Arterial and Venous system Flashcards
function of elastin fibres in aorta
Elastin fibres provide elasticity
– as blood is ejected the aorta expands, the rebound in diastole propels the blood onward
important structure in arteries
Arteries have a thick layer of smooth muscle
– allows them to withstand high pressures
collagen fibres function
Collagen fibres provide strength
how does collagen and elastin change throughout arteries
this and elastin decrease in abundance as arteries get smaller
how does collagen and elastin change WITH AGE
As we get old vessels get stiffer and less compliant
– one of the reasons blood pressure increases
Important structure of arterioles
Arterioles have a thick layer of smooth muscle
– as a total amount it is less than the large arteries but it is greater proportional
of the total wall
difference between arteries and arterioles
• Less elastin and collagen fibres
– less compliant compared to larger arteries
arterioles are site of
These are the site of total peripheral resistance
– think back to the Poiseuille’s Law (1 / r
4)
• Tone on these vessels determines where blood flows
– it always takes the path of least resistance
vascular tone
the level of constriction applied across vessels
state of arteries at rest
are slightly constricted meaning they can both
constrict and dilate
arterial tone
the balance of constrictors and dilators that are acting on the vascular smooth muscle
arterial constriction leads to..
decrease radius
increase resistance
decrease flow
arterial dilation
increase radius
decrease resistance
increase flow
what does vascular tone respond to
responds to both intrinsic (local) and extrinsic (systemic) factors
2 types of intrinsic factors
- intrinsic: mechanical stimuli E.G. stretch and shear
2. intrinsic: endothelial regulation plus other metabolites and autocoids in response to local demand
extrinsic
extrinsic: systemic regulation (nerves & hormones)
organs involved in primary intrinsic regulation of vascular tone
brain, kidney and heart
– local control regulating flow -
brain does not require external stimuli
primarily extrinsic regulation of vascular tone
skin
– think hypothalamus and temperature regulation
– also think cool peripheries following BP crash
interactions of regulation of vascular tone
skeletal muscle
– at rest systemic regulation
– during exercise local metabolites dominate
when do smooth muscles constrict
constricts when stretched
– occurs in most smooth muscles including vascular
– due to opening of Ca2+ channels
where does constriction occur
• Occurs in a number of vascular beds
– such as cerebral, renal and coronary
what does myogenic response of constriction of smooth muscle contribute to
This contributes to the basal tone of arteries and stabilises flow and prevents excessive perfusion
– it is an important feature of autoregulation
role of vascular endothelium
– interface between blood and body tissues – control of blood coagulation – regulates vascular structure – mediates inflammatory responses – regulates vascular tone
endothelium performs thru the release of what factors
paracrine factors
acting nearby; either the smooth muscle or platelets
endothelial mediators. - dilators
nitric oxide (NO) and prostacyclin (PGI2)
vasoconstrictors
such as endothelins (ET), Ang II and thromboxane (TxA2)
what does nitric oxide synthase enzyme produce
free radical nitric oxide
NO function
a vasodilator, relaxing vascular smooth muscle
– production increased by shear stress
– also agents such as ACh, histamine and bradykinin
NO is an anti-//
anti-thrombogenic and anti-atherogenic
– a healthy endothelium provides a non-thrombogenic surface
drugs interacting NO pathway -nitrates
– e.g. glyceryl trinitrate (GTN)
– used in angina
– assumed to act as NO is released via metabolism
– also available from dietary sources
drugs interacting NO pathway - phosphodiesterase inhibitors
– e.g. sildenafil (Viagra)
– erectile dysfunction and pulmonary hypertension
– prevents the breakdown of cGMP
what promotes vasodilation
Increased CO2, K+ , H+ and adenosine as well as decreased O2 all promote vasodilatation
– increased tissue metabolism increases perfusion
vasoactive substances
histamine, bradykinin, serotonin (5-HT) and
eicosanoids/prostanoids
metabolic hyperaemia
increased metabolic rate in tissue
accumulation of metabolites CO2 H+ K+ adenosine
local vasodilation
increased blood flow
accumulated metabolites flushed out
appropriate blood flow match metabolic rate
what nervous system is responsible for maintenance of vascular tone
SympatheticNS
most arteries are innervated by what fibres
sympathetic fibres
constriction is due to what hormone and what receptor
noradrenaline acting at α1
-adrenoceptors
increased sympathetic activity increases
will increase vasoconstriction
– cold, clammy peripheries
what receptors lead to dilation in arteries
β-adrenoceptors (mainly β2
-)
arteries are a target for circulating what hormone and what do they prevent
mainly a target for circulating adrenaline (adrenal medulla)
– prevalent in the skeletal muscle vascular beds and heart
vasodilator innervated by
parasympathetic innervation
organs innervated by PNS
face
gut
penis
PNS innervated vessels mediated by what hormone
ACh & nonadrenergic non-cholinergic (NANC)
– NANC transmitters include NO, substance P, VIP
mechanism of action of vasoactive hormones
Adrenaline from adrenal medulla.
– tends to act via β adrenoceptor
– constriction or dilation is vascular bed dependent
• Angiotensin II
– acts on AT receptors potent vasoconstrictor
• Vasopressin (anti-diuretic hormone, ADH)
– vasoconstrictor
• Insulin and oestrogens
– dilators by various mechanisms
function of venules and veins
carry blood from capillaries back to the heart
right atrium
structural difference between veins and arteries
Structurally veins are similar to arteries but have much thinner walls
– very little smooth muscle, small amounts of collagen/elastin
what gives veins their capacitance function
distensibility gives then a capacitance function
– two thirds of the blood volume is held in the venous system
– x20 compliance of arteries
what are the veins innervated by and what hormones and receptors mediate them
• Like arteries, veins are innervated by SNS fibres
– noradrenaline acts at ɑ1
-adrenoceptors to constricts veins
are veins capable of constricting
yes
affect of SNS fibres and noradrenaline
The effect of this is to raise pressure and decrease venous
capacitance
– redistributing the blood
function of valve
prevent backflow, blood is moved towards the heart
– increasing cardiac output via Starling’s Law
venous return is altered by
Skeletal muscle and thoracic pumps
– vary the pressure gradient during their activity
• Venous pressure/venoconstriction
gravity
how does gravity influence pressure
Hydrostatic pressure increases 0.74 mmHg for every 1 cm beneath the heart
– venous pressure the foot 100 mmHg, yet -10 mmHg in brain
how does gravity influence venous return and veins
• This increased transmural pressure distends the veins and venous return temporarily decreases
– this is venous pooling
how does gravity influence muscle, valves and thoracic pump
The valves and muscle and thoracic pump break up the column into smaller sections aiding return
– lack of movement (and muscle pump) increases ankle oedema
impact of failure of of valves
• Failure of valves also decrease return and increase venous pooling/oedema
– varicose veins
what is triggered when pressure falls
Baroreceptor reflex is triggered as cardiac output and pressure fall
– increased vaso/venoconstriction, heart rate and contractility
– this should be imperceptible
what happends when baroreceptors cannot respond
In states where the baroreceptors cannot respond then there is
postural drop and possibly syncope
– dehydration, already low pressure, old age (stiffer vessels)
affect of positive g force - pilot in a steep climb
– black out as venous pooling increases
– venous return drops as does cerebral perfusion
– in a suit pilots can tolerate ~9 G
affect of negative g force - pilot in a steep dive
“red out” and blood rushes to head (red eyes)
– even in suit can only tolerate about 3 G
what does central venous pressure measure -CVP
measures right atrial pressure via
catheter in central vein
what does CVP reflect and what is used to assess
it reflects the venous return and cardiac function
– can be used to assess fluid volume in fluid replacement
how does CVP change in heart failure
CVP increases in heart failure due to volume expansion
where is jugular venous pressure - JVP
seen in the internal jugular vein
of a person sitting
A,C,V waves of the jugular venous pulse in the ..
right atrium
how to measure jugular venous pressure
• Sit patient at 45 degrees
• The internal jugular veins fills from above
– where can you visualise is the filling point?
• The sternal angle is the zero point, more than 3 cm above is abnorma
what does increased jugular venous pressure suggest
A raised JVP suggest increased right atrial pressure
– fluid overload
– RV failure
– tricuspid valve stenosis/regurgitation
hepatic portal vein function
carries blood from the gastro-intestinal tract to the liver
– from intestinal capillaries to liver capillaries via portal vein
– two capillary beds in series
what type of capillaries are the capillaries in the liver
sinusoidal type
– large gaps allows large substances to be absorbed
how do diseases like cirrhosis impact hepatic portal circulation and how is it corrected
, resistance in the hepatic portal system increases
– to maintain flow pressure must increase (Q = ΔP ÷ R)
– pressure increases giving portal hypertension
how are nutrients absorbed in the hepatic portal circulation
All substances absorbed from the intestines pass through the liver
– this includes orally taken drugs – first pass metabolism
high portal pressure leads to
shunt vessels (varices) that bypass the liver back into systemic venous system
what can shunt vessels lead to
this leads to morbidity
– bleeding abnormalities and toxins damaging other organs
– (hepatorenal syndrome and hepatopulmonary syndrome)
