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NURS 2500 > Class 22: Arrythmias > Flashcards

Class 22: Arrythmias Flashcards

1
Q

what is the difference between a 12-lead ECG and cardiac monitoring

A
  • 12-lead ECG = moment in time, very detailed

- cardiac monitoring = continuous, less detailed

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2
Q

what is the path of transmission for conduction

A

SA –> AV –> Bundle of His (splits into R and L) –> purkinje fibers
“save his kin”

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3
Q

where is the SA node located? how does correlate to this function

A
  • RA

= causes atria to contract

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4
Q

what does it mean that the SA node is the pacemaker? what does it conduct impulses?

A
  • sets the pace (HR) of the heart
  • it is also the fastest pacing
  • 60-100 bpm
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5
Q

where is the AV node located

A
  • in the septum

- how you get from the atria to ventricles

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6
Q

what is meant by the AV node being the gatekeeper? why is this important?

A
  • at the AV node, it causes a slight delay
  • this is important because it allows the atria to fully empty into the ventricles
  • also prevents the atria & ventricles from contracting at the same time
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7
Q

where is the bundle of his located

A
  • in between the ventricles

- branches off into R and L bundle braches

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8
Q

where are the purkinje fibers located

A
  • in the ventricles
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9
Q

where does contraction of the heart begin? describe how contraction spreads?

A
  • at the apex

- it then fans out & up the ventricle wall to push blood up so it can leave the aortic & pulmonic valve

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10
Q

describe the difference between where conduction vs contraction begins

A
  • conduction = base of heart (SA node)

- contraction = apex

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11
Q

what is the difference between depolarization & repolarization

A
  • depolarization = contraction

- repolarization = relaxation

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12
Q

why is it important that electrical conduction follows the normal pathway

A
  • it is the most efficient

- impulses travel fast down the septum

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13
Q

how does SNS and PSNS effect the SA rate

A
  • SNS = increased

- PSNS = decreased

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14
Q

is it only certain cardiac cells that can initiate cardiac depolarization? what does this mean?

A
  • any cardiac cell can spontaneously depolarizae & initiate cardiac depolarization
    = although SA node is the pacemaker, cell in the AV node, etc. also have the capacity to become the pacemaker
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15
Q

how fast do SA cardiac cells depolarize compared to other cardiac cells

A
  • they are faster
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16
Q

what is overdrive suppression

A
  • the faster frequency in SA node cells suppresses other pacemaker sites thru this
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17
Q

explain how overdrive suppression works

A
  • the faster conduction of the SA node causes all the other myocytes to contract
  • after they contract, they enter a refractory period where they cannot contract again
  • this means that the other myocytes do not have a chance to fire at their own rate
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18
Q

what is ectopic focus

A
  • when a conraction is initiated by different cells other than the SA node cells
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19
Q

what is ectopic focus

A
  • when a contraction is initiated by different cells other than the SA node cells
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20
Q

what can cause an ectopic beat

A
  • ischemia
  • stretch
  • drugs
  • electrolyte imbalance
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21
Q

what can cause an ectopic beat

A
  • ischemia
  • stretch
  • drugs
  • electrolyte imbalance
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22
Q

how are the atria & ventricles electrically insulated from each other

A
  • by the AV valves
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23
Q

what is the only electrical path from the Atria to ventricles?

A
  • AV node
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24
Q

what is wolfe parkinson white syndrome

A
  • syndrome in 1 in 1000 individuals where they have a second electrical pathway between teh atria & ventricles`
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25
Q

how does SNS affect the AV node

A
  • decreases the delay by increasing the speed

- decreased refractory period = speeds recovery

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26
Q

how does PSNS affect the AV node

A
  • increases the delay

- increasing the refractory period = slows recovery

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27
Q

what are vagal maneuvers

A
  • stimulation of the vagal nerve to lower HR by causing PSNS stimulation
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28
Q

who are vagal maneuvers used in

A
  • pts with bursts or rapid HR
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29
Q

what are examples of vagal manuevers

A
  • bearing down (“giving birth feeling”)
  • coughing, gagging
  • cold stimulus to face (ex. cold water)
  • carotid massage (physician only)
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30
Q

what contraction/conduction correlates with the P wave

A
  • SA node fires

= atria contract

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31
Q

what occurs druing the PR interval

A
  • AV node delay
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32
Q

what occurs during the QRS complex

A
  • ventricles contract
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33
Q

what occurs during the T wave

A
  • ventricles repolarize (rest)
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34
Q

what influences the size of waves during an ECG

A
  • more cells involved = bigger wave

- why P wave is smaller than QRS, because atria are smaller

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35
Q

why dont we see atrial repolarization in an ECG

A
  • occurs at the same time as ventricles contracting =

it is hidden by the QRS wave because ventricles are bigger

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36
Q

explain the action potential in 1 myocyte

A
  • depolarization = Na & Ca into cell

- repolarization = K+ leave the cell (?)

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37
Q

what is an electrocardiogram (ECG)

A
  • when electrodes are placed on the skin to capture & map electrical activity of the heart on continuously running paper
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38
Q

how many electrodes vs leads are used?

A
  • 10 electrodes
  • 12 leads

think: 10 windows on a house, but can see 12 different views of the house

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39
Q

what are the electroduces

A
  • the pads place directly on the skn
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40
Q

what are the leads

A
  • the specific angle of electrical activity captured by the electrodes
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41
Q

what can a ECG detect

A
  • abnormalities in cardiac conduction
  • hypertrophy
  • electrolyte abnormalities
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42
Q

what is normal sinus rhythmn (NSR)

A
  • term used to describe a normal ECG rate and rhythmn

- generated in the SA node

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43
Q

what does each different lead do

A
  • gives info about a very specific area of the heart
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44
Q

what happens if we see ST changes in a specific view of an ECG

A
  • since different areas of the heart are supplied by a specific coronary artery, if see ST changes in a specific view, we can tell which artery in being blockedq
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45
Q

what is an ECG rhythm strip

A
  • simple, single view of the hearts electrical conduction

- may only have 3 or 5 leads attached

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46
Q

what is a positive or upward deflection

A
  • electrical activity moving toward an electrode
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47
Q

what is a negative or downward deflection

A
  • electrical activity moving aware from the lead

ex. from atria to ventricle

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48
Q

what do upward and positive deflections cause

A
  • some views are mirror of each other

ex. lead II and aVR

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49
Q

what are the 2 primary purposes of an ECG

A
  1. identify ischemia = ST changes

2. identify arrhythmias –> abnormal beating

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50
Q

when is ST change present? what does this mean?

A
  • only during active ischemia or angina
    = must get a STAT 12-lead ECG during angina to capture it
  • may always use cardiax monitoring
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51
Q

each is lead is in the ____ moment of time

A

same –> like a snapshot in time

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52
Q

what do we use if we want continuous monitoring

A
  • cardiac monitoring

- 3 or 5 leads & let it run continuously

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53
Q

what are 3 different ways that ECGs are used

A
  1. telemetry
  2. holter monitor
  3. stress/exercise test
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54
Q

what is a telemetry

A
  • where a pt has ECG monitoring that is transmitted to a local receiver and played on a monitor
  • like a portable ECG
  • often used in acute care wards
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55
Q

what are the benefits of telemetry

A
  • allows patients to get up & move around

- allows them to test their heart function b4 going home

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56
Q

what is a holter monitor

A
  • at home monitor
  • record an ECG 24 h a day & patient will keep a log book of activity which can be matched to the ECG recording and any changes
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57
Q

what is a stress/exercise test

A
  • patient will exert themselves & the ECG will record ant changes
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58
Q

what are stress/exercise tests used for

A
  • determine if meds are controlling angina well
  • or for intial diagnosis of stable angina
  • only on stable patients
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59
Q

what happens if the SA node fails to fire

A
  • the next fastest node will become the pacemaker

- in this case, the AV node

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60
Q

what is the intrinsic rate of the SA, AV, and purkinje fibers

A
  • SA= 60-100
  • AV = 40-40
  • purkinje = 20-40
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61
Q

what might sinus brady & tachy be used for

A
  • functional compensation = useful
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62
Q

when might sinus tachycardia be used

A
  • during activity

ex. if running, need increased cardiac output = HR increases

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63
Q

when might sinus bradycardia be used full

A
  • at rest

ex. when sleeping at night

64
Q

what is ST elevation a sign of

A
  • stemi
65
Q

when do we see ST depression

A
  • Non-STEMI
  • unstable angina
  • stable angina
66
Q

why do we get ST depression with unstable angina & Non-STEMI

A
  • get ischemia caused by partial occlusion of a coronary artery
67
Q

why do we get ST elevation with STEMI

A
  • bc get complete occlusion of the coronary artery & the entire thickness of the myocardium becomes ischemic
68
Q

describe the evoluation of a STEMI

A
  1. NSR
  2. ST elevation peaked T-wave
  3. ST elevation lessons & deep Q-wave, inverted T-wave
  4. resolving ST elevation, inverted T wave
  5. pathological Q wave (may be permanent)
    (look at pics in slides)
69
Q

what might pathological Q wave indicate

A
  • past MI bc may be permanent
70
Q

describe the PR interval

A
  • starts with atrial contraction
  • end before ventricular contraction
    = during the delay of AV nodes
71
Q

describe the ST segment

A
  • starts at end of ventricular contraction

- ends before ventricular repolarization

72
Q

is the inside of the cell (+) and (-) during resting membrane potential

A

(-) bc 3 Na out and only 2 K+ in

73
Q

what occurs during depolarization

A
  • Na coming in = membrane potential becoming more (+)

= ventricular contraction = QRS complex

74
Q

what occurs during repolarization

A
  • K+ coming out of the cell = becomes more (-)

= ventricular relaxation = T wave

75
Q

what occurs during the plateau of action potential

A
  • Ca flows in
  • K+ starts to flow out
    = correlates with ST segment
76
Q

what are arrhythmias

A
  • alterations in cardiac rhythm
77
Q

what are dysarrhythmias

A
  • loss of rhythm
78
Q

what is sinus bradycardia

A
  • sinus rhythm with a resting rate less than 60 per min
79
Q

who do we see sinus bradycardia in

A
  • trained athletes
  • during sleep
  • MI
  • resp. depression
  • hypothyroidism
  • drug toxicity
  • can be compensation for an underlying disorder
80
Q

what is sinus tachycardia

A
  • sinus rhythm above 100 per min
81
Q

when do we see sinus tachycardia

A
  • w exercise
  • fever
  • CHF
  • MI
  • hyperthyroidism
  • drug toxicity
  • hypovolemia
82
Q

do we usually directly treat sinus brady and tachy

A
  • no bc usually occur secondary or as compensation

- will treat the underlying cause tho

83
Q

what does excitability mean

A
  • ability of a cell to respond to an impulse & generate an AP
84
Q

what does conductivity mean

A
  • ability to conduct impulses
85
Q

what does refractoriness mean

A
  • extent to which the cell is able to respond to an incoming stimulus
86
Q

what are the 3 main mechanisms of arrhythmias

A
  1. increased automaticity
  2. triggered activity
  3. re-entry
87
Q

what is increased automaticity? when does this occur? what does it cause?

A
  • increase in the natural depolarization rate of nodal cells
  • occur in response to SNS
    = uncontrolled electrical activity
88
Q

what is triggered activity

A
  • when after depolarization of an action potential, a myocyte depolarizes spontaneously
    “twitchy”
89
Q

what are 2 types of after depolarization

A
  • early

- delayed

90
Q

what can cause triggered activity

A
  • ischemica or fibrosis

- or HF

91
Q

what does triggered activity cause

A
  • ectopic or premature beats
92
Q

what occurs with reentry

A
  • in injured tissue, it sets up a condition for a recurrent circuit
  • this causes an area of muscle to repeatedly contract
  • so instead of the impulse leaving, it just re-enter to where it came from
93
Q

explain how conduction moves in normal tissue

A
  • electrical waves move & when meet in the middle they cease due to the absolute refractory period
94
Q

explain what happen with conduction in necrotic tissue

A
  • when an impulse runs into necrotic tissue, the impulse is blocked bc necrotic tissue does not have intact cell membranes for an action potential
95
Q

what does a pacemaker do

A
  • helps to control ur hearbeat

- primarily for bradycardia

96
Q

what is cardiac resynchronization therapy

A
  • used when ventricles are out of sync to resync them

- form of pacemaker

97
Q

who is an implantable cardioverter defibrillator used in

A
  • pts with frequent fatal arrhythmias
  • or HF pts with EF of <30%
    ex. VT and VF
98
Q

what is cardioversion

A
  • procedure using external electrical shocks to restore a normal heart rhythm
  • often done in synchronization to R wave = must be able to recognize QRS
  • lower energy used
  • delay in delivery
  • may be planned or scheduled
99
Q

what is defibrillation

A
  • emergency life saving procedure using electrical shocks
  • not synchronized to R wave
  • immediate delivery
  • higher energy
100
Q

what is an AED

A
  • automated external defibrillator
101
Q

when is an AED used

A
  • in public buildings
102
Q

what is CPR

A
  • cardiopulmonary resuscitation
103
Q

describe use of an external pacemaker

A
  • for short term emergency use only
  • for unstable, symptomatic, slow rhythmns
  • very uncomfortable & painful
104
Q

describe use of a temporary pacemaker

A
  • wire inserted thru large blood vessel

- tip goes to apex of heart and delivers and electrical stimulus to pace the ventricle

105
Q

what is a capture

A
  • anytime an artificial stimulus is used & the heart responds by contracting
106
Q

what is a non-capture

A
  • when a stimulus does not respond in contraction
107
Q

describe use of an internal pacemaker

A
  • permanent, surgically implanted device w 2 wires

- one to pace the atria & one for the ventricle

108
Q

where is the generator of an internal pacemaker placed

A
  • below the clavicle

- under the skin but above the muscle wall so it can be accessed for replacement but also less invasive

109
Q

describe how cardiac resynch therapy work

A
  • adds a pacing lead to each ventricle (and the usual atrial) to recoordinate the ventricles & increase patient’s CO
110
Q

what do we see on an ECG before CRT

A
  • a bundle branch block = jagged look in the R wave
111
Q

what is an implantable cardioverter defibrillator

A
  • when lead is place on the heart to allow for monitoring of fatal arrhythmias
  • when the arrhythmias occur, the heart sends a jolt of electricity to reset the hearts electrical conduction & return to NSR
  • can be synchronized to R wave with cardioversion or random with defibrillation
112
Q

who is cardioversion used in

A
  • sustained SVT
  • A-fib
  • monomorphic VT
113
Q

what is defibrillation used in

A
  • v-fib
  • polymorphin VT
  • pulseless VT
  • for emergencies & fatal arrhythmias
114
Q

what is meant by avoid R on T when shocking

A
  • shocking the heart causes depolarization

- want to avoid doing this during T wave bc it can initiate an arrhytmias, specifically a bad one like VT/VF

115
Q

how do we avoid shocking the T wave?

A
  • find the R waves, easy to see bc tall

- the machine will also calculate when the T waves are

116
Q

is defibrillation synchronized?

A
  • no, often no R wave present bc no ventricular contraction w VF
117
Q

what are 3 concerns with arrhytmias

A
  1. sustainability
  2. cardiac workload & ischemia
  3. thrombus/emboli formation
118
Q

describe the concern of sustainability with increased Hr

A
  • increased HR = increased workload & decreased filling
119
Q

describe the concern of sustainability with decreased HR

A

= decreased CO

120
Q

describe hemodynamic instability with arrhytmias

A

= decreased CO = decreased bp = decreased perfuson = multiorgan failure (shock)

121
Q

describe cardiac workload & ischemia in arrhythmias

A

increased workload = ischemia & angina

acute MI = further ischemia = extended MI

122
Q

why is there a concern for thrombus/emboli formation w arrhythmias

A
  • weak contraction = blood stasis

- atrial fibrillation = blood statis in the atria

123
Q

what part of an ECG do we use to calculate HR/min

A
  • R wave to r wave = ventricle rate (usually match pulse)
124
Q

how do measure atrial rate

A
  • P to P
125
Q

what is an artifact rhythm on ECG

A
  • extra activity on ECG from either
    1. skeletal muscle activity (person moving around)
    2. loose electrodes
126
Q

what is sinus arrhythmia

A
  • variation of NSR
  • includes R to R variation that changes with breathing
  • not pathological, otherwise normal
127
Q

describe sinus arrhythmias during inspiration vs expiration

A
  • inspiration = faster due to less vagal tone

- expiration = slower due to increased vagal tone = PSNS

128
Q

what is a way to estimate vent or atria rate off an ECG

A
  • 15 boxes = 3 sec & usually 2 per strip = 6 sec

- count how many R or P waves during 6 sec & multiply by 10

129
Q

what is the box method to determine HR

A
  • measure how many big boxes between R and R

- use formula: (60sec/1m) (1 beat/ (0.2 x # of boxes))

130
Q

what is sinus bradycardia

A
  • heart rhythmn regular
  • but HR <60 beats/min
  • everything else normal
131
Q

what is sinus tachycardia

A
  • heart rhythm normal
  • but HR >100 beats/min
  • everything else normal
132
Q

what does sinus mean in sinus brady, tachy, etc.

A

sinus = originates from SA node

133
Q

what is a key characteristic of atrial rhythmns

A
  • abnormal P wave
134
Q

what is premature atrial contraction

A
  • abnormally early P wave
  • looks like it kinda interupts the T wave
  • otherwise everything else looks normal for the most part
135
Q

what causes a PAC?

A
  • premature atrial beats that originates in the atria but outside of the Sinus node
  • automaticity or triggering
  • stimulants: emotion, tobacco, coffee
  • hypoxia/ischemia, electrolyte imbalances, cardiac condition
136
Q

what are key ECG features of a PAC

A
  • underlying NSR
  • P-P interval shorted on premature beat
  • narrow QRS
137
Q

what are key assessment of a PAc

A
  • pulse primarly regular
  • occassional early beat
  • otherwise asymptomatic
138
Q

describe treatment for PAC

A
  • remove stress/stimulant

- otherwise, no treatment

139
Q

what is paroxysmal supraventricular tachy

A
  • starts and stops aruptbly
140
Q

what causes PSVT

A
  • re-entry at the AV node
141
Q

what are key ECG features of PSVT

A
  • narrow QRS
  • P hidden/distorted
  • 170-250 rate
  • starts & stops abruptly
  • burst
  • self limiting
142
Q

what can we do to treat stable PSVT

A
  • vagal maneuvers
143
Q

how can we treat unstable PSVT

A
  • adenosine IV bolus

- cardioversion

144
Q

what is long term control for PSVT

A
  • CCB/BB

- alblation therapy

145
Q

what symptoms may be seen in PSVT

A
  • drop in CO
  • palpitations
  • dizziness
  • angina & dyspnea if +CAD
146
Q

what is atrial flutter

A
  • atria contract much quicker than should ~300 bpm
  • creates F waves with a saw like appearance
  • get increase in A:V ratio ex. 4:1
147
Q

describe cause of atrial flutter

A
  • fleeting
  • re-entry
  • ischemic, stretch
  • usually resolves or converts to A fib
148
Q

what are key ECG features of Atrial flutter

A
  • sawtooth
  • A-rate up to 300
  • ratio of A:V changes
  • narrow QRS
  • regular/irregular variable
149
Q

what are key assessments for atrial flutter

A
  • senses flutter in chest = palpitation
  • possible drop in CO with S/S from low perfusion –> weak pulses, low BP, sluggish cap refill, cyanosis, pale, syncope, low urine output
150
Q

what is atrial fibrillation

A
  • chaotic atrial contraction
  • sometimes dont contract or signals do or not go to ventricles
  • multiple uncontrolled re-rentry circuits
151
Q

what determines our CO

A
  • ventricles
152
Q

what can cause atrial fibrillation

A
  • acute or chronic
  • multiple uncontrolled re-entry
  • ischemia, stretch
  • HTN/volume
  • no a-kick
153
Q

describe key ECG features in A-fib

A
  • irregular V rate (due to contraction sometimes go thru, sometimes not)
  • narrow QRS
  • pulse deficit
  • cant determine A rate
  • bunch of F waves before QRS
  • can be tachy or brady response
154
Q

what are key assessment for afib

A
  • rapid V response then drop in CO

- increased pulse deficit

155
Q

what kind of meds for afib

A
  • pre rate control meds: ex. digoxin, BB, CCB
  • risk of thrombus = anticoag, antiplt
  • rhythm-control with cardioversion and/or antiarryhthmics

NURS 2500 (5 decks)

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