Regional Circulation and their control - L10 Flashcards
CO distribution at rest:
Equal driving pressures across all organs
Parallel circuits: precise control within serial
circuits
Is CO distribution independent of altered MAP?
What is it dependent on for alteration?
What happens with increased organ activity?
If MAP remains the same, what allows altered CO distribution
Yes
We have an altered CO distribution irrespective of MAP it is regards to TPR instead
With increased organ activity (i.e. ↑ed metabolism - increased O2 and nutritional demands at that level)
Then CO distribution is altered
Organ BF increase occurs via active hyperaemia
Vasoactive components: some arterioles vasodilating to allow blood flow towards organ that will travel via capillary bed and vasoconstriction of less active organs
Active hyperaemia results in what for local capillary flow and why?
↑ Local capillary blood flow
Responds to ↑ed organ/tissue metabolism
Active hyperaemia is mediated by metabolic factors which act on:
Endothelial cells to release
Nitric Oxide (NO) – vasodilator
Metabolic factors that mediate active hyperaemia may include?
↓ O2 and/or ↑ CO2
↑ acid (carbonic [H2CO3] or lactic)
↑ K+ via repeated AP’s
↑ Osmolarity
What is reactive hyperaemia?
What happens to BF?
It is exaggerated hyperaemia
BF over and above that predicted by metabolism
What is reactive hyperaemia usually a result of?
What happens to blood flow during this?
Tissue hypoxia
Blood flow is restricted for a defined time period
What kind of effect foes reactive hyperaemia provide?
Provides a flushing effect
What is reactive hyperaemia mediated via? 2 things
Local metabolite accumulation similar to active hyperaemia
Myogenic relaxation - Arteriolar smooth muscle response to reduced stretch
Name 3 other vasoactive conditions:
Shear stress, local temperature and histamine
When is shear stress exeperinced and what does it induce in terms of vasoactivity?
Experienced with high blood flows, increase in blood velocity
Compensates for changes in longitudinal force of blood flow, the faster the velocity. For example during exercise
Induces endothelial cell NO release → local vasodilation
When is local temperature experienced and what are the 2 types?
Therapeutic during injury;
Heat-vasodilation; cold-vasoconstriction
What is histamine important for?
What is it derived from?
What does it do to smooth muscle?
What does it do to capillary permeability and give an example with allergic reaction?
Important in pathological conditions
Derived from connective tissue (mast cells) & basophils (circulation)
Increases smooth muscle dilation
Increases capillary permeability (induces oedema in allergic reactions)
What does autoregulation of blood flow utilise?
Myogenic mechanism
Autoregulation of blood flow is an inherent property of?
Vascular (arteriolar) smooth muscle
Increased pressure of this autoregulation of blood flow causes?
→ initial ↑ BF & increased stretch
→ compensatory contraction
→ limited ↑ BF
What defence does this autoregulation of BF provide, and is overriden by? give an example
Provides defence against change in MAP and is overridden by essential ↑’s BP, for e.g. active hyperaemia, exercise
Active hyperaemia factors main role is to bring about:
vasodilation to increase blood flow, brought about by factors that influence the endothelial cells and endothelial cells then release NO and that brings about active hyperaemia and vasodilation
Region circulations we have the renal system, what is this BF at rest?
What does it utilise?
Kidney (renal) blood flow (RBF)
At rest 20-25% of all CO (0.5% body mass) comes to kidney region purely due to role of filtration of blood - 180L of blood travels through the kidney throughout the day - not diffusion gradient as much
Utilises autoregulation
Constant flow of blood per minute is?
5L of blood per minute
Rental Blood Flow indirectly determines?
Glomerular Filtration Rate
Does histamine change systemically?
No it acts locally
EXAM Q Asks about contributions of TPR in relation to meeting metabolic demands of tissue:
Need to mention all these factors from diagram but main emphasis on sympathetic activity for extrinsic control and local control - at level of local metabolic changes that bring about the increase in endothelial cell activity via NO and endothelin
Address 3 factors: histamine, shear stress and local temperature that have vasoactive contributions
Autoregulation of BF?
Regulation of BF is about precise control and this is just a contributory mechanism - built in mechanism to help meet the demands of increases in BP but not to the extent that another area of the body suffers
Do all areas of the body have the same autoregulation of BF?
No different levels of the body all have different levels of autoregulation such as the renal system has very tight regulation
Does renal system have sympathetic innervation? what does this mean?
Is there active hyperaemia, why or why not?
High sympathetic innervation means that we can limit BF when high MAP’s are required (e.g. exercise)
Not as important to make urine when exercising for example
No active hyperaemia as it is not required with such a high resting BF as they have ample BF to meet demands
In addition to RBF indirectly determining GFR, this sympathetic innervation what other feedback is utilised by renal system?
Utilised tubuloglomerular feedback which increases GFR
How does Tubuloglomerular feedback increase GFR?
→ ↑tubular fluid flow detected by Macula Densa - senses glomerular filtration rate
→ feedback signals constricting afferent arteriole
→ ↓GFR
Other region circulations includes cerebral: CBF - Cerebral blood flow at rest?
Does it use autoregulation?
At rest it takes 15%-20% of all CO (2% body mass)
Utilises autoregulation
The way that autoregulation comes into play with CBF what is it purely based on?
What happens when we have decreased O2 what happens?
Decreased and increased partial pressure of CO2 causes?
Sensitivity to arterial partial pressures of CO2 and O2
Need to increase BF to counteract that as at all stages we need to make sure that the brain is accurately perfused: ↓pO2 <50 mmHg → ↑BF
Decreased CO2 =>↓BF (light headedness with hyperventilation) and ↑pCO2 → ↑BF as more CO2 means less O2
When range in mmHg CPP or MAP is CBF stable?
What happens above or below these ranges?
CBF is stable between 50 and 150 mmHg CPP (cerebral perfusion pressure) or 60 and 160mmHG (MAP)
When we are above/below these levels, we lose that capability to autoregulate, we lose that ability to meet the demands of the BF in relation to meeting the demands of increase or decrease in MAP
In hypoxic cases what happens to BF?
We have a huge increase in BF - 400 times its resting BF, the ability is there just need to make sure the supplies are there
Upright cerebral arterial pressure?
~77 mmHg
Where does autoregulation fail - give some examples?
When does fainting occur?
50 mmHg
e.g. sudden postural changes (supine to upright)
e.g. excessive peripheral dilation (high ambient temperature)
e.g. stress/emotion induced vasovagal (↓HR → ↓CO → ↓MAP) -> called vagal response: sympathetic activity is withdrawn and parasympathetic activity kicks in and we are not sure why
40 mmHg: fainting -> brings o2+CO2 back to normal, Only way to get them to go back to normal, compensatory mechanism as autoregulatory mechanism failed, the only issue with this is the fall that you have
Region circulations - dermal: skin blood flow what is it at rest?
What is the metabolic requirement?
Does it use autoregulation?
At rest: 5% CO (3% body mass)
Consistent metabolic requirement → 250 ml/min BF
Yes and it utilises sympathetic innervation (via hypothalamus)
How does skin blood flow protect core temperature, in terms of hot and cold exposure?
- Constricts arterio-venous anastamoses (noradrenergic) to limits blood flow to skin during a cold stress
- Stimulates sweat glands (preganglionic cholinergic)
Release bradykinin (vasodilator) – pseudo active hyperaemia causes a redenning - potent vasodilator that offsets the heat, sweat gland releases enzyme to trigger vasodilation mechanism to offset the build up of heat within the system
Regional circulations - splanchnic - splanchnic blood flow at rest?
Splanchnic blood flow
At rest 25% of all CO (5% body mass)
(Typically 30 ml min−1 100 g−1 of tissue)
Is this splanchnic BF adaptive?
What kind of control?
Yes -> Highly adaptive: decrease to to <10 ml min−1 100 g−1 in low cardiac output, peaks locally at 250 ml min−1 100 g−1 after a meal
Diverse control
Spanchnic BF has a diverse control - does it have sympathetic innervation?
When MAP is elevated in exercise for example what does it do?
Can it restrict bf?
Is there active hyperaemia, if so when?
Yes, there is sympathetic innervation
Involved in diverting BF when MAP is elevated – e.g. exercise
Can restrict blood flow almost completely
Some active hyperaemia - e.g. during digestion
1 role of skin?
Thermoregulation - it is a protective barrie - main role is for temperature control
We must keep our core organs at 37 ish degrees
It is exposed to different variations in ambient temperature and must be able to respond
What is one of the first systems to be targeted when the body is stressed?
Digestive system
What is the big thing with splanchnic BF?
Huge reserve that we can tap into if we need to
Coronary circulation at rest get how much of our CO?
When does it happen?
What % of cardiac cells have mitochondria and what does this mean in terms of energy?
What happens when metabolic activity of cardiac muscle increases?
What causes an increase in O2 and nutrient delivery to epicardial vessels?
Coronary blood flow - at rest 5% CO (0.5% body mass)
Happens during this phasic flow of systolic compression and diastolic dilation - about 40% of cardiac muscle cells are filled with mitochondria so they are energy rich and energy requiring structures
When this metabolic activity of cardiac muscle increases so does the oxygen supply that is needed - its O2 demand increases.
Anything that causes our heart rate to increase causes an increase in O2 and nutrients needed and delivered to those epicardial vessels
When the heart contracts itself for its own blood supply what happens to normal blood flow?
What happens to coronary heart supply during normal cardiac cycle such as the systole portion?
When the heart contracts itself and compresses the coronary vessels itself so it impedes blood flow whilst its contracting
Similarly the actual aortic valve during systole blocks entrance to the coronary artery so it deprives the coronary circulation of O2 delivery during systolic phase - 30% of circulation that gets to coronary vessels and 70% happens when the heart is relaxing during diastole
Does the coronary BF use active hyperaemia?
Yes it utilises it
What does reduced O2 supply cause in terms of coronary BF?
Adenosine is released and acts as a potent vasodilator and allows increases blood vessels and causes an increase in BF so we have increase O2 to meet O2 demand
Does the heart itself have any sympathetic innervation?
What does altered HR affect in terms of coronary flow?
The heart itself has a high sympathetic innervation
Altered HR affects time available for coronary flow, but overridden by metabolic active hyperaemia
Acute CVS changed during exercise -
When HR increases what is this due to?
Occurs as a result of increased sympathetic and decreased parasympathetic activity to SA node
Acute CVS changed during exercise -
What occurs when venous return is increased?
Occurs as a result of sympathetically induced venous vasoconstriction and increased activity of the skeletal muscle pump and respiratory pump
Acute CVS changed during exercise - increase in stroke volume occurs due to?
Occurs both as a result of increased venous return by means of the Frank-Starling mechanism and as a result of a sympathetically induced increase in myocardial contractility
Acute CVS changed during exercise -
What does increase in CO occur as a result of?
Occurs as a result of increases in both HR and SV
Acute CVS changed during exercise -
What does increase in blood flow to active skeletal muscles and heart occur as a result of?
Occurs as a result of locally controlled arteriolar vasodilation, which is reinforced by the vasodilatory effects of adrenaline and overpowers the weaker sympathetic vasoconstrictor effect
Acute CVS changed during exercise -
What is the change in blood flow to brain and what does this occur as a result of?
It is unchanged and this occurs because the sympathetic stimulation has no effect on brain arterioles, local control mechanisms maintain a constant CBF
Acute CVS changed during exercise -
What does increase in blood flow to skin occur as a result of?
Occurs the hypothalamic temperature control centre induces vasodilation of skin arterioles, increased skin blood flow brings heat produced by exercising muscles to the body surface where the heat can be lost to the external envioronment
Acute CVS changed during exercise -
What change occurs to blood flow to the digestive system, kidneys and other organs and what causes this to occur?
Blood flow is decreased
Occurs via generalised sympathetically induced arteriolar vasoconstriction
Acute CVS changed during exercise -
What change occurs to TPR and what causes this to occur?
Decreases - occurs because resistance in skeletal muscles, heart and skin decreases to a greater extent than resistance in the other organs increases
Acute CVS changed during exercise -
What change occurs to MAP and what causes this to occur?
Increases - modest
Occurs because CO increases more than TPR decreases
