PHYSIOL [C] cardiovascular Flashcards

0
Q

what is the light filament in muscle?

A

actin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

what is the dark filament in muscle?

A

myosin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

describe cardiac muscle?

A

striated
involuntary control
storing of Ca2+ for contraction is similar to skeletal but release mechanism is different

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

describe the tropomyosin and troponin action in contraction:

A

tropomyosin(blocks binding site @ rest) will move out of the way when Ca2+ binds to troponin(allows muscle to contract with Ca2+ binding)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

steps of the cross bridge binding cycle:

A
  1. energised (no Ca2+)
  2. binding (Ca2+ present excitation)
  3. bending (power stroke in response to presence of Ca2+)
  4. detachment (fresh ATP will detach)
  5. 2 no fresh ATP = rigor mortis complex …in death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

where does the Ca2+ come from?

A

Ca2+ stored in sarcoplasmic reticulum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what triggers Ca2+ release?

A

triggered by extracellular Ca2+ entering the cell through L-type calcium channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what causes the influx of Ca2+ through L-type calcium channels in the t-tubules?

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is the difference between Ca influx in cardiac muscle and skeletal muscle?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what are the steps of calcium induced calcium release in CARDIAC muscle?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

3 main points of cardiac control of contraction:

A

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 well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

how does neuronal input modulate force of contraction?

A

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

why are tetanic contractions not possible in cardiac muscle?

A

refractory period is too long, by the time another action potential can be fired the contraction is long gone
- contractions cannot summate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How are tetanic contractions possible in skeletal muscle?

A

another action potential can be fired BEFORE pervious contraction is finished

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what happens during PLATEAU phase of action potential in cardiac muscle?

A

Ca is flowing in keeping cell polarised

Ca coming into the cell is a slow process

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what can we conclude knowing tetanic contractions are not possible in cardiac muscle?

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

state the Frank-Starling law:

A

the force of contraction of the heart(blood pumped out) increases when the end-diastolic pressure and volume is increased (ie. muscle stretched)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

explain the Frank-Starling law in basic terms:

A

the output of the heart must match the input, and the two sides have to match each other

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is end-diastolic?

A

end of diastole
relaxed
in between heart beats

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

why does this happen?

A

unequal pumping would increase size of one side of heart and blood pooling in systemic veins(deoxygenated) or arteries(oxygenated)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

where on the body would blood pool in veins and arteries?

A
veins = fat ankles/lower legs
arteries = fluid build up in lungs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is the normal cardiac output per minute? (at rest)

A

4 L/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is the mechanism that ensures both sides of the heart match?

A

length tension relationship

stretch => force of contraction will go up

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

describe the length tension relationship in the heart:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
what is stroke volume?
amount of blood pushed out with each beat | -> around 60-70 ml per beat
25
what effect do heart problems have on the frank-starling relationship?
the relationship stops working | -> curve flattens and blood pools
26
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
27
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)
28
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
29
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
30
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
31
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
32
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
33
what is calmodulin?
calcium binding protein
34
what is kinase?
enzyme that sticks phosphates onto other proteins
35
what must happen to myosin heads in smooth muscle in order for them to contract?
they must be phosphorylated
36
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
37
what is the electrical activity in the heart?
the heart generates its own intrinsic electrical activity
38
Why is the action potential in the heart delayed at the AV node?
the delay allows atria to contract THEN ventricles
39
what keeps heart rate controlled? and how?
the Vagus nerve keeps the heart rate down @ rest HOW? via the release of Ach
40
what does the bundle of His branch off to? describe appearance
purkinje fibers | white thin visible on heart
41
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
42
which nerve systems innervate the SA node?
parasympathetic(vagus) sympathetic
43
how do parasympathetic fibres innervating the SA node effect heart rate?
release Ach | acts via muscarinic receptors to SLOW heart rate
44
how do sympathetic fibres innervating the SA node effect heart rate?
noradenaline acts via BETA 1 receptors to INCREASE heart rate
45
does the heart empty with each beat?
nope! around 60% of blood is ejected from the heart 60mls left in heart
46
what is the normal heart rate?
120/80 | systolic over diastolic
47
what is cardiac output effected by?
heart rate and stroke volume
48
what happens to an electrocardiogram when there is a partial AV block?
extra P wave after T mini hill
49
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
50
how are cardiac muscles connected?
via GAP junctions
51
parasympathetic stimulation of the heart effects which parts of the heart?
SA node AV node Atrial muscle
52
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
53
what does the flow of blood depend on?
length diameter pressure gradient (^pressure = ^flow) viscosity of blood (only for unhealthy people)
54
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
55
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
56
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
57
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
58
how can blood flow in capillary beds be controlled independently?
as the blood flows in parallel
59
describe arteries:
carry blood AWAY from heart act as pressure reservoir compliant, due to elasticity(absorbs pulse of blood) elastic walls
60
what is the equation for mean arterial pressure?
MAP = diastolic pressure + 1/3 pulse pressure
61
where does the largest drop in pressure occur in vessel system?
arterioles, | they are the major resistance vessels
62
why can radius be controlled independently in arterioles?
- regulate flow to individual organs | - regulate arterial blood pressure
63
what is vasoconstriction?
increased contraction of circular smooth muscle in arteriolar wall, which leads to increased resistance and decreased flow through vessel
64
what is vasoconstriction caused by?
increased: myogeic activity, O2, sympathetic stimulation, vasopressin(eg. epinephrine) decreased: CO2 and other metabolites
65
what is vasodilation?
decreased contraction of circular smooth muscle in the arteriolar wall, which leads to decreased resistance and increased flow through vessel
66
what causes vasodilation?
increased: CO2 and other metabolites, sympathetic stimulation decreased: myogenic activity, O2, Histamine release
67
how is the heart nourished?
blood in chambers do not provide nutrients to heart | nutrients are perfused through coronary arteries
68
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
69
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
70
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
71
what condition is often related with coronary artery problems? and how is it treated?
angina causing shortness of breathe | treated with nitrates - GTN
72
what can having an embolus lead to?
MI | Myocardial Infarction
73
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
74
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 ```
75
define preload:
load on ventricular muscle imposed BEFORE it starts to contract
76
define AFTERLOAD:
load on ventricular muscle imposed DURING contraction
77
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
78
5 L/min flow through aorta - > branch branch branch (FASTER) - > capillaries - short (SLOW) - > branch branch branch (FASTER)
bleh
79
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
80
why do capillaries only have a single endothelial cells layer?
minimise distance between RBC & wall | facilitating MAX gas exchange
81
describe the movements of solutes across capillary wall:
glucose goes INTO tissue cell Oxygen goes INTO tissue cell CO2 goes OUT OF tissue cell
82
what is the reaction constantly occurring within tissue cells?
glucose + O2 -> CO2 + H2O + ATP
83
define osmosis:
water moves from dilute solution to concentrated solution | V follows salt!
84
what is the role of lymph?
return of excess fluid | 20L filtered, 17 resorbed, 3 absorbed
85
what adverse effects are there from the lymph system being blocked?
severe fluid imbalance | ...think of elephantitis!
86
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
87
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
88
how does the exchange of solutes occur?
diffusion through endothelial cells
89
how do plasma proteins leave capillary?
generally plasma proteins cannot cross capillary wall
90
how do small water soluble substances pass through?
Na+, K+, proteins, glucose, amino acids | pass through the pores in capillary walls between endothelial cells
91
how do exchangeable proteins leave capillaries?
moved across capillary wall via vesicular transport
92
describe veins:
- low pressure - blood goes to heart - larger radius - thinner walls - little elasticity(more collagen) - valves
93
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
94
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)
95
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
96
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
97
what is the lower, middle and upper limits of capillary pressure:
``` lower = 17 middle = 26 upper = 37 ```
98
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)
99
describe possible pressures in left ventricle:
0 to 120
100
describe possible pressures in large arteries:
80-120
101
describe possible pressures in arterioles:
110 -> 40 | decreasing as you get closer to capillary system
102
describe possible pressures in capillaries:
37 -> 17 | decreasing as it get closer to venules and veins
103
describe possible pressures in veins and venules:
17 -> 0
104
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
105
what is the blood pressure that is monitored and controlled by the body?
mean arterial pressure
106
what does low MAP mean?
insufficient perfusion of tissues
107
what is perfusion:
process of body delivering blood to the capillary bed
108
what does high MAP mean?
increased workload on heart, vascular damage
109
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
110
what is the sensor in MAP control?
carotid sinus and aortic arch baroreceptor
111
what is the role of the control center in the feedback loop?
to assess the difference between the set point and the actual value
112
what is the control centre in MAP control?
medulla
113
what is the control output system in MAP control?
the sympathetic nervous system
114
what is the equation of Cardiac Output?
stroke volume X heart rate
115
what effects heart rate?
sympathetic and parasympathetic nerves
116
what effects stroke volume?
intrinsic(in heart) | extrinsic(sympathetic, circulated hormones)
117
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
118
what mainly controls total peripheral resistance?
``` Austonomic NS(short term) - sympathetic stimulation causes vasoconstriction of arterioles => increased resistance Hormonal control ```
119
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
120
what happens to blood pressure as you age?
medulla set point creeps up | => body maintains too high Blood Pressure
121
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
122
what area of the heart increase force of contraction if its diastolic volume increases?
an increase in left ventricular volume increases force of contraction
123
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
124
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)
125
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
126
on an ECG what does P-Q interval indicate?
it indicates AV nodal delay