Practical Procedures: Cardioversion and Pacing

I very much didn't like doing cardioversions, or pacing until I actually did them! I still find it difficult to remember the numbers, so I've got myself a special memory card - it's duplicated information elsewhere, but better too many times than not enough.

Syncope

Syncope is common, and difficult to investigate because by definition, the patient has recovered from the event! It is summarised here. There are five main causes to consider:

1. Neurocardiogenic or vasovagal (emotional, situational or orthostatic triggers)
2. Cardiac
3. Orthostatic
4. Neurological / psychiatric (5%). Neurological causes of syncope include basilar artery migraine, vestibular dysfunction and vertebrobasilar ischaemia. Psychiatric syncope is a recognised syndrome consisting of syncopal episodes found in anxiety, depression and conversion disorder that resolve with treatment of the psychiatric disorder.
5. Essential (no cause found -35-50%).

These will all be covered in turn, and separately. There are scoring systems used to help risk-stratify syncope (very important).  I do like EM Basic's quick approach:

Syncope + headache= subarachnoid or intracranial hemorrhage

Syncope + neuro deficit= stroke/TIA or intracranial bleed

Syncope + confusion= seizure

Syncope + chest pain= MI, PE, or aortic dissection

Syncope + back/abdominal pain in older patient= abdominal aortic aneurysm (AAA)

Syncope + positive HCG= ectopic pregnancy

Young with Syncope R/O: Structural heart prob HOCM Elect (brugada, prolonged QT, arrhythmia) Hypoglycaemia CNS insult Abnormal Lytes #FOAMed
— Meshal AlBassam (@meshal_albassam) March 16, 2014

OESIL (Osservatorio Epidemiologico della Sincope nel Lazio) Score

• age over 65 years;
• previous history of cardiovascular disease;
• syncope without prodrome and
• abnormal ECG

The score predicts 12 month mortality which rises from under 1% for patients with no risk factors to over 50% in patients with all 4 risk factors. I've never seen this used in clinical practice, or heard of it.

The San Francisco Rule
The San Francisco rule identifies high risk patients based on the presence of the following factors:

• History of congestive cardiac failure
• Haematocrit < 30%
• Abnormal ECG
• Complaint of shortness of breath
• Systolic Blood Pressure < 90 mm Hg

The presence of any factor is considered sufficient for the patient to be high risk.The rule is 98% sensitive and 56% specific to predict adverse events.

The EGSYS (derived from patients enrolled in the Evaluation of Guidelines in SYncope Study 2 trial) Score

Predictor	Score
Palpitations preceding syncope	4
Syncope during effort	3
Heart disease/ abnormal ECG	3
Syncope while supine	2
Precipitating/ predisposing factors	-1
Autonomic prodromes	-1

This specifically identified cardiac syncope with a score of 3 or more being 99% sensitive and 65% specific for identifying cardiac syncope (positive and negative predictive values 33% and 99%). Again, I've never seen this used in clinical practice.

Investigations
A completely normal ECG makes a cardiac cause of syncope other than transient arrhythmia unlikely.

Echocardiography should be performed in any patient with a cardiac murmur and to diagnose and quantify suspected heart failure. If aortic stenosis is suspected, echocardiography should be performed urgently.
Carotid sinus massage for 5 to 10 seconds with continuous ECG and blood pressure monitoring can be used to diagnose carotid sinus syndrome. It is considered positive if it produces a drop in systolic blood pressure of 50 mm Hg or a period of asystole of 3 seconds.
Ambulatory 24 hour ECG recording may be considered in patients with a high pre-test probability of arrhythmia.
Tilt table testing is not used much any more

@drsuneet @SergioPinski @MGKatz036 To me, tilts worthless in eval of syncope. Not reproducible and high false pos/neg rates.
— Westby Fisher, MD (@doctorwes) April 6, 2014

Management
Think about all causes - 18% of patients with syncope in one study had more than one cause.

Driving - consider whether the patient should refrain from driving

Other guidelines can be found here.

Orthostatic Syncope

Orthostatic syncope (10%) is defined as an orthostatic drop of >20mm systolic blood pressure or >10 mm diastolic blood pressure. This may be due to absolute volume depletion from dehydration or haemorrhage or to venodilatation caused by medications or autonomic insufficiency (eg as occurs in Parkinson’s Disease). It is NOT the same as reflex syncope caused by orthostatic stresses, although the clinical presentation is very similar.

Pathophysiology
Sympathetic activity is chronically impaired, so vasoconstriction can't happen. This means when you stand, the BP falls.

Clinical Features
Syncope is one symptom, others include dizziness/ lightheadedness, pre-syncope; weakness, fatigue, lethargy;palpitations, sweating; (iv) visual disturbances (including blurring, enhanced brightness, tunnel vision); hearing disturbances (including impaired hearing, crackles, and tinnitus); and pain in the neck (occipital/paracervical and shoulder region), low back pain, or precordial pain.

Cardiac Causes of Syncope

There are lots of cardiac causes of syncope, and they account for 10 - 30% of syncopal episodes. Cardiac causes include: arrhythmias, cardiac failure, ventricular dysfunction (eg. hypertrophic obstructive cardiomyopathy HOCM) and valvular heart disease.

Arrhythmias
The most common cardiac causes of syncope, and the arrhythmia should be treated.
Bradycardias - Mobitz II and complete AV block are most likely to cause syncope.
Tachycardias - Narrow and Broad
Sick sinus syndrome - the sinoatrial node is damaged,because of either abnormal automaticity or sinoatrial conduction abnormalities.Syncope is due to long pauses caused by sinus arrest or sinoatrial block and a failure of escape mechanism. It is a completely different pathogenesis to carotid sinus syndrome. It is more likely to happen in people >65 years old, with ischaemic heart disease risk factors. ECGs can show many things, including sinus bradycardia.

Arrhythmia related syncope can be diagnosed on ECG in the presence of:
    Sinus bradycardia rate under 40 bpm
    Mobitz II second degree block or above
    Alternating right and left bundle branch block
    Ventricular tachycardia or rapid supraventricular tachycardia
    Pacemaker malfunction

Cardiac Failure
This will be diagnosed as normal.

Ventricular Dysfunction
The ECG needs careful scrutiny.

Valvular Problems
Aortic stenosis needs excluding. What better summary than the one from The Calgary Guide here. 

Reflex syncope

This is one of the most common causes of syncope, estimated at 35-50%, and about 30% of people have survived at least one faint - and many more will have witnessed fainting! Vasovagal syncope is the "common faint" but it can be difficult to differentiate "faints" from other causes of syncope.

Reflex syncope is neurally modulated and can be split into three main groups:
- Vasovagal (emotional eg Blood and orthostatic stress)
- Situational (cough, sneeze, defaecation, micturition, post-exercise, post-prandial)
- Carotid sinus syncope

Signs and Symptoms
Transient loss of consciousness
Jerky movements similar to a seizure
May be associated with palpitations, blurred vision, and feelings of nausea, warmth and light-headedness prior to the syncope episode, and patients are more likely to have had previous syncopal episodes.

Pathophysiology
This arises from an initial increase in sympathetic outflow followed by a rebound reduction in sympathetic activity leaving unopposed parasympathetic activity causing vasodilatation, bradycardia and hypotension.
In other word, you get worried about something, so get the flight or fight response. This then stops, and the unopposed activity makes you collapse. 

Investigations
Look for carotid sinus hypersensitivity in any patient older than 40. A ventricular pause lasting >3 seconds or fall in BP of 50mmHg defines carotid sinus hypersensitivity.


Treatment
Exercises to improve blood flow
Driving - no restriction

Pacemakers

"Understand pacemakers and their failure" - what a broad statement to put in a syllabus. Luckily, some excellent resources exist to help us to do just that. The best resource has to be from EnlightenMe (especially good as that's for EM docs anyway).

EnlightenMe
http://www.enlightenme.org/knowledge-bank/cempaedia/cardiac-implantable-devices


GoogleFOAM
http://www.eperc.mcw.edu/EPERC/FastFactsIndex/ff_111.htm
http://journals.lww.com/em-news/Fulltext/2007/01000/Diagnosis__Pacemaker_Failure_to_Capture.9.aspx
http://lifeinthefastlane.com/education/ccc/pacemakers/ 
http://www.cardiacengineering.com/pacemakers-wallace.pdf
http://lifeinthefastlane.com/education/ccc/temporary-pacemaker-troubleshooting/
http://emcrit.org/blogpost/understanding-pacemakers/
http://www.mededmasters.com/sgarbossa-criteria---ami-in-presence-of-pacemaker.html http://lifeinthefastlane.com/ecg-library/pacemaker-malfunction/
http://expensivecare.com/2013/12/03/pacemakers-defibrillators-and-immortality/
http://archinte.jamanetwork.com/article.aspx?articleid=1783304
http://annals.org/article.aspx?articleid=706782
http://drgdh.wordpress.com/2011/07/11/pacemaker-emergencies/  

BMJLearning - nothing
Doctors.net - nothing

Pacemakers

 There are lots of different types of pacemakers, and these are catagorised using "NGB codes". The code should be in the patient's passport. This NGB code explains which chambers of the right heart are involved, as well as the way in which the device interprets electrical signals. Modern pacemakers are able to recognise intrinsic depolarisations (“sensing”) and provide artificial stimuli (“pacing”).

1st letter: the chamber paced: A(trium), V(entricle), or D(ual)
2nd letter: the chamber sensed: again, A,V, D, or very occasionally, neither (O)
3rd letter: the way in which the signals determine the activity of the pacemaker itself: I(nhibited), T(riggered), or D(ual). The differences between these are not relevant here.
       
Common modes of pacing are
- VVI: a single lead to the RV provides both sensing information and pacing 
- DDD: leads are positioned in both the RA and RV, and can both sense and pace 

Pacemaker problems
Device failure: failure to sense and/or pace appropriately. Don't be mislead by hysteresis. Consider a patient with a pacemaker and a lower acceptable heart rate of 50/min would start pacing as soon as the intrinsic rate fell to 49/min. Hysteresis is the separation of the lower pacing rate from the lower sensing rate. meaning that the device will pace at 50/min, but only when the intrinsic rate drops to, for example, 40/min. It is easy to see why this might give the impression that the device has malfunctioned, if the patient’s own rate is perhaps 42/min, but the pacemaker has not stepped in.
Lead failure: in the immediate post-implant period the leads may displace which might be quite subtle. Displacement can cause "Twiddler's Syndrome" where the patient manipulates the pulse generator, the pacemaker rotates and the leads dislodge. This can cause diaphragmatic or brachial plexus pacing!
Pocket problems: the pacemaker is implanted in a pocket in the deep issues of the chest. This may get infected. Antibiotics may help but the pacemaker may need changing.  


Questions
Check:

1. What device is implanted, and when?
   
2. How is the device set up, in terms of mode and rate etc.?
   
3. What is the patient’s own intrinsic rhythm and rate?
   
4. Is there evidence of appropriate pacing activity on the surface ECG?
   
5. Is there evidence of appropriate sensing on the surface ECG?
   
6. If no to 4 and 5, is there evidence of inappropriate pacing/sensing?
   
7. Is there any evidence of a mechanical complication, i.e., lead displacement, fracture etc.?
   
8. Is there evidence of a local complication such as infection

Presenting Complaints
 Delivered shock therapy whilst conscious
- Was this appropriate (for VF/untreated VT), or inappropriate (usually due to misidentification of the rhythm, or “noise” artifact secondary to lead fracture).
Clinical assessment within the ED will include the following:

• Check electrolytes, especially magnesium and potassium
• Look for myocardial ischaemia - if in doubt, treat as ACS
• Look for lead fracture: a plain chest x-ray is helpful
  
  A patient who is well, with a stable rhythm, and who has had a very limited number of shocks, does not necessarily require admission and can be discharged with next day follow up.

Syncope
Check syncope is really due to a cardiac cause. Remember: 

• Sustained bradycardia is unlikely if the ICD has pacing functions, but is possible if there is any evidence suggestive of pacemaker failure
• VF will rapidly lead to loss of consciousness.
• Patients who have had sustained VT  may or may not be aware of palpitations immediately beforehand, and there is often a degree of retrograde amnesia following a shock / collapse; a normal ECG at presentation does not exclude this as a cause

Associated cardiac symptoms
Chest pain, palpitations and dyspnoea may all be seen in ICD patients attending the ED, either from the underlying cardiac condition, or as a manifestation of issues around therapy from the device. In general, these should be approached as they would for any other patient.

Palliative PatientsIf possible, reprogramme the ICD with the tachyarrhythmia therapy disabled. If this isn't possible, tape an external magnet above the device.
Pacemakers don't keep dying patients alive as terminal events are normally associated with such a sick myocardium that the patient doesn't respond to the pacemaker.
If the patient is not imminently going to die, don't automatically switch off the pacemaker as you may cause symptomatic bradycardia and heart failure.

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).