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66 Cards in this Set

  • Front
  • Back
what does the cardiac conduction system do
generates and transmits electrical impulse and stimulates myocardium
what are the specialized cells that allow automaticity, excitability, and conductivity
nodal
purkinje
generates electrical impulse
automaticity
can be stimulated
excitability
stimulated to send electrical impulse on
conductivity
what do electrical impulses stimulate
cardiac myocytes
what does stimulation exchange occur through
na
k
ca
what is phase 4
resting phase
inside of cell is negatively charged and outside is positive
phase 4
final repolarization phase
phase 3
what happens in phase 3
repolarization causes sodium to move out of cell and let K move in
AKA plateau phase
phase 2
when does Ca move into cell
phase2
sodium enters cell and K leaves causing cell to become positive inside and negative outside
phase 0
what must myocardial cells do before being depolarized again
repolarize
cell unable to respond to electrical stimulus
absolute refractory
when is the phase considered absolute refrac.
phase 0-3
a stronger than normal electrical stimulus may cause premature depolariztion
relative refrac.
location of Sa nod
upper right atrium
functions normal pacemaker as highest rate automaticity
Sa node
in the lower right atrium
AV node
what does the AV node do
slows conduction impulse from atria to vents allowing filling
what happens if SA node not working
AV takes over
short fibers below AV node leading to branches
bundle of HIS
what does B HIS do
accelerates conduction velocity
rapidly conduct impulse per right bundle branch
bundle branches
has 2 branches
left side
automaticity of 20-40bpm
purkinje fibers
SA node firing
atria contract
slows down impulse of atria to allow vents to fill and contract for good C.O
AV node
where does AV node send signal to speed it up and send to body
bundle of his
decrease in HR causes what
increase in interval
decrease in interval
increase in HR
Autonomic NS controls what
rate of impulse
speed of conduction
strength of contraction
para NS causes
decrease rate
slow impulse conduction
decrease contraction
sympa NS causes
increase rate
increase contraction
direct result of directional flow of the hearts electrical impulse
upward or downward EKG movement
what affects waveforms on EKG
neg and pos electrode
above baselin
postive
below baseline
negative
what is the Pwave
atrial depolarization
QRS complex
ventricle depolarization
t wave
ventricle repolarization
u wave
repolal of purkinje fibers
pr interval t
travel of impulse from atria through av node to purkinje system
ST segment
early vent repolar
qt interval
vent depolar and repolar
should be at isoelectric line
St segment
what do the leads do on an EKG
6 measure electrical forces in the frontal plane
6 measure in the horizontal plane
NSR
60-100
characteristics of NSR
60-100
P---> P interval is same
R--->R interval is same
PR and QRS are normal
follows normal conduction
what is sinus bradycardia
<60 bpm
same NSR criteria
who usually has sinus bradycardia
athletes
how can one recognize sinus brady
decrease cardiac output
what are some things that sinus brady occur in response to
hypoxia
hypothermia
acidosis
hyper/hypo kalemia
hypovolemia
vagal stim
toxins/trauma/tamponade
hypothyroidism
what causes vagal stim
para symp
valsava
lifting
NG/OG/Endo tubes
Sx of sinus brady
hypotension
pale cool skin
weakness
angina
dizziness
confusion
Decreased LOC
SOB
Tx for sinus brady
atropine
EPI
dopamine
pacemaker
goal for tx of sinus brady
increase HR and contractility to improve CO
characteristics of sinus tachy
>100bpm
NSR criteria
r/t clinical cause
what is sinus tachy associated wth
exercise
pain
hypovolemia
myocardial ischemia
heart failure
fever
drugs (atroping/epi/dop/caff)
fear
Sx of sinus tachy
dizziness/hypotension d/t decreased CO
what does decreased perfusion cause
increased HR
Tx for sinus tachy
tx underlying cause
B-adrenergic blockers
verapamil
antipyretics
analgesics
decrease automaticity of SA node
verapamil
reduces HR and myocardial O2 consumption
B adrenergic blockers