11. Basic ECG Flashcards
Cardiac conduction pathway
SA node
internodal fascicles
bachmann’s bundle
AV node
Bundle of His
Right Bundle branch
Left bundle branch
purkinje fibers
where does the electrical current slow down in the heart
AV node
allows for atria to fully contract before the ventricles contract
maximizes ventricular filling
pacemaker cells
initiate heart beat
set heart rate
SA node
AV node
primary pacemaker of heart
SA node
SA node beats per min
60-100 bpm
sinus beats
AV node beats per min
40-60 bpm
junctional beats
ventricular muscle beats per min
30-40 bpm
p wave
atrial contraction
QRS
ventricular contraction
premature atrial contractions
heartbeats initiated by atrial myocardium
retrograde current is seen in
junctional beats initiated by AV node
retrograde current on ecg
inverted p wave
upright p wave
heartbeat originated from SA node or atria
ategrade conduction
inverted p wave
heartbeat originated from AV node
retrograde conduction
wide QRS
slow ventricular depolarization
heartbeat initiated by ventricular myocardium
1 large box
0.2 sec
1 small box
0.04 sec
1 second
5 large boxes
1 min
300 large boxes
RR interval
heart rate
300/#lg boxes
intervals include
a wave
normal p wave
3 small boxes
<0.12s
normal QRS
<0.12s
1.5-3 sm boxes
T wave
ventricular repolarization
normal T wave
<5mm height
U wave indicates
hypokalemia
J point
point where S wave returns to baseline
Delta wave
upward slurring Q wave
wollff parkinson white syndome
J wave
hypothermia
bump on S wave
PR interval
beginning of P to start of Q
normal PR interval
0.12-0.2s
3-5 sm boxes
long PR interval
indicates delayed conduction in AV node
QT interval
begining of Q wave to end of T wave
what prolongs QT interval
zofran
phenergan
subarachnoid hemorrhage
PR segment
end of P wave to beginning of Q wave
ST segment
J point to start of T wave
premature beat
heartbeats happens before expected
“fast”
PAC
PVC
PJC
escape beat
heartbeat that comes oafter long pause
“slow”
ventricular
junctional
systole
heart contraction
heart is not perfusing
organs are perfused
diastole
heart relaxation
heart is perfused
organs are not perfused
slower heart rate
increases coronary perfusion
faster heart rate
worse coronary perfusion
ventricular filling
amount of blood that fills the ventricles prior to ventricular contraction
preload
decrease ventricular filling
decreased SV
decreases CO
active ventricular filling
during atrial contraction
incr preload
normal SV
normal CO
passive ventricular filling
when atria dont contract
decr preload
decr SV
decr CO
heart conditions that reduce ventricular filling
- heartbeat w/o atrial contraction (no p wave)
- premature heartbeat
- rapid heart rate
do premature heartbeats produce a pulse
no
ECG leads detect
electrical difference (voltage) between 2 limbs
3 lead ECG limitation
not as sensitive for detecting myocardial ischemia occuring in left ventricle
lead 1
white to black
(-): RA
(+): LA
lead 2
white to red
(-): RA
(+): LL
lead 3
black to red
(-): LA
(+): LL
what additional leads are in 5 lead ECG?
green
brown (V5)
green lead
neutral grounding lead
brown lead
V5
precordial lead
helps detect left ventricular ischemia
lead locations
white - right
green - below green
black - left
brown - below black
red - below brown
how to get best ECG connection
cleanse site of application w/alcohol
exfoliate skin layer
avoid placing over hair
irregular sinus
HR fluctuating w/inspiration and expiration
inspiration: faster
expiration: slower
why is inspriation HR faster
decrease intrathoracic pressure
increases preload
increases HR
why is expiration HR slower
increase intrathoracic pressure
decreases preload
decreases HR
sinus tachy
P wave
HR>100 bpm
sinus tachy etilogies
hypovolemia
hypotension
pain/light anesthesia
sinus tachycardia causes
incr cardiac O2 demand
decr cardiac O2 supply
hypovolemia
sinus tachy treatment
give fluids
deepen anesthetic
beta blocker
sinus brady
p wave
HR <60bpm
sinus brady is good for what pts
healthy pts who exercise
pts w/CAD
lower HR
incr O2 supply
decr O2 demand
bradycardia is bad in what pt population
kids
what heart rate is always a cause for concern
<=30bpm
bradycardia treatment
robinul
atropine
epinephrine
cardiac pacing (unresponsive to meds)
temporary transcutaneous pacing
SA node pacing pads via defibrillator
pacemaker
implantable device to act as artificial SA node
ectopy
any heartbeat that orginates outside the SA node
- AV node
- atrial myocardiaum
- ventricular myocardium
PAC
premature beat
upright p wave
normal/narrow QRS
when are PACs concerning
when they start occuring frequently
PJC
premature beat
missing/inverted p wave
normal QRS
retrograde
when are PJCs concerning
when they start occuring frequently
PVC
premature beat
no p wave
wide/bizarre/different QRS
what can trigger PVC
ischemia
pH imbalance
electrolyte abnormalities
caffeine
stress
abnormal electrical pathways
do PVCs produce a pulse
no
what is the pulse rate for bigeminal PVCs
half of what the ECG says the pulse rate is
bigeminal PVC
every other beat
unifocal PVC
same shape = same origin
multifocal PVC
different shape = different origin
what is more concerning: unifocal or multifocal PVC?
multifocal
couplet PVC
2 in a row
salvo PVC
3 in a row
PVC treatment
antiarrythmics
- lidocaine (100mg)
- amiodarone
robinul (speed HR up)
junctional escape beat
escape beat
inverted/missing p wave
normal QRS
junctional escape beat physiology
SA node failed
AV node starts heartbeat
SA node starts working again
when should we be concerned w/junctional escape beats
if they occur frequently
treat w/robinul/atropine/pacing
junctional escape beat treatment
robinul/atropine
pacing
ventricular escape beat
long pause
wide QRS
no p wave
ventricular escape beat physiology
SA and AV node fail
ventricular myocardium initiates beat
SA node works again
atrial flutter
sawtooth p waves (250-350/min)
wide p waves
atrial flutter physiology
decr ventricular filling
decr CO
incr O2 demand
when are we concerned about atrial flutter
would not do an elective case until pt has been evaluated by a cardiologist
type 1 atrial flutter
<350bpm
type 2 atrial flutter
> 350bpm
atrial flutter treatment
amiodarone, sotalol, digoxin
synchronized cardioversion (for hypotensive pts)
shocking heart
treats unstable fast rhythms
pacing heart
treats unstable slow rhythms
Afib
no p waves
narrow QRS
may or may not have fibrillation waves
irregularly irregular rhythm
Afib physilogy
atria quivering w/500 atrial impulses/min
Afib risks
clot formation in LA (blood pooling)
CO decr
hypotension
Afib CO decreases by
25-50%
what type of afib is more concerning: chronic or acute?
acute afib is more concerning
suffer significant drop in CO
controlled afib
ventricular rate <100bpm
uncontrolled afib
ventricular rate >100bpm\
rapid ventricular response
afib treatment
medications
synchronized cardioversion
how long should a pt be anticoagulated prior to cardioversion
3 weeks prior
4 week post
junctional rhythm
inverted/absent P
normal QRS
normal junction
40-60bpm
accelerated junctional
60-100 bpm
junctional tachycardia
> 100bpm
junctional rhythm concerns
slower HR
reduced ventricular filling
junctional rhythm treatment
robinul to incr HR
SVT
HR >150bpm
normal QRS
may or may not have P waves
SVT concerns
decr ventricular filling
decr CO
SVT treatment
vagal maneuvers
adenosine (slows SA/AV)
synchronized csrdioversion
antiarrythmics
ventricular escape rhythm (idoventricular)
no p wave
wide WRS
slow HR <60bpm
ventricular escape physiology
SA and AV node failed
ventricular myocardium is beating
ventricular escape concerns
no active ventricular filling
HR is low
low CO
ventricular escape treatment
cardiac pacing
epinephrine
avoid lidocaine (suppresses ventricular beat)
accelerates idivoentricular rhythm
60-100bm
Vtach
> 100bpm
no p waves
wide QRS (same shape)
polymorphic Vtach
torsades de pointes
twisting
Vtach physiology
ventricular myocardium initiates heart beat at rapid rate
high O2 consumption
minimal ventricular filling
does vtach have a pulse?
potentially
Vtach treatment
electrical cardioversion
monomorphic vtach treatment
amiodarone
lidocaine
polymorphic vtach
magnesium
amiodarone does what to QT interval
prolongs it
Vfib
no real p waves or QRS complexes
shorter deflections
Vfib physiology
quivering ventricles
rapid rate
high O2 consumption
no pulse
no CO
Vfib treatment
defibrillation
CPR
agonal rhythm
slow complex rhythm immediately preceding asystole
do agonal rhythms produce cardiac output
nope
asystole
cardiac arrest
CPR
epinephrine
do not defibrilate
pulseless electrical activity (PEA)
pt has no pulse
ECG shows electrical activity
PEA is most likely seen with what rhythms
sinus
bradycardish
ventricularish
AV blockish
slowish type
cause of PEA
heart does not contract
insufficient cardiac output to generate pulse and supply blood to organs
PEA treatment
CPR
epinephrine
NO defibrillation
1st Deg AV block
long PR interval
>200msec (1 lg box)
2d Deg AV block
dropped QRS complex
2d Deg AV Type 1
dropped QRS
increasingly long PR intervals
2d Deg AV Type 2
dropped QRS
unchanging PR intervals
where is the block in 2d deg type 2
below the AV node
in bundle of his or bundle branches
3d deg AV block
wandering P waves
slow ventricular rate
3d deg AV block physiology
AV node completely blocekd
ventricles must initiate heart beat
atria and ventricals are not synchronized
decreased CO
treatment for complete heart block
cardiac pacing
epinephrine
AVOID lidocaine
pacemaker atrial lead
sense when atria is contracting
pacemaker ventricular lead
paces 120-200msec after each atrial beat
Ischemia/Infarction ECG indications
ST segment changes
abnormal T waves
abnormal Q waves
ST depression indicates
ischemia
ST elevation indicates
infarction
myocardial ischemia treatment: increase O2 supply
- 100% FiO2
- decrease HR
–give beta blockers - mx normal BP
—avoid hypotension - give NTG
- give aspirin
myocardial ischemia treatment: decrease O2 demand
- decr HR
–give beta blockers - avoid pain/anxiety/tachycardia
–give narcs/sedatives - avoid high afterload
–avoid HTN