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
how are cardiac muscles connected?
via GAP junctions
parasympathetic stimulation of the heart effects which parts of the heart?
SA node
AV node
Atrial muscle
what part of the heart/circulatory system can be effected by NS stimulation?
SA node, AV node
atrial muscle
conduction pathway, ventricular muscle
veins, arteries
what does the flow of blood depend on?
length
diameter
pressure gradient (^pressure = ^flow)
viscosity of blood (only for unhealthy people)
pressure isn’t the same through out the whole of vessels so how is pressure gradient calculated?
pressure at the start minus pressure at the end:
eg.
—————
90^ ^10 therefore pressure gradient = 80mmHg
what is blood flow proportional to? and which law is it?
Poiseuille’s Law
flow is proportional to radius to the 4th power
=> this means a small radius change will lead to a large change in flow
where is friction the highest in vessels?
friction is far greater in small vessels as RBCs are in contact with a larger amount of surface area
how does blood flow change around the body during exercise?
increases: skin, heart and skeletal muscle
decreases: digestive, kidney and bone
no change in brain! brain always needs a constant flow
how can blood flow in capillary beds be controlled independently?
as the blood flows in parallel
describe arteries:
carry blood AWAY from heart
act as pressure reservoir
compliant, due to elasticity(absorbs pulse of blood)
elastic walls
what is the equation for mean arterial pressure?
MAP = diastolic pressure + 1/3 pulse pressure
where does the largest drop in pressure occur in vessel system?
arterioles,
they are the major resistance vessels
why can radius be controlled independently in arterioles?
- regulate flow to individual organs
- regulate arterial blood pressure
what is vasoconstriction?
increased contraction of circular smooth muscle in arteriolar wall,
which leads to increased resistance and decreased flow through vessel
what is vasoconstriction caused by?
increased:
myogeic activity, O2, sympathetic stimulation, vasopressin(eg. epinephrine)
decreased:
CO2 and other metabolites
what is vasodilation?
decreased contraction of circular smooth muscle in the arteriolar wall, which leads to decreased resistance and increased flow through vessel
what causes vasodilation?
increased:
CO2 and other metabolites, sympathetic stimulation
decreased:
myogenic activity, O2, Histamine release
how is the heart nourished?
blood in chambers do not provide nutrients to heart
nutrients are perfused through coronary arteries
describe the coronary arteries:
- very high pressure
- high intrinsic tone
- high O2 extraction (65% vs. 25%)
- flow reduces during systole
- controlled mainly by local factors (esp adenosine & nitric oxide)
- > 70% of flow is during diastole
what does it mean by 70% of flow through coronary arteries is during diastole?
pressure inside muscle during contraction(systole) is so high blood cant get through
this is why heart stresses the fuck out when it beats faster because its not getting as much nutrients and has to work harder
what can go wrong with the coronary arteries?
insufficient flow: vascular spasm, coronary artery disease
Blockage of flow: embolus(ball blocking vessel), thrombus(hill on side of the vessel)
due to plaque build up just behind endothelium
what condition is often related with coronary artery problems? and how is it treated?
angina causing shortness of breathe
treated with nitrates - GTN
what can having an embolus lead to?
MI
Myocardial Infarction
what does the severity of Myocardial Infarction depend on?
how big of an area of myocardium is effected
this will depend solely on the location of the embolus in the artery
what are some of the consequences of Myocardial Infarction?
breathlessness pain dizziness (fall in cardiac output...less blood(nutrients) to brain) shock arrhythmias -> death death due to contractile failure
define preload:
load on ventricular muscle imposed BEFORE it starts to contract
define AFTERLOAD:
load on ventricular muscle imposed DURING contraction
explain the relationship between number of branches and area of vessels:
at each branch point the total area goes up
=> in order to maintain the same resistance as pre-branch
5 L/min flow through aorta
- > branch branch branch (FASTER)
- > capillaries - short (SLOW)
- > branch branch branch (FASTER)
bleh
describe capillaries:
- very thin walled
- single endo cells layer
- smaller than RBC in diameter(slightly elastic)
- only holds around 250ml of blood volume(like 5%)..nothing! so they are very short
why do capillaries only have a single endothelial cells layer?
minimise distance between RBC & wall
facilitating MAX gas exchange
describe the movements of solutes across capillary wall:
glucose goes INTO tissue cell
Oxygen goes INTO tissue cell
CO2 goes OUT OF tissue cell
what is the reaction constantly occurring within tissue cells?
glucose + O2 -> CO2 + H2O + ATP
define osmosis:
water moves from dilute solution to concentrated solution
|
V
follows salt!
what is the role of lymph?
return of excess fluid
20L filtered, 17 resorbed, 3 absorbed
what adverse effects are there from the lymph system being blocked?
severe fluid imbalance
…think of elephantitis!
describe the change in total cross sectional area as blood flows from aorta to vena cava:
increases from aorta to capillaries
then
decreases from capillaries to vena cava
describe the change in blow flow from aorta to vena cava:
it doesn’t change! lel trick question
remains 5 L/min
as velocity of flow decreases, total cross sectional area increases
=> counter acting each other to maintain same resistance and therefore same flow
how does the exchange of solutes occur?
diffusion through endothelial cells
how do plasma proteins leave capillary?
generally plasma proteins cannot cross capillary wall
how do small water soluble substances pass through?
Na+, K+, proteins, glucose, amino acids
pass through the pores in capillary walls between endothelial cells
how do exchangeable proteins leave capillaries?
moved across capillary wall via vesicular transport
describe veins:
- low pressure
- blood goes to heart
- larger radius
- thinner walls
- little elasticity(more collagen)
- valves
why are veins low pressure? and what does this result in?
less resistance(bigger) to allow same amount of blood flow
low pressure results in easier backflow of blood..VALVES prevent this
factors effecting venous return:
changes in pressure gradient
- cardiac driving pressure - elevated atrial pressure
changes in venous capacity
cardiac suction effect(as it springs back to shape is sucks blood in)
skeletal muscle pump(enhances venous return)
describe gravity and venous return:
pressure gradient far lower in person lying down, in comparison with person standing up
when standing up pressure is high near feet
how can the effect of blood pooling be reduced?
by contraction of skeletal muscles,
reducing height of column of blood
*** think of sausage diagram lol
what is the lower, middle and upper limits of capillary pressure:
lower = 17 middle = 26 upper = 37
describe fluid movement across capillary wall above and below 26mmHg(capillary pressure)
below 26, water is resorbed, fluid moves IN to capillaries(outward pressure)
above 26, water is absorbed, fluid moves OUT of capillaries(inward pressure)
describe possible pressures in left ventricle:
0 to 120
describe possible pressures in large arteries:
80-120
describe possible pressures in arterioles:
110 -> 40
decreasing as you get closer to capillary system
describe possible pressures in capillaries:
37 -> 17
decreasing as it get closer to venules and veins
describe possible pressures in veins and venules:
17 -> 0
veins have a much larger radius, what does this allow?
it allows veins to act as a reservoir for blood,
veins hold over 60% of the body’s blood
what is the blood pressure that is monitored and controlled by the body?
mean arterial pressure
what does low MAP mean?
insufficient perfusion of tissues
what is perfusion:
process of body delivering blood to the capillary bed
what does high MAP mean?
increased workload on heart, vascular damage
what 4 things must every feedback loop control system have?
- a sensor
- a “set point”
- control centre to assess difference between the set point and actual value
- control (output) system
what is the sensor in MAP control?
carotid sinus and aortic arch baroreceptor
what is the role of the control center in the feedback loop?
to assess the difference between the set point and the actual value
what is the control centre in MAP control?
medulla
what is the control output system in MAP control?
the sympathetic nervous system
what is the equation of Cardiac Output?
stroke volume X heart rate
what effects heart rate?
sympathetic and parasympathetic nerves
what effects stroke volume?
intrinsic(in heart)
extrinsic(sympathetic, circulated hormones)
in terms of baroreceptor(found in carotid sinus and aortic arch) reaction what happens after you stand up?
- > stand up
- > blood pressure drops
- > increase cardiac output
what mainly controls total peripheral resistance?
Austonomic NS(short term) - sympathetic stimulation causes vasoconstriction of arterioles => increased resistance Hormonal control
steps in baroreceptor reflex:
1) fluctuations in pulse pressure
2) generate action potentials through afferent pathways
3) medulla alters ratio of sympathetic and parasympathetic activity to heart and blood vessels
4) heart and blood vessels are the effector organs that respond to control blood pressure
what happens to blood pressure as you age?
medulla set point creeps up
=> body maintains too high Blood Pressure
contraction of cardiac muscle is caused by a rise in intracellular calcium, using percentages, where does this calcium come from?
about 5% of the calcium comes from outside the cell, about 95% from intracellular stores
what area of the heart increase force of contraction if its diastolic volume increases?
an increase in left ventricular volume increases force of contraction
what does the vagus nerve release and what is it’s effect on heart rate?
when the vagus nerve to the heart is stimulated the nerve terminals release Ach which decreases heart rate
what is blood flow through vessels proportional to?
proportional to the pressure gradient from one end of the vessel to another
also proportional to the radius of the vessel to the 4th power (so small change in radius = large change in flow)
describe what happens to the cross-sectional area as one progresses from the aorta to the capillaries:
total cross sectional area goes up, so that the velocity of flow decreases
on an ECG what does P-Q interval indicate?
it indicates AV nodal delay
