Cardiac Excitation And Contraction Flashcards
Cardiac output split between atria and ventricles (CO)
Atria/ventricles = 10/90
P-wave (EKG)
The first ‘bump’ on the EKG
Represents the wave of depolarization across the atria
Signal starts at SAN —> hits all parts of the atria and converges at the AVN
Fibrous ring keeps the conduction from traveling to the ventricles…and only to the AVN
I.e. the signal conduction can only get to the ventricles through the AVN
Role of AVN
Slows down conduction
‘Electrical filter’ to protect the ventricles
Structurally it can do this because…
- Fewer gap junctions
- Low expression levels of Na+ channels
THEREFORE Ca2+ is the dominant current, which has a smaller amplitude
Flat line immediately after P-wave
Signal is limited to the small area of the AVN…
So small that cannot detect electric potential on machine
QRS interval
Time taken for ventricular depolarization
AVN —> bundle of His (Purkinje Fibers)
Very very fast
Flow of conductance: endocardium —> epicardium
Gap junctions / intercalated discs in muscle cells
Highly permeable
Protein = connexons
Open condition = low [Ca2+] and normal pH
Closed = high [Ca2+] and low pH
—> mechanism to protect neighboring cells…so dangerous environment conditions don’t spread uncontrollably
Relationship between ATP levels and gap junction conformation
Low ATP —> increase [Ca2+] —> lower pH —> closed channels
T-wave
After QRS interval
Repolarization of ventricles
Flow: epicardium —> endocardium (reverse of depolarization)
—> due to the fact that APs have a shorter duration in the epicardium
Why T-wave is upright
What does a large P-wave indicate (amplitude)
Large Atria
= congestive heart failure
Abnormally wide QRS interval =
LV hypertrophy
If T-wave too high
Hyperkalcemia
If QT (ventricular repolarization) is too prolonged…
Rish for death!!! AAAHHHHHH
Regional differences in AP duration
Purkinje > ventricular»_space;> atrial
Regional differences in phase 1 notch
Epicardial»_space; endocardial
Regional differences in unstable diastolic potential
SAN > AVN > purkinje
They have to ability to spontaneous depolarized
Ionic basis of cardiac action potential
- K+ outflow (I-k1)
- Na+ influx (I-Na)
(Then most Na+ channel close)
- Some transient outflow of K+ (I-to)
(Then Ca2+ channels start to open)
- Ca2+ influx
(Ca2+ influx (+) K+ outlfow —> ‘plateau’ in graph ‘#2’)
- I-k activates outflow —> rapid repolarization
Relationship between conduction velocity and Na+ current
Direct relationship
Steps 0 —> 4 of cardiac AP
And their corresponding responsible current
0 = I-Na+ (influx)
1 = ‘notch’ = I-to (outflow)
2 = I-Ca2+ (influx)
3 = I-K (outflow)
4 = RP = I-K1 (@ E-k)
Effects of voltage and time on Na+ availablity
At -40mV = all channels inactivated
Cannot initiated AP until atleast 50% of channels are rested (RRP) - not ideal thou
