ECG Flashcards
1
Q
normal PR interval length
A
0.12-0.2 s
2
Q
normal sinus rhythm pattern
A
upright p wave
each p wave followed by a QRS
each QRS preceded by a P wave
PR interval length = 0.12-0.2 s
3
Q
how much time is denoted by 5 little horizontal squares
A
0.2 s
4
Q
how much voltage is denoted by 5 little vertical squares
A
0.5 mV
5
Q
in what order do you assess aspects of a rhythm strip
A
rate rhythm P wave PR interval QRS complex
6
Q
what 4 questions do you ask yourself about P waves
A
present?
same shape and size?
how many P waves per QRS?
what is the relationship between P waves and the QRS?
7
Q
what do P waves of the same P wave type indicate
A
1 atrial pacemaker
8
Q
what do P waves of different types on the same strip indicate?
A
more than 1 atrial pacemaker
9
Q
if there are no P waves, is there a PR interval?
A
NO
10
Q
what two questions do you ask yourself about PR intervals
A
short or long?
constant or changing?
11
Q
what is the normal length of the QRS complex?
A
0.12 s (3 small squares)
12
Q
what does a wide (>0.12 s) QRS indicate
A
LBBB
RBBB
ventricular pacemaker
13
Q
what does a narrow (
A
indicates pacemaker and conduction along His-Purkinje pathway (likely SA node pace)–> NORMAL
14
Q
what is a delta wave
A
a gradual incline in the QR segment
15
Q
what condition exhibits a delta wave in the ECG
A
wolff-parkinson-white syndrome
congential accessory pathway and episodes of tachyarrhythmia
16
Q
sinus bradycardia on ECG
A
only abnormality is rate
17
Q
sinus tachycardia on ECG
A
only abnormality is rate is >100
normal P waves, QRS complex, and PR interval
SA node is pacemaker and is just firing at a higher rate
18
Q
what is the max sinus rate
A
180-200 bpm (except in babies)
19
Q
what is indicated when HR exceeds 180-200 on ECG?
A
anything above this rate, the sinus node is not involved
common during exercise, fear and pain
other causes: volume depletion increased metabolic demand impaired cardiac filling decreased afterload
20
Q
1st degree AV block on ECG
“1st degree heart block”
A
wife = P wave husband = QRS
Wife waits at home for husband, and he comes home late every night, but he makes it home every night and he comes home at the same (late) time every night
due to slow conduction at the AV node
- long PR interval
- each P wave is associated with a QRS
- SA node = pacemaker
can coexist with other abnormalities (i.e sinus brady)
21
Q
what can cause 1st degree heart block
A
ischemia or fibrosis of AV node
22
Q
2nd degree AV block Type I
“2nd degree heart block Type I”
A
“Wenchebach” or “Morbitz”
wife = p wave husband = QRS
QRS comes home later and later every night until one night he doesnt come home at all
- irregular rhythm with pattern–> regularly missing QRS complexes
- more P waves than QRS complexes
- PR interval increases with each heart beat until it is so long that the signal doesnt reach the ventricles and the depolarization is “blocked” at the AV node
- SA node is the pacemaker
23
Q
2nd degree AV block Type II
“2nd degree heart block Type II”
A
wife= p wave husband = QRS wave
QRS sometimes comes home and sometimes doesn’t–> when he does come home, its always at the same time
- irregularly irregular (NO pattern) rhythm–> randomly missing QRS complexes
- more P waves than QRS complexes
- PR interval = constant (when a QRS is present)
- SA node = pacemaker
- more likely to develop into Type III heart block
24
Q
3rd degree AV block
“complete heart block”
A
wife = p wave
husband =QRS
P wave no longer waits on QRS. P wave and her husband are on completely different schedules and they are not associated at all. They are completely independent of each other and live totally separate lives
- atrial rate = faster than ventricular rate
- P waves are no longer associated with QRS complexes–> they are not conducted to the ventricles, they may become buried in the QRS
- there are more P waves than QRS complexes
- PR intervals are random
- QRS complexes are usually wide (rarely are narrow)
- SA node + ectopic side are the pacemakers (SA for atria, ectopic for ventricles)
25
Atrial flutter on ECG
1. type of tachycardia?
2. pacemaker?
3. atrial rate?
4. ventricular rate?
5. rhythm
6. why are there two different rhythms atria/ventricle?
7. characteristic waves on ECG
8. common block patterns
1. supraventricular tachy
2. ECTOPIC atrial site = pacemaker--> too fast for sinus node, which maxes at 180-200 bpm
3. 300 bpm
4. 150, 100 or 75 usually, depending on the block pattern
5. rhythm usually is regularly irregular, but can be irregularly irregular if the AV block is variable (AV block is usually regular)
6. atrial rate exceeds the rate at which the AV node can conduct and therefore there is a physiological block at the AV node due to the inherent REFRACTORY PERIOD
7. SAW TOOTH P WAVES = characteristic of atrial flutter
8. 2:1 (AV node blocks every 2nd atrial impulse) or 3:1
26
atrial fibrillation on ECG
1. type of tachycardia?
2. pacemaker?
3. are there P waves?
4. rhythm?
5. what is the relationship between atrial and ventricular rhythm?
6. what is a risk of atrial fibrillation?
1. supreventricular
2. multiple ectopic atrial sites act as pacemaker
3. no p waves--> background noise is present due to the high amount of uncoordinated electrical activity in the atria from the multiple ectopic pacemakers--> this results in quivering
4. irregularly irregular
5. the electrical activity is uncoordinated in the atria--> the AV node conducts this activity when it can and as fast as it can
6. increases danger of blood clots forming--> can lead to embolism
27
what is a supraventricular tachycardia?
any narrow tachycardia where QRS complexes are narrow and P waves are not obvious/affected
tachycardic rhythm that originates from ABOVE the bundle of His
i.e sinus tachycardia, atrial tachycardia, atrial flutter, atrial fibrillation, multifocal atrial tachycardia (MAT) which has 3 or more P wave morphologies, junctional tachycardia, and re-entry tachycardia
28
ventricular tachycardia on ECG
1. rate?
2. are there P waves?
3. what does the QRS complex look like?
4. pacemaker?
5. what is the danger with this rhythm?
1. between 100-250 bpm
2. p waves are absent (just QRS complexes over and over)
3. QRS complex is wide
4. sustained VENTRICULAR ECTOPIC pacemaker
5. can easily cause cardiac arrest--> call code blue immediately
**bottom line: wide QRS and fast rate--> looks like just big up and down waves over and over
29
ventricular fibrillation on ECG
1. pacemakers?
2. are there ventricular contractions?
3. what is this an example of? (i.e in what condition/state might you see this rhythm?)
4. what do you do when you see this rhythm on a strip
1. MULTIPLE ECTOPIC VENTRICULAR sites= pacemakers
2. NO ventricular contractions--> no cardiac output, no BP, no pulse
3. one example of cardiac arrest
4. call a code blue and use a defibrillator
* *uncoordinated electrical activity only
* high amount of uncoordinated electrical activity in the ventricles which results in quivering
* just random ups and downs all over the place
30
describe the usual progression of "electrical failing" of the heart that can lead to asystole
brady or narrow complex tachy--> ventricular tachycardia--> ventricular fibrillation--> agonal --> asystole
asystole = flat line; no electrical activity in the heart, patient has been in a pulseless rhythm for quite some time; hypoxic damage to the heart and brain from which recovery is not possible
31
what is the most common cause of supreventricular tachycardias
AVNRTs--> AV nodal re-entrant tachycardias
32
what is an AVNRT
when there is a re-entry tachycardia where the re-entry pathways is localized to the AV node
2 pathways-->
Alpha = normal conducting and normal refractory
Beta = slow conducting and fast refractory
the re-entry circuit is triggered by a premature atrial impulse that sends impulses into this circuit
33
what is a sinus nodal re-entry tachycardia
same as AVNRT but localized in the SA node
34
what is the second most common cause of supreventricular tachycardias
AV re-entrant tachycardias (not localized to AV node)
35
what is an AVRT
occurs in the presence of ACCESSORY PATHWAYS/bypass tracts which are errant strands of myocardium that bridge the mitral or tricuspid valves
these bypass tracts mean that the bundle of His is now no longer the only way for impulses to get from the atria to the ventricles
the impulses usually travel anterograde down the AV node and retrograde via the accessory pathway from ventricles to atria (orthrodromic AVRT)--most common
if it travels anterograde down the accessory pathway, this results in pre-excitation of the ventricles and thus a delta wave as seen in WPW--excitation then travels retrograde through AV node (antidromic AVRT)
36
what 4 things cause abnormal heart rhythms/rates
1. problems with or alterations to the hearts automaticity
2. re-entry circuits (causing tachy)
3. after-depolarizations (causing tachy)
4. conduction block (usually causing brady)
37
what mechanisms can the body use to induce bradycardia
1. increase parasympathetic drive
2. decrease the phase 4 slope, by using the vagus nerve and cholinergic stimulation of the SA node to decrease the probability that pacemaker channels are open
3. increase the threshold value (i.e the probability of open Ca2+ channels in phase 0 decreases)
4. make the "resting membrane potential" more negative which increases the probability that K+ channels are open at rest
38
what can happen if SA node pacemaker cells are slowed enough
Escape rhythm
meaning other conducting tissues like the AV node or the His-Purkinje system can take over the pacemaker role except at the slower than normal rate compared to normal SA function
39
by what mechanisms can the body induce tachycardia
1. decrease parasympathetic drive
2. increase the phase 4 slope through Beta 1 adrenergic stimulation of the AV node to increase the probability that the pacemaker channels are open
3. make the threshold lower (more negative) to increase the probability that voltage sensitive channels are capable of opening in phase 0
4. make "RMP" more positive
5. can also be caused by ectopic beat formation along the conduction pathway faster than can be produced by the SA node--> happens with overstimulation of the SNS, in hypoxia, ischemia or with electrolyte disturbances or drug toxicities
6. injury to membranes causing them to become leavy and thus atrial or ventricular cells to become partially depolarized causing ectopic beats
40
name a condition that is characterized by early after-depolarizations
torsades de pointes
some Na+ channels become abnormally activated in plateau or phase 3 of depolarization leading to self-propagating AP
41
what physiological condition can contribute to late after-depolarizations
states where there is high intracellular Ca2+ concentrations or when there is excessive catecholamine stimulation
high Ca2+ concentrations in the cell activates the Na2+/Ca2+ exchanger, causing more Na+ to enter the cell, causing depolarization
(occurs after repolarization is complete, unlike early after-depolarizations)
42
in what type of heart block are escape rhythms usually seen
3rd degree
43
what aspect of heart function do changes in the following affect?
1. phase 0
2. phase 2/3
3. phase 4
1. changes in phase 0 affect conduction speed
2. changes in phase 2/3 affect the refractory period
3. changes in phase 4 affect/determine the rate of spontaneous depolarization (i.e pacemaker rate)
44
conservative Tx for brachycardia
stop any meds that may be contributing to the brady
treat any reversible conditions (hypothyroidism, ischemia)
45
invasive Tx of brady
pacemaker
46
would you treat an asymptomatic sinus node brady?
no
pacemaker for symptomatic sinus node brady
47
Tx for...
1. 1st degree AV block
2. 2nd degree AV block Type I
3. 2nd degree AV block Type II
4. 3rd degree AV block
1. no Tx
2. no Tx
3. pacemaker
4. pacemaker
48
pharmacologic Tx of sinus brady
i.e how to speed up the SA node
1. increase SNS activity with EPINEPHRINE
2. increase SNS activity with DOPAMINE
3. decrease PSNS activity with ATROPINE
atropine = muscarinic blocker ("resets" heart)
49
conservative Tx of tachycardias
Tx of medical conditions contributing to the tachy (i.e sepsis, hyperthyroidism)
avoid tachy-cardiogenic meds
50
pharmacological Tx of tachycardias
anti-arrhythmic meds
51
invasive Tx of tachycardias
cardioverter/defibrillator implantation
catheter ablation
52
pharmacologic Tx for tachys
1. sodium channel blockers
2. Beta blockers
3. potassium channel blockers
4. non-DHP Ca2+ channel blockers
others are digoxin and atropine
53
name some sodium channel blockers used for tachy Tx
```
procainamide
disopyramide
lidocaine
mexiletine
propafenone
flecanimide
```
54
name some beta blockers used for tachy Tx
acebutolol
| metoprolol
55
name some K+ channel blockers used to treat tachy
```
amiodarone
sotatol
dronedarone
ibutilide
dofetilide
```
56
name some non-DHP calcium channel blockers used to treat tachy
verapamil
| diltiazem
57
procainamide
sodium channel blocker
58
acebutol
beta blocker
59
amiodarone
K+ channel blocker
60
mexiletine
sodium channel blocker
61
lidocaine
sodium channel blocker
62
diltiazem
non-DHP calcium channel blocker
63
dronedarone
K+ channel blocker
64
sotatol
K+ channel blocker
65
flecainide
sodium channel blocker
66
metoprolol
beta blockers
67
disopyramide
sodium channel blocker
68
ibutilide
K+ channel blocker
69
verapamil
calcium channel blocker
70
dofetilide
K+ channel blocker
71
propafenone
sodium channel blocker
72
what would you use cardioversion to treat
good for supraventricular tachycardias or organized ventricular tachycardia
you have to sync the shock with the QRS complex
73
what do you use vagal maneuvers to treat
tachys
the AV node is well supplied by PSNS fibers and thus responsive to vagal maneuvers
these maneuvers terminate junctional (AV node) reentry tachycardias by increasing the cardiac parasympathetic tone via the vagal nerve
74
what phase do you target to treat sinus tachy
phase 4
75
what meds do you use to treat sinus tachy
beta blockers and calcium channel blockers
76
which drugs alter the conduction speed
sodium channel blockers (because affect phase 0)
77
which drugs alter the refractory period
K+ channel blockers (because affect phase 2/3)
78
how does the carotid massage work to treat AV tachy
increases vagus nerve output
79
how does the valsalva maneuver work to treat tachys
changes the venous return to the heart and SVR
80
how done adenosine work to treat tachys
short (5-7 sec) inhibition of the AV node
81
what type of drug is atropine
anti-cholinergic
82
what classes of drugs would u use to treat atrial tachy
sodium and calcium channel blockers
83
what classes of drugs would you use to treat junctional/AV tachys
beta blockers, calcium channel blockers and digoxin
84
what classes of drugs would you use to treat ventricular tachys
sodium and potassium channel blockers
| affect conduction speed and refractory period
85
how does cardioversion work
give a huge electric current
depolarizes all cells
then there is simultaneous repolarization
entire heart is in refractory period during this time
after, the SA node, due to its automaticity, is the first to regenerate a beat and sinus rhythm is restored
86
what is the standard treatment for SVTs (i.e AVNRT) and typical atrial flutter
radiofrequency ablation
87
how does adenosine work u
IV adenosine causes transient heart block at the AV node
commonly administered to people with AVNRT
bind the ALPHA 1 receptor and inhibits ADENYLYL CYCLASE causing a reduction in cAMP--> causes HYPERPOLARIZATION by increasing the influx of K+
also causes endothelial dependent relaxation of smooth muscles surrounding the arteries (dilate)
SEs: facial flushing, temporary rash on chest, lightheadedness, diaphoresis or nausea + sense of impending doom
88
what drugs would you use to treat AVNRT
| from email from Courneya
beta blockers and non-DHP calcium channel blockers
adenosine
treats through suppression of AV node
89
what are the class Ia anti-arrhythmics?
how do they work?
Na+ channel blockers
moderate block
very much decrease the phase 0 upstroke rate and thus prolong AP duration
i.e quinidine, procainamide, dysopiramide
90
what are the class IIb anti-arrhythmics?
how do they work ?
Na+ channel blockers
mild block
slightly decrease phase 0 upstroke rate; shorten AP duration
lidocaine, mexiteline
91
what are the class Ic anti-arrhythmics?
how do they work?
Na+ channel blockers
MARKED block
very very much (more than Ia and Ib) decrease the phase 0 upstroke rate--> no change in AP duration
i.e flecainide
propafenone
92
```
what are the class II anti-arrhythmics?
how do they work?
```
Beta adrenergic receptor blockade
i.e pronanolol
esmolol
metoprolol
93
what are the class III anti-arrhythmics
how do they work
primarily K+ channel blockers
PROLONG AP duration
```
i.e amiodarone
sotalol
bretylium
ibutilide
dofetilide
```
serves to delay repolarization by inhibition of K+ ion channels (i.e in phase 2/3) and thus prolongs refractory period on all cardiac tissue and thus decrease HR
94
what are the class IV anti-arrhythmics?
how do they work
calcium channel blockers
95
what is the overall effect of digoxin
+ inotrope effect (stronger contraction)
prolong refractory period of AV node (slower HR)
96
what is the mechanism effect of digoxin?
increases contractility of the heart
inhibits the sarcolemmal Na+/K+ ATPase pump--> increased intracellular sodium concentration--> reduces Ca2+ extrusion from the cell by the Na+/Ca2+ exchanger--> more Ca2+ is thus pumped into the SR--> more Ca2+ is thus released at the next AP and thus greater force of contraction
97
what is the electrical effect of digoxin?
slows the conduction velocity and prolongs the refractory period at the AV node
does this by acting on cardiac tissue, enhancing vagal tone and inhibiting SNS activity
once it reaches the toxic range, digoxin has lots of toxic electrical effects (i.e causing re-entrant rhythms, complete heart block)
98
when is digoxin used clinically?
1. heart failure
- to increase contractility and augment cardiac output
2. as an anti-arrhythmic agent for atrial fibrillation and atrial flutter
- reduces the # of impulses through the AV node and therefore slows the ventricular rate
3. can be used to interrupt re-entrant circuits through AV node
99
what is atropine?
anti-cholinergic
competitively binds to muscarinic receptors and therefore suppresses vagal stimulation
increases HR and enhances AV node conduction
100
clinical uses of atropine?
symptomatic bradycardia that requires Tx
transient increase in HR only
pacemakers are needed for sustained brady Tx
101
how can you distinguished ventricular tachy from SVT on ECG
ventricular tachy = wide QRS
SVT = narrow QRS
SVT w/aberrancy has wide QRS but has normal QRS morphology and responds to vagal maneuvers
