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Cardiac Electrophysiology and the Electrocardiogram

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Page 1: Cardiac Electrophysiology and the Electrocardiogram

7/18/2019 Cardiac Electrophysiology and the Electrocardiogram

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Cardiac Electrophysiology and the Electrocardiogram

Slow action potentials

- SA nodes- AV nodes

Fast action potentials

- Atrial myocytes- Purkinje fbers- Ventricular myocytes

Electrophysiology o cardiac cells

- !he cardiac action potential starts in speciali"ed muscle cells o the sinoatrial

node# and then propagates in an orderly ashion throughout the hearto SA node

$roup o cells which cardiac action potential originates %ocated in the right atrium

Fire action potentials at a regular rate

• &'-('' times per minute

• )ntrinsic pacemaker or automaticity

• )n*uenced by both parasympathetic and sympathetic

neural inputo About one tenth o a second ater its origination# the signal arri+es at

the atrio+entrical ,AV nodeo  !he impulse does not spread directly rom the atria to the +entricles

because o the presence o a fbrous atrio+entricular ringo  !he only a+ailable pathway is or the impulse to tra+el rom the AV

node to the .is-Purkinje fber system- !he cardiac action potential conducts rom cell to cell +ia gap junctions

o /hm0s law

Current *owing between cell A and the adjacent cell 1 is

proportional to the +oltage di2erence between the two cells )n+ersely proportional to the electrical resistance between them

o )ntracellular current

Positi+e charge that enters cell A not only depolari"es cell A# but

also produces a *ow o positi+e charge to cell 1o E3tracellular current

 !he mo+ement o the e3tracellular positi+e charge rom aroundcell 1 toward the e3tracellular region around cell A

o  !he *ow o intra and e3tracellular current are e4ual and opposite

o )t is the *ow o this e3tracellular current in the heart that gi+es rise to

the electrocardiogram ,EC$- Cardiac action potentials ha+e as many as f+e distincti+e phases

o 5 major time-dependent and +oltage-gated membrane currents

6a7 current

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• 8esponsible or the rapid depolari"ing phase o the action

potential in atrial and +entricular muscle and in purkinje

fbers Ca97 current

• 8esponsible or the rapid depolari"ing phase o the action

potential in the SA node and AV node• Also triggers contraction in all cardiomyocytes

:7 current

• 8esponsible or the repolari"ing phase o the action

potential in all cardiomyocytes Pacemaker current

• 8esponsible in part or pacemaker acti+ity in SA nodal

cells# AV nodal cells# and purkinje fberso 9 electrogenic transporters carry current across plasma membranes

6a-Ca e3changer

6a-: pump

o Phases Phase '

• ;pstroke o the action potential

• ;pstroke is due only to Ca97 current

• Slow

Phase (

• 8apid repolari"ation component o the action potential

• <ue to almost total inacti+ation o 6a7 current and

Calcium current

• <epend on the acti+ation o a minor :7 current

Phase 9

• Plateau phase o the action potential• Prominent in +entricular muscle

• <epends on the continued entry o Ca97 and 6a7 ions

through their major channels

• /n minor membrane current due to the 6a-Ca e3changer

Phase =

• 8epolari"ation component o the action potential

• <epends on :7 current

Phase 5

• Constitutes the electrical diastolic phase o the action

potential

• <iastolic potential

o Vm during phase 5

• >a3imum diastolic potential

o >ost negati+e Vm during phase 5

• SA and AV nodal cells

o Changes in :7# Ca97# and pacemaker current

produce pacemaker acti+ity during phase 5

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• Purkinje fbers

o E3hibit pacemaker acti+ity

o ;se only pacemaker current

• Atrial and +entricular muscle

o 6o time-dependent currents during phase 5

- !he 6a7 current is the largest current in the hearto Abundant in

Atrial muscle

Ventricular muscle

Purkinje fbers

o 6ot present in

SA node

AV node

o  !he depolari"ation produce by the 6a7 current acti+ates 6a7 current

but also Ca97 current and :7 current- !he Ca97 current in the heart primarily through %-type Ca97 channels

o Present in all cardiac myocytes

o Current source o SA and AV nodes

o ;pstrokes are slower than those in atrial and +entricular muscle

o Ca97 current sums with 6a7 current during the upstroke o the action

potentials o the +entricular and atrial muscle and the purkinje fberso 1lockers o %-type Ca97 channels ,inhibits Ca97 current

Verapamil

<iltia"em

6iedipine

- !he repolari"ing :7 current turns on slowlyo Found in all myocytes

o 8esponsible or repolari"ing the membrane at the end o the action

potentialo )n SA and AV nodal cells# it contributes to pacemaker acti+ity by

deacti+ating at the diastolic +oltageo Early outward :7 current ,A-type current

o $ protein-acti+ated :7 current

o : A!P current

- !he pacemaker current is mediated by a nonselecti+e cation channelo Pacemaker current

Found in SA and AV nodal cells and in purkinje fbers

.C6

•  !he channel underlying this current is a nonspecifc cation

channel• 8elated to the cyclic nucleotide-gated channels

• Conduct both : and 6a

Produces an inward# depolari"ing current as it slowly acti+ated at

the end o phase = Also contribute signifcantly to the phase 5 depolari"ation

- <i2erent cardiac tissues uni4uely combine ionic currents to produce

distincti+e action potentials

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- !he sinoatrial node is the primary pacemaker o the hearto  !he concept o pacemaker acti+ity

= intrinsic pacemaking tissues

• SA node

• AV node

Purkinje fbers Pacemaker acti+ity

• 8eers to the spontaneous time-dependent depolari"ation

o the cell membrane that leads to an action potential in

an otherwise 4uiescent cell SA node is the astest pacemaker

o Sinoatrial node

Found in the right atrium

 !he primary site o origin o the electrical signal in the

mammalian heart Smallest electrical region o the heart and constitutes the astest

normal pacemaker )ntrinsic rate o &' beats?min or aster

Stable oscillators

 !he interaction among three time-dependent and +oltage-gated

membrane currents control the intrinsic rhythmicity o the SA

node

• Calcium current

• :7 current

• Pacemaker current

 !he sum o a decreasing outward current ,:7 current and 9

inward currents ,Ca97 and Pacemaker current produces the

slow pacemaker depolari"ation associated with the SA nodeo Atrio+entricular node

%ocated just abo+e the atrio+entricular ring

 !he secondary site o origin o the electrical signal in the

mammalian heart  !he interaction among three time-dependent and +oltage-gated

membrane currents control the intrinsic rhythmicity o the SA

node

• Calcium current

• :7 current

• Pacemaker current

SA and AV nodes share many properties• Similar action potentials

• Pacemaker mechanisms

• <rug sensiti+ities

• Similarly slow conduction o action potentials

o Purkinje fbers

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/riginates at the AV node with the bundle o .is# splits to orm

the

• %et bundle branches

o Conducts the signal to the let +entricle

o <i+ides into two main branches

%et anterosuperior ascicle ,hemibundle %et posteroinerior ascicle

• 8ight bundle branches

o Conducts the signal to the right +entricle

.a+e slowest intrinsic pacemaker rate

• 9' beats?min or less

Considered as tertiary pacemakers

<epends on our time- and +oltage-dependent membrane

currents

• 6a7 current ,not present in SA and AV nodal cells

• Calcium current

•:7 current

• Pacemaker current

>a3imum diastolic potential is -@' mV

- Atrial and +entricular myocytes fre action potentials but do not ha+e

pacemaker acti+ityo Atrial muscle

Action potential spreads +ia a direct cell-to-cell pathway

<epends on three primary time- and +oltage-dependent

membrane currents

• 6a7 current

• Calcium current

• :7 current 6o normal spontaneous acti+ity in atrial muscle

.as our special conducting bundles

• 1achman0s bundle

o Also known as Anterior interatrial myocardial band

o )nteratrial# and conducts the cardiac action

potential rom the SA node to the let atrium

• = other intermodal pathways

o Anterior

o >iddle

o Posterior

o Appear to conduct the action potential rom the SAnode to the AV node

o Ventricular muscle

Ventricular acti+ation is completed in appro3imately ('' ms

Step 9 the septum depolari"es rom let to right

Step = the anteroseptal region depolari"es

Step 5 depolari"e bulk o +entricular myocardium# rom

endocardium to epicardium

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Step B depolari"e posterior portion o base o the let +entricle

•  !he last region to depolari"e is the posteriobasal region o 

the let +entrical Step & the +entricles are now depolari"ed

 !hree major time- and +oltage-gated membrane currents

6a7 current• Calcium current

• :7 current

6o pacemaker current

6o pacemaker acti+ity

8esting potential is -@' mV

E2ecti+e respiratory period

• Arises because the inward currents that are responsible

or acti+ation are largely inacti+ated by the membrane

depolari"ation

• Same as the absolute reractory period in ner+e and

skeletal muscle 8elati+e reractory period

• Ca97 current and 6a7 current begin to reco+er rom

inacti+ation- Acetylcholine and catecholamines modulate pacemaker acti+ity# conduction

+elocity# and contractilityo SA node can slow the fring rate o its pacemaker by three mechanisms

 !he steepness o the depolari"ation during phase 5 # thereby

lengthening the time necessary or Vm to reach threshold  !he ma3imum diastolic potential can become more negati+e

 !he threshold or the action potential can become more positi+e

o Acetylcholine Vagus ner+e

• Parasympathetic

• 8eleases acetylcholine unto SA and AV nodes and slows

intrinsic pacemaker acti+ity by = mechanismso Ach decreases pacemaker current in the SA node

reducing the steepness o the phase 5

depolari"ationo Ach open $)8: channels# increasing relati+e :7

conductance and making the ma3imum diastolic

potential o SA nodal cells more negati+eo Ach reduces Calcium current in the SA node#

thereby reducing the steepness o the phase 5

depolari"ation and also mo+ing the threshold to

more positi+e +alueso Catheloamines

8eleasing mostly norepinephrine and epinephrine

hich act through D(- adrenergic receptors

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Produce increase in heart rate by 9 mechanism

• Catecholamines increase pacemaker current in the nodal

cells# thereby increasing the steepness o the phase 5

depolari"ation

• Catercholamines increase Calcium current in all

myocardial cells !he electrocardiogram

- An electrocardiogram generally includes f+e wa+eso ;sed to measure the electrical acti+ity o the heart

o A recording o the small e3tracellular signals produced by the

mo+ement o action potentials through cardiac myocyteso Electrodes on the e3tremities generate the si3 limb leads

,three standard and three augmented

o Chest electrodes produce the si3 precordial leads

o %ead records the *uctuation in +oltage di2erence between positi+e and

negati+e electrodeso

a+es *uctuations in e3tracellular +oltage recorded by each lead P wa+e

• 8e*ects depolari"ation o the right and let atrial muscle

8S comple3

• 8epresents depolari"ation o +entricular muscle

 ! wa+e

• 8epresents repolari"ation o both +entricles

; wa+e

• 8are

• >ay re*ect repolari"ation o the papillary muscle

o  !he signal measure on an EC$ is a +ector

.as both a three-dimensional direction and a magnitude- A pair o electrocardiogram electrodes defnes a leado Frontal plane

<efned by the si3 limb leads

o  !rans+erse plane

<efned by the si3 precordial leads

o  !he torso and limbs are +iewed as an e4uilateral triangle

Eintho+en0s triangle

• /ne +erte3 on the groin

• 9 +ertices on the shoulder joints

• Electrical attachment to an arm is to shoulder joint

Electrical attachment to a leg is to groino 8ight leg used or electrical grounding

o = initial limb leads represent between two o the limb electrodes

%ead )

• Positi+e connection to let arm

• 6egati+e connection to right arm

• %ead defnes an a3is in the rontal plane at ' degrees

%ead ))

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• Positi+e to let leg

• 6egati+e to right arm

•  !his lead defnes an a3is in the rontal plane at &'

degrees %ead )))

•Positi+e to let leg

• 6egati+e to let arm

•  !his lead defnes an a3is in the rontal plane at (9'

degreeso = augmented unipolar limb leads compare one limb electrode to the

a+erage o the other two aV8

• Positi+e connection to right arm

• 6egati+e connection is electronically defned in the middle

o the heart

•  !he a3is defned by this limb lead in the rontal plane is

-(B' degrees• a

o Stands or augmented

• V

o  represent unipolar

aV%

• Positi+e to let arm

• 6egati+e is middle o the heart

•  !he a3is is defned by this limb lead in the rontal plane is

-=' degrees aVF

• Positi+e to let leg

• 6egati+e is middle o the heart

•  !he a3is defned by this limb lead in the rontal plane is

7G' degrees- !he precordial leads

o %ie in the trans+erse plane# perpendicular to the plane o the rontal

leadso Positi+e connection

/ne o si3 di2erent locations on the chest wall

o 6egati+e connection

Electronically defned in the middle o the heart by a+eraging

the three limb electrodeso V(

5th intercostal space to the right o the sternum

o V9

Fourth intercostal space to the let o the sternum

o V5

Fith intercostals space at the midcla+icular line

o V=

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.alway between V9 and V5

o V&

Fith intercostals space at the mida3illary line

o VB

.alway between V5 and V&

o Special leads that are used include

Esophageal leads

)ntracardiac leads

• ;sed to obtain a recording rom the .is-bundle- A simple two-cell model can e3plain how a simple EC$ can arise

o hen a lead is perpendicular to the wa+e o depolari"ation# the

measured de*ection on that lead is isoelectricCardiac arrhythmias

- Arrhythmiao Any change in cardiac rhythm rom the normal sinus rhythm

- 6ormal arrhythmiaso Sinus tachycardia

.eart rate aster than normal <ri+e by the sinus node

Seen in rightened or startled indi+iduals or during e3ercise

Can be pathologic

• Acute hyperthyroidism

o Sinus arrythmias

A substle change in heart rate with each respiratory cycle

)nspiration accelerates the heart rate

E3piration slow the heart rate

 !he loss o sinus arrhythmia can be a sign o A6S dysunction

• Seen in diabetes

- Conduction abnormalities are a major cause o arrhythmiaso Conduction disturbances can be partial or complete

o 9 major causes

<epolari"ation

Abnormal anatomy

• ol2-Parkinson-hite syndrome

o .a+e a bypass pathway called the bundle o :ent

o Partial ,or incomplete conduction block

= major types

• Slowed conduction

o  !he tissue conducts all the impulses# but more

slowly than normalo (st Hdegree AV block

8e*ects a slowing o conduction through the

AV node Appears as an unusually long P8 inter+al

• )ntermittent block

o  !he tissues conducts some impulses but not others

o %eads to 9nd-degree AV block

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>obit" type ) block ,enckebach block

• P8 inter+al gradually lengthens orm

one cycle to the ne3t until the AV node

ails completely# skipping the

+entricular depolari"ation

>obit" type )) block•  !he P8 inter+al is constant rom beat

to beat

• 1ut e+ery nth +entricular

depolari"ation is missing

• E+ery second 8S is dropped ,9(

block 8ate dependent block

• 8e*ects pathology oten seen in the

large branches o the .is-Purkinje fber

system 1undle branch block

• Appears in EC$ as an intermittently

 wide 8S comple3

• ;nidirectional block

o Complete conduction block

Also called as =rd-degree AV block

6o impulse conduct through the a2ected area in either direction

AV dissociation

• AV nodal block electrically se+ers the atria and +entricles

• Each o which beat under control o its own pacemakers

• /n EC$# appears as regularly space P wa+e# and as

irregularly space 8S and ! wa+es that ha+e a low

re4uency and no f3ed relationship to the P wa+eso 8e-entry

8e-entrant e3citation or circus mo+ement

/ccurs when a wa+e o depolari"ation tra+els in an endless

circle = re4uirements

• Close conduction loop

• 8egion o unidirectional block

• A suIciently slow conduction o action potentials around

the loop ;nidirectional block

• A type o partial conduction block in which impulses tra+el

in one direction but not in the opposite one

• Arise as a result o a local depolari"ation or maybe due to

pathologic changes in unctional anatomy

• 8e-entry e3citation may be responsible or

o Atrial and +entricular tachycardia

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o Atrial and +entricular fbrillation and

o >any other arrhythmias

o Accessory conduction pathways

ol2-Parkinson-hite syndrome

• Pro+ides short circuit around the delay in the AV node

Early depolari"ation# or pre-e3citation appears as a smallpositi+e delta wa+e at the beginning o the 8S comple3

• )nter+al between the P wa+e and the 8S comple3 is

shortened

• >ay be associated with supra+entricular tachycardia

o  9 most common

Atrial fbrillation

Paro3ysmal supra+entricular tachycardia

• E3ceeding (B' beats per minute

o Fibrillation

Atrial fbrillation

Commonly ound in elderly patientso Sometimes with mitral +al+e or coronary artery

disease

• 8esulting in the irregular appearance o 8S comple3es

without any detectable P wa+eso 1aseline appears straight or may show small rapid

*uctuation Ventricular fbrillation

- Altered automaticity can originate rom the sinus node or rom an ectopic

locus