There are many causes of syncope. Syncope is the medical term for fainting. Most of us are pretty familiar with the common vasovagal cause. Fortunately syncope is often self-correcting; the patient hypo-perfuses, they blackout and fall, their body perfuses better, they wake up. This post will be dedicated to 12-lead presentations that may indicate causes of syncope.
I have decided to use some exerts from my favorite emergency physician/presenter, Dr. Amal Mattu. Dr. Mattu has spoke and written on these topics multiple times.
This first one is easy, and you wouldn't even need a 12-lead to determine it's malignancy.
What do you notice about the 12-lead above? How about the rate? This is an example of bradycardia. Bradycardia may cause hypo-perfusion, leading to syncope. This would classify them as symptomatic, and they may require treatment.
*It is important to remember that there are many tachycardic arrhythmias that could cause syncope as well.
Acute Myocardial Infarction
An acute myocardial infarction (AMI) is the most common reason we use a 12-lead for diagnostic purposes. An AMI may cause syncope amongst many other signs and symptoms. Syncope would be an atypical (not usual) presentation for an AMI. I am not going to elaborate much on this presentation because it requires much teaching for those who are unfamiliar with STEMIs (ST-Elevated Myocardial Infarction). Please head over to the prehospital 12-lead blog for some great education on STEMIs.
Long QT Syndrome
Long QT Syndrome, or LQTS may lead to arrhythmias that lead to syncope. This happens due to something called an R on T phenomenon. The most common arrhythmia due to LQTS is Torsades de Pointes, however monomorphic ventricular tachycardia is possible. Syncope and/or seizures are common symptoms of the rhythms associated with LQTS.
Torsades de Pointes
From Dr. Amal Mattu
•Prolonged QT-interval predisposes to torsades de pointes •One of the key “can’t miss” diagnoses associated with syncope •Perhaps a more common cause of syncope and sudden death than previously recognized?
Causes of QT-prolongation •Electrolyte abnormalities (hypokalemia, hypomagnesemia, hypocalcemia) •Sodium channel blocking medications (many!) •Includes Type IA medications, anticholinergics, cocaine, many antipsychotics, some antibiotics •Acute myocardial ischemia (usually associated with inverted T-waves) •CNS lesions, e.g. intracerebral hemorrhage (often associated with giant inverted T-waves) •Hypothermia •Congenital
How long is too long? •QT-interval will vary based on patient’s heart rate •Measure QT from beginning of the QRS complex to the end of the T-wave, and average over 3-5 beats •“Corrected” QT-interval (Bazett formula): QTc = QT/√(RR) •QTc is considered prolonged when > 450 msec in men and > 460 msec in women and children •Major risk occurs in patients with QTc > 500 msec
Treatment •Search for and correct underlying cause (e.g. correct electrolyte abnormalities, discontinue responsible medications, etc.) •Congenital or idiopathic causes: beta-blocking medications attenuate adrenergic-mediated trigger mechanisms •Treatment of torsades de pointes: cardioversion/defibrillation, magnesium if relatively stable (e.g. intermittent torsades): 2 grams IV over 2-3 minutes followed by infusion •Overdrive pacing? Isoproterenol? Atropine? These are listed as possible treatments in acquired (not for congenital) cases, but rarely needed •Post-conversion treatment with magnesium, not lidocaine/amiodarone/ procainamide! (unlike other forms of ventricular tachycardia); for congenital cases, add beta-blocking medications
Brugada syndrome is becoming more and more well known recently. It is associated with specific ECG changes and an increased risk for sudden cardiac arrest. Only known cause of Sudden Unexpected Death Syndrome (SUDS)--according to Wikipedia . The ECG changes associated with Brugada Syndrome are most visible in V1, and V2. Non-STEMI-like ST-elevation that cannot be explained by another pathological cause (ie. LVH, LBBB, BER) may be Brugada Syndrome. These individuals may be otherwise very healthy and/or young.
Some features of the different types of Brugada Syndrome include
a RBBB pattern in V1 without terminal S-waves in lead I and V6.
A saddleback ST-elevation pattern (type 2 below)
Coved J-point elevation in V1, V2, V3 that gradually slopes down (type 1 below)
From Dr. Amal Mattu
More common cause of sudden death than previously recognized •May be responsible for up to 20% of sudden deaths in individuals without structural heart disease •Responsible for 4-5% of all sudden deaths •Incidence varies in different populations (some genetic factors involved) •Most common in young males (< 50 yo.) •First onset of symptoms approximately 40 yo. •Mortality approximately 10% per year if not treated with an internal cardioverter-defibrillator (ICD), regardless of whether or not antiarrhythmics are used
Syndrome characterized by •ECG abnormalities in leads V1 – V3 •Polymorphic or monomorphic (less common) ventricular tachycardia •Causes syncope if self-terminating •Causes sudden death if persists and not terminated by treatment •Structurally normal heart •Familial occurrence in approximately half of patients
ECG findings in leads V1 – V3 •Right bundle branch block (RBBB) or incomplete RBBB pattern •ST-segment elevation — 2 types •“coved-type” (most common) •“saddle-type” •ECG findings can vary with time depending on the autonomic balance, administration of antiarrhythmic and other drugs affecting channel function, body temperature, and other unknown factors
Definitive diagnosis can be made with electrophysiologic testing •Challenge with an intravenous class I medication (e.g. ajmaline, procainamide, flecainide) •Will induce increased ST-segment elevation and “coving” •Programmed electrical stimulation of the heart •Can induce ventricular tachycardia
Treatment •Placement of an ICD is the only effective treatment •Antiarrhythmic drugs (including beta blockers, amiodarone, etc.) ineffective
•Prevalence — 0.02% – 0.2% of the general population •Genetic factors involved •Hypertrophied but nondilated left ventricle •Thickening is usually asymetric, involving the septum to a greater extent than the free ventricular wall •Cardiomegaly usually not present on chest x-ray •Mortality 3.5% per year •Diagnosis often made only when the patient experiences sudden death •Usually occurs during exertion \ •Average age at diagnosis is 30 – 40 yo. •Patients may also experience syncope, angina, palpitations, dyspnea (often associated with exertion)
ECG findings •Normal in 7% – 15% •Typical abnormalities •Deep narrow Q-waves in the inferior and/or lateral leads – I, aVL, V5-6 (simulates MI, but Q-waves are “too narrow” for MI) •Very specific for this condition •Q-waves in lateral leads are more common than inferior leads, very commonly misdiagnosed as lateral MI •Left atrial enlargement •High left ventricular voltage/left ventricular hypertrophy •Other less common abnormalities •Tall R-wave in lead V1 (simulates posterior MI) •Deep narrow Q-waves in the inferior leads (simulates inferior MI) •Don’t rely on your cardiologists to make the Dx on ECG! Clinical diagnosis •Systolic murmur at apex or LLSB •Murmur increases with valsalva, standing •Murmur decreases with trendelenburg position, isometric exercise, squatting •Definitive diagnosis — doppler echocardiography
Treatment •Beta blockers, calcium channel blockers to improve LV filling and diastolic \function ] •Amiodarone if ventricular dysrhythmias present
Unrecognized Killers in Emergency Electrocardiography