integration of cardiovascular mechanisms (CVS 9&10)

Question 1

components of CVS/cardiovascular system

Answer 1

• 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

Question 2

heart

Answer 2

=pump of cardiovascular system

-CO must match needs

Question 3

arteries

Answer 3

=passageways of blood from the heart to the tissue

-pressure must be maintained, but not too high

Question 4

arterioles

Answer 4

=major resistance vessels of cardiovascular system

Question 5

capillaries

Answer 5

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

Question 6

veins

Answer 6

=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

Question 7

regulation of heart rate (HR)

Answer 7

-mainly autonomic nervous system

Question 8

regulation of stroke volume (SV)

Answer 8

-pre-load/myocardial contractibility/after-load

Question 9

MAP =

Answer 9

• mean arterial blood pressure

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

Question 10

cardiac output (CO) =

Answer 10

HR x SV

Question 11

regulation of MAP

Answer 11

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

Question 12

how is MAP approximated

Answer 12

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

Question 13

eg. of approximation of MAP

Answer 13

-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

Question 14

how is the total peripheral resistance (TPR) regulated

Answer 14

• 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

Question 15

main site of TPR (total peripheral resistance)

Answer 15

arterioles

Question 16

components of total peripheral resistance (TPR)

Answer 16

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

Question 17

resistance to blood flow

Answer 17

• 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

Question 18

extrinsic control of vascular smooth muscles

Answer 18

-this involves nerves and hormones

Question 19

nerves involved in the extrinsic control of vascular smooth muscles

Answer 19

• 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

Question 20

vascular

Answer 20

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

Question 21

vasomotor tone

Answer 21

• 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

Question 22

hormones involved in the extrinsic control of vascular smooth muscles

Answer 22

• 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

Question 23

intrinsic control of vascular smooth muscles

Answer 23

• 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

Question 24

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

Answer 24

• 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)

Question 25

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

Answer 25

- 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

Question 26

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

Answer 26

- 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

Question 27

dilatation

Answer 27

= means the same as dilation | -the action of dilating a vessel or opening or the process of becoming dilated

Question 28

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

Answer 28

- 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)

Question 29

physical factors involved in intrinsic control of vascular smooth muscles

Answer 29

- 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)

Question 30

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

Answer 30

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

Question 31

MAP

Answer 31

-MAP = CO x TPR

Question 32

main site of TPR

Answer 32

arterioles

Question 33

control of TPR

Answer 33

- 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)

Question 34

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

Answer 34

- 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

Question 35

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

Answer 35

- 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)

Question 36

venomotor tone

Answer 36

- 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

Question 37

effect of increased vasomotor tone on MAP

Answer 37

-increases TPR and MAP

Question 38

effect of increased venomotor tone on MAP

Answer 38

-increased venous return, SV and MAP

Question 39

'the skeletal muscle pump'

Answer 39

- 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

Question 40

acute cardiovascular/CVS responses to exercise

Answer 40

- 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

Question 41

hyperaemia

Answer 41

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

Question 42

effect of sympathetic stimulation on the heart

Answer 42

- 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

Question 43

effect of sympathetic stimulation on pacemaker cells

Answer 43

- slope of pacemaker potential increases - pacemaker potential reaches threshold quicker - frequency of action potentials increases (positive chronotropic effect/increase HR)

Question 44

effect of sympathetic nerve stimulation on ventricular contraction

Answer 44

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

Question 45

effect of EDV on SV (frank starling curve)

Answer 45

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

Question 46

frank starling curve

Answer 46

stroke volume against EDV

Question 47

chronic cardiovascular/CVS responses to exercise

Answer 47

- 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

Question 48

summary of control of blood pressure/mean arterial blood pressure

Answer 48

- 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