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30 Cards in this Set
- Front
- Back
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SA Node
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- spontaneous generation of excitation
- right atrium |
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Excitation pathway
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- 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 |
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CICR
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-Ca induced Ca release
- opens ryanodine receptors on Sr - cardiac muscle dependent on extracellular Ca - mechanical coupling between DHP receptors and ryanodine receptors |
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Relaxation
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- 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 |
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passive tension
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- resistance to stretch of muscle cells to blood filling relaxed ventricles
- produced by connective tissue of ventricular wall |
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end-diastolic volume
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- amount of blood in ventricle immediately before ventricular contraction
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Starling's Law of the heart
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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 |
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active tension
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- magnitude depends on extent of ventricular filling (end diastolic volume)
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Intrinsic regulation of cardiac performance
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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 |
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phospholamban
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- 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 |
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Bowditch Effect
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- 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 |
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increased contractility
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incrased in active tension at a given EDV
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sympathetic nerve stimulation
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- increase --> hypereffective
- decrease --> hypoeffective |
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Differences in Structure of Cardiac muscle (from skeletal)
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1) T tubules on Z lines not at junction of A and I bands
2) more Mitochondria 3) intercalated disks with gap junctions |
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pacemaker cells
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- 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 |
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AV node
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- can function as very slow pacemaker, causing slow regular contractions independent of atrial contractions
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Phase 0
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- depolarization
- transmembrane potential changes from -90 mv to +20 mv - upstroke of AP - Na conductance, inward current - at peak, approaches Na equilibrium potential |
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Phase 1
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- 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 |
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Phase 2
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- 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 |
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Phase 3
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- repolarization
- Ca conductance ↓ CaV1(DHP) channels close - ↑ in K conductance - large outward K current |
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Phase 4
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- resting membrane potential
- inward and out K currents are equal - membrane potential continues to approach K equilibrium potential |
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AV action potential
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- slow response
- found in purkinje fibers as well as AV - starts with opening of Cav1 channels, slower and smaller amplitude - |
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pacemaker current
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- 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 |
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Na Ca exchange pump
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- 3 Na in 1 Ca out
- ATP used to create the Na gradient - cell wide Ca content |
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Pressure Volume relationship
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- diastole: heart fills with blood against passive pressure
- end-diastolic volume like length of skeletal muscle before onset of contraction - pressure increases with EDV |
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mechanical properties
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- 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 |
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Sympathetic innervation
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- 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 |
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Parasympathetic innervation
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- 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 |
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tetrodotoxin
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- fast Na channels blocked
- similar effect to anoxia |
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digitalis
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- inhibits Na K pump allowing Na to accumulate in muscle fiber
- can't remove Ca, so contraction gets stronger |
