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IB physiology > Mammalian Cardiovascular 2 > Flashcards

Mammalian Cardiovascular 2 Flashcards

1
Q

what I observed in the period of the fall in pressure from systolic to diastolic?

A

dicrotic notch

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2
Q

what is the dicrotic notch a result of?

A

back flow of blood towards the end of systole. (Pressure in aorta begins to exceed pressure in ventricle)

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3
Q

what terminates the dicrotic notch

A

(back flow of blood) terminated by closure of aortic valve.

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4
Q

what is the mean blood pressure approximated by?

A

diastolic pressure + 1/3 (systolic - diastolic)

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5
Q

what is pulse pressure ?

A

systolic - diastolic

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6
Q

cause of increase in mean blood pressure

A

age, slightly higher in men than women.

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7
Q

cause of increase of pulse pressure (different to mean blood pressure due to diastolic single factor)

A

reduction in arterial compliance. e.g. atherosclerosis

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8
Q

how does an increase in pulse pressure affect mean pressure? what does this suggest

A

mean pressure remains constant - systolic pressure rises as diastolic falls. Suggesting that mean ABP us principle regulated variable.

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9
Q

equation that links ABP, CO and TPR

A

ABP = CO x TPR ( think Darcy’s equation)

[ note: CO and TPR can be thought of as being independent of each other]

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10
Q

3 methods of MONITORING blood pressure

A

high pressure baroreceptors, low pressure baroreceptors and arterial chemoreceptors.

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11
Q

where are the HIGH pressure baroreceptors for monitoring blood pressure located?

A

carotid sinus and aortic arch.

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12
Q

what is required for the short term control of ABP?

A

high-pressure baroreceptors and chemoreceptors.

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13
Q

which baroreceptors are more sensitive from carotid and aortic?

A

carotid. (but aortic can respond to pressures above which those in carotid sinus will saturate)

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14
Q

how was it shown experimentally that an increase in blood pressure a carotid sinus produces a reflex reduction in blood pressure?

A

Cross circulation experiment with two dogs.

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15
Q

primary role of chemoreceptors in carotid and aortic bodies

A

regulate ventilation

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16
Q

when are the chemoreceptors in carotid and aortic bodies important for blood pressure control?

A

when blood pressure is very low or if PO2 is significantly reduced. High pressure baroreceptors are also relatively unresponsive under conditions of severe hypotension.

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17
Q

what is used for monitoring and influencing longer term control of ABP ?

A

low pressure baroreceptors

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18
Q

what are cardiopulmonary baroreceptors?

A

low pressure baroreceptors located in junctions of atria with their corresponding veins and in the atria themselves.

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19
Q

what do cardiopulmonary baroreceptors (low pressure) essentially detect?

A

RAP (firing rate of receptors increases with pressure)

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20
Q

how would RAP be detected by cardiopulmonary baroreceptors in heart failure and oedema (capillary pressures rising) ?

A

raised - circulation is over filled, heart can not maintain low venous pressures.

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21
Q

what does low RAP suggest?

A

cardiac output is maximal for current MSFP.

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22
Q

by what SYSTEMS do baroreceptors and chemoreceptors work?

A

feedback systems.

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23
Q

what kind of experiments shows the importance of baroreceptors and chemoreceptors for regulating arterial blood pressure?

A

denervation experiments

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24
Q

why can’t some stresses on ABP such as exercise and standing up be regulated by FEEDBACK systems ?

A

don’t cause detectable drops in ABP, can not be entirely reliant on feedback.

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25
mechanisms are used to preserve ABP due to changes from exercise, standing up, pain and emotions?
feedFORWARD.
26
example mechanism of feedforward control of ABP - exercise
drop in ABP prevented by inputs to medulla from cortex ("decision" to exercise) from cerebellum and from muscle and joint receptors.
27
where do all the feedforward mechanisms feed into ?
cardiovascular centre of medulla. (same as baroreceptors and chemoreceptors)
28
by what efferent pathways does the medulla control ABP?
sympathetic and parasympathetic
29
where do sympathetic and parasympathetic outflows work on the heart ?
sympathetic - vasculature and the heart | parasympathetic - only on heart
30
what does sympathetic activity generally cause on vasculature?
vasoconstriction (including venoconstricition) through action of noradrenaline on alpha 1 receptors
31
how does arteriolar vasoconstriction and venoconstriction differ in there effects?
vasoconstriction increases TPR, venoconstriction increases MSFP.
32
other effects of sympathetic activity to maintain ABP
redistribution of blood flow, some organs receive little effect. E.g. arteries and arterioles supplying the brain and heart.
33
what is the resting action potential frequency of tonically active sympathetic vasoconstrictor nerves?
1-4 Hz (increasing to 10 Hz which can reduce blood flow in extremis to almost zero)
34
what does the resting tone in sympathetic fibres allow for?
inhibition of sympathetic activity (from the baroreceptor reflex) to reduce ABP.
35
where do the sympathetic fibres innervate the heart? what are the effects)
SA node, atria and ventricles (increase heart rate and contractility, have a low resting frequency)
36
what innervates chromaffin cells in adrenal medulla, stimulating release of adrenaline into the circulation ? [ABP control]
preganglionic sympathetic fibres in the splanchnic nerves.
37
how does adrenaline act in terms of ABP?
similar to direct sympathetic innervation, via alpha1 receptors. However coronary blood vessels and skeletal muscle have more Beta2 receptor, triggering vasodilatation.
38
where does the vagus nerve innervate (parasympathetic control of circulation)
SA node, AV node and cardiac conducting system.
39
effect of vagus nerve activity on heart
slows heart rate and conduction, lengthening cardiac cycle. Does not influence force !!
40
how is vagal supply to heart different from most parasympathetic pathways?
shows tonic activity. Inhibition of vagus at rest using atropine, accelerates heart rate.
41
what is used to inhibit vagus nerve at rest ? (to heart)
atropine
42
a fall in TPR must be accompanied by an increase in CO ( ABP = TPR x CO) , how is this achieved?
sympathetic venoconstriction to increase MSFP, reduced vagal and increased sympathetic activity to heart to increase heart rate and contractility.
43
what happens in end-stage heart failure?
failure to adequately perfuse organs, organ failure and death if untreated
44
what is implied by heart failure ? (inability to pump blood from veins to arteries)
ATRIAL pressure is too high and ARTERIAL pressure is too low.
45
what constitutes as too high atrial pressure? (RAP)
should be close to 0. (RAP)
46
when is ABP too low?
when it is lower than a set point and can not be raised.
47
how does body respond to low ABP?
increased sympathetic drive causing vent constriction, arteriolar vasoconstriction and retention of fluid. (Raising TPR and MSFP, causing atrial pressure to rise )
48
what is CO limited by in heart failure ?
the heart (usually MSFP) [increase in MSFP due to low ABP does NOT result in increase in CO]
49
what are the primary causes of symptoms of heart failure?
inability to increase CO, increased atrial pressure.
50
what symptoms are present due to inability to increase CO in heart failure?
reduces exercise capacity, feelings of fatigue.
51
what results from raised atrial pressures?
raised venous pressures and raised capillary pressures, causing oedema.
52
which oedema is due to right sided heart failure? (raised atrial pressure)
peripheral oedema
53
which oedema is due to left sided heart failure? (raised atrial pressure)
pulmonary oedema
54
what drugs are used to inhibit RESPONSES to low blood pressures and produce symptomatic relief by lowering MSFP and TPR
ACE (angiotensin converting enzyme) inhibitors, diuretics and beta adrenergic blockers.
55
what is functional hyperaemia? when does it occur?
an increase in blood flow to a tissue due to the presence of metabolites and a change in general conditions. Occurs during strenuous exercise.
56
how much does blood flow increase from resting to during exercise ? (ml/min/100g)
2-3 to 35. (17 fold increase)
57
how does intense exercise affect TPR?
can cause it to drop to ~20% of its resting value.
58
how is a drop is TPR in intense exercise counteracted to maintain ABP?
increase in cardiac output and mechanisms to partially oppose local vasodilatation in muscle.
59
how can blood flow through a muscle differ when exercising in isolation compared to whole body?
in isolation blood flow can exceed flow through same muscle in whole body exercise.
60
what is the main difference in events occurring in phase 1 and 2 of functional hyperaemia
blood flow increases rapidly in phase 1, then a slower increase in phase 2 to sustained levels. (slower plato)
61
other than functional hyperaemia, what happens in muscles during exercise to affect vessels?
local factors influencing arteriole diameter (reduced Po2, increased Pco2, decreased pH, increased extracellular K+, lactic acid and increased extracellular ADP,AMP and adenosine.)
62
in phase 1 of hyperaemia, what is the effect of a rise in interstitial [K+]?
hyperpolarises arteriolar smooth muscle, closing voltage-gated Ca2+ channels, relaxing the muscle. (note: odd as would expect K+ to cause depolarisation)
63
what is the hyperpolarisation observed in phase 1 of functional hyperaemia?
raised extracellular K+ enchnaces Na+/K+ ATPase activity. Also enhances activation of inwardy-rectifying K+ channels. { leadind to increased intracellular K+ and increased K+ permeability} - AND MUSCLE PUMP. (muscle contractions accelerate venous return)
64
what can be used to reduce hyperpolarisation during phas I of functional hyperaemia? (Attenuates vasodilation by around 60%)
ouabain or barium
65
how does muscle contractions accelerate venous return?
enhances CO and reduces local venous pressures - enhancing pressure gradient through capillaries.
66
what is also observed in some animals such as cats in phase 1 of functional hyperaemia
neurogenic vasodilatation. [ sympathetic cholinergic nerves cause rapid increase in blood flow to muscle at start of exercise]
67
mechanisms involved in maintenance phase of exercise hyperaemia (phase II)
- raised extracellular K+ - increased O2 offloading; release of NO and ATP from Red blood cells. - low O2 enhances activity of ectoneucleotideases producing vasodilatory adenosine from ATP. - adenosine acculuates around muscle fibres.
68
How does adenosine act as a strong vasodilator?
acts on A(2a) receptors to increase cAMP levels in smooth muscle. (leading to hyperpolarisation)
69
function of exercise (functional hyperaemia)
exercising muscle receives a blood supply closely matched to metabolic demand. - increase in blood flow results largely from local vasodilatory influences. - systemic control to prevent TPR being too low
70
key method to increase CO
sympathetic venoconstriction (increasing MSFP), reduced cardiac vagal stimulation (increase heart rate), increase in cardiac sympathtic stimulation (increase HR and myocardial activity)
71
what allows the muscle pump action of contracting muscles on nearby veins to push blood towards the heart?
venous valves (reducing resistance to venous return)
72
what happens to ABP during exercise?
rises slightly - CO can increase 6 fold despite reduction in TPR.
73
what can be used to separate the central command to exercise from the actual occurrence of exercise ? (demonstrating that increase in heart rate can occur without any exercise occurring)
curare to block the neuromuscular junction
74
what is the effect of the baroreceptors during exercise (ABP)
maintain stability of blood pressure around a slightly raised point.
75
when can you observe the highest cardiac outputs?
during exercise
76
for a fit, healthy person, what provides the greatest limitation on whole-body power output during exercise?
circulation (can't let ABP drop too far) | [therefore, feeling fatigue mist relate to circulatory capacity]
77
What two stimuli does the body respond to in a haemorrhage?
reduced blood volume and pain/emotional state
78
How is a haemorrhage detected?
reduction in MSFP, venous return and blood pressure. Both baroreceptors detect changes, reducing inhibition of medullary vasomotor areas. (cortex and hypothalamus may also respond to fear/pain)
79
rapid responses to a haemorrhage
increase in arteriolar and venous tone and heart rate. (vagal tone decreases) - vasoconstrictory effects due to ADH, catecholamides and angiotensin II
80
changes in microvascular due to a haemorrhage (response after minutes)
- reverse stress relaxation (smooth muscle contracts when stretch is reduced) - mobilisation of tissue fluid (reabsorption due to shift in starling forces, around 500ml - 1l of circulating volume )
81
longer term responses to a haemorrhage
- renal conservation of water and salt, thirst and sodium appetite. (+10 mins) - (24-48 hours) ; plasma proteins replaced by liver synthesis, increased RBC production
82
what stimulates red blood cell production to restore lost erythrocytes ?
erythropoietin released from kidneys in response to low oxygen delivery.
83
what are the 2 types of external stress that can induce hypoxia?
- inability to breathe e.g. breath-hold diving | - reduced concentration in inhaled air. e.g. altitude
84
what is the bodys priority for 2 types of hypoxia ?
inability to breathe - conserve O2 to brain | reduced concentration - increase CO (o2 delivery = flow x conc)
85
primary chemoreceptor response (hypoxia due to inability to breathe)
reduction of cardiac work to a minimum, sympathetic drive overwhelms metabolic vasodilatation to divert blood to heart and brain (little sympathetic vasoconstriction innervation)
86
secondary chemoreceptor response (hypoxia due to reduced O2 concentration)
- increased rate and depth of breathing - pulmonary stretch receptors send info via vagus nerve to medulla, stimulating vasomotor centre causing venoconstriction - inhibits cardio-inhibitory centre (increasing HR) - causes pattern of vasodilatation and vasoconstriction that favours vital tissues. - RISE IN CO

IB physiology (4 decks)

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