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1

REGULATION OF BLOOD FLOW

- INTRINSIC
- EXTRINSIC

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intrinsic

- AUTO-REGULATION
- MYOGENIC HYPOTHESIS
- METABOLIC HYPOTHESIS
- cerebral circulation
- coronary circulation
- exercising muscle

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extrinsic

- ANS
- skin
- resting muscle

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INTRINSIC- cerebral circulation

- PaCO2 arterial carbon dioxide is the main factor regulating cerebral blood flow
hypoventilation- increases arterial PCO2, thus increase cerebral flow
hyperventilation- decreases arterial PCO2, thus decrease cerebral flow

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INTRINSIC- coronary circulation

- Adenosine is the by product of ATP breakdown
- vasodilate
- anti-arrhythmias
- recalcitron arrhythmias
- slowing conduction in the heart

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INTRINSIC- exercising muscle

- lactic acid

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INTRINSIC- MYOGENIC HYPOTHESIS

- has stretch receptors dilate by increase flow to the organ to control the flow, pressure related

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INTRINSIC- METABOLIC HYPOTHESIS

- vasodilatory metabolite, dilates, chemical induce pressure, MOST COMMON

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exercising individual

- blood flow to the CEREBRAL circulation REMAIN THE SAME PaCO2 is normal
- PaCO2 is the one that auto regulate the cerebral circulation
- increase metabolism will increase carbon dioxide will be poured into the veins
- INCREASING VENOUS CARBON DIOXIDE which then goes to the lung causing hyperventilation blowing excess CO2 out then PaCO2 will remain the same
- INCREASE oxygenation of the flow to the brain

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exercising individual

MAP= CO x TPR
CO= HR x SV
- increase HR
- increase SV
- increase CO
- increase production of lactic acid (vasodilator increase radius decreasing resistance)
- normal MAP

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normal exercise

- INCREASE systolic pressure (aka CO, HR, SV)
- DECREASE diastole (aka TPR) increase lactic acid
- NORMAL/SAME MAP

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RESTING MUSCLE (EXTRINSIC)

- controlled mainly by increasing or decreasing sympathetic alpha 1 adrenergic activity (ANS)
- in small contribution beta receptors also contribute tot blood flow

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EXERCISING MUSCLE

- mainly by vasodilatory (LACTIC ACID) metabolites
- increase CO
- beta 2 activation via EPINEPHRINE release via medulla of the ADRENAL GLAND hormonal causing increase flow
- beta 2 agonist (albuterol, salbuterol) can activate the beta 2 receptor in the blood vessels causing vasodilation
- decrease TPR causing diastolic hypotension
- sympathetic adrenergic alpha 1 receptors NO EFFECT ON FLOW due to action of lactic acid

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TPR proportional to

- aka BLOOD PRESSURE

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coronary circulation

- controlled by ADENOSINE
- pattern of control LV is most powerful than RV
- thereby LV contracts it squeezes the large coronary vessels that control the systole, flow to the left side of the heart is diminished.

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during diastole

- most of the blood supply is abundant due to is relaxation states

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coronary circulation

- 5-10% of CO
- by increasing the extraction of O2 from the blood
- causing extremely LOW PO2 to compensate increase blood flow
- A-V difference is LARGE

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kidney receives

- 20-25% CO

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A-V DIFFERENCE

- O2 extraction

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in the kidney

- A-V difference is small
- because the kidney receives large amount CO 20-25%
- extraction is minimal

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in the heart

- A-V difference is large
- because the heart receives small amount of CO 5-10%
- extraction is maximum

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pumping action CO

SV x HR

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hypertension

- increase pressure work
- increase afterload
- increase O2 demand

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INTRINSIC- cerebral circulation

- intracranial pressure is an important pathophysiologic factor that can affect cerebral blood flow

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hypoventilation (alveolar ventilation is inverse to arterial CO2)

- increases arterial PCO2, thus increase cerebral flow

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hyperventilation (alveolar ventilation is inverse to arterial CO2)

- decreases arterial PCO2, thus decrease cerebral flow

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during normal exercise

- arterial CO2 remains the same
- cerebral flow is normal

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cutaneous circulation(skin) (EXTRINSIC)

- controlled by SYMPATHETIC ADRENERGIC NERVES
- constriction of arterioles decreases blood flow
- constriction of venous plexus decrease blood volume in the skin
- increase skin temperature directly causes VASODILATATION, increase heat loss
- innervated by alpha 1 constricts (ANS)
brain + alpha 1 vasoconstriction, decrease flow increase TPR - alpha 1 increase blood flow to the skin
- beta 2 receptors non innervated, dilate, non ANS, + via hormones EPINEPHRINE causing vasodilation or drugs BETA 2 AGONIST ALBUTEROL decrease TPR, increase flow
- AT II constriction of blood vessel decrease flow to skin

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controlling temperature

via ETC
via HEAT LOSS thru skin

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main source of heat in our body

- OXIDATIVE PHOSPHORYLATION
- taking place electron transport chain
- ADP==> ATP
- O2 supply
- heat is released