14 EKG Basics

EKG components

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• SA to LA and RA myocytes

• HIS bundles, left and right BBB, purkinje embedded in myocytes

• time x axis, electrical activity in y axis

• P: atrial depolarization

• flat after P: time for electrical activity to go to ventricles

• QRS: ventricle depolarize

• T: repolarization of ventricle. Atrial repolarization happens during QRS

Pacemaker and Hr

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• speed by which electricity moves through heart

• most of time between P and QRS is by AV nodal conduction

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• small box: 40 ms

• big box: 200 ms

• 300 / # of big boxes

EKG lead

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• some electrical activity to left, right

• sum of all activity: arrow

• each of 12 EKG leads look at summation from different POV = different QRS shape

• AVR: summation away, negative QRS

• 1, AVL: summation towards, positive

QRS Axis

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• -30 and -90

• V tach, activity not from SA node but from ventricle itself

• 90 and 180

• positive lead 1: toward 0

• negative lead 1: towards 180

• positive lead 2: going down

• negative lead 2: going up

• added lead 1 and 2 vectors to have summation vector

• exception: part up part down, physiologic, slightly to left, nl

Intervals

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• PR: shorter than 1 big box

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• less than 3 small boxes

• Inactivated peanut butter jar: TCAs block the cardiac fast Na+ channels, decreased contractility, QRS, QT propagation

• Wide QRS crack: TCAs can widen the QRS complex on ECG

• Twisted torsades streamer: TCAs can induce torsades

• Lightly held peanut butter jar: class IA antiarrhythmics have an intermediate binding affinity for the Na+ channel (intermediate use-dependence, moderate slowing of the phase 0 upstroke)

• Pushing away the curtain: class IA antiarrhythmics also block K+ channels, prolonging phase 2 and 3 of the cardiac action potential -> prolonged refractory period

• Twisted torsades streamer: class IA antiarrhythmics can cause Q-T interval prolongation (precipitates torsades) (K channel prolongation)

• Wide QRS shaped crack: class I antiarrhythmics widen the QRS complex on the ECG (decreased AP conduction velocity) (faster cells bind more and slow down more) (QRS widen as HR increases)

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• less than half QRS - QRS

• left: T begin immediately without flat portion

• hypocalcemia: less driving force to move Ca in, longer for Ca to go in, longer for QT interval to occur (myocyte in ventricles to depolarize, repolarize )

• Torsades strip: risk of prolonged Q-T interval

• Twisted streamer: FGAs can cause torsades de pointes

• Lightly held peanut butter jar: class IA antiarrhythmics have an intermediate binding affinity for the Na+ channel (intermediate use-dependence, moderate slowing of the phase 0 upstroke)

• Pushing away the curtain: class IA antiarrhythmics also block K+ channels, prolonging phase 2 and 3 of the cardiac action potential -> prolonged refractory period

• Twisted torsades streamer: class IA antiarrhythmics can cause Q-T interval prolongation (precipitates torsades) (K channel prolongation)

• Wide QRS shaped crack: class I antiarrhythmics widen the QRS complex on the ECG (decreased AP conduction velocity) (faster cells bind more and slow down more) (QRS widen as HR increases)

• Pushing away the curtain: class III antiarrhythmics block K+ channels prolonging phase 2 and 3 of the cardiac action potential -> prolonged refractory period

• Twisted streamer: sotalol, dofetilide, and ibutilide can induce torsades (although all type III antiarrhythmics can widen the QT interval)

• Inactivated peanut butter jar: TCAs block the cardiac fast Na+ channels, decreased contractility, QRS, QT propagation

• Wide QRS crack: TCAs can widen the QRS complex on ECG

• Twisted torsades streamer: TCAs can induce torsades

_..

• Torsades strip: risk of prolonged Q-T interval

• Twisted streamer: FGAs can cause torsades de pointes

• Lightly held peanut butter jar: class IA antiarrhythmics have an intermediate binding affinity for the Na+ channel (intermediate use-dependence, moderate slowing of the phase 0 upstroke)

• Pushing away the curtain: class IA antiarrhythmics also block K+ channels, prolonging phase 2 and 3 of the cardiac action potential -> prolonged refractory period

• Twisted torsades streamer: class IA antiarrhythmics can cause Q-T interval prolongation (precipitates torsades) (K channel prolongation)

• Pushing away the curtain: class III antiarrhythmics block K+ channels prolonging phase 2 and 3 of the cardiac action potential -> prolonged refractory period

• Twisted streamer: sotalol, dofetilide, and ibutilide can induce torsades (although all type III antiarrhythmics can widen the QT interval)

• Inactivated peanut butter jar: TCAs block the cardiac fast Na+ channels, decreased contractility, QRS, QT propagation

• Wide QRS crack: TCAs can widen the QRS complex on ECG

• Twisted torsades streamer: TCAs can induce torsades

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• longer to depolarize/repolarize, longer QT

• not really seizures, passing out from torsades

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• hyperacute: precede ST elevation in ischemia