Control of Blood Flow Flashcards
Resistance=
4 general blood flow control mechanisms
Resistance = 8 x n x L/ pi r^4
n (fluid viscosity) and L (vessel length)
1) Local
Metabolic mech
Myogenic mech
They autoreg. Blood flow in the face of changing perfusion pressure or inc. blood flow in response to inc. in metabolic demand
2) endothelial
Release of NO or prostaglandins (vasodilator)
3) Hormonal
ADH, Adrenaline, AngII
4) Central neural
Sympathetic NS
How does increase in sympathetic nerve outflow cause arteriolar vasoconstriction?
6 steps
1) Post- ganglion sympathetic neurones a1 adrenoreceptors + NA
2) stim. of adrenorecpetors causes rapid inc. [Ca2+]cyt in arteriolar smooth muscle cells
3) stimulate contraction of smooth muscle in arteriolar
4) vasoconstriction
5) Dec. Lumen radius
6) inc. resistance and dec. blood flow
Intrinsic Factors
Definition
Autoreg. 3 examples
Another 2 examples which are linked
Def- regulates blood flow to organ by factors originating from within the organ
Autoreg:
Metabolic mechanism
Myogenic mechanism
Endothelial mechanism
Metabolic and active hyperaemia
Extrinsic factors
Definition-
Neural-> 4 types of fibres/ actions
Endocrine 3/5 examples
Notable extrinsic and intrinsic factor examples depending on location 1/2
Definition- Regulation of blood flow to an organ by factors originating from outside the organ.
Neural Sympathetic vasoconstriction fibres Parasympathetic vasodilator fibres Sympathetic vasodilator fibres ->sweat glands Nociceptive fibres
Endocrine
ADH, Ang II, Oestrogen, Relaxin, Catecholamines
Notables examples:
Adenosine (- vasodilator) everywhere else but renal afferent arteriole (+)
Endothelial secretions: NO (-) endothelin (+)
Classic over arching equation
Central command definition
Via (2 areas!)
what else does central command do during exercise + why? 1,2,3
3 types of receptors during exercise further control feedback mechanisms via inc. sympathetic outflow, what are the receptors?
ABP = CO x TPR
Definition- feedback anticipatory response before exercise to increase HR
Via motor cortex and assoc. regions
Medullary CV control centres lead to inc. HR
triggers central resetting of arterial baroreflex -> therefore allows for greater hypertension during exericse.
increase in sympathetic outlfow, inc. temporary driving force/ pressure gradient, inc blood flow during exercise.
Mechanoreceptors
Metabaroreceptors
Arterial barorecpetors
3 ways venous return is significantly increased during exercise:
1
2
3- 3 steps
1) sympathetic vasoconstriction: NA + a1 (arteries and veins)
2) skeletal muscle pump-> inc. pressure in veins as muscles compress, inc. venous return
3) Resp. muscle pump-> inspiration triggers dec. in intrapleural pressure, dec. in pressure in vena cava, creates a pressure gradient and drives venous return.
pulmonary circulation:
Pulmonary BP is low, what is it?
2 reasons why it is low
But it has a high flow, meaning…
when exercising, blood flow inc so resistance must drop to maintain same pressure, how? (2 methods)
active or passive?
which part of the lung has the most perfusion and why?
1)
also
2,3,4
25/8 mmHg
- prevents oedema in lungs as inc. in hydrostatic pressure will push fluid out, inc. diffusion pathway for O2 and decrease perfusion
- also limits after-load in right ventricle (would cause RV hypertrophy)
meaning very low resistance ( x5 less than systemic)
methods to decrease resistance: PASSIVE
1) recruitment of more capillaries
2) distention of the capillaries
most at base of the lungs
pulmonary artery pressure dec. as you go up the lungs to apex as it works against gravity
also
intrapleural pressure grater at base of lungs as weight of lungs is pushing it down -> decreases intrapleural space -> more perfusion
How does functional (metabolic) hyperaemia increase blood flow to active skeletal muscles?
5 steps
intrinsic or extrinsic?
INTRINSIC
1) inc. O2 demand
2) inc. blood flow compensates for inc. CO2 prod
3) inc. metabolite prod: Adenosine, K+, Lactate
4) vasodilator effect
5) further inc. blood flow so washes metabolites away
Hyperaemia:
Active Hyperaemia: 5 steps
Reactive hyperaemia: 6 steps
active hyperaemia:
1) inc. tissue metabolism
2) inc. metabolic vasodilators into ECF
3) dilation of arterioles
4) dec. resistance and inc. blood flow
5) O2 and nutrient supply to muscles continues as long as metabolism continues
reactive hyperaemia: 6 steps
1) dec. blood flow due to occlusion
2) metabolic vasodilators accumulate in ECF
3) dilation of arterioles but occlusion prevents blood flow
4) removal of occlusion
5) dec. resistance and inc. in blood flow
6) as vasodilators wash away arterioles constrict and blood flow returns.
Coronary Circulation
cardiac perfsion is dependant on…
perfusion effected when: 1,2,3
where are coronary arteries found?
Diastolic pressure
effected when:
1) tachycardia -> decrease time for diastolic filling
2) hypertension/ elevated end diastolic pressure
3) reduced arterial BP
in subendocardial region
What happens to inactive muscles and the renal/ splanchnic arteries during exercise and why?
1,2,3,4(also)
explain the changes in blood flow to cutaneous circulation initially in exercise and then later in exercise
initially:
1)
later:
1,2,3
until:
1,2
1) vasocontriction via sympathetic activity
2) maintain TPR and ABP
3) allows for maximal blood flow to be redirected to active muscles
4) also baroreflex resets allowing for small rise in arterial pressure
Initially:
sympathetic vasoconstriction of cutaneous blood vessels to decrease flow, inc TP resistance and maximise flow to active muscles
later:
core body inc.
blood flow to skin inc. to thermoreg
TPR will dec so HR inc. to maintain ABP
until:
blood flow to skin rises linearly with body temp until it wont go any higher- sacrifices thermoreg for ABP maintenance.
this level of plateau is dependant on hydration.
