Intro
Myocardium |
middle of heart wall, contains cardiac muscle |
How are CM cells connected? |
intercalated discs, forms desmosomes and gap-junctions |
Functional Syncytium |
group of CM cells that contract in coordination with each other (gap junctions) |
Autorhythmicity |
creates its own electrical activity (no NS input) |
Pacemaker Cells |
creates pacemaker activity, grouped together in nodes |
Cardiac Contractile Cells |
99% of cardiac muscle cells, actually performs contraction but is not autorhythmic |
Other Characteristics |
involuntary (autonomic neuro fibers), striated, lots of mito + myoglobin, longer AP than smooth/skeletal muscle |
Pacemaker Flow
SA Node |
70 APs/min, main node |
Where is SA node? |
right atrium near superior vena cava |
AV Node |
50 APs/min, follows SA node |
Where is AV node? |
base of right atrium |
Bundle of His |
tract of pacemaker cells that start at AV node -> ends at left and right ventricles |
Purkinje Fibers |
30 APs/min, follows SA node |
Where are Purkinje Fibers? |
from end of Bundle of His through ventricular myocardium |
Interatrial Pathway |
pacemaker pathway from right to left atrium |
Internodal Pathway |
pacemaker pathway from SA node to AV node |
AV Nodal Delay |
activity delay of 100ms going through AV node |
Why is AV Nodal Delay important? |
allows for ventricles to contract after atrial contraction |
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Pacemaker Activity
Nodes |
controls rate and coordination of contractions |
How many nodes? |
2 nodes, SA and AV |
Pacemaker potentials |
depolarization of membrane potential until threshold (triggers AP) |
First half of pacemaker potential |
funny channels open -> Na+ in, K+ channels close (K+ remains inside) |
Second half of pacemaker potential |
funny channels close, T-type Ca2+ channels open -> takes potential to threshold |
Threshold |
T-type Ca2+ channels close, L-type Ca2+ channels open -> potential reaches peak |
Falling Phase |
K+ channels open (K+ out), L-type Ca2+ channels close --> fall back to original potential |
Major ions for pacemaker activity |
K+, Na+, Ca2+ |
Timing |
both Ca2+ channels are crucial for keeping rhythm (T-type channels: gradual depolarization, L-type: fast depolarization) |
Pacemaker potential value |
-60mV |
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Contractile Cardiac Muscle Cells
Resting potential value |
-90mV |
Rapid rise |
opening fast Na+ channels, Na+ in |
Brief repolarization |
limited K+ efflux, coupled with inactivation of Na+ channel |
Plateau Phase |
Ca2+ entry (opens L-type channels), coupled with reduced K+ efflux (K+ channels close) |
Rapid falling |
opening ordinary voltage-gated K+ channels (K+ out) |
Resting potential |
back to resting potential by closing ordinary K+ channels and opening leaky K+ channels |
AP and Contractile response |
contraction happens during plateau phase |
Contractile AP vs. Pacemaker AP
Excitation-Contraction Coupling
Dyhydropyridine receptors |
acts like voltage-gated Ca2+ channels. When AP reaches T-tubules, these receptors activate and allows Ca2+ flow |
Sarcoplasmic Reticulum |
entry of Ca2+ causes calcium release from Sarcoplasmic Reticulum |
Contraction |
number of activated cross-bridges is proportional to Ca2+ conc. in cytosol |
Calcium-Induced Calcium-Release |
opening of L-type Ca2+ channels -> activation of dyhydropyridine receptors -> amplified release of Ca2+ from sarcoplasmic reticulum |
Refractory Period and Contraction |
refractory period and length/strength of contraction is directly proportional (longer refractory period = contractile length/strength increases) |
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