Exam 8 - Blood Flow Control Flashcards
3 principles of blood flow
- Local flow depends on local need
- VR/CO is the sum of flow through all local tissues
- Control of BP is independent of local flow and VR/CO
~Pressure drop kept constant across tissues….R changes
When does external contractility change
- In times of emergency / out of ordinary situations
Types of flow control
- Acute: moment to moment situations
can’t compensate 100% - Chronic: long term mechanism
What tissues need from blood flow
- Oxygen
- Nutrients (glucose, amino acids, fatty acids)
- Waste removal
- Maintain [ion]
- Supply hormones
Demand between tissues
- Tissues have different functions, thus, different demands
- Demand varies over time (local flow adjusts for this)
- Ensure that each tissue gets its needs without overworking heart
- EXCEPTION: some organs get flow based on function…not need
- Kidneys, liver, adrenal glands
Distribution of flow
- Heart: 4%
- Brain: 14%
- Muscle: 15% (can go up to 80%)
- Bone: 5%
- Liver: 27% (6% arterial / 21% GI and Spleen)
- Kidney: 22%
- Skin: 6%
- Other: 8%
Flow range on skeletal muscle
750 - 16,000 mls/min
Acute (metabolic control)
- Response within seconds
- Not 100% compensation
- Control via dilation/constriction of metarterioles/pre-cap sphincters
- Arterioles can be overridden by sympathetic tone/ANS
Long-term (chronic control)
- Slow response…days to weeks
- More permanent changes in metabolism/O2 content/input pressure
- Infinite response…close to 100% compensation
- controlled via increase/decrease # and/or size of vessels
Acute Control response to metabolism
- 8x increase in metabolism causes 4x increase in flow
- achieved by decreasing venous sat (taking out more O2) and increasing flow
Acute control response to Oxygen
- decrease in arterial sat results in increase blood flow
~ high altitude
~ Pneumonia
~ CO poisoning (HgB can’t carry O2)
~ Cyanide poisoning (tissues can’t use O2) - Increased flow almost makes up for decreased O2
~ Acute cannot fully compensate
Branching in capillary bed
- Arterioles: flow to whole bed
- Metarterioles: flow to branches
- Pre-cap sphincters: flow to individual vessels in bed
- No ANS innervation….acute response is innate to vessels
Precapillary Sphincters
- Either completely closed or open
- Open/Close multiple times/min (vasomotion)
- If open more….flow increases
- Time open proportional to waste…inversely to O2 content
~ Waste = CO2 and H+ (in form of Lactic Acid)
Two theories that explain response to O2/metabolism
- Oxygen Demand Theory (Nutrient demand theory)
- Muscles use O2 to contract (other nutrients as well)
- More O2/less metabolism -> more contraction -> less flow
- As O2 decreases/metabolism increases -> less contraction -> more flow
- Vasodilator theory
- Metabolism increase -> waste formation increase
- Waste interacts with smooth muscle and causes vasodilation
- Mostly affects metarterioles and precap sphincters
- tone of arterioles depends on tone of ANS
- Control probably a mixture of both theories
Vasoactive substances
- Adenosine: released when [O2] down
- released when flow is down, ATP is down too - CO2: Vasodilator especially in brain
- Adenosine phosphate compounds:
- released when ATP broken down or Adenosine released - Histamine: vasodilator from mast cells/basophils
- K ions: vasodilator in brain and heart (causes hyperpolarization)
- makes it harder to contract - H ions: released from tissue in form of lactic acid when [O2] down
Active Hyperemia
- Internal change
- response to increased metabolic demand in a tissue
- like in skeletal muscle - Plateau flow determined my local need/demand
Reactive Hyperemia
- Response of tissue to period of ischemia
- Flow can bump to 4-7x normal after ischemic period
- Longer the ischemic period….longer reactive Hyperemia period
- bigger oxygen debt to repay to tissue
How does cardioplegia help?
- Keeps the O2 debt down while we have no flow through heart
- Lessens the O2 debt
Autoregulation and MAP
- Local control only function if MAP is constant
- If MAP changes…ALL tissues/flow will change
- If MAP up…constrict to try and keep flow through tissue normal
- Gets close to 100% compensation but not quite
- Can autoregulate only over a range of BP
Myogenic Theory
- Sudden stretch of small vessels -> SM contract -> flow down
- stretch will happen if BP increases
- If BP down…stretch down…triggers SM relax…flow up
- Only allows vessels to respond to changes in P….not flow
Special acute flow control
- Kidney: tubuloglomerular feedback control
- Brain: CO2 and H+ [ ] sensitivity as well as normal control
- Skin: control linked to temperature regulation
Tubuloglomerular feedback in Kidneys
- Macula Densa monitor filtrate in distal tubule
- If flow of filtration increases…Na increases…trigger afferent arterioles to constrict….reduce flow
- Opposite is true if too little flow/filtration
Brain and CO2/H+
- If either increase…vasodilation…increase flow to remove them
- ideal level of cerebral activity requires fixed CO2 level
- essentially operates at an optimal pH
Endothelial derived control factors
- endothelial cells release and interact directly with SM
- NO (vasodilator) and Endothelin (vasoconstrictor)