cardiac muscle Flashcards
what is the function of conductile cells of cardiac muscle? Name the different kinds
- function: rapid spread of electrical signal (action potential) through myocardium
- kinds
- bundle of his
- purkinje fibers
- SA node
- AV node
conducting cells can generate what type of action potentials
spontaneous
what conductile cells are the primary pacemakers
Sinoatrial (SA) node
function of cardiac myocytes
contractile cells: contraction
list the spread of excitation
- SA node: initiates action potential
- spread to atria and AV node
- AV node: slow conduction
- bundle of his and purkinje fibers : fast conduction

depolarization of ventricular myocardium goes from what level to what level
from endocardium to epicardium
what is conduction velocity
speed of action potential propagation through heart
what conductile cells have the fastest and slowest conduction velocity
slowest: AV node: 0.01-0.05 m/sec
fastest: Bundle of his and purkinje fibers: 2-4 m/sec
what dictates the conduction velocity
- rate of change in membrane potential as a function of time (i.e. upstroke phase of action potential)
- resistance
compare duration of action potentials of cardiac vs skeletal muscle
cardiac AP have a longer duration

compare action potentials between contractile cells and pacemaker cells
- contractile cells: fast AP
- pacemaker cells: slow AP
what is phase 0 of fast action potential
- upstroke, rapid depolarization
- fast inward Na+ current

what is phase 1 of fast action potential
- early repolarization
- activation of K+ channels: K+ moves out
- inactivation gates on Na+ channels close

what is phase 2 of fast action potential
- Plateau phase
- responsible for the very long AP
- due to balance between Ca2+ (L-type channel: inward) current and K+ outward current
- L-type = long lasting: have slower kinetics than “fast” Na+ channels

what is phase 3 of fast action potential
- repolarization
- turn off of Ca2+ current and further increase in K+ current
- K+ current reduced near end of phase 3 because membrane potential closer to K+ equilibrium

what is phase 4 of fast action potential
- resting potential
- caused by K+ outward current
- different channels thatn phase 3
- balanced by inward Na2+ and Ca2+ current

why is summation and tetanus of cardiac muscle unlikely
because long refractory period occurs in conjunction with prolonged plateau phase
* this is good because it ensures alternating periods of contraction and relaxation which are essential for pumping blood

Key differences of sinoatrial (SA) node slow action potential
- automatically
- unstable resting membrane potential
- no sustained plateau
* phase 1 and 2 are absent

what is phase 0 in SA node slow action potential
- upstroke
- slow due to inward long-lasting Ca2+ current

what is phase 3 in SA node slow action potential
- repolarization
- turn-off of Ca2+ current
- further increase in K+ current

what is phase 4 in SA node slow action potential
-
pacemaker potential
- spontaneous depolarization
- longest portion
- (If) inward Na+; inward T-type Ca2+ current
- If turned on by repolarization from preceeding AP

rate of what phase sets heart rate
phase 4 in SA node slow action potential
cardiac muscle cells are interconnect by what feature that helps form functional syncytium
intercalated disc

within the intercalated discs, there are two kinds of membrane junctions, name them
- desmosomes: mechanical junctions
- gap junctions: electrical junctions
what molecule initiates excitation-contraction coupling in cardiac contractile cells? What is the source?
- CA2+
- extracellular Ca2+ (differs from intracellular Ca2+ used in skeletal muscle)
list the steps of excitation-contraction coupling in cardiac contractile cells
- excitation: AP causes the depolarization of the membrane
- Ca2+ channels open (during plateau of AP)
- Ca2+ enters cell
- Ca2+ - induced Ca2+ release form SR
- Ca2+ binds to troponin
- crossbridge cycling
how is calcium removed from cytoplasm during relaxation
- uptake into SR: SERCA pump contributes to majority of CA2+ flux
- uptake into mitochondria
- Na+/K+ ATPase and NCX pump which create gradient for calcium removal

function of drugs Digitalis and Digoxin
- mechanism: inhibit the Na+/K+ ATPase and therefore reverse the Na+/Ca2+ exchanger so that now there is higher intracellular CA2+
- result: enhances force of contraction (contractility)
