Arteries and Arterioles

hemodynamics

pressure, flow, resistance of cardiovascular system

What promotes flow through vasculature?

What impedes flow?

pressure gradient: difference between ends of tube (high to low)

Resistance: friction between outer fluid layer and wall, fluid layers themselves

Flow =

Delta P/R (pressure gradient / resistance)

Things that affect resistance + what can cause them to change

1. Blood viscosity: directly proportional

   1. change in hematocrit (% RBC)

2. Length of Tube: directly proportional

   1. Doesnt change

3. Radius of tube: Inversely proportional

   1. contraction/relaxation of smooth muscle

How does pressure change going from aorta to vena cava

How does resistance Change?

Pressure high in large elastic arteries → falls off in arterioes + continues to fall off into the veins

Low resistance in arteries, high resistance in arterioles, low resistance in veins

What is compliance

Volume/Pressure : (transmural pressure)

how easily a blood vessel can distend; depends on stiffness of BV wall

how does compliance change

High in arteries, low in arterioles, very high in veins

Structure of large artery

Inner single layer of endothelial cells: endothelium

Many layers of smooth muscle, elastic fibers, and CT

Outer layer of CT

What enables large arteries to have low resistance and high compliance

Low resistance: arteries have a large diameter or radius

High compliance: arterial wall contains lot of elastic fibers

Conductance vessels Functions

Large arteries

1. Rapid transit for passage of Blood from heart to organs: large diameter w/ low resistance

2. Pressure reservoir (high compliance): driving force for blood during diastole

During systole: some energy is stored ?

in stretched wall, helps maintain blood flow during diastole

(elastic recoil is pump during diastole)

What happens to BP if large arteries become sitffer?

Systolic pressure and diastolic pressure?

pulse pressure?

MAP?

• Systolic pressure increase

• Diastolic pressure decrease

• pulse pressure = systolic - diastolic, so increase

• 1/3 SP + 2/3 DP (amount of time in each) = no change

Why is MAP important?

Why is pulse pressure important?

Tells you whether or not you are perfusing your organs (supplying organs with blood)

It is an important predictor of mortality, better indicator of arteriosclerosis than MAP

Arterioles: what is the wall of an arteriole like?

inner endothelium, lumen, one to a couple of layer of smooth muscle cells

Arterioles are __ resistance and _ compliance

high, low

What controls the amount of blood delivered to capillaries at any given MAP?

arterioles

How does body ensure that particular organ is supplied with sufficient blood to meet its metabolic demands?

By changing the resistance of the arterioles that supply that organ

What causes the contraction or relaxation of arteriolar smooth muscle to change resistance and hence blood flow?

Arteriolar smooth muscle is __ contracted

tonically (independent of neuronal or or hormonal stimulation

Local control and ANS hormones

• vasodilate: increase radius, decrease resistance, increase flow

• Vasoconstrict: decrease radius, increase resistance, decrease flow

Active hyperemia

Metabolic activity increase → blood flow to tissue increase

(vasodilation)

Autoregulation involves two mechanisms

Same metabolic factors as active hyperemia

myogenic response

when does a person have a chronic increase in afterload?

Hypertension

Myogenic response with flow autoregulation

Pressure is too high → stretches arteriole → vasoconstrict cerebral arterioles to reduce flow to brain and vice versa

Reactive hyperemia mechanism

Loss of blow flow causes tissues to

• use up all of O2

• Accumulate more CO2m waste products

Localized relaxation of arteriolar smooth muscle and vasodilation in ischemic tissue

Occlusion → use up O2, build up CO2 → vasodilation to increase flow

Increase metabolic activity (less O2, More Co2) → vasodilation to increase flow

Change in perfusion pressure → myogenic response/metabolic changes → flow returns to normal

Active hypermia

Reactive hyperemia

Autoregulation

What happens to smooth muscles when you are cold?

Smooth muscle on arterioles contain mostly A1 receptors

Cold → activates SNS to release NE → activates A1 → vasoconstriction`

where does extra blood come from during excecise?

Skin, gut: vasoconstrict: NE on A1, vs Epi vasodilate on B2 in skeletal muscle