lecture 19- cardiovascular foundations II Flashcards
myocaridal cells (myocytes)
99% of the cells
contractile force
the force producing cells: striated muscle fibers
autorhythmic (pacemaker) cells
generate spontaneous, rhythmic APs
–> do not contribute to the contractile force of a muscle
both myocytes and pacemaker cells can generate…
APs
ventricular myocyte APs
(myocardial contractile cells)
- resting membrane potential is -90mV
- AP is initated when wave of depolarization enters cells
- AP divided into 4 phases
- long AP duration (about 200msec)
What are the 3 channels in generating ventricular action potential
- voltage gated Na+ channels
- voltage gated Ca2+ channels
- a number of different voltage-gated K+ channels
ventricular AP: what are the diff types of voltage gated K channels?
slow
medium
fast
leak
ventricular AP shape (curve on graph) is due to
time-dependent opening and closing of different voltage-gated ion channels
- speed of opening is different for every channel
Ventricular AP: Na+ channels
similar function to those in neurons:
-fast activating
-fast inactivating
-membrane must repolarize for them to reset (refractory period)
Ventricular AP: Ca2+ and K+ channels
also open w membrane depolarization but take longer to open
(Ca2+ is faster than K+ though)
5 phases of ventricular AP
*starts at 4
0= rapid upstroke/depolarization
1= notch
2= plateau (tug of war)
3= rapid repolarization
4= at rest
ventricular AP phase 0
Na+ channels open
Na+ in (upstroke/depolarization, was -90mV at resting)
ventricular AP phase 1: notch
Na+ channels inactivate. Fast K+ channels open (repolarization).
Na+ flow stops. K+ flows out (brief)
ventricular AP phase 2: plateau
fast K+ channels close and slower K+ channels open.
Ca2+ channels open.
K+ flows out. Ca2+ flows in
initially Pk=Pca (equilibrium)
ventricular AP phase 3: repolarize
Ca2+ channels inactivate. Slow K+ channels open.
Ca2+ flow stops. K+ flows in
ventricular AP phase 4: at rest
slow K+ channels close.
(Kv close but K leak stay open)
K+ out through leak channels.
Na+-K+ATPase
tetanus
the fusion of contractions to produce a continuous contraction
the long cardiac AP prevents…
summation and tetanus
compare refractory period in cardiac muscle vs skeletal muscle AP
cardiac muscle fiber: refractory period is almost as long as the entire muscle twitch
skeletal muscle fast twitch fiber: refractory period is very short compared to amount of time needed for the development of tension
compare summation and tetanus in cardiac vs skeletal muscle AP
cardiac: long refractory period prevents tetanus
skeletal muscles are stimulated repeatedly, they will exhibit summation and tetanus
(tension sums w/ each twitch)
pacemaker APs are driven by
“funny” channels
pacemaker APs
- no stable resting membrane potential
- pacemaker potential between APs
- due to If current through “funny”/HCN channel:
–> HCN channels conduct both Na+ and K+ in.
Net Na+ IN leads to depolarization.
HCN channel=
hyperpolarization-activated cyclic nucleotide gated channels
(pacemaker channels, funny channels)
APs rhythmically initiated in —- cells set the pace of the heart
SA node
SA nodes lie at the junction between
superior vena cava and right atrium
where are autorhythmic cells localized to?
specialized tissues of conduction
(wiring and insulation for atria and ventricles to contract)
Ventricular conduction system
AV node –> the common AV bundle (bundle of His) –> divides into left and right bundles –> bundles give rise to Purkinje fibers
AV (atrio ventricular) nodes lie in the
inter-atrial septum
–> the only pathways for electrical conduction across connective tissue between atria and ventricles
SA node function
sets the pace of the heartbeat at 70 bpm
AV node function
routes direction of electrical signals
delays transmission of APs
(PAUSE! atria need to finish contracting before ventricles contract)
AV node can act as pacemaker under some pathological conditions (fires at 50 bpm) too slow!
what other fibers also have pacemaker properties?
Purkinje fibers (35 bpm)
what cells is HR set by?
the fastest pacemaker cells in the circuit
(SA node)
APs are continually and spontaneously initiated in the
SA node
APs spread through — system of the heart
electrical conducting
when APs pass across atria and ventricles….
depolarization spreads acorss myocytes
APs depolarize the myocyte membrane
myocyte contracts
Einthoven’s triangle and ECG
represents global electrical activity of the heart
- mostly measures spread of depolarization through heart muscle
ECG: P wave=
atrial depolarization
ECG: QRS complex=
atrial repolarization and ventricular depolarization
ECG: T wave=
ventricular repolarization
Tachycardia
HR is FASTER than normal
Bradychardia
HR is SLOWER than normal
Fibrilation=
electrogram is disorganized
Atrial fibrilation=
heart still functions as a pump
- atria keeps fluttering, doesn’t fully relax
- not life threatening
Ventricular fibrilation=
heart does not function as an effective pump
- life threatening
- ventricles fluttering
