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30 Cards in this Set

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SA Node
- spontaneous generation of excitation
- right atrium
Excitation pathway
- SA node --> via transverse tubules -->depolarization opens L type Ca channels (dihydroyridine receptors)in T- tubules
- T tubules through Ca induced Ca release open ryanodine receptors on SR membrane
CICR
-Ca induced Ca release
- opens ryanodine receptors on Sr
- cardiac muscle dependent on extracellular Ca
- mechanical coupling between DHP receptors and ryanodine receptors
Relaxation
- cytoplasmic Ca must return to resting values (<10^-7M)
- 1) SR Ca- ATPase reputakes
2) Na-Ca antiport
3) Ca pump sequesters Ca within SR via calreticulin and calsequestrin
passive tension
- resistance to stretch of muscle cells to blood filling relaxed ventricles
- produced by connective tissue of ventricular wall
end-diastolic volume
- amount of blood in ventricle immediately before ventricular contraction
Starling's Law of the heart
energy of contraction of the muscle is related/proportional to the initial length of the muscle fibre
- EDV icreases as active tension increases
- what goes in must come out
active tension
- magnitude depends on extent of ventricular filling (end diastolic volume)
Intrinsic regulation of cardiac performance
1) starlin's law,
heterometric autoregulation
- instrinsic propery of muscle, soley dependent on stretched length in muscle cells

2) sympathetic nerve stimulation
- NE on B1 R coupled to Gs receptors --> CAMP --> protein kinase A cascade --> Ca release from SR
- additive effect from multiple action potentials
1) SR Ca-ATPase activity increased
2) L type Ca channels are P, increasing open time --> more Ca influx
- CICR increase, SR more loaded, more Ca released
3) T type Ca Channels and non-selective channel If are P, increasing heart rate, more Ca enters cell per minute
phospholamban
- SR protein normally limits SR Ca Atpase activity
- Inhibition increases SR Ca-ATPase increases rate of muscle relaxation and loads the SR wtih more Ca
- phosphorylation inhibits the inhibitor
Bowditch Effect
- increase in HR increases myocardial contractility, by allowing more Ca in per minute, further loading SR to make Ca more available
- offsets decreased ventricular filling time by shortening length of systole, and increasing the amount of time in diastole
- shift to the L in P-V curve
increased contractility
incrased in active tension at a given EDV
sympathetic nerve stimulation
- increase --> hypereffective

- decrease --> hypoeffective
Differences in Structure of Cardiac muscle (from skeletal)
1) T tubules on Z lines not at junction of A and I bands
2) more Mitochondria
3) intercalated disks with gap junctions
pacemaker cells
- generate AP
- cardiac cells have continuous cytoplasm through gap junctions
- SA node
- contain small round cells that probably are pacemakers
- ANY cardiac cell can fire if not stimulated by another cell, so ANY can become pacemakers
AV node
- can function as very slow pacemaker, causing slow regular contractions independent of atrial contractions
Phase 0
- depolarization
- transmembrane potential changes from -90 mv to +20 mv
- upstroke of AP
- Na conductance, inward current
- at peak, approaches Na equilibrium potential
Phase 1
- fast decrease in potential to +10 mv
- up til now looks like any AP
- brief period of initial repolarization
- outward current, due to K outflow (chemical and electrical gradient)
- ↓ Na conductance
Phase 2
- long plateau at +10 mv
- transient ↑ in Ca conductance
- inward Ca current
- ↑ in K conductance
- outward and inward currents are equal so stable membrane potential
Phase 3
- repolarization
- Ca conductance ↓ CaV1(DHP) channels close
- ↑ in K conductance
- large outward K current
Phase 4
- resting membrane potential
- inward and out K currents are equal
- membrane potential continues to approach K equilibrium potential
AV action potential
- slow response
- found in purkinje fibers as well as AV
- starts with opening of Cav1 channels, slower and smaller amplitude
-
pacemaker current
- If f=funny
- non specific cation channel permeable to K and Na, opened by high transmembrane potentials
- slowly activated, and does not inactivate
- in SA and AV Ca and K channels contribute to progressive depolarization
Na Ca exchange pump
- 3 Na in 1 Ca out
- ATP used to create the Na gradient
- cell wide Ca content
Pressure Volume relationship
- diastole: heart fills with blood against passive pressure
- end-diastolic volume like length of skeletal muscle before onset of contraction
- pressure increases with EDV
mechanical properties
- low [Ca} graph of L v Tension steeper but shifted to the right than skeletal
- Cardiac muscle less sensitive to Ca than skeletal
- increasing length increases sensitivity to Ca
- due to cardiac troponin having several sites for P, regulate sensitivity to Ca
Sympathetic innervation
- β1 adrenergic R
- Gs protein R that elevate cyclic AMP and Phophokinase A
- Pacemaker: ↑ Ca current through Cav3 channels
- If: ↑
- higher frequency of AP
- Sarcoplasmic Ca pump is activated --> shorter AP and contractions
- P of α1 activates Cav1 Ca channels --> ↑ contractile force
- higher HR and stronger contractions
Parasympathetic innervation
- muscarinic 2 cholinergic R
- G protein R
- Gβγ open K (inward rectifying)
- Pacemaker: If and Ica reduced
- lower frequency of AP
- slower HR, longer weaker contractions
tetrodotoxin
- fast Na channels blocked
- similar effect to anoxia
digitalis
- inhibits Na K pump allowing Na to accumulate in muscle fiber
- can't remove Ca, so contraction gets stronger