6. The electrical Conducting System of the Heart

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Last updated 4:04 PM on 5/25/26
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26 Terms

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<p>structure of electrical conducting system of heart</p>

structure of electrical conducting system of heart

<p></p>
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function of elements of conducting system

  • SAN→ generates electrical impulse

  • AVN→ mode of passage of impulse from atria to ventricles

  • bundle of his, right bundle branch, left bundle branch→ specialised conducting system to transmit impulse

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action potential

  • transient depolarisation of a cell as a result of activity of ion channels

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types of cardiac action potentials

  • pacemaker action potential

  • non pacemaker action potential

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pacemaker action potentials

  • autorhythmic

  • controlled by If (funny) channels

<ul><li><p>autorhythmic</p></li><li><p>controlled by I<sub>f</sub> (funny) channels </p></li></ul><p></p>
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stages in pacemaker action potential generation

  1. funny channels allow Na+ influx into membrane

  2. depolarises membrane

  3. as membrane potential reached until threshold reached→ action potential generated

    1. Ca2+ channel open

  4. at top of depolarisation, K+ channels open and Ca2+channels close

  5. K+ leave→ causes repolarisation

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non-pacemaker action potentials

  1. sodium ions influx into cell membranes, rapidly depolarising membrane

  2. sodium channels close, potassium channels open so K+ moves out of cell

  3. calcium channels open, so lots of calcium moves in, little bit of potassium leaving to allow electrochemical balance

  4. calcium channels close and potassium channels open→ lots of potassium exits to repolarise

  5. potassium leaves channel slowly from potassium channel

<ol start="0"><li><p>sodium ions influx into cell membranes, rapidly depolarising membrane</p></li><li><p>sodium channels close, potassium channels open so K+ moves out of cell</p></li><li><p>calcium channels open, so lots of calcium moves in, little bit of potassium leaving to allow electrochemical balance</p></li><li><p>calcium channels close and potassium channels open→ lots of potassium exits to repolarise</p></li><li><p>potassium leaves channel slowly from potassium channel</p></li></ol><p></p>
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pacemaker activity

  • intrinsic, spontaneous time dependant depolarisation of a cell membrane that leads to an action potential

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hierarchy of pacemakers

  • primary pacemaker→ highest firing frequency (fastest pacemaker):

    • SAN→ 100bpm

  • secondary pacemaker:

    • AVN→ 40bpm

  • tertiary pacemaker:

    • purkinje fibres→ 20bpm

  • SAN under constant vagal stimulation which suppresses its intrinsic frequency to approx. 60 bpm

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drugs affecting cardiac action potential

  • Class 1→ Na+ channel blocker

  • class 2→ Beta blocker

  • Class 3→ K+ channel blockers

  • Class 4→ Ca2+ channel blocker

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examples of class 1 channel blockers

  • 1a→ moderate:

    • quinidine

    • procainamide

  • 1b→ weak:

    • lidocaine

    • phenytoin

  • 1c→ strong:

    • flecainide

    • propafenone

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examples of class 2 heart drugs

  • propranolol

  • metoprolol

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examples of class 3 heart drugs

  • amiodarone

  • sotalol

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examples of class 4 heart drugs

  • verapamil

  • diltiazem

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conduction of action potentials

  • pass through gap junctions located at intercalated disks

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components of ECG

  • P wave→ atrial depolarisation

  • PQ interval→ AV nodal delay

  • QRS→ ventricular depolarisation

  • ST→ interval between depolarisation and repolarisation

  • T wave→ repolarisation

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normal sinus rhythm

knowt flashcard image
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atrial fibrillation

  • no ordinated atrial contraction

  • sinus node no longer in charge

  • ventricular rate is irregular

  • AVN important in regulation of atrial signals

<ul><li><p>no ordinated atrial contraction</p></li><li><p>sinus node no longer in charge</p></li><li><p>ventricular rate is irregular</p></li><li><p>AVN important in regulation of atrial signals</p></li></ul><p></p>
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atrial flutter

  • abnormal rhythm in atrium

  • regular but fast→ 300ppm

  • AV node is vital

<ul><li><p>abnormal rhythm in atrium</p></li><li><p>regular but fast→ 300ppm</p></li><li><p>AV node is vital</p></li></ul><p></p>
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ventricular fibrillation

  • cardiac arrest rhythm

  • no regularity

  • shockable

<ul><li><p>cardiac arrest rhythm</p></li><li><p>no regularity</p></li><li><p>shockable</p></li></ul><p></p>
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ventricular tachycardia

  • associated w cardiac arrest

  • shockable

<ul><li><p>associated w cardiac arrest</p></li><li><p>shockable</p></li></ul><p></p>
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1st degree heart block

  • long time between P wave and QRS

  • aka 1st degree AV block

  • AVN takes longer to produce ventricular depolarisation

  • always QRS after p wave

<ul><li><p>long time between P wave and QRS</p></li><li><p>aka 1st degree AV block</p></li><li><p>AVN takes longer to produce ventricular depolarisation</p></li><li><p>always QRS after p wave</p></li></ul><p></p>
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Second degree AV block→ Mobitz I)

  • progressive lengthening of PR interval, then missed QRS complex

<ul><li><p>progressive lengthening of PR interval, then missed QRS complex</p></li></ul><p></p>
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secondary degree AV block→ Mobitz II

  • PR interval normal, then absent QRS after P wave

<ul><li><p>PR interval normal, then absent QRS after P wave</p></li></ul><p></p>
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second degree AV block→ 2:1 block

  • absent QRS after alternate P waves

<ul><li><p>absent QRS after alternate P waves</p></li></ul><p></p>
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third degree block with junctional escape

  • no relationship between P waves and QRS complexes

<ul><li><p>no relationship between P waves and QRS complexes</p></li></ul><p></p>