Components of Cardiovascular System Flashcards
Components of CVS
Heart Arteries Veins Arterioles Capillaries
Arteries
Passageway of blood from heart to tissue
pressure must be maintained
Arterioles
Major resistance Vessels
Capillaries
Site of exchange of gas, nutrients and water between blood and tissue
Veins
contain most blood volume at rest- capacitance vessels
blood from tissue to heart
Regulation of SVR
Vascular smooth muscles
- contraction increases SVR and MAP
- controlled by intrinsic and extrinsic mechanisms
Relationship between blood flow and resistance
R is directly proportional to blood viscosity and blood vessel length and inversely proportional to the radius of blood vessel^4
Which nerve fibres control vsm? Which nt is involved?
sympathetic nerve fibre
noradrenaline acting on alpha receptors
Vasomotor tone
vascular smooth muscle is partially constricted at rest
What causes vasomotor tone?
tonic discharge of sympathetic nerves resulting in continuous release of noradrenaline
* increasing sympathetic discharge increases vasomotor tone-> vasoconstriction
Hormones involved in control of VSM
Mainly adrenaline
also angiotensin II, andiuretic hormone (vasopressin)
What effect does adrenaline acting on alpha receptors have?
Vasoconstriction
What effect does adrenaline acting on beta-2 receptors have?
Vasodilation
Where are alpha receptors predominantly found?
skin, gut, kidney arterioles
Where are beta-2 receptors predominantly found?
cardiac and skeletal muscle arterioles
Effect of angiotensin II on VSM
vasoconstriction
Effect of vasopressin on VSM
vasoconstriction
Intrinsic control of VSM
matches blood flow of different tissue to their metabolic needs
can override extrinsic mechanisms
includes chemical and physical factors
Local metabolites
these chemical changes influence contraction of arteriolar smooth muscle
Factors causing vasodilation and metabolic hyperaemia
- Decreased local PO2
- Increased local PCO2
- Increase local [H+]/ decreased pH
- Increased ec [K+]
- Increased ECF osmolality
- ATP release of adenosine
Influence of local humoral agents
contraction of arterial and arteriolar smooth muscle
When are local humoral agents released?
Response to injury or inflammation
Humoral agents which cause vasodilation
Histamine
Bradykinin
NO (constantly released by endothelial cells in arteries and arterioles)
Production of NO
constantly produced from L-argenine in vascular endothelium through action of Nitric Oxide Synthase
Is NO a vasodilator or constrictor
Potent vasodilator
Has life of only a few seconds
Flow dependent NO formation
Stress, due to increased flow, on vascular endothelium causes vascular endothelial cells to release calcium. This activates NOS
Receptor stimulated NO formation
Chemical stimulation allows vasoactive substances to act
Activation of formation of cGMP
NO diffuses from vascular endothelium to surrounding smooth muscle cells, activating formation of cGMP
Role of cGMP
second messenger for signalling smooth muscle relaxation
Humoral agents which cause vasoconstriction
Serotonin
Thromboxane A2
Leukotrienes
Endothelin
Endothelin
potent vasoconstrictor released from endothelial cells
Characteristics of endothelial produced vasodilators
anti-thrombotic
anti-inflammatory
anti-oxidants
Characteristics of endothelial produced vasoconstrictors
pro-thrombotic
pro-inflammatory
pro-oxidants
Effect of temp of VSM
cold- vasoconstriction; warm- vasodilation
Myogenic response to stress
MAP rises= automatic constriction of resistance vessels
Important in tissue like brain and kidneys
Sheer stress in terms intrinsic control of vascular smooth muscle
Dilation of arterioles causes stress in arteries upstream, making them dilate also
- increases blood flow to metabolically active tissue
Autoregulation of Cerebral blood flow
Myogenic response keeps cerebral blood flow constant over wide range of MAPs
Sympathetic nervous system role
primarily role of the control of arteriolar radius and SVR (the brain is an exception)
Factors which cause an increase in venous return
Increase in venomotor tone
increase in blood volume
increase in respiratory pump
increase in skeletal muscle pump
Impact of increased venous return on stroke volume
causes increase on arterial pressure-> increased EDV-> increased SV
Increased Venomotor Tone
Increased venous return, SV and MAP
What happens to intrathoracic and intraabdominal pressure during inspiration? What impact does this have on venous return?
ITP decreases
IAP increases
increases pressure gradient for venous return and creates suction effect, moving blood from veins to heart
Effect of increasing rate and depth of breathing on venous return?
Increases venous return
Impact of increased muscle activity on venous return
increases venous return to heart
large veins limbs lie between skeletal muscles
Acute CVS responses to exercise
increase in sympathetic nerve activity
->increase in HR, SV and hence CO, causing increased SBP
->reduced flow to kidneys and gut
metabolic hyperaemia overcomes vasomotor drive in skeletal and cardiac muscle
-> vasodilation in proportion to metabolic activity
-> decreased SVR and DBP (PP increases)
Effect of sympathetic stimulation on heart
increases HR by increasing firing rate of SAN and decreasing AVN delay
Increases force of contraction
Effect of noradrenaline on pacemaker cells
increase in slope of pacemaker potential, causing pacemaker potential to reach threshold quicker and frequency of action potential to increase (+ve chronotropic effect)
Effect of sympathetic stimulation on ventricular contraction
Peak ventricular pressure rises, causing contractility of heart at given EDV to rise
FS curve shifts to left
Chronic CVS responses to exercise
reduced sympathetic tone and noradrenaline levels
increased parasympathetic tone to heart
cardiac remodelling
Reduced plasma renin levels
Improved endothelial function (increase in vasodilators; decrease in vasoconstrictors)
Decrease in arterial stiffening
