regulation of BLOOD FLOW Flashcards
REGULATION OF BLOOD FLOW
- INTRINSIC
- EXTRINSIC
intrinsic
- AUTO-REGULATION
- MYOGENIC HYPOTHESIS
- METABOLIC HYPOTHESIS
- cerebral circulation
- coronary circulation
- exercising muscle
extrinsic
- ANS
- skin
- resting muscle
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
INTRINSIC- coronary circulation
- Adenosine is the by product of ATP breakdown
- vasodilate
- anti-arrhythmias
- recalcitron arrhythmias
- slowing conduction in the heart
INTRINSIC- exercising muscle
- lactic acid
INTRINSIC- MYOGENIC HYPOTHESIS
- has stretch receptors dilate by increase flow to the organ to control the flow, pressure related
INTRINSIC- METABOLIC HYPOTHESIS
- vasodilatory metabolite, dilates, chemical induce pressure, MOST COMMON
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
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
normal exercise
- INCREASE systolic pressure (aka CO, HR, SV)
- DECREASE diastole (aka TPR) increase lactic acid
- NORMAL/SAME MAP
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
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
TPR proportional to
- aka BLOOD PRESSURE
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.
during diastole
- most of the blood supply is abundant due to is relaxation states
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
kidney receives
- 20-25% CO
A-V DIFFERENCE
- O2 extraction
in the kidney
- A-V difference is small
- because the kidney receives large amount CO 20-25%
- extraction is minimal
in the heart
- A-V difference is large
- because the heart receives small amount of CO 5-10%
- extraction is maximum
pumping action CO
SV x HR
hypertension
- increase pressure work
- increase afterload
- increase O2 demand
INTRINSIC- cerebral circulation
- intracranial pressure is an important pathophysiologic factor that can affect cerebral blood flow
hypoventilation (alveolar ventilation is inverse to arterial CO2)
- increases arterial PCO2, thus increase cerebral flow
hyperventilation (alveolar ventilation is inverse to arterial CO2)
- decreases arterial PCO2, thus decrease cerebral flow
during normal exercise
- arterial CO2 remains the same
- cerebral flow is normal
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
controlling temperature
via ETC
via HEAT LOSS thru skin
main source of heat in our body
- OXIDATIVE PHOSPHORYLATION
- taking place electron transport chain
- ADP==> ATP
- O2 supply
- heat is released
hyperthyroidism
- increase ETC
hypothyroidism
- decrease ETC
increase heat loss
- increase blood flow to the skin
- ANS inhibit alpha 1
- vasodilate
decrease heat loss
- decrease blood flow to the skin
- ANS stimulate alpha 1
- vasoconstrict
under normal circumstances KIDNEYS and SPLANCHNIC ORGANS blood supply is controlled by
- intrinsic circulation
under ABnormal circumstances KIDNEYS and SPLANCHNIC ORGANS blood supply is controlled by
- EXTRINSIC CIRCULATION
- e.g. severe hemorrhage causing decrease perfusion, and BP
pulmonary circuit is a
- low pressure circuit
- small pressure gradient
PA= pressure 15 mm Hg
PV= pressure 5mm Hg
pressure gradient= 10 mm Hg
MOST IMPORTANT FACTOR HAS A VERY HIGH COMPLIANCE (change in volume/small change in pressure) - it respond to PO2 hypoxic vasoconstriction causing decrease flow
- lung receives 100% CO large compliance inverse to resistance
- very low resistance
sympathetic has no role in
- BLOOD FLOW
CO =
HR x SV
exercising LUNG
- increase HR
- increase SV
- increase CO
- increase blood flow to the lung
- increase compliance accommodate thus pressure kept almost NORMAL to slightly increase reason for not developing pulmonary hypertension
smoking, calcification of the arteries in the lung during exercise
- pressure increase due to loss of compliance in the lung
- due to stiffness of the lung
- causing pulmonary hypertension
deoxygenated(pulmonary artery) blood flow from
- RV (25 mm Hg) to the lungs (5-10 mm Hg) then back to oxygenated blood(pulmonary vein 5mm Hg pressure) to LA (5-10mm Hg)
pressure gradient in the lungs
- 5-10 mm Hg
artery pressure
- 15 mm Hg
lungs respond to hemorrhage
- is through COMPLIANCE nature circuit
- increase constriction of blood vessel to maintain pressure
- decrease volume, decrease CO
