Lecture 8: Haemodynamics II Flashcards
1. Describe the structure, function & properties of arterioles 2. Discuss how the radius of arterioles is regulated. 3. Describe the structure, function & properties of veins. 4. Discuss the factors that influence venous return
Describe the overall function of arterioles
Part of microcirculation
- connect arteries to capillaries
Major resistance vessels
- greatest resistance to blood flow
- largest pressure drop in vasculature ->93 mmHg to 37 mmHg
- radius is small enough to create large enough resistance to flow
- contribute 60% of TPR
List the properties of arterioles
Main differences from arteries:
- Smaller radius
- Thinner walls
- Less elastic -> no expanding + recoiling- only in aorta
- Rich supply of sympathetic nerve fibres
- Thick layer of smooth muscle around vessels
State the functional significance of changing the radius of arterioles
- Functional significance of changing the radius of arterioles -> blood flow to different regions of the body may be independently regulated
Describe the use of sympathetic nerve fibres in arterioles
-regulation of radius-via contraction of smooth muscle ->regulation of resistance ->regulation of BF
Explain the functional significance of arterioles
Pressure differential- move blood towards organs
-> Primary resistance vessels- establish pressure differential moving the blood towards the organs
->convert the pulsatile systolic-to-diastolic pressure swings in arteries into nonfluctuating pressure present in capillaries.
Control cardiac output distribution
Regulate arterial blood pressure
Describe the relationship between vascular tone and vasodilatory capacity
- Arterioles always exhibit tone
- Basal vascular tone = some degree of smooth muscle contraction
- > gives indication of vasodilatory capacity
- High vascular tone = large vasodilatory capacity
- Low vascular tone = low vasodilatory capacity
Explain the causes of basal vascular tone
Tonic smooth muscle of arterioles produces myogenic partial contractions
->has sufficient surface-membrane voltage-gated Ca2+ channels open even at resting membrane potential -> trigger partial contraction
-> myogenic activity independent of neural or hormonal influence -> self-induced contractile activity
Sympathetic fibres supplying most arterioles continually release norepinephrine -> further enhances vascular tone
Describe the variation of vascular tone in different organs of the body
- Brain-> has low basal vascular tone + low vasodilatory capacity (constant+ same BF)
- Basal vascular tone differs among organs
- Organs that have large vasodilatory capacity ->e.g., myocardium, skeletal muscle, skin, gastrointestinal circulation= have high vascular tone
- Organs have relatively low vasodilatory capacity ->e.g., cerebral and renal circulations= have low vascular tone
State how vascular tone can be controlled intrinsic and extrinsic mechanisms
- Vascular tone controlled by: –intrinsic mechanism
- > controls blood flow to local area/organ/individual capillary beds
- extrinsic mechanisms
- > controls systemic vascular resistance
State what type of control for radius is chemical factors and explain how it does so
Local metabolic changes->Match blood flow to momentary metabolic needs
- Decrease in O2=
- increase in CO2 =Generated as byproduct with more oxidative phosphorylation
- increase in acid=more carbonic acid generated from increased CO2, + lactic acid (lactate) accumulates when glycolysis pathway used for ATP production
- increase in K+= repeated AP that outpace the Na+ K+ pump ability to restore resting membrane potential ->more K+ in interstitial fluid
- Increase in osmlarity= concentration of osmotically active solutes – >increases during elevated cellular metabolism
- increase adenosine release= concentration of osmotically active solutes – >increases during elevated cellular metabolism
- Active hyperemia= active increase in blood flow
Endothelial-derived vasoactive paracrines
- do not act directly on smooth muscle
- endothelial cells release chemical mediators
- act on arteriolar endothelial cells
- respond to changes in cell environment
->reduction in O2
->physical changes: increase in frictional force of blood as it flows over surface of vessel lining
• nitric oxide = NO = small, highly reactive short-lived gas molecule
- numerous functions of NO as signalling molecule in physiological and pathological processes.
- Vasodilation-> increases conc. of intracellular 2nd messenger cyclic GMP in smooth muscle
-> activation of enzyme that reduces phosphorylation of myosin (necessary for cross bridge cycline)
=causing smooth muscle relaxation
- Released in response to local metabolic changes-> to further enhance vasodilation in area
- Plays role in regulating mean arterial pressure
• Endothelin
- Released from endothelial cells
- Potent vasoconstrictor
Histamine induces vasodilation
- Important in certain pathological conditions
- synthesized & stored in mast cells in many tissues & circulating WBCs
- When tissues are injured/damaged histamine is released
- Promotes arteriolar smooth muscle relaxation
- Increased blood flow, redness, swelling –> signs of inflammatory response
State what type of control for radius is physical factors and explain how it does so
- Myogenic response
- Shear stress
- Heat
Myogenic response ( inherent property of smooth muscle)
- blood flow > blood pressure > stretch
- mechanically gated cation channels open
- small depolarisation
- opens surface-membrane voltage-gated Ca2+ channels
- cytosylic Ca2+
- contraction of smooth muscle
- Vasoconstriction > radius > resistance >
- blood flow
- Important for regulation of hypertension
- Myogenic response works simultaneously with local chemical mechanisms ->return blood flow to normal within minutes
- Skeletal muscle doesn’t have myogenic response
- Myogenic response important in:
- brain
- kidney
- heart
= Purpose = keep blood flow constant = autoregulation -> no hormonal/ neural control
Shear stress - Release of NO -> response to increased shear stress of blood flow
- Endothelial cells shed due to friction
Temperature Heat: - ↑ blood flow - useful therapeutic agent ->remove waste+ increase travel of hormones + circulation
- Cold
- ↓ blood flow
- useful therapeutic agent
- > reduce swelling
- counteracts histamine-induced vasodilation
Derive MAP=CO x TPR
F=deltaP/R F=CO delta pressure= MAP R=TPR CO=MAP/TPR MAP=CO/TPR
Explain how neural controls can be used to affect TPR
Sympathetic system
- Controlled by cardiovascular control centre in brain stem
- Innervation of smooth muscle of arterioles
- sympathetic activity
- > vasoconstriction of systemic arterioles
- > TPR
Explain how TPR for brain is controlled using neural control
- Except brain-> BP remains constant
- Cerebral vessels controlled by local mechanisms ->maintains constant bf
=support constant level of brain metabolic activity
Explain how blood can be redistributed to vital organs
- Joint activity of systemic and local controls-> allow redistribution of blood
- To increase BF to vital organs-> local metabolic factors released to cause vasodilation of arterioles of those organs
= increase CO to vital organs + increase TPR+ MAP - Exercise
- NA + adrenaline= chemical mediators
->Noradrenaline (NA), (neurotransmitter +hormone), released from sympathetic nerve endings (NT) & adrenal medulla (hormone)
->NA binds with α adrenergic receptors on arteriolar smooth muscle
= general vasoconstriction in all systems through Phosphatidyl inositol triphosphate signaling system - Noradrenaline is the primary extrinsic factor affecting TPR and MAP
- Adrenaline is a hormone produced by the adrenal glands
+ acts as a neurotransmitter for nerve cells - Adrenaline weakly binds the α adrenergic receptor
+ strongly binds β adrenergic receptors in the arteriolar smooth muscle in the heart and skeletal muscles
= local vasodilation
= the local effect of adrenaline in heart and skeletal muscle overrides the systemic effect of noradrenaline (and to a smaller extent adrenaline)
Explain how hormonal controls can be used to affect TPR
- When NA + adrenaline released from adrenal medulla= hormone
- When from synapse= NT
- Adrenaline release only as hormone for local arteriole control
- Vasopressin (vasoconstriction)
- > Posterior pituitary gland
- > Maintain water balance via kidney water retention
- Angiotensin II (vasoconstriction)
- > Renin-angiotensin-aldosterone system (RAAS)
- > Regulation of body salt and water balance in kidneys
- Both promote systemic vasoconstriction of blood vessels= important for haemorrhage when need to maintain BP
List the properties of veins
- Large radius =less loss due to friction
= little resistance to BF-> lower pressure gradient required for BF - Small amount of smooth muscle
- Thin walls -> high compliance
- Blood reservoir – capacitance vessels
-> 60% of total blood volume (TBV) in systemic veins at rest - Has valves
- Venous flow is dependent on the pressure gradient between veins & right atrium
Explain the function of valves
- prevent backflow
- temporarily supports column of blood
- unidirectional BF -> towards heart only
Define venous return
- Venous return = volume of blood/min entering atrium from veins
Describe how venous return affects BF to organs
-decrease VR > decrease end- diastolic volume > decrease SV > decrease CO > decrease BF to organs
List the factors that affect venous return
- blood volume
- respiratory pump
- skeletal muscle pump
- sympathetic vasoconstriction activity
- pressure imparted to blood by cardiac contraction
- cardiac suction effect
- venous valves
Explain these factors affect venous return
Factor= Cardiac suction effect
- Pressure gradient between central veins (high) & atria (low) drive blood back to heart
venous pressure -> driving force for venous return
= CVP influences venous return
- CVP increased with heart failure/congestive heart failure, heart congested/overfilled
->overfilled/congested heart because: ventricular muscle not contracting forcefully enough
= can’t eject all blood
= reduced CO
Factor=sympathetic vasoconstrictor activity:
- Venomotor tone: Smooth muscle in walls of veins innervated by sympathetic NS (a adrenergic receptors)
- Norepinephrine stimulates contraction of smooth muscle =venous constriction
->Increases central venous pressure
->Decreases venous compliance
=Increases venous return
Factor= Skeletal muscle pump
- Many of the large peripheral veins lie between skeletal muscles
Skeletal muscle contracts ->compression of the veins:
venous capacity
venous pressure
= Essentially squeezing fluid in veins towards heart
- Exercise: muscle activity blood pushed out of veins blood to heart = Increase in venous return
Factor=Respiratory pump
- Inspiration
Pressure in thoracic cavity
- Pressure in chest cavity ~ 5 mmHg less than atmospheric P -> pressure gradient between atmosphere + thoracic cavity
- Blood from lower regions of body at higher pressure
Because lower region blood-> has external pressure of atmospheric
= pressure gradient exists between lower veins & chest veins
- Blood squeezed from lower veins chest veins
CVP
= venous return
