Mod3NotesFall09Carolyn.doc

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RNSG 2432 ONLINE NOTESModule 3: Cardiac Rhythm Disorders

Carolyn Morse Jacobs, RN, MSN, ONC

Etiology/Pathophysiology of Cardiac Rhythm isord!rs

1. Normal conduction system of the heart as it relates to dysrhythmia !e"is #.

$%1&$%' ( )%'&)%3* +i 3'&- ( 3'&/ 0 no" normal conduction of heartbeat& S2, 2, 4undle of 5is etc & ho" each com#onent is re#resented on 67

Net"or8 s#eciali9ed cells and conduction #ath"ays that initiate and s#readelectrical im#ulses causin heart to beat

a. 0Cardiac muscle: uniue& enerate electrical im#ulse and contractioninde#endent of ner;ous system

b. Cardiac muscle: uniue& enerate electrical im#ulse andcontraction inde#endent of ner;ous system

c. 2bnormal cardiac rhythms< dysrhythmias'. =ro#erties of cardiac cells >able 3&1 #. )%3/

a. 2utomaticity"# s#ontaneous* 0S2 node hihest le;el automaticity

2# stimulated by ner;ous system ;ia ;aus ner;e3# sym#athetic increases rate of firin* #arasym#athetic decreases

rate4# 0cardiac cells in a$y#art of heart #acema8er cells or non&

#acema8er/ cells can ta8e on role of a #acema8er& bein

eneratin e?traneous im#ulses, called !ctopics% &'($y

cardiac m)scl! ca$ g!$!rat! a$ !l!ctrical imp)ls! a$dco$tractio$ i$d!p!$d!$t of $!r*o)s syst!m+#

b. 6?citability& ability of myocardial cells to res#ond to stimuli eneratedby #acema8er cells action #otential/&be electrically stimulated

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c. Conducti;ity& ability to transmit im#ulse from cell to cell, orderlymanner

d. Contractility&ability of myocardial fibers to shorten in res#onse tostimulus* mechanical

e. Refractory absolute ( relati;e/ =. )%&)%$3. Cardiac (ctio$ Pot!$tial+i 3&1 #. )%3/ 0See 3 !ead 67 ;ideo 44

a. Measured in milli;olts m/, ;ertical a?is 67 #a#er, time sec/,hori9ontal a?is

b. 06lectrical acti;ity < "a;eforms on 6C7 stri#s due to ion mo;ement

across cell membranes stimulatin muscle contraction

c. =hases"# R!sti$g stat!,polari-!d stat!

a/ =ositi;e and neati;e ions alin on either side of cellmembrane* Na hih, lo"* relati;ely neati;e chare

"ithin cell* #ositi;e chare e?tracellularlyb/ Neati;e restin membrane #otential

2# Co$tractio$, d!polari-atio$0im#ortant& consider ho" meds"or8 to affect heart rhythm and #um#in action/

a/ Restin cell stimulated by chare

1/ Na ions enter cell throuh fast sodium channels'/ Calcium enter cells ;ia slo" calcium&sodium

channels

3/ Membrane less #ermeable to ions%/ Membrane #otential chane to slihtly #ositi;e

at @'A & @3A m

(5) Dysrhythmic meds as era#amil Calan,Bso#tin/ control dysrhythmia hat dru class*

ho" te?t #. )-/3# Thr!shold pot!$tial

a/ Cell more #ositi;eoint reached "hen action #otentialenerated

b/ Cause chemical reaction of Ca "ithin cell(1) 2ctin and myosin filaments slide toether&

#roduce cardiac muscle contraction

(2) Once myocardium com#letely de#olari9ed,re#olari9ation bein

4# R!polari-atio$#rotect heart muscle from s#asm, tetany/

a/ Cell return to restin, #olari9ed stateb/ +ast sodium channels close abru#tly

c/ Cell reains neati;e chare ra#id re#olari9ation/d/ Muscle contraction #roloned&slo" calcium&sodium

channels remain o#en #lateau #hase/e/ Once closed, sodiumotassium #um# restore ion

concentration & cell membrane #olari9ed aain.# R!fractory p!riod >ab 3.3 #. )%$/

a/ Myocardial cells resisti;e to stimulation* 00dysrhythmiastriered durin relati;e refractory and absolute

refractory #eriods1/ 2bsolute refractory #eriod: no de#olari9ation

can occur& from E "a;e until middle of > "a;e

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'/ Relati;e refractory #eriod: reater than normalstimulus needed for de#olari9ation

contraction/* oes throuh 'nd half > "a;e

%. Ner;ous System Control

a. 2utonomic

"# Rate of im#ulse formation2# S#eed of conduction3# Strenth of contraction

b. =arasym#athetic ner;ous system: 00aus ner;e

1) Decreases rate

2) Slo"s im#ulse conduction3) Decreases force of contraction

c. Sym#athetic ner;ous system1/ Bncreases rate'/ Bncreases force of contraction

-. 6tioloy of ysrhythmiaa. Causes ;ary* treatment based u#on causati;e factors

b. Cardiac cells either contractile cells influencin #um#in action or#acema8er cells influencin electrical acti;ity of heart

c. +actors that trier"# 5y#o?ia

2# Structural chanes atherosclerosis, atrial fibrillation, chanesafter MB etc/

3# Electrolyte imbalanceses#ecially altered0#otassium,0calcium,0manesium, sodium le;els/

4# CNS stimulation as caffeine, nicotine, cocaine*.# !ifestyles beha;iors

# Medications 0dio?in, recall thera#eutic le;els/, beta bloc8ers&end in FlolG, drus that slo" do"n or drus that s#eed&u# heart

rate.d. Bdentify, e;aluate, treat dysrhythmia&determined by client res#onse

. Sinificance of dysrhythmias&a. Dec. cardiac out#ut and cerebralH;ascular #erfusion

b. Normal Sinus Rhythm& NSR/, atria fill, stretch ;entricles "ith about3AI more blood* 0atrial 1ic1G occurs* im#ro;es contractility of;entricles* increases cardiac out#ut. ie& if im#ulse start in 2 node or

;entricles, atrial and ;entricular contraction not coordinated* Fatrial8ic8G is lost& cardiac out#ut falls.

RNSG 2432 3

6cto#ic stimuli occurrin durinrefractory #eriod e;en by

cardio;ersion/ allo" re&entryim#ulses&cause #remature beats,abnormal conduction #, )%$


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I$t!rpr!tatio$ of Cardiac Rhythms

1. 6C7& 7ra#hic recordin electrical acti;ity of heart'. 1'&!ead 6C7 +i 3 '(3 #. )%%/ 0Standard 1'&lead 6C7* simultaneous

recordin of limb leads and #recordial leads ;ie"s of electricalconduction/

a. Si l!adsmeasure electrical forces in frontal #lane Lim l!ads:bi#olar leads B, BB, BBB, and uni#olar leads or aumented limb leads:aR, a! and a+/

b. Si l!ads1 '3%-/ measure electrical forces in hori9ontal

#lane3. !ead =lacement& 3 leadH- lead +i 3.% #. )%-/ ( access lin8 &>heoretical

4asis for 67 ( 3 !ead 67 ;ideos&Bntroductiona. 6ach lead has #ositi;e, neati;e and round electrode

b. 6ach lead loo8s at a different area of heart.c. Can be dianostic recall MB ie S> ele;ation/

d. 4est& lead BB and MC! modified chest lead/ or 1 leads& lead BB easy tosee = "a;es. MC! or 1 easy to see ;entricular rhythms. ;ie" each

com#onent of 67. !ead BB& use "ith 3 !ead system ref 3 !ead 67

;ideo/e. Bf im#ulse oes to"ard #ositi;e electrode&com#le? #ositi;ely deflected

or u#riht

f. Bf im#ulse oes a"ay from #ositi;e electrode&com#le? neati;elydeflected or oes do"n form baseline

2ssess lin8&>heoretical 4asis for 67 ( 3 !ead 67 ;ideos& Bntroduction 0ideos

located "ith Module 3 in 4lac8board* ui9 items also in 4lac8board/ 0as8 if difficultyin locatin

EG Sta$dard L!ads 'from Th!or!tical 5asis for EC#

>hese leads& usually desinated as B, BB and BBB.

1. 4i#olar i.e., detect a chane in electric #otential bet"een t"o #oints/ anddetect an electrical #otential chane in frontal #lane.

!ead B& bet"een riht arm and left arm electrodes,& left arm bein #ositi;e.

!ead BB is bet"een riht arm and left le electrodes, leftle bein #ositi;e.

!ead BBBis bet"een left arm and left le electrodes, leftle aain bein #ositi;e.

2 diarammatic re#resentation of these three leads&

termed 6intho;enKs trianle sho"n in blue belo"/, afterDutch doctor "ho first described the relationshi#. Central

source of electrical #otential in trianle is heart.

RNSG 2432 5
http://www.technion.ac.il/~eilamp/EKGtheory.htmlhttp://www.technion.ac.il/~eilamp/EKGtheory.htmlhttp://www.technion.ac.il/~eilamp/EKGtheory.htmlhttp://www.technion.ac.il/~eilamp/EKGtheory.htmlhttp://www.technion.ac.il/~eilamp/EKGtheory.htmlhttp://www.technion.ac.il/~eilamp/EKGtheory.html


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EG ()gm!$t!d Lim L!ads

1. Same three leads that form standard leads also formthe three uni#olar leads& 8no"n as aumented

leads: aRriht arm/, a!left arm/ and a+left le/* also record chane in electric #otential

in frontal #lane.

'. Lni#olar leads& measure electric #otential at one #oint"ith res#ect to a null #oint one "hich doesnKt reister any

sinificant ;ariation in electric #otential durin contractionof heart/.

3. Null #oint& obtained for each lead by addin #otentialfrom the other t"o leads. +or e?am#le, in lead aR,

electric #otential of riht arm is com#ared to a null #oint"hich is obtained by addin toether the #otential of lead

a! and lead a+.

EG Pr!cordial L!ads

1. Si? uni#olar leads, each in different #osition on chest'. Record electric #otential chanes in heart in a cross sectional #lane

3. 6ach lead records electrical ;ariations that occur directly under electrode.

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(ss!ssm!$t of Cardiac Rhythm

1. &(ss!ss cli!$t first& "hat res#onse to dysrhythmia connected to monitor/'. 67 stri# reconition: "a;eforms& reflect direction of electrical flo" "hat

seen on 67 stri#/a. =ositi;e u#"ard/ "a;eform is to"ard #ositi;e electrode

b. Neati;e do"n"ard/ "a;eform is a"ay from #ositi;e electrodec. 4i#hasic both #ositi;e and neati;e/ "a;eform sho"s #er#endicular

to #ositi;e #ole

d. Bsoelectric line straiht line/ absence of electrical acti;ity

3. Bdentify com#onents 67 0electrical #recedes mechanical/ 0>ab 3&'.)%$/

0Refer to #. )%$ >able 3&'& alues may ;ary slihtly "ith different sources&use te?t

boo8 for test #ur#osesa. = "a;e: atrial de#olari9ation and contraction< F#G , u#riht A.A&

A.1'/b. =R inter;al&time for sinus im#ulse to tra;el from S2 node to 2 node

and into bundle branches beinnin of = "a;e to beinnin of ERScom#le?/ A.1' & A.'A seconds

c. ERS Com#le?&;entricular de#olari9ation and contraction* transmissionof im#ulse throuh ;entricular conduction system 0A.A% A.1'/

secondsd. S> sement&beinnin of ;entricular re#olari9ation* end of ERS

com#le? to beinnin of > "a;e* isoelectric* 0Recall sinificance ofele;ated S> sement "ith MB A.1'/

e. > "a;e& ;entricular re#olari9ation* smooth and round, 1A mm tall*

same direction as ERS com#le?* abnormalities due to myocardial

inury or ischemia, electrolyte imbalances. 0Daner area if Fshoc8G on> "a;e

f. E> inter;al& total time ;entricular de#olari9ation and re#olari9ation*

beinnin of ERS com#le? to end of > "a;e* #roloned E>: #roloned

relati;e refractory #eriod < reater ris8 for dysrhythmias* shortenedE>: due to medications or electrolyte imbalance* 0measure E> inter;al

#rior to admin. some meds A.3% A.%3 seconds/. L "a;e& re#olari9ation of terminal =ur8ine fibers* same direction as >

"a;e* seen "ith hy#o8alemia contact healthcare #ro;ider/

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%. Calc)lat! rat! &$o6 ho6 to do this+#. )%3&)3* fi. 3.-&3.P/

a. 6C7 "a;eforms recorded on #a#er& mar8in re#resentati;e of time8no" this/

b. 6ach small bo? < A.A% seconds sec/* one lare bo? - small bo?es/ able 3.$ #. )%P/ 0ey reference

Si$)s Rhythms ,electrical stimulus oriinates at S2 nodes

"% Si$)s 5radycardia

a. Characteristics: Sinus node fires A b#m* Normal conduction* rate

less than A b#m* rhythm reular* =: ERS: 1:1* =R inter;al: A:1' to .'A sec.* ERS com#le?: A.A% to A.1' sec

b. Clinical 2ssociationsHsinificance: normal in aerobically trained athletesand durin slee#* inc. ;aal #arasym#athetic/ acti;ity* inury or

ischemia to sinus node* inferior "all damae "ith acute MB* increasedintracranial #ressure* medications such as beta&bloc8ers and dio?in*

hy#othermia* acidosis* res#onse to carotid sinus massaec. 0>reatment: determine cause* treat if sym#tomatic, can lead to

decreased CO* use &atropi$! to i$cr!as! rat! or )s! pac!ma1!r

2% Si$)s Tachycardia

a. Descri#tion: normal conduction* e?ce#t rate reater than 1AA b#m

b. Clinical associationsHcauses: sym#athetic ner;ous system stimulation*bloc8ae ;aal acti;ity* body res#onse to #hysioloical stressors:an?iety, #ain, caffeine, hy#o;olemia, MB, heart failure, fe;er, etc

c. Clinical Manifestations: #al#itations* shortness of breath* di99iness,lead to inc. myocardial o?yen consum#tion may lead to anina

d. >reatment: eliminate cause as caffeine, adm drus to reduce heart

rate as &2dreneric bloc8ers and myocardial o?yen consum#tion,

anti#yretics to treat fe;er, analesics to treat #ain. Note&2denosine2denocard/ B (Hor bata bloc8ers may be indicated. see #. )-A/

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3% Si$)s (rrhythmia

a. Descri#tion: normal conduction, ho"e;er irreular rhythm& rate A&1AA, increases "ith ins#iration, decreases "ith e?#iration* =, ERS,>

"a;e normalb. Clinical associationHcauses& normal in children, dru effect as MSA%/,

MB

c. >reatment& none

S)pra*!$tric)lar dysrhythmias 'atrial arrythmias/ Can be serious: atriaco$tri)t!s 2.,3=ase, dec. 2 conduction s#eed/, amiodarone Cardarone/ Class BBB #otassium

channel bloc8er/, dofetilide >i8osin/ #otassium channel bloc8er/, ;era#amil 0Calan/calcium channel bloc8ers 0 no" these

4% Pr!mat)r! (trial Co$tractio$

a. Descri#tion: atria is pac!ma1!r: P>?RS> ">"* ecto#ic atrial beatoccurs earlier than ne?t e?#ected sinus beat* = "a;e&abnormallysha#ed, or = "a;e lost in ERS* =R inter;al shorter* ERS normal A.A

to A.1'/* ha;e a non&com#ensatory #ause early beat affects = "a;ea##earance/

b. Clinical associations&due to emotional stress, caffeine, tobacco,alcohol, hy#o?ia, electrolyte imbalances, CO=D, ;al;ular disease

c. Clinical sinificance& Bsolated =2Cs &not sinificant if healthy hearts&heart disease may reuired trt.

RNSG 2432 11


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d. >reatment&de#ends on sym#toms: &2dreneric bloc8ers to dec. =2Cs,

reduce or eliminate caffeine See #. )- >ab 3&)/

.% S)pra*!$tric)lar Tachycardia 'S@T#/Paroysmal S)pra*!$tric)lar

Tachycardia 'PS@T#, hy im#ortant Tdecreases cardiac out#ut

a. Descri#tion: oriinates in ecto#ic focus any"here abo;e bifurcation ofbundle of 5is&Rate 1-A&'-A* atria is #acema8er, may not see = "a;es

due to ra#id rate ecto#ic foci abo;e ;entricles/* Run of re#eated

#remature beats< usually =2Csb. Descri#tion contaro?ysmal& abru#t onset and termination* some

deree of 2 bloc8 may be #resent* occur in #resence of olff&=ar8inson&hite =/ syndrome

c. Clinical 2ssociations& initiated by a 0r!,!$tryA loopin or around 2node* #reci#itated by sym#athetic ner;ous system stimulation and

stressors includin fe;er, se#sis, hy#erthyroidism* heart diseasesincludin C5D, diitalis to?icity, myocardial infarction, rheumatic heart

disease, myocarditis or acute #ericarditis* cor #ulmonale, olff&=ar8inson&hite syndrome =/

d. Clinical Sinificance: #al#itations, Fracin heartG, an?iety, di99iness,dys#nea, aninal #ain, e?treme fatiue, dia#horesis, #roloned heart

rate abo;e 1)A lead to decreased CO

e. >reatment:2# &@agal stim)latio$> @alsal*a, couhin* I@ ad!$osi$!

ho" does it "or8/

3# Bf ;aal maneu;ers andHor dru thera#y ineffecti;e andHor#atient hemodynamically unstable, DC cardio;ersion needed

4# &(d!$oci$ '(d!$ocard#I@ stops h!art,& allo"s S2 node toreset brief asystole/* similar to electrical cardio;ersion* short

term use only* i;e only in BCL, 6R, monitored situations.tem#orary/* also dio?in, ;era#amil, inderal, cardia9em

ti8osyn to #re;ent recurrance.# 0=S> recurs in olff&=ar8inson&hite syndrome, may need

radiofreuency catheter ablation of accessory #ath"ay

12 RNSG 2432
http://en.wikipedia.org/wiki/Wolff-Parkinson-White_syndromehttp://en.wikipedia.org/wiki/Wolff-Parkinson-White_syndrome


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% (trial Bl)tt!r

a. Descri#tion: origi$at!s i$ atria from si$gl! !ctopic foc)s* ra#id,

reular atrial rhythm due to i$tra,atrial r!,!$try m!cha$ism* atrialrate '%A&3AA, ;entricular rate de#ends u#on deree of 2 bloc8,

usually 1-A 4=M* = "a;es Fsa"& toothedG, ratio ':1, 3:1, %&1*flutter "a;es* =R inter;al not measured

b. Clinical associations: C2D, hy#ertension, mitral ;al;e disorders,#ulmonary embolus, chronic lun disease, cardiomyo#athy,

hy#erthyroidism, ;al;ular diseases, =* due to sym#athetic ner;ousstimulation

c. Cli$ical Sig$ifica$c!:1/ 5ih ;entricular rates T1AA/ and loss of the atrial F8ic8G &

decrease CO ( #reci#itate 5+, anina'/ Ris8 for stro8e &ris8 of thrombus formation in the atria 0not

as bad as "ith atrial fibrillation0d. >reatment: =rimary oal& slo6 *!$tric)lar r!spo$s!by increasin

2 bloc8

1/ 7!ds to slo6 *!$tric)lar r!spo$s! as &adreneric

bloc8ers or calcium channel bloc8er follo"ed by uinidine,

#rocainamide, flecainide or amiodarone. 0>hin8 about "hy,ho" these meds "or8

'/ Sy$chro$i-!d cardio*!rsio$& con;ert the atrial flutter to

sinus rhythm emerently and electi;ely* maintain rhythm"ith antidysrhymic meds

3/ 2lation to obliterate abnormal conduction #ath"ays

% &(trial Birillatio$a. >otal disorani9ation atrial electrical acti;ity due to multi#le ecto#ic foci

lead to loss of effecti;e atrial contraction* no = "a;es, 0garag!

as!li$!A:atrial rate 3AA&AA* too ra#id to count* ;entricular rate"


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b. Clinical associations: underlyin heart disease, rheumatic heart disease

heart disease, C2D, 5>N cardiomyo#athy, thyroto?icosis, caffeine use,5+, #ercarditis, Q1 arrhythmia in elderly

c. Clinical Significance: lead to d!cr!as! i$ COdue to ineffecti;e

atrial contractions loss of atrial 8ic8 and ra#id ;entricular res#onseRR/*

1/ &Thromi form in atria due to blood stasis'/ &Emol)sde;elo# and tra;el to brain cause 0stro8e

d. >reatment: 7oals&decrease ;entricular res#onse* #re;ent emboli1/ &Pr!*!$t lood clots,anti#latelet, anticoaulation* reduce

ris8 of stro8e0'/ Co$*!rt to si$)s rhythm or g!t to co$troll!d rat!

of"he

scar tissue directs electric sinals throuh a controlled #ath, orma9e, to ;entricles.

D% F)$ctio$al ysrhythmiasa. Descri#tion: 02 node& #acema8er* S2 node failed to fire or im#ulse

bloc8ed at 2 node* rate& %A&A 4=M, can ha;e unctional tachycardiaor A&1%A 4=M* = "a;e #atterns ;ary, may be absent or #recede ERS

in;erted in BB, BBB and 2+, or hidden in ERS or follo" ERS/* =Rinter;al is absent or hidden .1A* ERS normal at A.A&A.1A sec

14 RNSG 2432
http://www.webmd.com/heart-disease/atrial-fibrillation/maze-procedure-for-atrial-fibrillationhttp://www.webmd.com/hw-popup/atrial-fibrillationhttp://www.webmd.com/heart-disease/atrial-fibrillation/maze-procedure-for-atrial-fibrillationhttp://www.webmd.com/hw-popup/atrial-fibrillation


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b. Clinical 2ssociationsHcauses: dru to?icity Dio?in, am#hetamines,caffeine, nicotine/, hy#er8alemia, increased ;aal tone, cardiac

causes* hy#o?ia, hy#o?ia, ischemia, inferior MB, electrolyte imbalancesc. Clinical Sinificance

1/ Ser;e as safety mechanism "hen S2 node has not beeneffecti;e

'/ 6sca#e rhythms should not be su##ressed3/ Bf rhythms ra#id, may result in reduction of CO and 5+

d. >reatment often none reuired/"# If symptomatic 'slo6 rat!#, atropi$!

2# 2ccelerated unctional rhythm and unctional tachycardiacaused by dio?in to?icity&, hold dio?in

3# &2dreneric bloc8ers, calcium channel bloc8ers, amiodarone&

for control of unctional tachycardia not caused by dio?in

to?icity4# No DC cardio;ersion

(trio*!$tric)lar '(@# Co$d)ctio$ 5loc1s> Delayed or bloc8ed transmission ofsinus im#ulse throuh 2 node due to tissue inury or disease, increased ;aal tone,

dru effects

% Birst,!gr!! (@ 5loc1a. Descri#tion& 0E*!ry imp)ls! co$d)ct!d to *!$tricl!s, d)ratio$

(@ co$d)ctio$ prolo$g!d* transmission throuh (@ $od! d!lay!d.1/ ERS normal, = "a;e normal* rate: A&1AA 4=M* slo"ed

transmission throuh 2 node* =R inter;al is T A.'A

b. Clinical 2ssociations: MB, C2D, Rheumatic fe;er, hy#erthyroidism,

;aal stimulation, drus as Dio?in, &adreneric bloc8ers, calcium

channel bloc8ers, flecainide li8e #ro#afenone&Rythmol class 1C/

&Hhy th!s! dr)gs implicat!d

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c. Clinical Sinificance1/ Lsually asym#tomatic

'/ May be pr!c)rsor to high!r d!gr!!s of (@ loc1d. >reatment

1) Chec8 medications 0 Bf on diitalis or beta bloc8ers, holdmeds

2) Continue to monitor

""J 4>"

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b. Clinical 2ssociations* Rheumatic heart disease, C2D, 2nterior MB,Diitalis to?icity

c. Clinical Sinificance* &Progr!ss to third,d!gr!! (@ loc1*associated "ith a #oor #ronosis* reduced 5R result in dec. CO "ith

hy#otension and myocardial ischemia

d. >reatment: If symptomatice.., hy#otension, anina/ before#ermanent #acema8er, use tem#orary trans;enous or transcutaneous#acema8er* 7ay try atropi$! li8ely not to be effecti;e# J Is)pr!l

'6hy th!s! dr)gs #: lo$g t!rm,&P!rma$!$t pac!ma1!r

"2% &Third,!gr!! (@ !art 5loc1 'Compl!t! !art 5loc1#

a% Descri#tion: Borm of (@ dissociatio$, &$o imp)ls!s from atriaco$d)ct!dto ;entricles* atria stimulated, contract inde#endently of

;entricles

1/ entricular rhythm& Fesca#eG rhythm'/ 6cto#ic #acema8er &abo;e or belo" bifurcation of bundle of

5is3) 2tria and ;entricles beat inde#endently se#arate rates for

each/* rhythm from unctional fibers rate %A A 4=M/ or

;entricular 3A 4=M/* No PR i$t!r*al: 6id! ?RS

RNSG 2432 17
http://en.wikipedia.org/wiki/Artificial_pacemakerhttp://en.wikipedia.org/wiki/Artificial_pacemaker


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% Clinical 2ssociations: Se;ere heart disease: C2D, MB, myocarditis,

cardiomyo#athy* Systemic diseases: 2myloidosis, scleroderma* Drus:

Dio?in, &adreneric bloc8ers, calcium channel bloc8ers

c% Clinical Sinificance: fatiue, SO4, faintin* Sy$cop!from se;erebradycardia or e;en #eriods of asystole: if )$tr!at!d ,d!cr!as!d

cardiac o)tp)t a$d shoc1d% >reatment:

1) &Tra$sc)ta$!o)s pac!ma1!r )$til a p!rma$!$tpac!ma1!r

2) Drus e.., atro#ine, e#ine#hrine/: >em#orary &increase 5Rand su##ort 4= until tem#orary #acin is initiated then

#ermanent

3) =ermanent #acema8er reuired

&@ENTRICML(R SRT7I(S 'origi$at! i$ *!$tricl!s: most s!rio)s+#,Disru#tion of ;entricular rhythm& s!rio)s im#act cardiac out#ut and tissue

#erfusion. 6C7 Characteristics of ;entricular rhythms: Wide and bizarre QRS

compl! ' sement, > "a;e deflected in o##osite direction from ERS

com#le?

"3% &Pr!mat)r! @!$tric)lar Co$tractio$s '&need to recognize)

a% Descri#tion: 0Co$tractio$ origi$ati$g i$ !ctopic foc)s of*!$tricl!s% Pr!mat)r! occ)rr!$c! of a 6id! a$d distort!dJ 6id!

i-arr! ?RS compl! 'ri#let or sal;o: 3 =Cs in a ro"

4ieminy: =C e;ery other beat>rieminy: =C e;ery third beat

Lnifocal =Cs: arise from one site* all =Cs loo8 sameMultifocal =Cs: from different ecto#ic sites all =C s

loo8 different arise from different foci

2) Rate ;aries, rhythm irreular, =C interru#t underlyinrhythm* follo"ed by com#ensatory #ause* No = "a;e before

=C* no =R inter;al

3/ Due to enhanced automaticity or a re&entry #henomenon

18 RNSG 2432


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% Cli$ical (ssociatio$s: Stimulants: Caffeine, alcohol, nicotine,amino#hylline, e#ine#hrine, iso#roterenol, Dio?in, electrolyte

imbalances, hy#o?ia, fe;er, disease states: MB, mitral ;al;e #rola#se,

5+, C2Dc% Clinical Sinificance: normal heart, usually benin1/ 5eart disease, =Cs may decrease CO ( #reci#itate anina

and 5+* must monitor #atient res#onse to =Cs'/ =Cs often do not enerate sufficient ;entricular contraction

to result in #eri#heral #ulse3/ 2#ical&radial #ulse rate assess to determine #ulse deficits

%/ Re#resents ;entricular irritability-/ May occur after lysis of coronary artery clot "ith thrombolytic

thera#y in acute MBUre#erfusion dysrhythmias and after#laue reduction "ith #ercutaneous coronary inter;ention

/ 0#ost MB PAI de;elo# =Cre#resent ;entricular irritability&

lead to lethal dysrhythmias @TJ @Bi gr!at!st ris1 of

d!ath+# & &&'R o$ T# ph!$om!$o$ 'P@Cs falli$g o$ T6a*!K%l!ad to fatal *!$tric)lar firillatio$+

d% Tr!atm!$t, as!d )po$ ca)s!1/ O?yen thera#y for hy#o?ia

'/ 6lectrolyte re#lacement

3/ r)gs>Class BB*&2dreneric bloc8ers as meta#rolol/* Class

I(/I5,sodi)m cha$$!l loc1!r& !idocaine, #rocainamide*#henytoin Dilantin#, "stli$! for *!$tric)lar: Class III

potassi)m Cha$$!l 5loc1!r& amiodarone/&1stline for

RNSG 2432 19


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;entricular 0Must treat if reater than - =C a minute, runs of=C, multifocal =Cs See #. )- >ab 3&) 2ntidysrhythmic

meds%/ (latio$

"4% @!$tric)lar Tachycardia '@TJ @Tach#

a. Descri#tion: R)$ of thr!! or mor! P@Cs:monomor#hic,#olymor#hic, sustained, and non&sustained* life&threatenin due to

decreased CO* 00d!t!riorat! to *!$tric)lar firillatio$

1/ ra#id ;entricular rhythm of 3 or more =Cs* Rate T 1AA&'-A"ith reular rhythm* no = "a;e, ERS T.1'* "ide and bi9arre*

may occur in short bursts, runs or T 3A seconds.'/ due to re&entry #henomenon

b. Clinical 2ssociationsHcauses: electrolyte imbalance, cardiomyo#athy,

mitral ;al;e #rola#se, lon E> syndrome, diitalis to?icity, MB, dito?icity, mechanical irritability, dysfunctional F#acema8erG* MB most

common factor

c. Cli$ical Sig$ifica$c!, @T Q 0stal!A 'pati!$t has p)ls!# or0)$stal!A 'pati!$t p)ls!l!ss/

1/ S)stai$!d @T> s!*!r! d!cr!as! CO, se;ere hy#otension,"ea8 or non& #al#able #ulse, loss of consciousness,

#ulmonary edema, decreased cerebral blood flo", ;entricular

fibrillation, cardiac arrest.'/ >reatment must be ra#id, "ill recur

d% Tr!atm!$t1/ =reci#itatin causes &identify and treat e.., hy#o?ia/

'/ Monomor#hic > anda/ 5emodynamically stable e.., @ #ulse/ @ #reser;ed !

left ;entricular/ function> gi*! I@ procai$amid!JsotalolJ amiodaro$!J or lidocai$!

b/ 5emodynamically unstable or #oor ! function: gi*! I@amiodaro$! or lidocai$! follo6!d y cardio*!rsio$

3/ =olymor#hic > "ith a normal baseline E> inter;al: &

2dreneric bloc8ers, lidocaine, amiodarone, #rocainamide, or

sotalol* cardio;ersion used if dru thera#y ineffecti;e%/ =olymor#hic > "ith a #roloned baseline E> inter;al: B

manesium, iso#roterenol, #henytoin, lidocaine, or

20 RNSG 2432
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antitachycardia #acin: stop dr)gs that prolo$g th! ?Tinter;al* cardio;ersion if rhythm does not con;ert. >orsades

de #ointes, #. )-- 3&1)/-/ &@T 6itho)t p)ls!,lif!,thr!at!$i$g sit)atio$ '$o$,

r!spo$si*!/a# Cardiop)lmo$ary r!s)scitatio$ 'CPR# a$d rapid

d!firillatio$# Epi$!phri$! if d!firillatio$ )$s)cc!ssf)l

".% @!$tric)lar Birillatio$& @Bi#Se;ere deranement of heart rhythm*

6C7 sho"s irreular undulations of ;aryin contour and am#litude& noeffecti;e contraction or CO occurs

a% Descri#tion: e?tremely ra#id, chaotic rhythm & ;entricles ui;er, do notcontract* 0cardiac arrest and death result "ithin % minutes if rhythm

not terminated* %AA&1AAA beats #er minutetoo ra#id to count

1) 7arbae baseline: $o P 6a*!sJ $o ?RSSJ NO cardiaco)tp)t

% Clinical 2ssociations: 2cute MB, C2D, cardiomyo#athy, may occurdurin cardiac #acin or cardiac catheteri9ation, "ith coronary

re#erfusion after fibrinolytic thera#y, accidental electrical shoc8,hy#er8alemia, hy#o?ia, acidosis, dru to?icity

c% Clinical Sinificance: )$r!spo$si*!J p)ls!l!ssJ ap$!ic stat!J)$tr!at!dd!ath

d% >reatment:

1/ COE sit)atio$,Bmmediate initiation of C=R and ad;ancedcardiac life su##ort 2C!S/ measures "ith immediate use ofdefibrillation and definiti;e dru thera#y

&ca$$ot cardio*!rtK$o rhythm to cardio*!rt

"% (systol!, total absence of ;entricular electrical acti;ity, no ;entricularcontraction CO/ occurs& no de#olari9ation

RNSG 2432 21


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a. Descri#tion: No electrical conductionH no ;entricular acti;ity* C2RDB2Carrest, death* no rate* no F#G "a;e, or e;en if F#G "a;e, no ;entricular

res#onse* no ERS, no conduction* no rhythm

b. Cli$ical associatio$: most commonly after termination of atrial, 2

unctional or ;entricular tachycardias* usually insinificant in those

cases 0adenosinewas used to stopthese abnormal rhythms/1/ aysystole of loner duration in #resence of acute MB and C2D

freuently fatal'/ ad;anced cardiac disease, se;ere cardiac conduction system

disturbance

3/ end&stae 5+c. Clinical sinificance: unres#onsi;e, #ulseless, and a#neic state

1/ #ronosis for asystole& e?tremely #oord. >reatment

1) &CPR 6ith i$itiatio$ of (CLS m!as)r!s '!%g%J i$t)atio$Jtra$sc)ta$!o)s paci$gJ a$d I@ th!rapy 6ith

!pi$!phri$! a$d atropi$!#

"% EG cha$g!s r!lat!d to (c)t! Coro$ary Sy$drom! CS #. )1 +i3.'), 'P, 3A and >ab. 3.13/ 0Re;ie" #re;ious notes n MB

a. 6C7 chanes in res#onse to ischemia, inury, or infarction ofmyocardial cells

b. Chanes in leads that face area of in;ol;ementc. Reci#rocal o##osite/ 6C7 chanes often seen in leads facin o##osite

area in;ol;edd. =attern of 6C7 chanes& information on coronary artery in;ol;ed in

2CS

22 RNSG 2432


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e. ST s!gm!$t !l!*atio$ is sig$ifica$tif T1 mm abo;e isoelectric line1/ Bf treatment #rom#t, effecti;e, may a;oid infarction

'/ Bf serum cardiac mar8ers #resent, ha;e S>&sement&ele;ationMB S>6MB/

f. =hysioloic E "a;e & first neati;e deflection follo"in = "a;e, smalland narro" A.A% second in duration/* #atholoic E "a;e is dee# and

TA.A3 second in duration. =atholoic E "a;e &at least half thic8ness of heart "all in;ol;ed E

"a;e MB/, May be #resent indefinitelyh. > "a;e in;ersion related to infarction&occurs "ithin hours* may #ersist

for months

RNSG 2432 23


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P)ls!l!ss El!ctrical (cti*ity ,6lectrical acti;ity can be obser;ed on the 6C7, butthere is no mechanical acti;ity of the ;entricles and the #atient has no #ulse*

>reatment& C=R follo"ed by intubation and B e#ine#hrine* 2tro#ine is used if the;entricular rate is slo"* directed to"ard correction of the underlyin cause

S)dd!$ Cardiac !ath 'SC#, Death from a cardiac cause* maority of SCDs due

to ;entricular dysrhythmias ;entricular tachycardia, ;entricular fibrillation/

Prodysrhythmia , 2ntidysrhythmic drus may cause life&threatenin dysrhythmias

es#. Dio?in and class B2, BC, and BBB antidysrhythmia drus* first se;eral days of

dru thera#y most ;ulnerable #eriod for de;elo#in #rodysrhythmias. 0ideally bemonitored in hos#ital.

Collaorati*! Car! for ysrhythmias

"% Boc)s

a. Reconition and identification of dysrhythmia

b. 6;aluatin the effects, es#ecially lethalityc. >reatment of underlyin causesd. Nursin assessment: a#ical rate and rhythm* a#icalHradial deficit*

blood #ressure* s8in, urine out#ut, sins of decreased cardiac out#ute. Bnter;ention in dysrhythmia

1/ 2ntidysrhythmia drus'/ Defibrillation

a/ Cardio;ersion

b) Bm#lantable cardio;erter&defibrillatorc/ =acema8er

d/ Radio&freuency catheter ablation thera#y

2% ECG rhythm a$alysis proc!ss as co;ered/a. Rate determination

b. Reularity determinationc. = "a;e assessment

d. 2ssessment of = to ERS relationshi#e. Determination of inter;als

1/ =R inter;al'/ ERS com#le? duration

3/ E> inter;alf. Bdentification of abnormalities

3% iag$ostic T!sts as co;ered&see also #. $-3&$-- >ab 3'&$/a% "2 l!ad El!ctrocardiogram

1/ Bdentification of rhythm'/ Bnformation about underlyin disease #rocesses

3/ Monitor effects of treatment

% Cardiac St)di!s re;ie" all/1/ Continuous cardiac monitorin

'/ 2mbulatory 6C7 monitorin 5olter monitorin or>ranstele#honic e;ent recorder/

3/ 6?ercise >readmill test

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%/ 6chocardiocram HStress echocardioramH=harmacoloic 6C5O"hat dru/

-/ >ranseso#haeal 6chocardioram >66// Nuclear Cardioloy includin #harmacoloical nuclear imain

"hat dru/ ML72, =6>$/ MR2, MRB

)/ Cardiac Catheteri9ation etc

I$t!r*!$tio$s/Th!rapy for ysrhythmia

"% !firillatio$6merency deli;ery of direct current 6itho)t r!gard to cardiac cycl!

'*!$tric)lar firillatio$#: #erformedimm!diat!ly"hen rhythmreconi9ederformed e?ternally or internally surery, o#en chest/* also

automatic e?ternal Defibrillators. 00Note "here #addles are #laced =, )-$fi 3&'P&Read te?t

a% !firillatio$ &$o$,r!spo$si*!J p)ls!l!ss cli!$t

1/ Most effecti;e method &terminate + and #ulseless >'/ =assae of DC electrical shoc8 throuh heart to de#olari9e cells

of myocardium to allow SA nodeto resume role of #acema8er3/ Deli;er enery usin a mono#hasic or bi#hasic "a;eform

Mono#hasic Deli;er enery one direction* bi#hasic deli;erenery t"o directions successful shoc8s at lo"er eneries,

fe"er #ostshoc8 6C7 abnormalities/%/ O)tp)t,measured in;o)l!s/6atts#er second

% Recommended enery for initial shoc8s1/ 4i#hasic +irst and successi;e shoc8s: 1-A to 'AA oules

'/ Mono#hasic&Bnitial at 3A oules3/ 2fter initial shoc8, chest com#ressions C=R/

2% Sy$chro$i-!d Cardio*!rsio$

Direct electrical current synchroni9ed "ith heart rhythm: a*oid shoc1 d)ri$g*)l$!ral! p!riod of r!polari-atio$ 'R o$ T#

El!cti*! proc!d)r!,tr!at S@TJ a,fiJ fl)tt!rJ h!mody$amically stal!@T

0Cli!$ts i$ afi-; need anticoagulation several wees beforecardioversion, dec. ris8 for thromboembolism #ost cardio;ersion

RNSG 2432 25
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1/ Choice of thera#y for hemodynamically unstable ;entricular or

su#ra;entricular tachydysrhythmias

2) Synchroni9ed circuit &deli;ers countershoc8 on R "a;e of ERScom#le? of 6C7

3) Synchronizer switch must be turned on

3% Impla$tal! Cardio*!rt!r, !firillator'IC# 0ho is a candidate for

one & read #. )-$P)ls! g!$!rator impla$t!dsurically into client "ith lead electrodes forrhythm detection and current deli;ery* senses rate and "idth of ERS,

combined #acema8er* senses life&threatenin rhythm chanes* deli;ersautomatic electric shoc8 to con;ert dysrhythmia

a! +or clients "ho sur;i;ed SCD Sudden cardiac death/b! 5a;e s#ontaneous sustained >, synco#e "ith >, fib durin 6=S

c! 2t hih ris8 for future life&threatenin dysrhythmias;"#f fires$ contacthealth care %rovider$ or &''(

d! Consists of lead system #laced ;ia subcla;ian ;ein to endocardiume! 4atteryo"ered #ulse enerator im#lanted subcutaneously

f! #C) sensing system- monitors *R and rhythm$ identifies +, or+

g! 2##ro?. '- sec. after detectin > or +, BCD deli;ers '- oules* iffirst shoc8 unsuccessful, BCD recycles and deli;ers successi;e shoc8s

h! 6ui##ed "ith antitachycardia and antibradycardia #acema8ersi! Bnitiates o;erdri;e #acin of S> and >

.! =ro;ides bac8u# #acin for bradydysrhythmias! 6ducation critical* fear, body imae alteration, an?iety, su##ort rou#

/"See ,ab 01-2 %! 2324

26 RNSG 2432

1. =ro;ides #acin on demand

'. Stores 6C7 records of rhythms3. Can be re#rorammed at bedside "hen

necessary

%. Needs to be surically re#laced e;ery -years
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4% Pac!ma1!rs 'Bndications & >ab 3&1A #. )-P/0=ulse enerator, pro*id!s !l!ctrical stim)l)s to h!art 6h!$ h!art fails

to g!$!rat! or co$d)ct o6$ at a rat! for ad!9)at! cardiac o)tp)t

a. Lsed to #ace heart "hen normal conduction #ath"ay damaed ordiseased*

1/ =acin circuit consists of #o"er source, one or more conductin

#acin/ leads and myocardium'/ 6lectrical sinal stimulus/ tra;els from #acema8er, throuh

leads to "all of myocardium* myocardium Fca#turedG

&stimulated to contract

3) Bnitially for sym#tomatic bradydysrhythmias* no"antitachycardia and o;erdri;e #acin antitachycardia

#acin


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Clic8 for more #acema8er information3/ Pac!ma1!rs see +i 3&'% #. )-P/

a/ Modes: aynchronousreset time "ithout fail or

synchronous or demand&"hen heart rate oes belo" setrate

b/ Sense acti;ity in and #ace ;entricles only

c) 0Most no" sense acti;ity in and #ace both atria and;entricles atrio&;entricular seuential #acin stimulatesin seuence that imitates normal seuence of atrial

contraction follo"ed by ;entricular contraction/%/ Cardiac r!sy$chro$i-atio$ th!rapy 'CRT#>=acin techniue

a/ Resynchroni9es& cardiac cycle by #acin both ;entricles

b/ Combined CR> "ith an BCD for ma?imum thera#yc/ &Importa$t for h!art fail)r! ma$ag!m!$t

-/ ECG charact!ristics +i 3.3, )-)/

a/ Paci$g d!t!ct!dby #resence of #acin artifact&0sharp spi1! occur before = "a;e in atrial #acin or

before ERS com#le? in ;entricular #acinb/ Ca#ture noted by contraction of chamber follo"in the

s#i8e seen as = "a;e in atrial #acin or ERS com#le? in;entricular #acin/

/ >eachinSee >ab 3&1' #. )1/ 0Read carefully

a# Pr!,op* teach, e?#lain #rocedure* #lace electrodes a"ay

from #otential incision site* teach ROM e?ercises for affectedsite& hel# #re;ent shoulder stiffness.

28 RNSG 2432
http://www.heartpoint.com/pacerintro.htmlhttp://www.hrspatients.org/patients/treatments/resync.asphttp://www.heartpoint.com/pacerintro.htmlhttp://www.hrspatients.org/patients/treatments/resync.asp


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b/ Post Qop&c hest ?&ray* mi$imi-! mo*!m!$t of aff!ct!darmdurin initial #ost&o# #eriod&decrease ris8 of

dislodin #acer* monitor #acer "ith 6C7* re#ort failure to#ace, etc* assess for dysrhythmia, ta8es '&3 days for

FseatinG* document* date of #acer insertion, model etc.

a) om! Car!: ho" it "or8s, ho" #laced, battery

re#lacement, ho" to ta8e and record #ulse, incision sitecare, acti;ity restrictions, BD card, dont hold certainelectrical de;ices near itsets off security de;ices

b) 7ai$tai$i$g saf!ty* =re;entin infection andcom#lications

.% Cath!t!r (latio$Th!rapy 'Clic1 h!r! for *id!o#6lectrode&ti##ed ablation catheter FburnsG accessory #ath"ays or ecto#ic

sites in atria, 2 node, andHor ;entriclesa. No$pharmacologic tr!atm!$tfor 2 nodal reentrant tachycardia,

re&entrant tachycardia related to accessory by#ass tracts* control of;entricular res#onse of certain tachydysrhythmias

b. Com#lete ablation of 2 node or bundle of 5is& may be done in somecases of uncontrolled ;entricular res#onse in atrial fibrillation or flutter

unres#onsi;e to medical thera#y1/ I$*ol*!s locatio$/d!str)ctio$ ')r$ !ctopic path6ay# of

!ctopic foci i$ h!art&'/ iag$os!d i$ !l!ctrophysiology la/p!rform!din cardiac

cath lab

3/ Cardiac mappi$g: identification of sites "here im#ulseinitiated in atria or ;entricles&use internal or e?ternal catheters

%/ (latio$: destroy ecto#ic focus "ithradiofreuency enery "ith

catheters* 0anticoaulant thera#y may be started after"ard todecrease ris8 of clot formin at ablation site

% Oth!r m!as)r!s to stop dysrhythmias&Bor S@T

a. &@agal ma$!)*!rs, client Fbears do"nG: forced e?halation aainst a

closed lottis to slo" heart rateb. Carotid sinus massage$continuous monitorin& by #hysician onlyc. 7!dicatio$ssuch as ad!$osi$!J calci)m cha$$!l loc1!rs

d. 0See antidysrhtymic meds 8no"/ >ab 3.) #. )- and >ab. 3%&1' #.)AA and #. $P)&)A1 and list of meds as included.

N)rsi$g Car!1. Decrease ris8 for C5+HDec. CO, "hich is maor ris8 for dysrhythmias

RNSG 2432 29
http://my.clevelandclinic.org/heart/services/tests/procedures/ablation.aspxhttp://heartdisease.about.com/cs/heartfailure/a/CHF1.htmhttp://www.webmd.com/heart-disease/treating-arrhythmias-ablationhttp://my.clevelandclinic.org/heart/services/tests/procedures/ablation.aspxhttp://heartdisease.about.com/cs/heartfailure/a/CHF1.htmhttp://www.webmd.com/heart-disease/treating-arrhythmias-ablation


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'. Reduce sym#athetic ner;ous system stimulants li8e caffeine

N)rsi$g iag$os!s1. 0!cr!as!d Cardiac O)tp)t

a. 2l"ays assess the client before treatin the dysrhythmiab. Monitor ;ital sins, 6C7, and o?yen saturation freuently durin

antidysrhythmic dru infusionsc. Nurses carin for clients "ith dysrhythmias& need to be com#etent in

C=R and 2C!S

'. Bneffecti;e >issue =erfusion

3. 2n?iety and fear%. no"lede deficit

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