Specialised circulations Flashcards
Learning outcomes
- describe the circulation to special regions (skeletal muscle, skin, splanchnic & pulmonary areas, heart & brain) in terms of local & nervous factors & their control
- describe the influence of intracranial pressure on cerebral blood flow
- describe the effect of posture on the circulation (relate to fainting)
- explain fainting in relation to cerebral ischaemia, blood pressure & cerebral vascular resistance
Control of regional blood flow
Circulation to an organ depends on:
Perfusion pressure
Vascular resistance
Control of vascular resistance depends on:
Intrinsic/local factors (to tissue)
1. autoregulation – relatively stable blood flow to organ despite changing perfusion pressure: myogenic, metabolic & endothelial factors (NO, endothelin, EDRF)
2. mechanical compression (coronary/skeletal circulation)
Extrinsic/external factors (to tissue)
- nervous (Sympathetic)
- hormonal ( Adrenaline, vasopressin, angiotensin II)
What is autoregulation?
The ability of an organ to maintain blood flow despite changes in perfusion pressure
Myogenic, metabolic and endothelial(NO, endothelin, EDRF) factors
-Occurs in the absence of extrinsic factors (nervous/hormonal)
Features of Coronary Blood Flow (CBF)
High basal flow (80 mL/min/100g)
- High basal O2 consumption (10-25 mL/min/100g)
- High myocardial O2 extraction (70-80%; other tissues ~ 25%)
- High density of myocardial capillaries (3000-5000/mm2)
- O2 transport ↑by myoglobin in myocytes
- Little O2 in reserve if requirements ↑- blood flow must increase
- In exercise, CO ↑ x5, so O2 supply must ↑
Control of CBF
Flow is closely linked to O2 demand
Local/Metabolic primarily: ↓ O2, ↑ CO2, NO, H+, K+, lactate, prostaglandins, & adenosine -vasodilation
Neural indirectly
Sympathetic activation to heart results in coronary vasodilation & ↑ CBF. WHY?
-↑ metabolic activity
vasodilation > SNS vasoconstriction
B1 receptors on heart react to noradrenaline, tachycardia during exercise ( through C. vasodilation and metabolite production)
CBF in different states
At rest: 5% CO ( circulating oxygen) Moderate exercise: 5% CO Mechanical compression is important CBF At rest: 5% CO Moderate exercise: 5% CO Mechanical compression is important -Tachycardia significant in patients with coronary artery disease where coronary flow reserve is ↓: restricted myocardial bloodflow (most through diastole)- less relaxation between contractions, shorter diastolic phase, less blood flow to subendocardium in LV- angina and MI can follow
Skeletal muscle contraction
At rest:18% CO
Moderate exercise: >70% CO
Skeletal muscle vascular resistance can affect BP. Why?
- SM makes up 40% of body weight- if there is reduction in V. resistance in SM, it will affect BP- vasodilation in SM bed is 40% of BM, the decrease in resistance will affect BP ( MAP= c.ouput/ total peripheral resistance)
Local metabolic control
Metabolic vasodilatation –
(active/functional/exercise hyperaemia- increase in BF)
Important vasoactive metabolites- e.g. K+, PO43-, pH, hypoxia &lactic acid (H+)
Neurohormonal control in Skeletal muscle circulation
Neurohormonalcontrol: action of sympathetic nerves & hormones
-Sympathetic noradrenergic vasoconstrictor nerves–α1 adrenoceptors on surfaces of vascular SM
Adrenaline– β2 adrenoceptors on vascular SM: VASODILATION- noradrenaline to A1 receptors on Vascular SM causes vasoconstriction
Vasodilation in SMV bed, total peripheral resistance decreased, BP decreased
Sympathetic cholinergic vasodilator nerves
–Start of exercise
–Fainting
Compression of BV supplying muscle on SM contraction
Sphlanchnic ( GIT, liver, pancreas, spleen)
At rest: 30% CO
Moderate exercise: 5% CO
-Regulation
Local mechanisms - autoregulation
E.g. During digestion: local hormones, vasodilation, Inc BF to digestive tract
Nervous control - sympathetic vasoconstrictor nerves e.g. hypotension or exercise -↑ SV & CO. Why?
Alot of blood volume at rest in veins within these organs- venoconstriction- increased return to heart>inc. stroke volume> cardiac output- capacitance function of splanchnic system
Pulmonary circulation
Right side of heart- PC, left side Systemic C
BF through lungs = CO.
Heavy exercise: BF ↑ x 4-7 fold
Characterised by:High compliance & flow, low resistance & pressure (proximity to heart- vessels not as elastic, not as much smooth muscle compared to systemic- low BF resistance, so BF increased- all blood goes through PC)
Systemic C requires high pressure ( BF against gravity around body)
Control:
Local gas tensions
Hypoxic pulmonary vasoconstriction
allows perfusion/ventilation matching- if areas of lungs underventilated, blood flow redirected to better ventilated areas
low O2 pressure in arterties> vasoconstriction in lungs- vasodilation in Sys. C
Nervous control negligible
Cutaneous (skin) circulation
At rest: 4-10% CO
Moderate exercise: <20% CO
Range: 1-150mL/100g/min Venous plexus (deoxygenated blood- large SA which allows for heat loss)
Arteriovenous anastomoses- between arterioles and VP. when Arterioles are V.dilated and VP walls are vdilated, blood moves directly from arteriole> VP bypassing capillaries- inc amount of heat disappated
When AVA activated w sympathetic nerve supply, reduced BF between AVA to VP (cold weather)- withdrawal of SNS activity happens when body temp increased
Regulation
Local control – direct effect of temperature
Nervous control – hypothalamus output to sympathetic NS
Cerebral blood flow
At rest: 14% CO but only forms 2% body mass
Moderate exercise: 14% CO
Oxygen extraction relatively high- ischaemia even v temporarily> unconsciousness and the neurons intolerant to lack of oxygen
Control
Metabolic: ↓O2, adenosine, ↓ pH & ↑ CO-vasodilation
Myogenic: protect from changes in BP: ↓ MAP –cerebral vessels dilate; ↑ MAP – cerebral vessels constrict
Brain vulnerable under extreme systemic MAP changes: MAP < 60mmHg – syncope
MAP > 160mmHg – oedema
Unique characteristics of cerebral blood flow
- Active regions in the brain receive increased BF (active/functional hyperaemia)
- Blood-brain barrier
- Enclosed in the skull thus intracranial pressure influences cerebral perfusion
Cranial cavity – a brain (1400g), blood (75ml) & spinal fluid (75ml) –must remain constant
↑ in intracranial pressure can compress blood vessels thereby ↓ cerebral BF
e.g: 1.↑ brain volume – brain oedema
2.↑ CSF – hydrocephalus
3.↑ cerebral blood volume - blockage in venous drainage or vasodilation
Cerebral perfusion pressure= MAP- Intracranial pressure
In stressful circumstances flow to the heart & brain is maintained; reductions occur to other organs
Effect of posture on circulation
Cardiovascular changes moving from supine to upright
Defenses against venous pooling
- Neurovascular effects –baroreceptors
- Muscle pump
- Hormones – renin-angiotensin-aldosterone system
Usually only transient loss in BF although cerebral BF ↓20%
Fainting
Fainting
Standing up> 300-500 ml of blood pools in leg veins> Fluid accumulates in interstitium > ↓ venous return
> ↓ SV, CO & BP leads to 2 changes:
1.↓ cerebral BP approx 20-40 mmHg- leads to decreased cerebral BF and loss of consciousness
and 2. ↓ jugular venous P approx. 5-8 mmH- decreased cerebral BF, > paCO2, ↓ paO2& pH > ↓ cerebral vascular resistance> decreased cerebral vascular resistance> increased BF
Compensations-
Baroreflex- leads to increased arteriolar vasconstriction and increased heart rate/ CO, leading to increased BP
