he done fell out

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“He done fell out. . .” Malachi Winters MICT I/C CCEMTP

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Discussion of syncope and sudden cardiac death syndromes.

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“He done fell out. . .”

Malachi Winters

MICT I/C CCEMTP

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Called for a fainting spell. . .

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Syncope Rule of 15%

• Subarachnoid Bleed• Acute Coronary Syndrome (AMI)• Thoracic Aortic Dissection• Pulmonary Embolism• AAA Rupture/Leak• Ruptured Ectopic Pregnancy

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Causes of sudden cardiac death

• Brugada Syndrome• Hypertrophic Cardiomyopathy (HCM)• Long QT Syndrome• Wolff Parkinson White Syndrome• Life threatening electrolyte abnormalities

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Brugada Syndrome

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Brugada Syndrome

• Discovered by the Brugada brothers in 1992.• Inherited defect of sodium channels (SCN5A

gene).• Epicardial area of the RV has repolarization

abnormality.• Prone to spontaneous Ventricular Arrhythmias.

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Brugada = Sailboat of DEATH in V1-V3.

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Post cardiac arrest 41 y/o

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Post cardiac arrest 41 y/o

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Brugada Syndrome

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Brugada Syndrome

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Brugada Syndrome

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Brugada Syndrome

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Brugada Syndrome

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Brugada Syndrome

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Brugada Syndrome

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Brugada Syndrome

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Brugada Syndrome leads to ventricular arrhythmias.

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When a patient begins showing signs of Brugada Syndrome (syncope), mortality increases by 10%

for every year Brugada is untreated.

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Ddon’t give Brugada patients Na+ Channel Blockers!

• TCAs • Flecinide• Procainamide• Bupivicaine• Lidocaine (recommended)• Amiodarone (recommended)

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Hypertrophic Cardiomyopathy (HCM)

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Hypertrophic Cardiomyopathy

• A leading cause of sudden cardiac death in young athletes.

• Can be familial or a spontaneous mutation.

• Risk for sudden ventricular arrhythmias.

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Hypertrophic Cardiomyopathy

• True diagnosis requires more than an ECG• Huge QRS in V leads (caused by left

ventricular hypertrophy).• Pathological Q waves (caused by septal

hypertrophy).

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Hypertrophic Cardiomyopathy

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Hypertrophic Cardiomyopathy

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Hypertrophic Cardiomyopathy

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Hypertrophic Cardiomyopathy

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Long QT Syndromes

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Inherited Long QT Syndromes

• Jervell and Lange-Nielsen Syndrome– Congenital defect affecting K+ channels in heart and ears. – Results in congenital deafness and sudden cardiac death

• Romano Ward Syndrome– Group of at least six genetic defects.– Only symptoms are syncope and sudden cardiac death.

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QT Segment

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A prolonged QT segment increases risk of R on T and thus SCD.

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QT Segment varies with HR

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QTc measurement corrects the QT interval for rate.

• Bazzett’s Formula• QT interval/√(RR Interval)

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QTc should not exceed 0.450s (or 450 ms)

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For rates between 60-100, the QT interval should NOT exceed ½ the RR interval.

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Prolonged QT interval

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Patient with a seizure

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Patient with a seizure

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Psych patient in triage “needs to be medically cleared”.

• Patient is somnolent, suicidal.• Not forthcoming with history.• Triage note: “Patient is faking syncope”.• Records indicate that patient is taking

antipsychotics.

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ECG from psych patient.

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Lovely Torsades De Pointes

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55 year old man taking methadone and complaining of syncope.

QTc is 551 ms

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A few minutes later. . .

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Wolff Parkinson White Syndrome

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Wolff-Parkinson-White Syndrome (WPW)

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Wolff Parkinson White Syndrome

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Bundle of Kent.

• In WPW, an accessory pathway (called a bundle of Kent) allows for the atrial activity to stimulate the ventricles without slowing at the AV node.

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WPW conduction

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EKG changes in WPW

• Characterized by a short PR interval and a delta wave.

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EKG changes in WPW

• Delta wave is caused by early aberrant depolarization of the ventricles starting at the Kent bundle.

• Soon the normal conduction via the Ventricular Conduction system depolarizes the rest of the ventricles.

• This causes a widening of the QRS at the beginning of the QRS. Last part of the QRS is normal.

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Significance of WPW

• While WPW is generally benign on a day to day basis, two major problems may arise.

• 1) A reentrant circuit may form with the AV node and the bundle of Kent, leading to SVT.

• 2) In the pressence of atrial fibrillation or flutter, there is a very fast uncontrolled ventricular response.

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WPW reentry circuit

• Reentrant circuit leads to SVT.

• Because electrical activity is passing retrogradely through Kent bundle, Delta wave may not be seen.

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Orthodromic AVRT

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Antidromic AVRT

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WPW with A-fib/A-flutter

• Very frequent electrical impulses are passed through Kent bundle without pause like in the AV node.

• Results in a VERY FAST ventricular response.

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WPW with A-fib

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Treatment WPW a-fib/a-flutter with WPW

• Avoid calcium channel blockers!• Calcium channel blockers decrease conduction

through AV node, not through Kent bundle. By giving calcium channel blockers, you can actually increase the conduction through the Kent bundle and increase ventricular response.

• The same applies with Adenosine.

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Treatment WPW a-fib/a-flutter with WPW

• Recommended first line treatment is cardioversion.

• If cardioversion is unsuccessful, Procainamide and Amiodarone may be used.

• Ultimate treatment is eblasion to get rid of the Kent bundle.

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Potassium changes

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Potassium Changes

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Hyperkalemia

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Potassium 7.5

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Severe Hyperkalemia

• After potassium levels exceed 7.5, some very drastic changes begin to occur.

• The QRS and T wave meld together into one monophasic wave that is called a sine wave.

• AV blocks, V-tach, and V-fib soon follow.

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Hypokalemia

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Hypokalemia

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Severe Hypokalemia

• AV blocks, bradycardias and asystole are common with severe hypokalemia.

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Hypokalemia prolongs the QT interval and increases PVC frequency.

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Summary

• Take syncope seriously!• Screen for:

– Brugada– HCM– Prolonged QT– WPW– Hyper/Hypokalemia

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[email protected]

Malachi Winters