Lecture 2: Conduction and ECG Flashcards
Cardiac Muscle Cells
*branched! (unique to only them)
striated, centrally located nucleus (or 2)
actin and myosin in myofibrils
Why branching in CM cells?
allows for communication between 1 cell and every cell it touches
transmit electrical impulses and pull in all directions, so no tearing
Gap Junctions
small tubes where ions travel from cell to cell
(electrical impulses) (sodium in first, depol., leaks into new cell, causing its depol
*** In intercalated discs between neighbors
spans 1 membrane, int. cell space, next membrane
Intercalated discs house
Gap Junctions
desmosomes
desmosomes
hold adj. cells together so they can pull w/o tearing
folds (in what)
inc SA, so more desmosomes and gap junctions
for more pulling
How cardiac muscle differs from skeletal
much reduced
fewer t tubules
lessened SR extensive network
1 triad per sarcomere
extracellular calcium also plays role (never in skeletal)purkinje
lots of extensive branching
carry signal to many places
Pacemaker
In cell wall of R atrium, always sending sequence
cells spontaneously discharge APs: 100-120/minute by themselves
When inbody, ANS regulate speed, more like 70 bpm (resting)
SA node, depol here first
Bundle of His
R & L bundles connected by it
Transmits AP to bundle branches, Purkinje fibers, and muscles of ventricles (lower parts first, blood pushes up.)
atria and ventricles
contract separate from each other
EKG/ECG
APs of all active cells that are detected and recorded
P wave
atrial depol (influx Na+)
PQ interval
time between initiation and ending of contraction of atria, ventricle excitation
QRS complex
repol of atria, deopl of ventricles
ST
period of time when vents contract
T wave
repolarization of ventricles (relaxation)
sarcomere
thick and thin filaments overlap
triad
terminal cisternae: lots of calcium
t-tubule
fluid inside, where the release of calcium is ordered
Conduction 1
AP starts at SA, impulse travels down acorss atria, causes more contraction
Conduction 2
AV node
AV border: cells (not PM) make a maze for AP to slow down impulse by 0.1 sec so the atria can fully empty and the vents can fill
3 AV bundles (bundle of His)
signal is traveling and insulated.
contraction begins at apex, goes toward base
Cardiac Muscle APs
polarize, plateau, repolarize, return to resting potential
Plateau
not in skeletal
LONG time (100 to 300 X longer break than skeletal)
in contracting state, due to Ca influx
Don’t want tetnus in heart!
avoided by long contraction period and a longer refractory period
Depolarization:
sodium influx
Repolarization
close Ca gates, open K+ gates
Refractory period
when muscle cell is unresponsive to stimulatin
absolute refractory period
cell won’t respond regardles of stimulus strength
very ling, about as long as AP (250 ms)
relative refractory period
cell will respond only if stim reaches suprathreshold
Pacemaker potentials
autorhytmic
innitiate APs
Unstable resting potentials = pacemaker potentials
Calcium influx used to raise phase of AP (not sodium)
Threshold: -60 mV (unstable)
depol then imediate repol (no waiting)
Pacemaker Gate opening
Voltage gated Ca+ ;ead to increased depol
Na, Ca, K (as opposed to cardiac muscle: Na, K, done only)
start-P
atrial systole
Q-T
ventricle systole
T- end
relaxation of ventricles
this gets shorter as heart speeds up
