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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
Q

mechanisms are used to preserve ABP due to changes from exercise, standing up, pain and emotions?

A

feedFORWARD.

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26
Q

example mechanism of feedforward control of ABP - exercise

A

drop in ABP prevented by inputs to medulla from cortex (“decision” to exercise) from cerebellum and from muscle and joint receptors.

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27
Q

where do all the feedforward mechanisms feed into ?

A

cardiovascular centre of medulla. (same as baroreceptors and chemoreceptors)

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28
Q

by what efferent pathways does the medulla control ABP?

A

sympathetic and parasympathetic

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29
Q

where do sympathetic and parasympathetic outflows work on the heart ?

A

sympathetic - vasculature and the heart

parasympathetic - only on heart

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30
Q

what does sympathetic activity generally cause on vasculature?

A

vasoconstriction (including venoconstricition) through action of noradrenaline on alpha 1 receptors

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31
Q

how does arteriolar vasoconstriction and venoconstriction differ in there effects?

A

vasoconstriction increases TPR, venoconstriction increases MSFP.

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32
Q

other effects of sympathetic activity to maintain ABP

A

redistribution of blood flow, some organs receive little effect. E.g. arteries and arterioles supplying the brain and heart.

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33
Q

what is the resting action potential frequency of tonically active sympathetic vasoconstrictor nerves?

A

1-4 Hz (increasing to 10 Hz which can reduce blood flow in extremis to almost zero)

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34
Q

what does the resting tone in sympathetic fibres allow for?

A

inhibition of sympathetic activity (from the baroreceptor reflex) to reduce ABP.

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35
Q

where do the sympathetic fibres innervate the heart? what are the effects)

A

SA node, atria and ventricles (increase heart rate and contractility, have a low resting frequency)

36
Q

what innervates chromaffin cells in adrenal medulla, stimulating release of adrenaline into the circulation ? [ABP control]

A

preganglionic sympathetic fibres in the splanchnic nerves.

37
Q

how does adrenaline act in terms of ABP?

A

similar to direct sympathetic innervation, via alpha1 receptors. However coronary blood vessels and skeletal muscle have more Beta2 receptor, triggering vasodilatation.

38
Q

where does the vagus nerve innervate (parasympathetic control of circulation)

A

SA node, AV node and cardiac conducting system.

39
Q

effect of vagus nerve activity on heart

A

slows heart rate and conduction, lengthening cardiac cycle. Does not influence force !!

40
Q

how is vagal supply to heart different from most parasympathetic pathways?

A

shows tonic activity. Inhibition of vagus at rest using atropine, accelerates heart rate.

41
Q

what is used to inhibit vagus nerve at rest ? (to heart)

A

atropine

42
Q

a fall in TPR must be accompanied by an increase in CO ( ABP = TPR x CO) , how is this achieved?

A

sympathetic venoconstriction to increase MSFP, reduced vagal and increased sympathetic activity to heart to increase heart rate and contractility.

43
Q

what happens in end-stage heart failure?

A

failure to adequately perfuse organs, organ failure and death if untreated

44
Q

what is implied by heart failure ? (inability to pump blood from veins to arteries)

A

ATRIAL pressure is too high and ARTERIAL pressure is too low.

45
Q

what constitutes as too high atrial pressure? (RAP)

A

should be close to 0. (RAP)

46
Q

when is ABP too low?

A

when it is lower than a set point and can not be raised.

47
Q

how does body respond to low ABP?

A

increased sympathetic drive causing vent constriction, arteriolar vasoconstriction and retention of fluid. (Raising TPR and MSFP, causing atrial pressure to rise )

48
Q

what is CO limited by in heart failure ?

A

the heart (usually MSFP) [increase in MSFP due to low ABP does NOT result in increase in CO]

49
Q

what are the primary causes of symptoms of heart failure?

A

inability to increase CO, increased atrial pressure.

50
Q

what symptoms are present due to inability to increase CO in heart failure?

A

reduces exercise capacity, feelings of fatigue.

51
Q

what results from raised atrial pressures?

A

raised venous pressures and raised capillary pressures, causing oedema.

52
Q

which oedema is due to right sided heart failure? (raised atrial pressure)

A

peripheral oedema

53
Q

which oedema is due to left sided heart failure? (raised atrial pressure)

A

pulmonary oedema

54
Q

what drugs are used to inhibit RESPONSES to low blood pressures and produce symptomatic relief by lowering MSFP and TPR

A

ACE (angiotensin converting enzyme) inhibitors, diuretics and beta adrenergic blockers.

55
Q

what is functional hyperaemia? when does it occur?

A

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
Q

how much does blood flow increase from resting to during exercise ? (ml/min/100g)

A

2-3 to 35. (17 fold increase)

57
Q

how does intense exercise affect TPR?

A

can cause it to drop to ~20% of its resting value.

58
Q

how is a drop is TPR in intense exercise counteracted to maintain ABP?

A

increase in cardiac output and mechanisms to partially oppose local vasodilatation in muscle.

59
Q

how can blood flow through a muscle differ when exercising in isolation compared to whole body?

A

in isolation blood flow can exceed flow through same muscle in whole body exercise.

60
Q

what is the main difference in events occurring in phase 1 and 2 of functional hyperaemia

A

blood flow increases rapidly in phase 1, then a slower increase in phase 2 to sustained levels. (slower plato)

61
Q

other than functional hyperaemia, what happens in muscles during exercise to affect vessels?

A

local factors influencing arteriole diameter (reduced Po2, increased Pco2, decreased pH, increased extracellular K+, lactic acid and increased extracellular ADP,AMP and adenosine.)

62
Q

in phase 1 of hyperaemia, what is the effect of a rise in interstitial [K+]?

A

hyperpolarises arteriolar smooth muscle, closing voltage-gated Ca2+ channels, relaxing the muscle. (note: odd as would expect K+ to cause depolarisation)

63
Q

what is the hyperpolarisation observed in phase 1 of functional hyperaemia?

A

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
Q

what can be used to reduce hyperpolarisation during phas I of functional hyperaemia? (Attenuates vasodilation by around 60%)

A

ouabain or barium

65
Q

how does muscle contractions accelerate venous return?

A

enhances CO and reduces local venous pressures - enhancing pressure gradient through capillaries.

66
Q

what is also observed in some animals such as cats in phase 1 of functional hyperaemia

A

neurogenic vasodilatation. [ sympathetic cholinergic nerves cause rapid increase in blood flow to muscle at start of exercise]

67
Q

mechanisms involved in maintenance phase of exercise hyperaemia (phase II)

A
  • 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
Q

How does adenosine act as a strong vasodilator?

A

acts on A(2a) receptors to increase cAMP levels in smooth muscle.
(leading to hyperpolarisation)

69
Q

function of exercise (functional hyperaemia)

A

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
Q

key method to increase CO

A

sympathetic venoconstriction (increasing MSFP), reduced cardiac vagal stimulation (increase heart rate), increase in cardiac sympathtic stimulation (increase HR and myocardial activity)

71
Q

what allows the muscle pump action of contracting muscles on nearby veins to push blood towards the heart?

A

venous valves (reducing resistance to venous return)

72
Q

what happens to ABP during exercise?

A

rises slightly - CO can increase 6 fold despite reduction in TPR.

73
Q

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)

A

curare to block the neuromuscular junction

74
Q

what is the effect of the baroreceptors during exercise (ABP)

A

maintain stability of blood pressure around a slightly raised point.

75
Q

when can you observe the highest cardiac outputs?

A

during exercise

76
Q

for a fit, healthy person, what provides the greatest limitation on whole-body power output during exercise?

A

circulation (can’t let ABP drop too far)

[therefore, feeling fatigue mist relate to circulatory capacity]

77
Q

What two stimuli does the body respond to in a haemorrhage?

A

reduced blood volume and pain/emotional state

78
Q

How is a haemorrhage detected?

A

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
Q

rapid responses to a haemorrhage

A

increase in arteriolar and venous tone and heart rate. (vagal tone decreases)
- vasoconstrictory effects due to ADH, catecholamides and angiotensin II

80
Q

changes in microvascular due to a haemorrhage (response after minutes)

A
  • 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
Q

longer term responses to a haemorrhage

A
  • 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
Q

what stimulates red blood cell production to restore lost erythrocytes ?

A

erythropoietin released from kidneys in response to low oxygen delivery.

83
Q

what are the 2 types of external stress that can induce hypoxia?

A
  • inability to breathe e.g. breath-hold diving

- reduced concentration in inhaled air. e.g. altitude

84
Q

what is the bodys priority for 2 types of hypoxia ?

A

inability to breathe - conserve O2 to brain

reduced concentration - increase CO (o2 delivery = flow x conc)

85
Q

primary chemoreceptor response (hypoxia due to inability to breathe)

A

reduction of cardiac work to a minimum, sympathetic drive overwhelms metabolic vasodilatation to divert blood to heart and brain (little sympathetic vasoconstriction innervation)

86
Q

secondary chemoreceptor response (hypoxia due to reduced O2 concentration)

A
  • 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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