Lecture 22 - Special Circulation Flashcards Preview

FHB Exam 1 - Cardiovascular Physiology > Lecture 22 - Special Circulation > Flashcards

Flashcards in Lecture 22 - Special Circulation Deck (42):
1

What is least tolerant tissue to ischemia?

BRAIN

2

What is the function of the BBB? What is it mainly composed of? What can pass through?

1. Limit the transport of substances from systemic circulation to the PARENCHYMA of the brain

2. Endothelial tight junctions (basement membrane, neuralgia, metabolic enzymes)

3. Ethanol, O2, CO2, glucose amino acids, steroids = lipid soluble

(nothing greater than 500 D)

3

What are the 5 factors that affect cerebral blood flow?

1. Autoregulation
2. Tissue Pressure (monroe Kellie doctrine)
3. Metabolism
4. Autonomics
5. Cushing's Response

4

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)

5

What is Cerebral perfusion Pressure normally between? What happens if CPP falls? Rises?
(vasoconstrict or dilate?)

80-100 mmHg

1. if CPP falls = vasodilator

2. CPP rise = Vasoconstrict (decrease flow)

6

What is the normal auto regulation range for the Cerebrum? What happens during hypertension?

70-140 mmHg

2. shifts the curve RIGHT
- blood flow normal at HIGHER pressures

(not as well maintained at lower mean arterial pressures)

JUST LIKE BARORECEPTORS

7

What happens when intracranial pressure increases?
- how does resistance change? What is this called?

increased pressure = vascular compression (tissue compression)

2. Resistance INCREASES

3. ISCHEMIA!

8

What is the equation for CPP?

CPP = MAP - Intracranial Venous Pressure

9

What can cause a reduction in Cerebral Perfusion Pressure?

1. Decrease in MAP (hypotension)

2. Increase in Venous Pressure (tumor, hydrocephalus, hematoma)

10

If tissue pressure increases, which vessels will be compressed first and why?

1. VENOUS SIDE

2. LOWEST pressure

- less blood flow so result: arterial vasodilation aka AUTOREGULATION to maintain flow

11

What is the result of increasing CSF pressure on:
1. Vascular Resistance
2. Cerebral Blood flow

1. Increase resistance
2. Decrease flow

12

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

13

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

14

What happens to brain volume, vascular volume & CSF volume during Hemorrhage? How is pressure changed?

1. Brain volume INCREASES
- CSF volume decreases
- Vascular volume decreases

2. PRESSURE INCREASES in CSF & Vascular

15

What is cerebral blood flow most sensitive to?

CO2 changes!

16

What happens to the following during HYPERVENTILATION:

1. pH
2. CO2 content
3. Blood flow (constrict/dilate)
4. Membrane Excitability
5. Binding of Calcium & Sodium Permeability

1. pH increases - Respiratory Alkalosis

2. CO2 decreases

3. VASOCONSTRICTION

4. Membrane excitability increases

5. calcium binding decreases and Na permeability increases! (hyper excited& anxiety)

- leads to decreased blood flow & DIZZINESS FAINTING

17

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)

18

What is the brain more responsive to, respiratory or metabolic acidosis/alkalosis?

RESPIRATORY!

- metabolites like H+ cannot cross the BBB

19

Decreases in O2 may cause what? Is the affect greater than CO2?

VASODILATIOn!

- less than CO2

20

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

21

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

22

What is the affect of:
1. Adenosine
2. K+
3. NO

VASODILATION

23

Which receptor does adenosine act on?

PURIGENIC on vascular smooth muscle to activate ATP-sensitive K+

(can also release NO)

24

What does an increase in extracellular K+ activate?

- Na/K ATPase
- inreases membrane conductance to K+

= HYPERPOLARIZE smooth muscle & RELAX

25

What does NO do to MLCK & MLC? How?

NO --> cGMP --> PKG

phosphorylates MLCK

which prevents phosphorylation (& activation) of MLC

- less actin-myosin cross bridges

26

What has a stronger affect in the BRAIN:
metabolic or autonomic control?

METABOLIC

- autonomic:

parasympathetic: CN 7 = vasodilation

Sympathetic = constriction (increase resistance)

27

What is the cushing response?
What is the sympathetic & parasympathetic response?

Increase in Intracranial Pressure = decrease in Cerebral Perfusion

1. S = BP increases

2. Para = HR decreases!

- can see this on an EKG when arterial pressure increases but HR decreases!

- response to ischemia

28

How does the compliance of the pulmonary system compare to the systemic arteries?

Pulmonary = 7 times more compliant!!

- due to low resistance, , low pressure, & HIGH FLOW

29

How is capillary resistance in pulmonary system different from the systemic circulation?

PULMONARY
- capillaries have a MAJOR influence on vascular resistance

(no autoregulation)

30

Do pulmonary vessels autoregulate?

NO

31

What does L. Ventricle HF do to pulmonary system pressure?

INCREASES pressure

(mitral stenosis)

- causes pulmonary edema

32

How does pulmonary resistance change as flow & pressure increase? (ex: exercise)

resistance DECREASES

since more capillaries open

33

What happens to the following upon INSPIRATION:
1. Alveola (capillaries)

2. Extra-Alveolar (venous/arterial)

3. Resistance

Is this an example of low volume or high volume?

1. Alveola = COMPRESSED

2. Extra-Alveolar - DISTEND

3. Resistance INCREASES (or no change)
- since capillaries compressed

4. HIGH VOLUME

34

What happens to the following upon EXPIRATION:
1. Alveola (capillaries)

2. Extra-Alveolar (venous/arterial)

3. Resistance

Is this an example of low volume or high volume?

1. Alveola = DISTEND

2. Extra-Alveolar - COMPRESSED

3. Resistance DECREASES (or no change)
- since capillaries compressed

4. LOW VOLUME

35

Where is normal breathing on the vital capacity & resistance graph?

FRC
- functional resistance capacity

36

Upon inspiration, resistance approaches alveolar or extra-alveolar values?

ALVEOLAR!

37

Where is hydrostatic pressure greatest in the lung? in an upright position

HIGHER AT THE BOTTOM

- due to gravitational force

38

Why do you hear RAULS at the bottom of the lung?

Because hydrostatic pressure is larger here

- edema fills up bottom to top

39

Where is blood flow greatest in the lung?

Blood flow is least at the top and greatest at the bottom of the lung

40

Describe the relationship between Pa, Pv, and PA in the 3 zones:

1. Zone 1

2. Zone 2

3. Zone 3

1. NOT NORMAL CONDITIONS
PA>Pa>Pv

2. Pa>PA>Pv
- capillaries partially collapsed & flow depends on pressure difference between arteries & alveoli
- increased Resistance
- independent of venous pressure

3. Pa> Pv > PA
NORMAL

- FLOW depends on pressure gradient between arteries & veins

41

When does ZONE 1 exist?

when Pa - arterial pressure decreases = HYPOTENSION

OR

PA increases = Positive Pressure increases
- by way of mechanical ventilation

42

Where is flow distributed in a normal upright person primarily?

Zone 2 and 3