PHYSIOL [C] cardiovascular Flashcards
what is the light filament in muscle?
actin
what is the dark filament in muscle?
myosin
describe cardiac muscle?
striated
involuntary control
storing of Ca2+ for contraction is similar to skeletal but release mechanism is different
describe the tropomyosin and troponin action in contraction:
tropomyosin(blocks binding site @ rest) will move out of the way when Ca2+ binds to troponin(allows muscle to contract with Ca2+ binding)
steps of the cross bridge binding cycle:
- energised (no Ca2+)
- binding (Ca2+ present excitation)
- bending (power stroke in response to presence of Ca2+)
- detachment (fresh ATP will detach)
- 2 no fresh ATP = rigor mortis complex …in death
where does the Ca2+ come from?
Ca2+ stored in sarcoplasmic reticulum
what triggers Ca2+ release?
triggered by extracellular Ca2+ entering the cell through L-type calcium channels
what causes the influx of Ca2+ through L-type calcium channels in the t-tubules?
opening of L-type(low threshold) calcium channels(DHP receptor equivalent) during plateau phase of the action potential allows calcium to flow down its electrochemical gradient (Ca inside the cell is very low in comparison with Ca outside cell)
what is the difference between Ca influx in cardiac muscle and skeletal muscle?
cardiac muscle has no direct link whereas skeletal muscle does have a direct link between DHP receptors* and Ca2+ release channels
in cardiac muscle coupling between the receptors and release channels is by calcium influx itself
*these are L-type voltage gated calcium channels in cardiac muscle
what are the steps of calcium induced calcium release in CARDIAC muscle?
1) voltage gated channels open due to action potential
2) rise in internal calcium allow Ca2+ to bind to receptors on surface of SER
3) upon this binding, calcium-induced calcium release occurs
3 main points of cardiac control of contraction:
1) cannot get tetnus - due to long action potential
2) no such thing as motor units - its a synciticum (network)
3) neuronal input modulates contraction (force and rate) - does not initiate it
how does neuronal input modulate force of contraction?
by changing the amount of Ca that comes IN:
- > sympathetic stimulation
- > noradrenaline(epinephrine) released
- > noradrenaline binds to BETA receptors
- > BETA receptors trigger mechanism(cyclic MP)
- > Ca channels open more readily -> calcium-induced calcium release
why are tetanic contractions not possible in cardiac muscle?
refractory period is too long, by the time another action potential can be fired the contraction is long gone
- contractions cannot summate
How are tetanic contractions possible in skeletal muscle?
another action potential can be fired BEFORE pervious contraction is finished
what happens during PLATEAU phase of action potential in cardiac muscle?
Ca is flowing in keeping cell polarised
Ca coming into the cell is a slow process
what can we conclude knowing tetanic contractions are not possible in cardiac muscle?
that one action potential in the heart will produce one contraction
- as action potential and contraction overlap
…although neuronal input can change length of overlap(changing the amount of Ca going in(released)
state the Frank-Starling law:
the force of contraction of the heart(blood pumped out) increases when the end-diastolic pressure and volume is increased (ie. muscle stretched)
explain the Frank-Starling law in basic terms:
the output of the heart must match the input, and the two sides have to match each other
what is end-diastolic?
end of diastole
relaxed
in between heart beats
why does this happen?
unequal pumping would increase size of one side of heart and blood pooling in systemic veins(deoxygenated) or arteries(oxygenated)
where on the body would blood pool in veins and arteries?
veins = fat ankles/lower legs arteries = fluid build up in lungs
what is the normal cardiac output per minute? (at rest)
4 L/min
what is the mechanism that ensures both sides of the heart match?
length tension relationship
stretch => force of contraction will go up
describe the length tension relationship in the heart:
when heart is stretched, Ca release increases,
the contractile proteins become MORE SENSITIVE to Ca when you pull on them therefore *greater force per amount of Ca released as proteins more sensitive
what is stroke volume?
amount of blood pushed out with each beat
-> around 60-70 ml per beat
what effect do heart problems have on the frank-starling relationship?
the relationship stops working
-> curve flattens and blood pools
what is the effect of increasing resting length in between contractions on the force of the next contraction?
the force of the next contraction will be larger
what are the similarities between contraction of cardiac and skeletal muscle?
- mechanisms of contraction (actin, myosin, sarcomeres etc.)
- source of calcium is similar (mostly from internal stores vs. entirely from internal stores)
list the differences in contraction of cardiac and skeletal muscle?
- triggering of Ca release (indirect vs. indirect)
- control of tension (action potential durations)
- length tension curve is different (no descending limb)
- Frank-starling law important to match pulmonary and systemic outputs
characteristics of smooth muscle
- not striated
- surrounds blood vessels, lungs and broncioles
- has tone = constant low level tension(no 1:1 relation between tension and action potentials)
- thick and thin filaments arranged in matrix rather than sarcomeres
describe the mechanism of contraction of smooth muscle:
no troponin, contraction depends on extracellular Ca almost exclusively and MUST be PHOSPHORYLATED before it can contract
describe steps of contraction in smooth muscle:
1) muscle excitation
2) rise in cytosolic Ca2+(mostly from extracellular fluid)
3) series of biochemical events
4) phosphorylation of myosin in thick filament
5) binding of actin and myosin at cross bridges
6) contraction
what are the series of biochemical events that lead to the phosphorylation of myosin in smooth muscle?
1) Ca2+ comes into cell and binds with Calmodulin
2) Calmodulin binds to kinase
3) activates myosin kinase
4) active myosin kinase phosphorylates inactive myosin
5) phosphorylated myosin can now interact with actin and start cycling
what is calmodulin?
calcium binding protein
what is kinase?
enzyme that sticks phosphates onto other proteins
what must happen to myosin heads in smooth muscle in order for them to contract?
they must be phosphorylated
in the heart, where does AP start and end?
action potentials originate at the SA node
- > atrio-ventricular node AFTER delay
- > carried down into ventricles by bundle of His
what is the electrical activity in the heart?
the heart generates its own intrinsic electrical activity
Why is the action potential in the heart delayed at the AV node?
the delay allows atria to contract THEN ventricles
what keeps heart rate controlled? and how?
the Vagus nerve keeps the heart rate down @ rest
HOW?
via the release of Ach
what does the bundle of His branch off to? describe appearance
purkinje fibers
white thin visible on heart
what is the bpm going through SA node, AV node and bundle of His/the purkinje fibres?
SA node = 70-80
AV node = 40-60
bundle of His/Purkinje fibres = 20-40
which nerve systems innervate the SA node?
parasympathetic(vagus)
sympathetic
how do parasympathetic fibres innervating the SA node effect heart rate?
release Ach
acts via muscarinic receptors to SLOW heart rate
how do sympathetic fibres innervating the SA node effect heart rate?
noradenaline acts via BETA 1 receptors to INCREASE heart rate
does the heart empty with each beat?
nope!
around 60% of blood is ejected from the heart
60mls left in heart
what is the normal heart rate?
120/80
systolic over diastolic
what is cardiac output effected by?
heart rate and stroke volume
what happens to an electrocardiogram when there is a partial AV block?
extra P wave after T mini hill
what happens to an electrocardiogram when there is a total AV block?
extra P wave after T mini hill
P and T = P+T combine