Function: to maintain levels of CO2 and O2 in body tissues via lungs

Homeostatic systems help maintain ideal levels of O2 and CO2

Pick up O2 from lungs & deliver it to tissues; pick up CO2 from tissues & deliver it to lungs

Maintenance of mean arterial pressure

Maintenance of adequate oxygen delivery to tissues during rest & exercise

Meaintenance of CO2 levels in tissues during rest & exercise

Lower altitude --> higher atmospheric pressure --> higher partial pressure of oxygen

Higher altitude --> lower atmospheric pressure --> lower partial pressuer of oxygen

How much gas can dissolve in a solution

C = k x P

C: molar concentration of dissolved gas

P: partial pressure of gas

k: solubility constant of gas in solvent

Equilibration

Relevance of equilibration to physiology

Gases move between water & air by going DOWN a partial pressure gradient - over time, partial pressure in water will equal that of air

Diffusion of O2 and CO2 from lungs (air) to blood (water)

How much more soluble are O2 and CO2 in water than in air?

Why is CO2 20x more soluble than O2 in water?

O2 is 1.7x more soluble in water than in air

CO2 is 34x more soluble in water than in air

CO2: H2O is slightly polar (negative O and positive Hs) --> weak hydrogen bonding between O in CO2 and H in H2O

O2: Weak Van der Waals bonding that is weaker than hydrogen bonds

Diffusion

• Energy
• Distance
• Movement based on what?
• Where does it occur (source to sink)? 

• Thermal energy (no muscle contraction so no ATP expenditure)
• Efficient over short distances & much less efficient as distance increases
• Based on individual partial pressure gradient (mmHg, not molarity when diffusion is occuring between 2 solutions in which the gas has different solubilities) based on how much gas is dissolved in a solution
• Capillaries - O2 diffuses from lungs into blood & from blood into tissues; CO2 does the opposite

For when source & sink concentrations are kept constant (as with blood/lung O2 levels etc.)

J = k x A(P₂-P₁)/D

• J: rate of diffusion (ml or cm³/sec)
• k: diffusion constant
• A: area over which diffusion occurs
• P₂-P₁: partial pressure gradient
• D: distance over which diffusion occurs

• Heart's muscle contractions require ATP to generate fluid pressure gradient (highest pressure upon leaving heart, lowest pressure upon entering heart)
• Efficient over longer distances
• Based on total pressure gradient
• Q (rate) = ∆P (change in fluid pressure)/R (resistance esp. frictional based on blood vessel diameter)

In the respiratory system, the pressure gradient for the movement of air is established by the _____________.

In the cardiovascular system, the pressure gradient for the movement of blood is established by the ___________.

Respiratory muscles

Heart

Partial pressures to know (sea level & at rest)

• Atmospheric oxygen
• Lung oxygen (alveolar)
• Systemic arterial oxygen
• Systemic venous oxygen
• Atmospheric carbon dioxide
• Lung carbon dioxide (alveolar)
• Systemic arterial carbon dioxide
• Systemic venous carbon dioxide

Distance between O2 source (alveoli)

(OR) sink (capillary blood) and between CO2 source (capillary blood) and sink (alveoli)

Secrete pulmonary surfactant (detergent - hydrophobic and -philic portions) to lower alveoli surface tension

Hydrophilic part buries itself in water surface - separates & prevents adhesion

Hydrophobic tail sticks up & pulls on surfactant molecule to prevent it from diving into the water column

Pleural sac

& structure

Surrounds lungs & separates them from chest wall

Visceral pleura lies directly on lung

Parietal pleura lies against chest wall

Intrapleural space filled with intrapleural fluid between visceral and parietal pleura

RR (breaths/minute) x IV (volume/breath)

RR is respiratory rate, IV is inspiratory volume

Quiet inspirations/expirations - inspiratory volume at rest

Does not normally change

Inspiratory volume

Relative to tidal volume?

TV + whatever else you breathe in (up to IRV)

Can be <, =, > tidal volume

TV + IRV + ERV

Upon reaching adult height, this cannot change much even with exercise. Smoking decreases it.

ERV + RV

Volume of lungs at the end of a tidal-volume expiration, doesn't normally change

Ventilation = RR (breaths/min) x IV (L/breath)

Equation for alveolar ventilation

What is ADS?

AV = RR x (IV-ADS)

ADS: anatomical dead space - space where air cannot diffuse in conducting zone (increased in smokers)

Increase respiratory rate from 12 to 35 breaths/min

Increase inspiratory volume from .5 to 3L/breath

Inspiration --> lung pressure < atmospheric pressure

Expiration --> lung pressure > atmospheric pressure

Diaphragm contracts

External intercostals contract

Chest wall/lungs expand

Sternum moves upward & outward

Diaphragm relaxes

External intercostals relax

Lungs/chest wall contract

Sternum moves downward & inward

At functional residual capacity, causes of negative intrapleural pressure

Negative pressure value to keep lungs at functional residual capacity

Elastic recoil of lungs (inward) & chest wall (outward) - opposite directions 

-4mmHg

Inspiration: respiratory muscles contract, intrapleural pressure becomes more negative, stronger vacuum pulls on alveoli, increase in alveolar volume, decrease in alveolar pressure (subatmospheric)

THEN air flows down the pressure gradient - from atmosphere to lungs

Expiration: respiratory muscles relax, intrapleural pressure becomes less negative, weaker vacuum causes alveoli to shrink, decrease in alveolar volume, increase in alveolar pressure (superatmospheric)

Elastic recoil of lungs would lead to their collapse

Maintains partial inflation of lungs (FRC) at the end of expiration to make sure oxygen is still reaching blood during expiration

Goes to all parts of body except lungs

Arteries with high oxygen and veins with low oxygen

Goes to lungs

Arteries with low oxygen and veins with high oxygen

Frictional

Elastic

• Minor: Elastic properties of lung tissue
• Dominant: surface tension (F/L)

Uneven forces on water surface molecules create strong attraction between water molecules

Interstitial fluid: thin layer of water on inside of alveoli/between alveoli and capillaries

Millions of alveoli --> high aggregate surface tension

Increases solubility of oxygen in blood (1g hemoglobin holds 1.3 ml oxygen) so that cardiac output does not need to be very high to meet metabolic oxygen consumption

4 globins (protein) & 4 ferrous hemes (+2 iron reversibly binds to oxygen - OXYGENATION, NOT OXIDATION)

Higher PO250

Lower PO250

& situations in which these occur

Rightward shift - hemoglobin has lower affinity for oxygen

• Higher temperature
• Lower pH (exercise --> H+ + HCO3- --> lower pH --> easier to unload oxygen)

Leftward shift - hemoglobin has higher affinity for oxygen

• Lower temperature
• Higher pH (CO2 removal --> less H2CO3 --> higher pH --> easier to pick up oxygen)

Asymptotically approaching 100% saturation

Allows us to travel: even if P(O2) is a bit less, if still on plateau, no significant decrease in % oxygen saturation of hemoglobin

Allows us to exercise: Steep curve below ~40 mmHg allows us to easily give up oxygen when exercising

Enzyme in RBCs that catalyzes:

• H2O + CO2 <--> H2CO3 <--> H+ + HCO3-

Ways to maintain partial pressure gradient/CO2 diffusion:

At tissues

At lungs

TISSUES: CO2 carried as HCO3- or carboamino reduces amount of dissolved CO2 in RBCs and sustains partial pressure gradient

Buffering of H+ by amino acids in hemoglobin --> continuation of conversion of CO2 into H2CO3 --> enables further diffusion

LUNGS: reverse reaction (production of CO2 and H2O from H+ and HCO3-)

Carrying O2 and CO2

Carrying fuel/hormones

Immunity

Heat transfer

DIFFUSION at lungs & tissues due to small distance

BULK FLOW - moving blood/contents from heart to tissues and back

Blood pressure potential energy, not blood velocity kinetic energy

Q = HR (beats/min) x SV (ml/beat)

Q = ∆P (MAP - central venous pressure)/TPR

∆P represents potential energy

Mean arterial pressure: blood pressure as blood enters aorta, usually 90-100

Central venous pressure: blood pressure as blood enters right atrium, usually around 0

Total peripheral resistance usually around 20

Branching/parallel circuit, not series

Allows blood to be distributed to many parts of the body as quickly/efficiently as possible

Allows changes in blood distribution to various tissues during various situations (e.g. exercise - skeletal muscle vessels dilate and kidney/GI tract vessels contract)

Difference between velocity and flow rate

Relationship between area and velocity

What would happen with an increaes in capillary beds?

Velocity = flow rate/cross-sectional area

Inversely proportional (think of capillaries, where diffusion is maximized, and aorta, where rapidity is maximized. Flow rate of all capillaries combined = flow rate of aorta)

Decrease in average velocity

Mechanically and electrically interconnected heart cells - allows for greater heart power

Pacemaker cells (spontaneously & always electrically active, set rhythm, found in sinoatrial node)

Conducting cells - modified muscle cells (conduct electrical activity from SA node with low resistance throughout heart)

Contractile cells - cardiac muscle cells (physical contraction as a result of electrical excitement)

Sends electrical impulses:

To left/right atrii (interatrial pathway)

To AV node (internodal pathway)

Atrioventricular node

AV bundle/Bundle fo His

Resistor - slows down SA node impulse so atrii & ventricles don't contract simultaneously (greater blood flow)

Bundle of His - thick fibers & many gap junctions (current travels quickly through septum) --> split into L/R bundle branches and electrical impulse carried quickly to all ventricular cells for almost-simultaneous activation

Diatole - ventricles are filling with blood

Systole - blood being pumped out of heart

Diastole twice as long as systole so ventricles will fill (AV node resistor)

Systole half as long as diastole so power (Energy/time) of contraction will be greater

Diastolic pressure: pressure as blood enters heart

Systolic pressure: pressure as blood leaves heart

Diastole

Ventricular pressure following

Ventricular volume unchanging

All valves closed

Isovolumetric relaxation & ventricular filling

Dicrotic notch - upward blip in aortic pressure because of blood rebound following aortic valve closing

Diastole

Ventricular filling & atrial contraction

Aortic pressure falling

Vent pressure < atrial pressure --> AV valves open, blood flows into ventricle --> increase ventricular volume to end-diastolic volume

Halfway through: start of atrial contraction --> active blood flow & increaesd ventricular pressure

Systole

Isovolumetric contraction

All valves closed

Start vent contraction --> rapid increase vent pressure till > atrial pressure --> AV valves close

"Phase 2" to "Phase 3" transition

"Phase 3"

Vent pressure exceeds aortic pressure --> aortic & pulmonary valves open

Systole

Ventricular ejection

L ventricular pressure increases & peaks dramatically (R peaks but less dramatically), then decreases

Ejection of blood from ventrical to aorta/pulmonary circuit

Rapid decrease to end-systolic volume

Blood constantly flowing into atrium (inferior & superior vena cava, pulmonary veins) 

Atrial pressure and volume don't change much

First sound: right AV valve closing

Second sound: aortic valve closing

Poiseuille's Law: 8ηL/πr^4 = R

Q = ∆P/8ηL/πr^4

η - viscosity

L - blood vessel length

r - radius

Series - sum each unit's resistance

Add new resistor --> total resistance increases

Innermost layer: endothelium (1 cell-thick layer) - all blood vessels have this

Smooth muscle wall controlled by sympathetic nerves (not consciously controlled, originate in spinal chord)

Connective tissue to maintain stucture

Arteries

Aging

Thickest walls (high systemic arterial pressure)

Highly elastic - stretch under high systolic pressure, rebound during diastole to add force to blood

Aging: hardening of the walls --> increase systolic pressure, decrease diastolic pressure (but other factors cause increase diastolic pressure)

Arterioles

What controls smooth muscle contraction?

Most smooth muscle relative to size - do most changes in blood vessel size (main resistors)

Increase resistance by contracting smooth muscles to decrease arteriole radius

Decrease resistance by relaxing smooth muscles to increase arteriole radius

Sympathetic nerves' basal tone discharge (discharge signal to contract when excited)

Decreased oxygen/high CO2/high pH --> smooth muscles relax (vessels dilate to increase blood flow to tissue)

Low O2/high CO2 --> arterioles in active (skeletal muscle) tissues dilate

Nerves try to constrict but are overridden by local

effects

Nerves to inactive tissues (kidney, GI tract) cause arteriole constriction so despite increase in cardiac output no increase in blood flow

Thin-walled - rapid diffusion

Molecules can pass through cell membranes, through pores, or between cells

Hyperventilation

Hyperpnea

Breathing more deeply/often than metabolically necessary - losing CO2 and gaining O2 overall

Breathing more deeply/often because metabolic rate has increased (e.g. exercise) -- CO2 and O2 levels match those at rest, but rates of CO2 and O2 disposal/acquisition increase

Thin, stretchable walls

COMPLIANT - can be distended without much change in vessel pressure (decreases as smooth muscles contract)

Contain 2/3 of vascular tree blood (capacitous)

Valves to prevent backflow

Too low --> tissues don't receive enough blood for metabolic functions

Too high --> tissues might be damaged by force of blood