Cardiophysiology Flashcards

1
Q

What are the leak ion channels? Which direction do the ions flow?

A

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

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2
Q

What factors determine resting membrane potential? What cells don’t have a RMP?

A
  • 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

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3
Q

Describe auto rhythmic cells. What is their function?

A

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

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4
Q

What is the cardiac skeleton and what is its function?

A

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

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5
Q

What is the sequence of excitation for auto rhythmic cells?

A

Sinoatrial node (100 BPM)
atrioventricular node
atrioventricular bundle
bundle branches
conduction myofibrils - brings depolarizing current to contrastive cells of the heart

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6
Q

Describe the sinoatrial node. Where is it located and what happens when it it triggers an action potential?

A

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

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7
Q

What is the role of the atrioventricular node and where is it located? What is AV nodal delay?

A

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

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8
Q

Describe the atrioventricular bundle, bundle branches, and conduction myofibers.

A

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

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9
Q

Describe funny channels. What ion does it allow to pass though? What kind of channel is it?

A

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

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10
Q

Describe the pre potential permeability in auto rhythmic cells

A

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

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11
Q

Describe the depolarization phase of autorhythmic cells

A

fast Ca channels open
- vg channels
- cause for action potential

voltage gated K channels closed

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12
Q

Describe the repolarization phase autorhythmic cells

A

Fast Ca channels (vg) close

Vg - K channels open, allowing K to move out and bring MP back to negative

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13
Q

Describe the opening/closing of channels in autorhythmic AP in order

A

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

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14
Q

Describe parasympathetic neuromodulation of auto rhythmic cells. What nerve and what NT is in charge of this, and what are the effects is has?

A

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

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15
Q

Describe the sympathetic neuromodulation of the autorhythmic cells

A

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

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16
Q

How does caffeine affect the sympathetic nervous system and increase heart rate?

A

caffeine blocks the activity of phosphodiesterase
- less cAMP deactivation: more funny channels open, more protein kinases activated to P transient Ca channels

17
Q

Describe the intercalated discs in cardiac muscle tissue. What are they made of and what are the function of the components?

A

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

18
Q

Describe the contractile muscle cell AP. Does it have a resting membrane potential? How does it compare to a skeletal muscle cell?

A

RMP: - 90 mv
1. transmission of AP via gap junctions - vg - Na open for rapid depolarization (Na IN)

  1. short repolarization due to vg K opening (K out)
  2. 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
  3. Ca ions activate Na-Ca ion exchangers - one Ca out for every 3 Na in
  4. repolarization - vg- Ca close, vg - K open
19
Q

What are the Ca transporters that are active during relaxation?

A

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

20
Q

Describe the effect of digiatlis and its effect on heart contractility

A

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

21
Q

Describe the sympathetic neuromodulation of cardiac contractile cells

A

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

22
Q

Do cardiac contractile cells have motor end plates?

A

no motor end plates
incoming depolarization comes from gap junctions or auto rhythmic cells