14 EKG Basics

  • 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

  • speed by which electricity moves through heart

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

  • small box: 40 ms
  • big box: 200 ms
  • 300 / # of big boxes

EKG lead

  • 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

  • -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

  • PR: shorter than 1 big box

  • 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)

  • 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

  • longer to depolarize/repolarize, longer QT

  • not really seizures, passing out from torsades

  • hyperacute: precede ST elevation in ischemia