CARDIOVASCULAR SYSTEM Flashcards
SA node
collection of special cells in upper R atrium that can generate their own APs
-don’t have resting membrane potentials; membrane potentials are always fluctuating
-frequency of APs determines heart rate (1 AP = 1 contraction of heart)
SA node fibers have what channels
-F-type/funny channels
-L-type channels
F-type channels
voltage-gated sodium channels
-funny because open as cell becomes more negative/hyperpolarizes
-most voltage-gated sodium channels open via depolarization
L-type channels
calcium channels
-stay open for long periods of time
how SA node generates its own APs
Funny channels open when interior reaches -60mV (peak negative value) ->
sodium enters + depolarizes to -50mV (threshold) ->
at threshold, funny channels shut + L-type open ->
calcium enters + depolarizes up to +10/20mV ->
calcium ions move to adjacent regions of SA node + depolarize them to open more L-type channels (this is how AP propagates through SA node) ->
at +20mV (peak positive value), L-type channels close + voltage-gated potassium channels open ->
potassium starts leaving the cell, repolarizing to -50mV - >
at -50mV, L-type channels reset ->
at -60mV, voltage-gated potassium channels shut + funny channels open -> process restarts
SA node (+ AV node) fibers propagate their APs using what
calcium
neurons propagate their APs using what
sodium
skeletal muscle fibers propagate their APs only using what
sodium
do cardiac contractile fibers have resting membrane potentials
yes
how is SA node attached to contractile fibers
intercalated discs
-desmosomes/gap junctions
desmosomes
staple; what attaches fibers together
gap junctions
tunnel for ions
how are APs passed from SA node to contractile fibers + rest of the heart
when AP reaches the intercalated discs between SA node + contractile fibers, calcium ions move through gap junctions + into the contractile fiber (via electrical driving force to enter because contractile fiber resting membrane potential is -90mV)
explain how APs propagate down contractile fibers
calcium ions enter contractile fiber via gap junctions + depolarize the region ->
when it hits threshold at -75mV, voltage-gated sodium channels open + depolarize even more ->
at -50mV, L-type channels open + depolarizes up to +10/20mV ->
sodium + calcium ions move to adjacent negative regions + propagate AP
describe cardiac + skeletal muscles structurally + functionally
-structurally the same
-functionally different (cardiac don’t need AMN to pass them APs; if 1 cardiac fiber contracts they all contract)
describe how contraction (excitation-contraction coupling) in occurs skeletal fibers
AP propagates down plasma membrane into T-tubule using only sodium channels ->
DHP receptors are physically linked to ryanodine receptors on SR ->
AP (sodium ions) open DHP receptor so it can pull on ryanodine receptors to let calcium into cytosol
-DHP receptors are only in T-tubule + pull on ryanodine to let calcium in; DHP receptor itself doesn’t let calcium in
describe how contraction (excitation-contraction coupling) occurs in cardiac fibers
-ryanodine receptors are embedded in SR membrane but aren’t physically attached to DHP receptors
-DHP receptors run the entire length of cardiac fibers + let calcium in
-influx of calcium through DHP receptors binds to troponin so that myosin/actin can interact
-also causes calcium induced calcium release because calcium binds to ryanodine receptors on SR causing them to open + spill out calcium
-calcium coming from DHP receptors + SR causes cardiac to contract
describe how relaxation of the heart occurs
-calcium is pumped back into SR via SERCA pumps
-SERCA pumps use ATP to pump calcium from low to high concentration
-also- there are various transporters for calcium in plasma membrane that pump calcium back into ECF
-calcium goes back to SR + ECF
what causes the plateau in AP
-after cardiac contractile fiber goes from -90mV to +10mV, there is a plateau
-between +10/20mV, voltage-gated sodium channels close but L-type are still open, giving fiber a continuous influx of calcium ->
-voltage-gated potassium channels are delayed so takes them a while to open; during this time calcium is still coming in + potassium isn’t leaving (this is what causes plateau)
plateau occurs in which fibers
ONLY cardiac contractile fibers
-not SA node fibers
why is the plateau important (3)
-allows calcium to continue flowing for extended period of time
-most of the calcium that allows for cardiac muscle contraction come from ECF, only some from SR- so you must allow for a large amount of calcium to enter from ECF for a meaningful contraction to occur
-cardiac contractions are much longer than skeletal contractions
AV node
-structurally identical to SA node- collection of pacemaker cells that can generate their own AP
-has funny channels
-only uses calcium to propagate AP just like SA node
difference between SA + AV node
AV node takes longer to get to threshold because not as many funny channels
AV node role
-AP propagates to L/R atrium first + does it so fast that it is basically in unison; conduction velocity of AP slows down at the AV node
-there is a break between atria + ventricular contraction so that atria can finish pushing blood into the ventricles before they contract
-SA node generates way more APs than AV node does -> so before AV node can get to threshold on its own, it receives AP generates by SA node
where are atria + ventricles connected
ONLY at the AV node
cardiac skeleton
large piece of kinetic tissue that separates atria + ventricles
P-wave
contraction of atrial fibers
QRS complex
contraction of L/R ventricles
describe a typical ECG
there is a P-wave then a break until QRS complex
-break represents the AP going through the AV node
if someone has a heart arrythmia + their SA node stops working, are they in immediate danger
no
-AV node fibers will eventually get to threshold on their own + generate an AP
-atrial fibers won’t contract; you will only see ventricular contractions on ECG
-not a big deal because R/L atria only push 20% blood into ventricles; person is fine as long as ventricles are still contracting
conduction fibers
-identical to contractile fibers but play a different role
-purpose is to propagate APs very quickly throughout atria/ventricles so that they contract in unison
AP generated by SA node will pass to which fibers
both contractile + conduction fibers
what would happen without conduction fibers
-heart would contract at different times
-no meaningful force would be generated
describe control center for ANS
hypothalamus controls ENTIRE ANS
-limbic system, PMC, + premotor cortex neurons synapse with hypothalamic neurons
nucleus tractus solitarius
region of brainstem in medulla that controls sympathetic/parasympathetic neurons at the heart
where is the cardiac control center
medulla
sequence of synapses to the heart
PMC ->
hypothalamus ->
medulla cardiac center ->
sympathetic/ parasympathetic neuron ->
release ACh/norepinephrine onto heart to increase/decrease heart rate
explain how sympathetic nervous system influences SA node fibers (complex explanation)
sympathetic neuron releases norepinephrine onto SA node ->
norepinephrine binds to adrenergic receptors (beta 1 cAMP pathway) ->
alpha subunit swaps GDP for GTP + disassociates away from beta/gamma ->
alpha activates adenylate cyclase to turn ATP into cAMP ->
cAMP activates pKa ->
pKa phosphorylates funny channels in SA node so that more open
-normally- funny channels open at -60mV but many don’t open until -61, 62, 63, 64mV
-pKa allows for these channels to be open at less negative value, which gets fiber to threshold faster
explain how sympathetic nervous system influences SA node fibers (simplified explanation)
pKa opens funny channels that don’t usually open which increases frequency of SA node APs
explain how parasympathetic nervous system influences SA node fibers (complex explanation)
parasympathetic neuron releases ACh onto SA node ->
ACh binds to muscarinic cholinergic receptors ->
alpha swaps out GDP for GTP + disassociates away from beta/ gamma ->
beta/gamma crawl to + activate GIRK channels ->
GIRK channels increase cells permeability to potassium so potassium leaves faster ->
potassium leaving at a fast rate causes hyperpolarization so this decreases the number of APs the SA node can generate
explain how parasympathetic nervous system influences SA node fibers (simplified explanation)
GIRK channels increase potassium permeability + hyperpolarizes SA node which decreases frequency of SA node APs
SA node fiber has only adrenergic/muscarinic receptors
has BOTH
describe sympathetic/parasympathetic systems at rest
-SA node fiber generates 100 APs per minute when taken out of heart but only 70 APs per minute when in the body
-this is because parasympathetic is more active than sympathetic at rest + there is always some ACh being released onto heart at rest
-most people with heart conditions have hyperactive sympathetic nervous systems + higher resting heart rate than normal people
reasons sympathetic stimulation of cardiac contractile fibers results in increased force production (7)
- exercise activates sympathetic nervous system, which increases heart rate, which ultimately increases cardiac output
- sympathetic releases norepinephrine which activates cAMP G-protein pathway, increasing pKa activity, opening more L-type channels so that more calcium will bind to troponin + myosin/actin can interact more -> more force
- pKa directly phosphorylates ryanodine receptors, increasing the # of receptors open so that more calcium can be released from SR to bind to troponin
- pKa phosphorylates troponin, increasing its affinity for calcium, causing more calcium to bind to troponin; also makes it easier for troponin to release calcium to go back to SR
- the increase in calcium influx triggers calcium included calcium release, so more ryanodine receptors will open + more calcium will be released from SR
- pKa phosphorylates phospholambin, making SERCA pumps more efficient at bringing calcium back to SR so fiber relaxes faster + therefore can contract faster
- calcium binds to calmodulin to form calcium-calmodulin complex which activates myosin light chain kinase to put myosin heads in a more perpendicular position to actin so they can bind faster + produce more force
systole
contraction of a chamber
diastole
relaxation of a chamber
end systolic volume
amount of blood in the chamber at the end of contraction
-chamber is empty
end diastolic volume
amount of blood in the chamber at the end of relaxation
-chamber is filled with blood
stroke volume
total amount of blood pumped out of a chamber when it contracts
stroke volume formula
stroke volume = end diastolic volume – end systolic volume
cardiac output
amount of blood circulating the body in 1 minute
cardiac output formula
cardiac output = heart rate x stroke volume
heart rate
the # of times the heart contracts per minute
-average 70 beats per minute
how will exercise influence heart rate, stroke volume, cardiac output
-solely anticipation of exercise causes inhibition of parasympathetic nervous system (the inhibition of parasympathetic is much more important than activation of sympathetic in this)
-sympathetic is activated when the person ACTUALLY starts exercising
-both heart rate + stroke volume increase during exercise, so cardiac output also increases
