Class 22: Arrythmias Flashcards
(155 cards)
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
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”
3
Q
where is the SA node located? how does correlate to this function
A
- RA
= causes atria to contract
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
5
Q
where is the AV node located
A
- in the septum
- how you get from the atria to ventricles
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
7
Q
where is the bundle of his located
A
- in between the ventricles
- branches off into R and L bundle braches
8
Q
where are the purkinje fibers located
A
- in the ventricles
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
10
Q
describe the difference between where conduction vs contraction begins
A
- conduction = base of heart (SA node)
- contraction = apex
11
Q
what is the difference between depolarization & repolarization
A
- depolarization = contraction
- repolarization = relaxation
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
13
Q
how does SNS and PSNS effect the SA rate
A
- SNS = increased
- PSNS = decreased
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
15
Q
how fast do SA cardiac cells depolarize compared to other cardiac cells
A
- they are faster
16
Q
what is overdrive suppression
A
- the faster frequency in SA node cells suppresses other pacemaker sites thru this
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
18
Q
what is ectopic focus
A
- when a conraction is initiated by different cells other than the SA node cells
19
Q
what is ectopic focus
A
- when a contraction is initiated by different cells other than the SA node cells
20
Q
what can cause an ectopic beat
A
- ischemia
- stretch
- drugs
- electrolyte imbalance
21
Q
what can cause an ectopic beat
A
- ischemia
- stretch
- drugs
- electrolyte imbalance
22
Q
how are the atria & ventricles electrically insulated from each other
A
- by the AV valves
23
Q
what is the only electrical path from the Atria to ventricles?
A
- AV node
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`
25
how does SNS affect the AV node
- decreases the delay by increasing the speed
| - decreased refractory period = speeds recovery
26
how does PSNS affect the AV node
- increases the delay
| - increasing the refractory period = slows recovery
27
what are vagal maneuvers
- stimulation of the vagal nerve to lower HR by causing PSNS stimulation
28
who are vagal maneuvers used in
- pts with bursts or rapid HR
29
what are examples of vagal manuevers
- bearing down ("giving birth feeling")
- coughing, gagging
- cold stimulus to face (ex. cold water)
- carotid massage (physician only)
30
what contraction/conduction correlates with the P wave
- SA node fires
| = atria contract
31
what occurs druing the PR interval
- AV node delay
32
what occurs during the QRS complex
- ventricles contract
33
what occurs during the T wave
- ventricles repolarize (rest)
34
what influences the size of waves during an ECG
- more cells involved = bigger wave
| - why P wave is smaller than QRS, because atria are smaller
35
why dont we see atrial repolarization in an ECG
- occurs at the same time as ventricles contracting =
| it is hidden by the QRS wave because ventricles are bigger
36
explain the action potential in 1 myocyte
- depolarization = Na & Ca into cell
| - repolarization = K+ leave the cell (?)
37
what is an electrocardiogram (ECG)
- when electrodes are placed on the skin to capture & map electrical activity of the heart on continuously running paper
38
how many electrodes vs leads are used?
- 10 electrodes
- 12 leads
think: 10 windows on a house, but can see 12 different views of the house
39
what are the electroduces
- the pads place directly on the skn
40
what are the leads
- the specific angle of electrical activity captured by the electrodes
41
what can a ECG detect
- abnormalities in cardiac conduction
- hypertrophy
- electrolyte abnormalities
42
what is normal sinus rhythmn (NSR)
- term used to describe a normal ECG rate and rhythmn
| - generated in the SA node
43
what does each different lead do
- gives info about a very specific area of the heart
44
what happens if we see ST changes in a specific view of an ECG
- 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
45
what is an ECG rhythm strip
- simple, single view of the hearts electrical conduction
| - may only have 3 or 5 leads attached
46
what is a positive or upward deflection
- electrical activity moving toward an electrode
47
what is a negative or downward deflection
- electrical activity moving aware from the lead
| ex. from atria to ventricle
48
what do upward and positive deflections cause
- some views are mirror of each other
| ex. lead II and aVR
49
what are the 2 primary purposes of an ECG
1. identify ischemia = ST changes
| 2. identify arrhythmias --> abnormal beating
50
when is ST change present? what does this mean?
- only during active ischemia or angina
= must get a STAT 12-lead ECG during angina to capture it
- may always use cardiax monitoring
51
each is lead is in the ____ moment of time
same --> like a snapshot in time
52
what do we use if we want continuous monitoring
- cardiac monitoring
| - 3 or 5 leads & let it run continuously
53
what are 3 different ways that ECGs are used
1. telemetry
2. holter monitor
3. stress/exercise test
54
what is a telemetry
- 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
55
what are the benefits of telemetry
- allows patients to get up & move around
| - allows them to test their heart function b4 going home
56
what is a holter monitor
- 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
57
what is a stress/exercise test
- patient will exert themselves & the ECG will record ant changes
58
what are stress/exercise tests used for
- determine if meds are controlling angina well
- or for intial diagnosis of stable angina
- only on stable patients
59
what happens if the SA node fails to fire
- the next fastest node will become the pacemaker
| - in this case, the AV node
60
what is the intrinsic rate of the SA, AV, and purkinje fibers
- SA= 60-100
- AV = 40-40
- purkinje = 20-40
61
what might sinus brady & tachy be used for
- functional compensation = useful
62
when might sinus tachycardia be used
- during activity
| ex. if running, need increased cardiac output = HR increases
63
when might sinus bradycardia be used full
- at rest
| ex. when sleeping at night
64
what is ST elevation a sign of
- stemi
65
when do we see ST depression
- Non-STEMI
- unstable angina
- stable angina
66
why do we get ST depression with unstable angina & Non-STEMI
- get ischemia caused by partial occlusion of a coronary artery
67
why do we get ST elevation with STEMI
- bc get complete occlusion of the coronary artery & the entire thickness of the myocardium becomes ischemic
68
describe the evoluation of a STEMI
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
what might pathological Q wave indicate
- past MI bc may be permanent
70
describe the PR interval
- starts with atrial contraction
- end before ventricular contraction
= during the delay of AV nodes
71
describe the ST segment
- starts at end of ventricular contraction
| - ends before ventricular repolarization
72
is the inside of the cell (+) and (-) during resting membrane potential
(-) bc 3 Na out and only 2 K+ in
73
what occurs during depolarization
- Na coming in = membrane potential becoming more (+)
| = ventricular contraction = QRS complex
74
what occurs during repolarization
- K+ coming out of the cell = becomes more (-)
| = ventricular relaxation = T wave
75
what occurs during the plateau of action potential
- Ca flows in
- K+ starts to flow out
= correlates with ST segment
76
what are arrhythmias
- alterations in cardiac rhythm
77
what are dysarrhythmias
- loss of rhythm
78
what is sinus bradycardia
- sinus rhythm with a resting rate less than 60 per min
79
who do we see sinus bradycardia in
- trained athletes
- during sleep
- MI
- resp. depression
- hypothyroidism
- drug toxicity
- can be compensation for an underlying disorder
80
what is sinus tachycardia
- sinus rhythm above 100 per min
81
when do we see sinus tachycardia
- w exercise
- fever
- CHF
- MI
- hyperthyroidism
- drug toxicity
- hypovolemia
82
do we usually directly treat sinus brady and tachy
- no bc usually occur secondary or as compensation
| - will treat the underlying cause tho
83
what does excitability mean
- ability of a cell to respond to an impulse & generate an AP
84
what does conductivity mean
- ability to conduct impulses
85
what does refractoriness mean
- extent to which the cell is able to respond to an incoming stimulus
86
what are the 3 main mechanisms of arrhythmias
1. increased automaticity
2. triggered activity
3. re-entry
87
what is increased automaticity? when does this occur? what does it cause?
- increase in the natural depolarization rate of nodal cells
- occur in response to SNS
= uncontrolled electrical activity
88
what is triggered activity
- when after depolarization of an action potential, a myocyte depolarizes spontaneously
"twitchy"
89
what are 2 types of after depolarization
- early
| - delayed
90
what can cause triggered activity
- ischemica or fibrosis
| - or HF
91
what does triggered activity cause
- ectopic or premature beats
92
what occurs with reentry
- 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
explain how conduction moves in normal tissue
- electrical waves move & when meet in the middle they cease due to the absolute refractory period
94
explain what happen with conduction in necrotic tissue
- 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
what does a pacemaker do
- helps to control ur hearbeat
| - primarily for bradycardia
96
what is cardiac resynchronization therapy
- used when ventricles are out of sync to resync them
| - form of pacemaker
97
who is an implantable cardioverter defibrillator used in
- pts with frequent fatal arrhythmias
- or HF pts with EF of <30%
ex. VT and VF
98
what is cardioversion
- 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
what is defibrillation
- emergency life saving procedure using electrical shocks
- not synchronized to R wave
- immediate delivery
- higher energy
100
what is an AED
- automated external defibrillator
101
when is an AED used
- in public buildings
102
what is CPR
- cardiopulmonary resuscitation
103
describe use of an external pacemaker
- for short term emergency use only
- for unstable, symptomatic, slow rhythmns
- very uncomfortable & painful
104
describe use of a temporary pacemaker
- wire inserted thru large blood vessel
| - tip goes to apex of heart and delivers and electrical stimulus to pace the ventricle
105
what is a capture
- anytime an artificial stimulus is used & the heart responds by contracting
106
what is a non-capture
- when a stimulus does not respond in contraction
107
describe use of an internal pacemaker
- permanent, surgically implanted device w 2 wires
| - one to pace the atria & one for the ventricle
108
where is the generator of an internal pacemaker placed
- below the clavicle
| - under the skin but above the muscle wall so it can be accessed for replacement but also less invasive
109
describe how cardiac resynch therapy work
- adds a pacing lead to each ventricle (and the usual atrial) to recoordinate the ventricles & increase patient's CO
110
what do we see on an ECG before CRT
- a bundle branch block = jagged look in the R wave
111
what is an implantable cardioverter defibrillator
- 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
who is cardioversion used in
- sustained SVT
- A-fib
- monomorphic VT
113
what is defibrillation used in
- v-fib
- polymorphin VT
- pulseless VT
- for emergencies & fatal arrhythmias
114
what is meant by avoid R on T when shocking
- 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
how do we avoid shocking the T wave?
- find the R waves, easy to see bc tall
| - the machine will also calculate when the T waves are
116
is defibrillation synchronized?
- no, often no R wave present bc no ventricular contraction w VF
117
what are 3 concerns with arrhytmias
1. sustainability
2. cardiac workload & ischemia
3. thrombus/emboli formation
118
describe the concern of sustainability with increased Hr
- increased HR = increased workload & decreased filling
119
describe the concern of sustainability with decreased HR
= decreased CO
120
describe hemodynamic instability with arrhytmias
= decreased CO = decreased bp = decreased perfuson = multiorgan failure (shock)
121
describe cardiac workload & ischemia in arrhythmias
increased workload = ischemia & angina
| acute MI = further ischemia = extended MI
122
why is there a concern for thrombus/emboli formation w arrhythmias
- weak contraction = blood stasis
| - atrial fibrillation = blood statis in the atria
123
what part of an ECG do we use to calculate HR/min
- R wave to r wave = ventricle rate (usually match pulse)
124
how do measure atrial rate
- P to P
125
what is an artifact rhythm on ECG
- extra activity on ECG from either
1. skeletal muscle activity (person moving around)
2. loose electrodes
126
what is sinus arrhythmia
- variation of NSR
- includes R to R variation that changes with breathing
- not pathological, otherwise normal
127
describe sinus arrhythmias during inspiration vs expiration
- inspiration = faster due to less vagal tone
| - expiration = slower due to increased vagal tone = PSNS
128
what is a way to estimate vent or atria rate off an ECG
- 15 boxes = 3 sec & usually 2 per strip = 6 sec
| - count how many R or P waves during 6 sec & multiply by 10
129
what is the box method to determine HR
- measure how many big boxes between R and R
| - use formula: (60sec/1m) (1 beat/ (0.2 x # of boxes))
130
what is sinus bradycardia
- heart rhythmn regular
- but HR <60 beats/min
- everything else normal
131
what is sinus tachycardia
- heart rhythm normal
- but HR >100 beats/min
- everything else normal
132
what does sinus mean in sinus brady, tachy, etc.
sinus = originates from SA node
133
what is a key characteristic of atrial rhythmns
- abnormal P wave
134
what is premature atrial contraction
- abnormally early P wave
- looks like it kinda interupts the T wave
- otherwise everything else looks normal for the most part
135
what causes a PAC?
- 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
what are key ECG features of a PAC
- underlying NSR
- P-P interval shorted on premature beat
- narrow QRS
137
what are key assessment of a PAc
- pulse primarly regular
- occassional early beat
- otherwise asymptomatic
138
describe treatment for PAC
- remove stress/stimulant
| - otherwise, no treatment
139
what is paroxysmal supraventricular tachy
- starts and stops aruptbly
140
what causes PSVT
- re-entry at the AV node
141
what are key ECG features of PSVT
- narrow QRS
- P hidden/distorted
- 170-250 rate
- starts & stops abruptly
- burst
- self limiting
142
what can we do to treat stable PSVT
- vagal maneuvers
143
how can we treat unstable PSVT
- adenosine IV bolus
| - cardioversion
144
what is long term control for PSVT
- CCB/BB
| - alblation therapy
145
what symptoms may be seen in PSVT
- drop in CO
- palpitations
- dizziness
- angina & dyspnea if +CAD
146
what is atrial flutter
- 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
describe cause of atrial flutter
- fleeting
- re-entry
- ischemic, stretch
- usually resolves or converts to A fib
148
what are key ECG features of Atrial flutter
- sawtooth
- A-rate up to 300
- ratio of A:V changes
- narrow QRS
- regular/irregular variable
149
what are key assessments for atrial flutter
- 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
what is atrial fibrillation
- chaotic atrial contraction
- sometimes dont contract or signals do or not go to ventricles
- multiple uncontrolled re-rentry circuits
151
what determines our CO
- ventricles
152
what can cause atrial fibrillation
- acute or chronic
- multiple uncontrolled re-entry
- ischemia, stretch
- HTN/volume
- no a-kick
153
describe key ECG features in A-fib
- 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
what are key assessment for afib
- rapid V response then drop in CO
| - increased pulse deficit
155
what kind of meds for afib
- pre rate control meds: ex. digoxin, BB, CCB
- risk of thrombus = anticoag, antiplt
- rhythm-control with cardioversion and/or antiarryhthmics
