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CVS physiology > integration of cardiovascular mechanisms (CVS 9&10) > Flashcards

integration of cardiovascular mechanisms (CVS 9&10) Flashcards

1
Q

components of CVS/cardiovascular system

A
  • heart = pump, CO must match needs
  • arteries = passageways of blood from the heart to the tissue, pressure must be maintained, but not too high
  • arterioles = major resistance vessels
  • capillaries = site of exchange of gas, nutrients and water between blood and tissues
  • veins = capacitance vessels (contain most of blood volume during rest), passageways of blood from tissues to heart, venous return must provide heard with sufficient blood to pump
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2
Q

heart

A

=pump of cardiovascular system

-CO must match needs

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3
Q

arteries

A

=passageways of blood from the heart to the tissue

-pressure must be maintained, but not too high

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4
Q

arterioles

A

=major resistance vessels of cardiovascular system

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5
Q

capillaries

A

=site of exchange of gas, nutrients and water between blood and tissues

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6
Q

veins

A

=capacitance vessels (contain most of blood volume during rest)

  • passageways of blood from tissues to heart
  • venous return must provide heard with sufficient blood to pump
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7
Q

regulation of heart rate (HR)

A

-mainly autonomic nervous system

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8
Q

regulation of stroke volume (SV)

A

-pre-load/myocardial contractibility/after-load

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9
Q

MAP =

A
  • mean arterial blood pressure

- MAP = CO (cardiac output) x TPR (total peripheral resistance)

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10
Q

cardiac output (CO) =

A

HR x SV

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11
Q

regulation of MAP

A

-if we regulate HR, SR and TPR, we will regulate MAP

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12
Q

how is MAP approximated

A

MAP = DBP + 1/3 of the difference between SBP and DBP (pulse pressure)

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13
Q

eg. of approximation of MAP

A

-a blood pressure of 110/80mHg, indicates:
->systolic BP = 110mmHg
->diastolic BP = 80mmHg
->pulse pressure = 110 - 80 = 30mmHg
->MAP = DBP + 1/3 pulse pressure
= 80 + (1/3 30) = 80 + 10 = 90 mmHg

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14
Q

how is the total peripheral resistance (TPR) regulated

A
  • TPR is regulated by vascular smooth muscles
  • contraction of vascular smooth muscles causes vasoconstriction and increases TPR and MAP (ie.pressure upstream)
  • relaxation of vascular smooth muscles causes vasodilation and decreases TPR and MAP
  • > vascular smooth muscles are controlled by extrinsic and intrinsic mechanisms
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15
Q

main site of TPR (total peripheral resistance)

A

arterioles

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16
Q

components of total peripheral resistance (TPR)

A
  • arteries (~20%)
  • arterioles (~50%)
  • capillaries (~20%)
  • veins (~10%)
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17
Q

resistance to blood flow

A
  • resistance to blood flow is directly proportional to blood viscosity and length of blood vessel, and inversely proportional to the radius of the blood vessel to the power of 4
  • the resistance to blood flow is mainly controlled by vascular smooth muscles through the changes in the radius of arterioles
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18
Q

extrinsic control of vascular smooth muscles

A

-this involves nerves and hormones

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19
Q

nerves involved in the extrinsic control of vascular smooth muscles

A
  • they are very important on blood pressure regulation (refer to baroreceptor reflex from previous lectures)
  • the vascular smooth muscles are supplied by the sympathetic nerve fibres, the neurotransmitter is noradrenaline acting on alpha receptors
  • increased sympathetic discharge will increase the vasomotor tone resulting in vasoconstriction
  • decreased sympathetic discharge will decrease the vasomotor tone resulting in vasodilatation
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20
Q

vascular

A

relating to, affecting, or consisting of a vessel or vessels, especially those which carry blood

21
Q

vasomotor tone

A
  • the vascular smooth muscles are partially constricted at rest, this is called the vasomotor tone
  • the vasomotor tone is caused by tonic discharge of sympathetic nerves resulting in continuous release of noradrenaline (which acts on alpha receptors)
  • increased sympathetic discharge will increase the vasomotor tone resulting in vasoconstriction
  • decreased sympathetic discharge will decrease the vasomotor tone resulting in vasodilatation
22
Q

hormones involved in the extrinsic control of vascular smooth muscles

A
  • effect of adrenaline (from the adrenal medulla) is largely organ specific, it depends on predominant type of receptor (adrenaline acting on alpha receptors causes vasoconstriction, adrenaline acting on beta receptors causes vasodilation) - alpha receptors are predominant in skin, gut and kidney arterioles, whereas beta receptors are predominant in cardiac and skeletal muscle arterioles (this helps with strategic redistribution of blood eg. during exercise)
  • angiotensin II causes vasoconstriction
  • antidiuretic hormone (vasopressin) causes vasoconstriction
  • > angiotensin II and antidiuretic hormone are important in the intermediate control of blood pressure
23
Q

intrinsic control of vascular smooth muscles

A
  • these controls match the blood flow of different tissues to their metabolic needs
  • they can over-ride the extrinsic control mechanisms
  • they include chemical and physical factors
24
Q

chemical factors involved in intrinsic control of vascular smooth muscles (local metabolites)

A
  • local metabolic changes within an organ influences the contraction of arteriolar smooth muscles
  • the following factors causes relaxation of arteriolar smooth muscles resulting in vasodilatation:
  • > decreased local PO2
  • > increased local PCO2
  • > increased local [H+] (decreased pH)
  • > increased extracellular [K+]
  • > increased osmolarity of ECF
  • > adenosine release (from ATP)
25
Q

chemical factors involved in intrinsic control of vascular smooth muscles (local humoral agents) causing vasodilation

A
  • in addition to metabolites, other local chemicals released within an organ (local humoral agents) influence the contraction of arteriolar smooth muscles
  • they can be released in response to tissue injury or inflammation
  • the release of the following humoral agents causes relaxation of arteriolar smooth muscles resulting in vasodilation:
  • > histamine
  • > prostaglandins
  • > bradykinin
  • > nitric oxide (NO) - this is continually released by endothelial cells of arteries and arterioles
26
Q

nitric oxide (NO) and involvement in intrinsic control of vascular smooth muscles

A
  • NO is continuously produced by the vascular endothelium from the amino acid L-arginine though enzymatic action of nitric oxide synthase (NOS)
  • NO is a potent vasodilator (with a short life of a few seconds) which is important in the regulation of blood flow and maintenance of vascular health
  • shear stress on vascular endothelium, as a result of increased flow causes the release of calcium in vascular endothelial cells and the subsequent activation of NOS ie. flow dependent NO (nitric oxide) formation
  • chemical stimuli can also induce NO (nitric oxide) formation- receptor stimulated NO (nitric oxide) formation- many vasoactive substances act through stimulation of NO (nitric oxide) formation
  • nitric oxide (NO) diffuses from the vascular endothelium into the adjacent smooth muscle cells where it activates the formation of cGMP that serves as a second messenger for signalling smooth muscle relaxation
27
Q

dilatation

A

= means the same as dilation

-the action of dilating a vessel or opening or the process of becoming dilated

28
Q

chemical factors involved in intrinsic control of vascular smooth muscles (local humoral agents) causing vasoconstriction

A
  • the release of the following humoral agents causes contraction of arteriolar smooth muscles resulting in vasoconstriction:
  • > serotonin
  • > thromboxane A2
  • > leukotrienes
  • > endothelin (this is a potent vasoconstrictor released from the endothelial cells, its production is stimulated by angiotensin II and vasopressin)
29
Q

physical factors involved in intrinsic control of vascular smooth muscles

A
  • temperature (cold causes vasoconstriction, warmth causes vasodilation)
  • myogenic response to stretch (if MAP rises resistance vessels automatically constrict to limit flow, if MAP falls resistance vessels automatically dilate to increase flow; myogenic response is important in tissues like brain and kidneys)
  • sheer stress (dilation of arterioles causes sheer stress in the arteries upstream to make them dilate, this increases blood flow to metabolically active tissues)
30
Q

regulation of cerebral blood flow (in order of contribution to control)

A
  • hypercapnia (cerebral blood flow and MAP are directly proportional to each other)
  • autoregulation of cerebral blood flow (myogenic response) (sigmoidal)
  • sympathetic nerve stimulation (sigmoidal)
31
Q

MAP

A

-MAP = CO x TPR

32
Q

main site of TPR

A

arterioles

33
Q

control of TPR

A
  • sympathetic nervous system plays the primarily role on the control of arteriolar radius and TPR (the brain is an exception)
  • local control of TPR aims to satisfy the intermediate demands of particular tissues, it often overrides the nervous control in these tissues (eg. skeletal muscle and heart during cycle)
34
Q

effect of end diastolic volume (EDV) on SV (frank starling curve)

A
  • end diastolic volume increases from ‘rest’ - ‘increased venous return’
  • as end diastolic volume (fibre length) increases, as does the stroke volume (tension), until a maximal force is generated at optimal fibre length
35
Q

factors influencing venous return (and an explanation of starlings curve)

A
  • increased venomotor tone increases venous return
  • increased ‘skeletal muscle pump’ increases venous return
  • increased blood volume increases venous return
  • increased ‘respiratory pump’ increases venous return
  • > an increase in venous return causes an increase in atrial pressure which causes an increase in end diastolic volume which causes an increase in stroke volume (starling)
36
Q

venomotor tone

A
  • the veins are capacitance vessels that contain most of the blood volume under resting conditions
  • venous smooth muscles are supplied with sympathetic nerve fibres
  • stimulation gives venous constriction
  • on account of venous valves, blood is driven to right atrium
  • increased venomotor tone increases venous return, SV and MAP
37
Q

effect of increased vasomotor tone on MAP

A

-increases TPR and MAP

38
Q

effect of increased venomotor tone on MAP

A

-increased venous return, SV and MAP

39
Q

‘the skeletal muscle pump’

A
  • large veins in limbs lie between skeletal muscles
  • contraction of muscles aids venous return
  • one way valves allow blood to move forwards towards the heart
  • muscle activity increases venous return to the heart
40
Q

acute cardiovascular/CVS responses to exercise

A
  • sympathetic nerve activity increases
  • HR and SV increase, this increases CO (CO=HRxSV)
  • sympathetic vasomotor nerves reduce flow to kidneys and gut (vasoconstriction)
  • in skeletal and cardiac muscle, metabolic hyperaemia overcomes vasomotor drive (vasodilation)
  • blood flow to skeletal and cardiac muscles increase in proportion to metabolic activity
  • > the increases in CO increases systolic BP
  • > the metabolic hyperaemia decreases TPR and decreases DBP (diastolic blood pressure)
  • > therefore pulse pressure increases
  • post exercise hypotensive (lowering the blood pressure) response
41
Q

hyperaemia

A

an excess of blood in the vessels supplying an organ or other part of the body

42
Q

effect of sympathetic stimulation on the heart

A
  • sympathetic stimultion increases heart rate (HR) by inreasing the rate of firing of SA node and decreasing AV nodal delay
  • sympathetic stimulation also increases force of contraction
43
Q

effect of sympathetic stimulation on pacemaker cells

A
  • slope of pacemaker potential increases
  • pacemaker potential reaches threshold quicker
  • frequency of action potentials increases (positive chronotropic effect/increase HR)
44
Q

effect of sympathetic nerve stimulation on ventricular contraction

A
  • peak ventricular pressure rises (contractility of heart at a given EDV rises)
  • frank-starling curve is shifted to the left
45
Q

effect of EDV on SV (frank starling curve)

A

-as EDV (fibre length) increases, as does SV (tension)

46
Q

frank starling curve

A

stroke volume against EDV

47
Q

chronic cardiovascular/CVS responses to exercise

A
  • regular anaerobic exercise helps to reduce blood pressure
  • mechanism not fully understood and controversial
  • likely to be multifactorial (due to more than one factor)
  • chonic cardiovascular responses to regular exercise may include:
  • > reduction in sympathetic tone and noradrenaline levels
  • > increased parasympathetic tone to the heart
  • > cardiac remodeling
  • > reduction in plasma renin levels
  • > improved endothelial function (increased vasodilators, decreased vasoconstrictors)
  • > decreased arterial stiffening
48
Q

summary of control of blood pressure/mean arterial blood pressure

A
  • MAP= CO x TPR
  • TPR is effected by arteriolar radius which is effected by local metabolites and extrinsic control
  • > local metabolites are effected by muscle activity
  • > extrinsic control is effected by sympathetics/adrenaline and ADH/angiotensin II
  • ADH and angiotensin II regulate salt and water balance which regulates blood volume (along with fluid shift across capillaries)
  • blood volume and muscle activity effect venous return and venous return and sympathetics and adrenaline affect stroke volume
  • sympathetics and adrenaline and vagus innervation effet HR
  • HR and SR effect CO
  • > CO x TPR = MAP

CVS physiology (11 decks)

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