Test 1: lecture 3 +4 ekg intro Flashcards
change from — to — happens inside cell during action potential
negative to positive
— is the ability of certain cardiac cells to initiate an electrical signal
automaticity
why is HR controlled by SA node
automaticity of those cardiac cells produce a signal at a faster rate then any other cell types in the heart, blocks out other signals
if SA node disfunctional heart will beat according to AV node
— is the ability of cardiac cells to respond to an electrical signal
excitability
resting cell at -70
Na/K pump pushed 3 Na out and 2 K in. results in net negative
K will diffuse into or out of the cell
out of cell
will keep inside of cell negative
what happens during depolarization
rush of Na and Ca into a cell makes it positive inside
what happens during repolarization
cell returns to resting negative
potasium(K) diffuses out of cell
explain fast response action potential
cell negative at rest at -90 mV
stimulus causes rapid depolarization as Na floods into cell
Ca slowly comes into cell- 2 steady state-then stops
K leaks out of cell- causing repolarization
Na/K pump returns cell to normal resting
explain slow response AP
pacemaker cells
can cause impulse on its own
resting at -60mV
DOES NOT need outside actional potential
steady influx of Calcium causes AP
repolarization caused by K leaking back out
slow or fast response AP causes automaticity
slow
think SA or AV node
can trigger itself by slow influx of Ca into the cell
what part of the heart has a slow conduction velocity
SA and AV node
controlled by slow response AP- slow influx of Ca into the cell
allows for the atria to empty into the ventricles before the ventricles contract
what part of the heart has a fast conduction velocity
purkinje fibers
atrial muscle
ventricular muscle
controlled by fast response AP- rapid influx of Na into the cell
explain cardiac excitation-contraction coupling
when cardiac cell is depolarized (becomes more +)
calcium comes into cell, increased intracellular calicum leads to increased sarcomere activation= contraction of the muscle cell
fast EKG paper speed
50 mm/s
1 small square= 0.02 seconds
BIC: # R-R intervals x 20 for bpm
instantaneous: 3000/RR interval= bpm
slow EKG paper speed
25 mm/s
1 small square = 0.04 seconds
BIC: # R-R intervals x 10 for bpm
instantaneous: 1500/RR interval= bpm
a voltage change of 2 mV would be how many squares
20 mm (20 small squares)
20 squares tall
what color electrodes on what limb
black- left arm
red- left leg
white- right arm
green- right leg
lead 1 has + and - where
R arm negative
left arm positive
lead 2 has + and - where
positive left leg
negative right arm
lead 3 has + and - where
positive left leg
negative left arm
how to form augmented leads
aVR= will have positive on right arm and average negatives of L arm and L leg
aVR, aVL, aVF will look at heart from different prospectives on frontal plane (cranial to caudal and left to right)
where are the leads in a hexaxial mapping system
depolarizing current will cause an internal change from — to — and if moving toward the positive electrode will be seen at —
negative to positive
toward positive = positive deflection
away form electrode = negative deflection
repolarizing current will cause an internal change from — to — and if moving toward the positive electrode will be seen at —
positive to negative
toward positive= negative deflection
away from electrode = positive deflection
what happens in phase 3 of action potential
repolarization (loss of K)
cell changes from + to negative
the change moves toward the + electode= negative deflection
phase 2 of fast AP causes what to EKG
phase 2= slow increase in Ca = plateau
no change in EKG
A vector parallel to the lead will cause a — deflection
larger
A vector perpendicular to the lead will cause a — deflection
smaller or no deflection
P wave represents
atrial depolarization
from SA to AV node (small positive bump)
QRS represents
ventricular depolarization
Q= intraventricular septal depolarization= small negative
R= ventricular depolarization= big +
S= depolarization of base of ventricles = small positive
PR interval/segment =
AV node holding signal
no change
flat line
QT interval=
ventricular depolarization and repolarization
— is between ventricular depolarization and repolarization
ST segment
— is ventricular depolarization and repolarization
QT interval
BIC pen on a 50 mm/sec paper is — long
150 mm= 150 small squares= 30 large squares = 3 seconds
count RR interval x 20 seconds= beats per minute
what is HR
7 beats in 3 seconds
7x20=140 bpm
paper speed 25 mm/sec
BIC pen =
150 mm= 150 small squares= 30 large squares= 6 seconds
RR interval x 10 = bpm
on 50 mm/sec paper a BIC pen is equal to how many seconds
on 25mm/sec?
50 mm/sec: 3 seconds
x 20 for bpm
25 mm/sec: 6 seconds
x 10 for bpm
vet use what paper speed for more spread out reading
50 mm/sec
faster
with irregular HR, max and min HR is found by measuring the —
longest and shortest RR interval
on 25 mm/sec paper how to calculate instantaneous HR
slow speed= 1 little square= 0.04 seconds
25 mm=1 sec
1500 mm=1 min
1500/RR interval= bpm (instant HR)
how to calculate instant HR with fast paper
50 mm/sec
1 small square= 0.02 second
50 mm= 1 second
3000 mm=60seconds
3000/RR interval = bpm instant HR
— ventricular enlargement leads to a MEA shift
right
left does NOT cause MEA shift
what are some causes of axis shift of MEA
right ventricular enlargement
RBBB or left anterior fasicular block
MEA for a dog points
40-100
MEA for a cat points
0-160
how to use isoelectric lead method
what lead is isoelectric?
lead 1
what lead is perpendicular to the iso lead?
aVF
Is the perpendicular + or negative?
positive
MEA= 90
how to determine MEA using pizza
look at lead 1 and aVF
what is polarity of lead 1?
positive
what is polarity of lead aVF?
positive
what is the overlap?
0-90
what is the MEA
pizza
lead 1= positive
lead aVF= negative
MEA =-90→0
left anterior axis shift
what can ventricular enlargement cause on an EKG
Increased R wave amplitude (Left sided)
Increased S wave (Right sided)
Prolonged QRS (rare)
what can atrial enlargement do to the EKG
P wave changes
Increased amplitude and/or increased duration
P mitrale is another name for
increased P wave duration
can happen with atrial enlargement
P pulmonale is another name for
increased amplitude of P wave
can be caused by atrial enlargement
if large P waves what might be happening?
atrial enlargement secondary to valve disease (regurgitation)
left ventricular enlargement will do what to EKG and MEA
increase R wave (gets taller/stronger)
rare prolonged QRS duration
NO change in MEA
LV enlargement in a dog will be seen as
— in lead 1
— in lead 2
60 msecds wide (rare)
over 1.0
over 3.0
LV enlargement in a cat will show as greater or equal to — in any lead
1 mV
greater then 60 msec wide (rare)
large R wave= LV enlargement
can be from hypertrophic cardiomyopathy
will still have normal MEA
right ventricular enlargement will cause — on the EKG
deep S wave
S>0.05 mV in lead 1
S> 0.35 mV in lead 2
right MEA shift
dog: MEA >103
what is MEA
what is wrong
deep S wave= right ventricular enlargement=pulmonic valve stenosis
MEA= lead 1 negative, aVF negative = 180 to -90
pulmonic stenosis will cause EKG —
right ventricular enlargement
leads to deep S in lead 1 and 2
right MEA shift
RBBB will do what to EKG
QRS prolongation
dog > 0.08 seconds
cat > 0.06 seconds
right axis shift
deep S waves
RBBB
long QRS
right axis shift
deep S waves (lead 1-3 and aVF)
right ventricular enlargement
deep S wave
right MEA shift
left ventricular enlargement
big R waves
NO change to MEA
normal QRS interval in dog is
70 ms
RBBB causes >80ms
normal QRS interval in cats
40 ms
RBBB causes >60ms
LBBB
normal MEA
long QRS
left or right BBB is always associated with underlying heart disease
LBBB
will cause QRS elongation
normal MEA
