Cardio Flashcards
What are the two levels of control over smooth muscle, surrounding arteries?
Local/intrinsic mechanisms- selfish needs
Central/extrinsic mechanisms- for TPR and therefore MAP of whole body
Increase of metabolites in the blood perhaps due to exercise, leads to what
Local intrinsic control
Endothelial cells sense and release EDRF, so arteriolar dilate
What are the four local intrinsic controls
Active metabolic hyperaemia
Pressure flow auto regulation
Reactive hyperaemia
Injury
Difference between the
local/intrinsic controls?
Active/metabolic - trigger is increase in metabolites
Pressure/flow auto regulation - MAP decrease is the trigger, so metabolites washed away less, but same response
Reactive hyperaemia - trigger is occlusion of the blood supply: causes subsequent increase in blood flow (metabolites were not being washed away- and as such, arteriolar became very dilated).
Also injury response
What’s the injury response
When you injure yourself, your C-fibres get activated, they fire action potentials, to brain (ouch) but also collateral branches = release substance p, acts on mast cells, triggers histamine release, histamine = smooth muscle relaxes, arteriolar dilate, increase blood flow. Permeability increase.
Central control of blood pressure, what’s the difference between what the sympathetic and parasympathetic does.
Sympathetic = noradrenaline, binds to alpha 1 receptors, causes arteriolar constriction
Parasympathetic = no effect.
Parasympathetic nerves have no effect on blood pressure, what affect DOES it have
Genitalia and salivary glands have increased fliw
Normal hormonal central control of blood pressure
Adrenaline
A1 receptors
Arteriolar construction
adrenaline hormonal central control of blood pressure: adrenaline and alpha 1 vs adrenaline and beta 2
Well it’s alpha 1 receptors that the adrenaline binds to. But some tissues eg some muscle also activated beta 2 receptors. Which means opposite affect- arteriolar dilation, not construction.
Eg during exercise
What happens to coronary circulation during systole?
It’s interrupted
Because pressure in ventricles squishes blood vessels
Still has to cope with increased demand during exercise
So active/metabolic hyperaemia
Where the local paracrine signal like nitric oxide is released, = arteriolar dilation
Smooth muscles in the arterioles = beta 2 receptors = smooth muscle relaxation, and arteriolar dilation
What’s special about the cerebral circulation
Needs to be kept stable
So good pressure auto regulation, where MAP decrease is triggered, so EDRF
How is pulmonary circulation kept okay?
Decrease in O2 = arteriolar constriction , shynt
What’s the auto regulation like in the renal circulation?
Fantastic
Filtration rate kept relatively constant during normal fluctuations in MAP
What does MAP = equation
MAP = CO x TPR
What happens if MAP is too low/too high
Too low = fainting/syncope
Too high = hypertension
Why syncope
Because removes gravity, so less pooling, EDV restored, preload restored, stroke volume restored
Short term way of sensing blood pressure / MAP is what?
Arterial baroreflex
The arterial baroreflex is essentially an integrating centre that’s looks at the info, decides what to do with it etc
Yes
What are the two sensing sets of baroreceptors
The carotid sinus baroreceptors
The aortic arch baroreceptors
Where are the carotid sinus baroreceptors
In the common carotid arteries
Where’s the carotid sinus
It’s where the common carotid arteries become the internal carotid arteries
How do the baroreceptors (carotid sinus and aortic arch) actually work?
They detect changes in pressure by detecting stretch, and when they detect change in stretch, they increase the firing rate of action potentials
Less pressure = less firing rate of baroreceptors, true or false
True
When during the cardiac cycle do the baroreceptors have the highest firing rate?
when walls most stretched, so that’s early in systole.
