Lecture 22 - Special Circulation Flashcards
What is least tolerant tissue to ischemia?
BRAIN
What is the function of the BBB? What is it mainly composed of? What can pass through?
- Limit the transport of substances from systemic circulation to the PARENCHYMA of the brain
- Endothelial tight junctions (basement membrane, neuralgia, metabolic enzymes)
- Ethanol, O2, CO2, glucose amino acids, steroids = lipid soluble
(nothing greater than 500 D)
What are the 5 factors that affect cerebral blood flow?
- Autoregulation
- Tissue Pressure (monroe Kellie doctrine)
- Metabolism
- Autonomics
- Cushing’s Response
How is auto regulation different in the brain then skeletal muscle?
Flow rates depend upon which part of the brain is active at any given time
- maintains constant flow to brain (55ml/min/100g)
What is Cerebral perfusion Pressure normally between? What happens if CPP falls? Rises?
(vasoconstrict or dilate?)
80-100 mmHg
- if CPP falls = vasodilator
- CPP rise = Vasoconstrict (decrease flow)
What is the normal auto regulation range for the Cerebrum? What happens during hypertension?
70-140 mmHg
- shifts the curve RIGHT
- blood flow normal at HIGHER pressures
(not as well maintained at lower mean arterial pressures)
JUST LIKE BARORECEPTORS
What happens when intracranial pressure increases?
- how does resistance change? What is this called?
increased pressure = vascular compression (tissue compression)
- Resistance INCREASES
- ISCHEMIA!
What is the equation for CPP?
CPP = MAP - Intracranial Venous Pressure
What can cause a reduction in Cerebral Perfusion Pressure?
- Decrease in MAP (hypotension)
2. Increase in Venous Pressure (tumor, hydrocephalus, hematoma)
If tissue pressure increases, which vessels will be compressed first and why?
- VENOUS SIDE
- LOWEST pressure
- less blood flow so result: arterial vasodilation aka AUTOREGULATION to maintain flow
What is the result of increasing CSF pressure on:
- Vascular Resistance
- Cerebral Blood flow
- Increase resistance
2. Decrease flow
What is the first mechanism that occurs when CSF pressure becomes larger than venous pressure?
What happens when CSF pressure overcomes ARTERIAL pressure? What pressure does this occur at?
1st = AUTOREGULATION
- arteries vasodilate to increase flow
2nd = once arteries are compressed, FLOW DECREASES!!!
- at 80 mmHg
- as CSF pressure increases toward arterial pressure, cerebral flow decreases rapidly
What is the basis of the Monro Kelli Doctrine? What are the 3 components?
when volume of one compartment increases, there must be a decrease in the volume of the other 2 compartments
Brain volume + CSF volume + Vascular Volume = CONSTANT
What happens to brain volume, vascular volume & CSF volume during Hemorrhage? How is pressure changed?
- Brain volume INCREASES
- CSF volume decreases
- Vascular volume decreases - PRESSURE INCREASES in CSF & Vascular
What is cerebral blood flow most sensitive to?
CO2 changes!
What happens to the following during HYPERVENTILATION:
- pH
- CO2 content
- Blood flow (constrict/dilate)
- Membrane Excitability
- Binding of Calcium & Sodium Permeability
- pH increases - Respiratory Alkalosis
- CO2 decreases
- VASOCONSTRICTION
- Membrane excitability increases
- calcium binding decreases and Na permeability increases! (hyper excited& anxiety)
- leads to decreased blood flow & DIZZINESS FAINTING
What is a way to decrease CEREBRAL EDEMA by way of utilizing CO2?
Cause artificial HYPERVENTILATION (decrease CO2)
low CO2 = vasoconstriction
- decreases flow & thus decreases hydrostatic pressure
= decreases EDEMA formaiton & pressure!
**Trade-off involves Monro Kelli Doctrine)
What is the brain more responsive to, respiratory or metabolic acidosis/alkalosis?
RESPIRATORY!
- metabolites like H+ cannot cross the BBB
Decreases in O2 may cause what? Is the affect greater than CO2?
VASODILATIOn!
- less than CO2
What is O2 content useful for in the brain?
fMRI studies to see the ratio of oxygenated/deoxygenated HEMOGLOBIN & thus the metabolic activity during different tasks
(more oxy= more lit up)
- speech, movement, reading
What metabolite is released upon a reduction in O2 or an increase in O2 demand?
ADENOSINE
- Katp channels open (hyper polarization)
- ->lowers intracellular calcium
= RELAXATION
What is the affect of:
- Adenosine
- K+
- NO
VASODILATION
Which receptor does adenosine act on?
PURIGENIC on vascular smooth muscle to activate ATP-sensitive K+
(can also release NO)
What does an increase in extracellular K+ activate?
- Na/K ATPase
- inreases membrane conductance to K+
= HYPERPOLARIZE smooth muscle & RELAX
