Action Potential/ECG Flashcards
hierarchy of conduction system
SA node - 60-80
AV node - 30-40
Purkinje - 20-30
Ventricular muscle - slowest
E-C coupling in the heart
AP - triggers Ca release - responsible for contraction
coupling! not same signal

Slow AP Conduction Tissues
SA Node
AV Node
I(k1)
highly expressed in most myocytes except the node!
keeps resting potential at about -80
basis of resting membrane potential in cell

Fast response action potential
Atrial, Purkinje, Ventricular Action Potentials
Phase 0
Fast response
Upstroke
Sodium is entering - I(Na)
I(K1) is closed - resting potential, close because Mg in the cell is trying to leave and it plugs the channel

Phase 1
Fast response
Early repolarization
I(to) - channel opens when in depolarized range and opens just for a short time
outward K+ current

Phase 2
Fast Response
Plateau
I(to) inactivated
I(k) - delayed rectifier! open and potassium leaves
I(ca) - trigger Ca - L type channels - voltage gated
plateau - balance of K out and Ca in
when inactivate I(Ca), delayed rectifier WINS and repolarization happens because K leaves

Phase 3
Fast Response
Final repolarization
I(k) [delayed rectifier] and I(k1) [resting current] both open and both letting out K!
back to rest

Phase 4
Fast response
Rest
I(K1) open - keeping resting potential
Na/K transporter working

Structure of Voltage gated K+ channel
4 separate subunits form channel
voltage sensor
Pore region
N-terminal - V-dependent inactivation

voltage sensor of K channel
S4

Pore region of votage gated K channel
S4-S5 linker

Voltage gated Na/Ca channel
same structure as K channel but single subunit has 4 repeats

I(K1)
inward rectifier current
resting membrane potential
outward current during phase 3
NOT voltage gated
closes at DEPOLARIZED membrane potentials
NOT in pacemaker cells
I(K)
delayed rectifier current
Outward current during phase 2 and 3
2 components:R and S
EXIST in pacemaker cells
Phase 0
Slow response
upstroke due to inward Ca current (L type Ca current
resting potential was already less negative (there is no I(K1))

Phase 3
Slow response

Phase 4
Slow response
slow diastolic depolarization

I(f)
current that contributes to phase 4 diastolic depolarization
inward Na+
induced by hyperpolarization and allows to oscillate toward depolarization
currents that contribute to diastolic depolarization in nodal cells
I(f) - inward Na - induced by hyperpolarization
I(ca) - inward Calcium
I(k) - outward delayed rectifier current (R and S

factors that influence pacemaker rate
slope of diastolic depolarization
threshold potntial
min diastolic potential

effect of parasympathetic stimulation
Activate I(k)ACH channels
lowers minimum diastolic potential
decreases slope of phase 4

effect of sympathetic stimulation
activate I(f) channels
Increases slope of phaes 4
no change in min diastolic potential

unipolar limb leads
aVR, aVL, aVF
Wilson’s Central Terminal - average the other two!
impossimble to flip

bipolar limb leads
I (right arm to left arm)
II (right arm to left leg)
III (left arm to left leg)
possible to flip - true + and true -

precordial leads
V1-V6

lead diagram

augmented lead
aVR, aVL, aVF
averaged vector

ventricle depolarization and ECG
starts on left side of septum moving toward right

Normal value of PR
.12-.2 seconds (less than 1 big box)

Normal QRS duration
.06-.10 seconds (less than half of a box

Normal QT interval duration
less than .44 in men and .46 in women (less than 2 boxes_

time on EKG
1 big box is .2 sec, 200 msec
1 small box is .04 sec, 40 msec
voltage on ECG
1 big box = .5 mV
Count off method for HR
300-150-100-75-60-50 from QRS to QRS
left axis deviation
inferior wall MI
left anterior fasciuclar block
LVH
-30 to -90
if up in I and down in II

right axis deviation
RVH
acute R heart strain (PE)
left posterior fascicular block
+90-+180
down in 1 and up in 2

normal axis
up in limb I and limb II
mean axis must fall between -30 and +90

RA enlargement on EKG
P wave
lead II - higher at neginning
V1 - biphasic

LA enlargement
P wave
Lead II - higher at end
V1 - p wave is negative!

Sign of RVH
R>S in lead V1
R axis deviation

LVH
S in V1 + R in V5
R in aVL>11 mm
or
R in I >15 mm

ECG Read Order
- rate
- rhythm
- axis
- intervals (PR, QRS, QT)
- Morphology - P, T, ST
RBBB
RSR’ in V1 (rabbit ears)
LV first (down in V1, Up in V6)
Widneed QRS
Prminent S in V5

LBBB
Early R added to big, late L and compound
deeply negative in V1
rS
Widened QRS
broad, notched R in V6
absent R and prominent S in V1

RBBB contraction pattern
starts on R side of septum
toward R
big toward L
then to R

LBBB contraction pattern
starts on right side of septum
depol R then big swing to L

Left Anterior Fasicular block
Posterior to Anterior
L axis deviation
Small Q in aVL and I (first depolarization is away)
Small R in inferior leads (II, III, aVF) - inital downward

Left posterior fasicular black
start anterior and swing posterior
R axis deviation
small R in aVL and I
Small Q in inferior leads (II,III, aVF)

ST Elevation
ischemia
acute-hours

Q wave
with ischemia
begins hours after ischemia and deepens
persists long after MI

T Wave Inversion
Days after ischemia
will normalize

Pathologic Q Wave
fibrotic/bad conduction system - can’t gt through (physical block)
eventually jumps over it
25% QRS amplitude if seen in V1-V3

Hyperkalemia on EKG
Tall, peaked T wave

anteroseptal leads
V1, V2
anterolateral leads
V5, V6
I
aVL
anteroapical leads
V3, V4
Inferior Leads
II, III, aVF