Cardiophysiology Flashcards
What are the leak ion channels? Which direction do the ions flow?
Na and K ion leak channels
- help maintain resting membrane potential
- Na goes into cell
- K goes out of cell
- more K than Na leak channeks
What factors determine resting membrane potential? What cells don’t have a RMP?
- K/Na leak channels
- Na/K-ATPase pump: 3 Na out for every 2 K in against their concentration gradient
- negatively charged proteins
auto rhythmic cells do not have RMP
Describe auto rhythmic cells. What is their function?
function: to regulate heart activity via AP’s
contain very little actin/myosin
- replaced with glycogen
capable of depolarizing on their own
- does not require NTs to have graded potential
- NTs can speed up rate
What is the cardiac skeleton and what is its function?
band of dense irregular CT around valves that gives structural support and does NOT conduct electricity
- the current through the atrial muscle cells are blocked
- once it reaches the AV node, it starts again via AV bundle
What is the sequence of excitation for auto rhythmic cells?
Sinoatrial node (100 BPM)
atrioventricular node
atrioventricular bundle
bundle branches
conduction myofibrils - brings depolarizing current to contrastive cells of the heart
Describe the sinoatrial node. Where is it located and what happens when it it triggers an action potential?
pacemaker of the heart - 100 BPM without regulation
located in wall of R atrium below superior VC
specialized muscle fibers of the heart with more leaky Na channels
AP spread downward through atria
- muscles cells joined by gap junctions at intercalated discs
What is the role of the atrioventricular node and where is it located? What is AV nodal delay?
located in the right atrial wall near interatrial septum
- depolarized by AP’s of R atrial contractile muscle cells
AV nodal delay: .1 seconds
due to AV autorhythmic fibers smaller in diameter, fewer gap junctions
Describe the atrioventricular bundle, bundle branches, and conduction myofibers.
AV bundle - located in iinteratrial septum
- only electrical connection btw atria and ventricles
bundle branches - AV bundle splits into two bundle branches that pass through the septum
conduction myofibers - contain few myofibrils
- supply cardiac and papillary muscles in ventricles
Describe funny channels. What ion does it allow to pass though? What kind of channel is it?
funny channels - Na ion channels that typically open at negative resting membrane potential
- voltage gated - opens during hyper polarization
- ligand gated - cAMP binding can open the channels
Describe the pre potential permeability in auto rhythmic cells
small # Na channels open - Na enters
- funny channels begin to open at (-) MP
vg - K channels that opened during depolarization phase begin to close
transient Ca channels begin to open
Describe the depolarization phase of autorhythmic cells
fast Ca channels open
- vg channels
- cause for action potential
voltage gated K channels closed
Describe the repolarization phase autorhythmic cells
Fast Ca channels (vg) close
Vg - K channels open, allowing K to move out and bring MP back to negative
Describe the opening/closing of channels in autorhythmic AP in order
at - 60 mV:
- funny channels open: some K leave but mainly Na enters - depolarization
- near - 40 mv: funny channels close, slow Ca open - continue depolarization
- 40 mv: threshold reached - Fast Ca open and depolarize
+ 5 mv: fast Ca close, VG K open and repolarize
Describe parasympathetic neuromodulation of auto rhythmic cells. What nerve and what NT is in charge of this, and what are the effects is has?
Postganglionic neurons from the VAGUS nerve release ACETYLCHOLINE
- bind to muscarinic GPCR in autorhytmic cells
- inhibitory alpha unit inhibits adenylate cyclase
- fewer cAMP = decreased number of funny channels
- beta/gamma subunits bind to K channels to cause them to open
takes longer for the cell to depolarize to the threshold potential - longer heart rate
Describe the sympathetic neuromodulation of the autorhythmic cells
postganglionic neurons of the sympathetic nervous system release norepinephrine - binds to beta 1 GPCR’s of auto rhythmic cells
- alpha unit activates adenylate cyclase = more cAMP = more/earlier funny channels = faster depolarization
- cAMP activates protein kinase A which P’s transient Ca channels = opens easier/longer
higher heart rate
How does caffeine affect the sympathetic nervous system and increase heart rate?
caffeine blocks the activity of phosphodiesterase
- less cAMP deactivation: more funny channels open, more protein kinases activated to P transient Ca channels
Describe the intercalated discs in cardiac muscle tissue. What are they made of and what are the function of the components?
join the short, fat, branched cells of cardiac muscle together
- gap junctions - allow communication from one cell to the next
- desmosomes - vertical aspect of desmosome - holds muscle together
Describe the contractile muscle cell AP. Does it have a resting membrane potential? How does it compare to a skeletal muscle cell?
RMP: - 90 mv
1. transmission of AP via gap junctions - vg - Na open for rapid depolarization (Na IN)
- short repolarization due to vg K opening (K out)
- slow vg Ca open - Ca flows into cell, slowing down repolarization - plateau
- additional Ca from SR
- lots of Ca in cytoplasm = activate interaction btw actin and myosin = more contraction - Ca ions activate Na-Ca ion exchangers - one Ca out for every 3 Na in
- repolarization - vg- Ca close, vg - K open
What are the Ca transporters that are active during relaxation?
Ca/ATPase pump - uses energy to move 2 Ca out of cell or into ST
Na/Ca cotransporter - removes one Ca from inside cell for every 3 Na to enter
- affected by digitalis
Ca mitochondrial uniport
- hypoxia - affects Na/K ATPase - increased Na = increased Ca
- damages mitochondria due to increase in Ca mitochondrial uniport
Describe the effect of digiatlis and its effect on heart contractility
blocks the activity of Na/K ATPase - increases [Na] in the cell
- increased Na means that the Ca/Na cotransporter will not work
- increases [Ca] in cardiac contractile cell - increases FORCE of contraction
Describe the sympathetic neuromodulation of cardiac contractile cells
Postganglionic sympathetic releases NE that binds to beta1 GPCR on cardiac contractile cells
- alpha subunit activate adenylate cyclase = more cAMP = more activated protein kinase A
- Protein kinase A increases intracellular Ca by opening Ca channels in SR and plasma membrane
- more Ca = increased contractility
ventricular muscle cells do not have receptors for ACh
Do cardiac contractile cells have motor end plates?
no motor end plates
incoming depolarization comes from gap junctions or auto rhythmic cells
