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19 Cards in this Set

  • Front
  • Back

Modified myocytes

-SA node


-more rapid rate of phase 4 depolarization

Ventricular myocytes

-contractile


-Fast response action potential

Ions

Na+- 150mM out 15mM in = depolarize


Ca2+ - 2mM out .0001mM in = depolarize


K+ - 5mM out 150mM in =Repolarize



-Potential depends on permeability to each ion

SA node


Slow response

Phase 0: Upstroke - opening of L-type Ca2+ and influx of Ca2+


Phase 3: Repolarization - Above 0, opening of delayed rectifier K+ channels - efflux of K+


Phase 4: Pacemaker - K+ close ; Funny (IF) open, Na+ influx and depolarize


-At -55 mV T type Ca2+ open to depolarize to -40 where L type open

Ventricle / Atrial


Fast response

Phase 0: depolarizing - opening of Na+ channels


Phase 1: Early repolarization- close of Na+ and open of transient K+


Phase 2: Plateau- Open Of L type Ca2+ channels and the open rectifier K+ (equal)


Phase 3: Rapid Repolarization - efflux of K+ dominates; L type Ca2+ closure


Phase 4: Resting potential - inward K+ rectifier open - maintain -90mV

Overdrive suppression

-SA node dictates firing frequencies of AV and Purkinje (tertiary pacemaker)


SA-60-100


AV-40-60


Purkinje-20-40

Conduction pathway

SA node---> AV node----> Bundle of HIS ---> Bundle Branches ----> Purkinje fibers

Action potential

Starts by going down T tubules (wider than skeletal)---> depolarizes ----> L type calcium channels (DHPR) in t tubules open ----> Ca2+ entry---> bind to Ryanodine receptor----> increase in opening SR Ca2+ release channels (RYR)



-DHPR and RYR not physically connected like in skeletal


Amplifier

-Calcium Induced Calcium release (CICR)


-30% calcium outside


-70% from SR

Diastole

-relaxation


-Calcium taken out

Mechanisms that take calcium out

-Back into SR via ATP-Ca2+ pumps


-3 Na+ ---> 1 Ca2+ exchanger (NCX)


-Sarcolemmal Ca2+ ATPase



The same that entered must leave

Troponin complex

-Tropomyosin bound to actin


-Troponin T bound to Tropomyosin and Troponin I


-Troponin I bound to actin in absence of Ca2+ (covers actin- myosin binding site)


-Troponin C weakly bound to Troponin I

Troponin complex (Continued)

1 Calcium binds to Troponin C---> Troponin C binds more strongly to Troponin I ----> Troponin I no more binds to actin----> Troponin I binds to Troponin T ---> Troponin T binds to tropomyosin ---->Tropomyosin binds to actin---> Tropomyosin moves into groove of actin and Troponin swings out uncovering myosin binding site

Cross bridge

1. Actin x Myosin x ADP x Pi


2. Actin x Myosin ( rigor mortis)


3. Actin x myosin x ATP


4. Actin x myosin x ADP x Pi

ATP

-needed for every contraction


-Aerobic metabolism and oxidative phosphorylation


- Fatty and lactic acids


Cardiac Contraction

-One can not build on the other


-Must have diastole for refill



-Absolute refractory period - Fast Na+ channels


-Relative refractory period - Large stimulus required

Cardiac tension

-During diastole = passive tension


-Diastolic volume is equivalent to muscle length


-Preload =EDV

Preload

-Rest length


-normal working range but not optimal length


- the more preload the more contraction

Afterload

-Pressure in aorta that must be overcome to open aortic valve


-Diastolic Pressure



-For a given afterword, as you increase preload you increase shortening velocity (shift to the right)