS slurring or notching with horizontal ST segment elevation in the inferolateral leads has been associated with an increased risk of arrhythmic death in one study of middle aged, non-athletic Finnish citizens. However, a significant percentage of young competitive athletes (25-30%) show early repolarisation with similar morphologic features in either the inferior or lateral leads.

Calculating the QTc

An accurate assessment of the QTc can be achieved by adhering to the following six principles.
1.  Bazett’s heart rate correction formula
     (QTc = QT/√RR; note the RR interval is measured in seconds).

2.  Bazett’s formula loses accuracy at slow heart rates and can underestimate the individual’s inherent QTc at heart rates <60 bpm, especially at heart rates <50 bpm.
3.  In sinus arrhythmia calculate an average QT interval. 
4.  Identifying the end of the T wave properly.
5.  It is incorrect to include the commonly seen low amplitude U wave in the QT calculation. Such U wave inclusion will inflate greatly the QTc. Instead, follow the “Teach-the-Tangent” or “Avoid-the-Tail” method as shown in Figure 4.

6.  The morphology of the T waves, not just the length of the QT interval, can suggest the presence of a QT syndrome. A notched T wave in the lateral precordial leads may be a tip off to LQTS even in the absence of overt QT prolongation.

LQTS is estimated to affect 1 in 2000 individuals. SQTS is much less common affecting less than 1 in 10000 individuals.LQTS is the most common channelopathy responsible for about 15-20% of SUD and is diagnosed based on a combination of symptoms, family history, electrocardiographic findings, and genetic testing. The Schwartz-Moss score is used to invoke low, intermediate, and high probability for LQTS. 

Genetic testing is recommended for:
1) any patient where a cardiologist has an index of suspicion for LQTS (intermediate or high probability score), or
2) an asymptomatic patient with no family history but an incidental ECG finding with a QTc >480 ms pre-puberty and >500 ms post-puberty that is confirmed on repeat ECG testing.
Genetic testing may be considered for individuals with an incidental QTc finding (repeated) of > 460 ms pre-puberty and >480 ms post-puberty.

Guidelines from the European Society of Cardiology for ECG interpretation in athletes define a QTc value of >440 ms in males and >460 ms in females (but <500 ms) as a ‘grey zone’ requiring further evaluation, and a QTc ≥500 ms, otherwise unexplained and regardless of family history and symptoms, as indicative of unequivocal LQTS.

SVT

When two premature ventricular contractions (PVCs) are recorded on a baseline (10 second) ECG, the likelihood is very high that the athlete has > 2,000 PVCs per 24 hours. In athletes with > 2,000 PVCs per 24 hours, underlying structural heart disease that may predispose to more life-threatening ventricular arrhythmias was found in 30% of cases.

HOCM
Symptoms of HCM (autosomal dominant) include chest pain, syncope, and exercise intolerance, but for many persons the disease can be asymptomatic and SCD may be the clinical presentation of the disease. However, the reported prevalence of HCM in competitive athletes is apparently lower, approximately 1 in 1,000 to 1 in 1,500 athletes.

Over 90% of patients with HCM will have an abnormal ECG including T wave inversion, ST segment depression, pathologic Q waves, conduction delay, left axis deviation, and left atrial enlargement.

The isolated presence of high QRS voltages fulfilling voltage criterion for LVH is regarded as a normal finding in athletes related to physiologic increases in cardiac chamber size and/or wall thickness and does not in itself require additional evaluation.


Ventricular fibrillation and sudden death in patients with Brugada syndrome occurs more commonly during rest and sleep and is unrelated to exercise.

CPVT should be considered in any person who experiences syncope during exercise or extreme emotion, particularly in those who experience syncope during maximal exertion or have repeated episodes of syncope with exercise. CPVT cannot be diagnosed on the basis of a resting ECG, as the resting ECG is normal. An echocardiogram is also typically normal. As ventricular ectopy occurs only in the face of increased emotion or exercise, exercise stress testing is the key test in the evaluation CPVT. As exercise workload increases, there is typically an increase in the amount of ventricular ectopy which ultimately may result in polymorphic ventricular tachycardia (Figure 7).