PHSL 3051 pulmonary

functions of the respiratory system

complience

• the change in pressure is needed to inflate the lungs to a certain volume

• lung tissue matrix is a weave of elastin and collagen fibers

• lungs that are more compliant are “stretchier” - it takes low pressure to inflate them

  • stiff lungs cause restrictive lung disease

  • emphysema destroys the weave (easy to stretch out, hard to recoil)

surface tension

• allows water particles to stick together - like beading of water on a slick window

• high surface tension makes alveoli more likely to collapse (harder to open)

• different sized alveoli have different collapsing pressures with equal ST

• surfactant lowers ST and lowers it more in the small alveoli so that pressures are equalized

surface tension in action - what if the water (saline) in your lungs formed beads?

• the alveoli would collapse and pull water in the lungs

• you would not be able to breath

• **this is why we need surfactant

law of laplace

when two alveoli with different sizes dont have surfactant, their surface tension will be the same; this then creates a pressure gradient between the two alveoli

• the small alveoli will collapse and blow up the big alveoli

the presence of surfactant (review)

1. lowers surface tension

2. increases compliance

3. equalizes pressures between two different areas of the lungs

4. overall stabilizes different areas of the lungs

atmospheric pressure (Patm)

airway resistance

• many of the same principles as vascular resistance

• flow = change in pressure/resistance

• most important influence on airway resistance is the size of the airways

• asthma and COPD cause high airway resistance

why does emphysema increase compliance

• emphysema destroys the lung matrix, the airways are very collapsable

• especially with forced expiration, the airways flatten out such that air is hard to get through

lung diseases (two categories)

1. obstructive

   1. something is obstructing the airflow

   2. characterized by high airway resistance

2. restrictive 

   1. something is restricting chest expansion

   2. characterized by low compliance

vital capacity

• total amount of air that can be moved in and out of the lungs

• 3.5 to 4.5 L is an estimated value depending on a persons height

• reduced with any kind of pulmonary disease

• the size of vital capacity is an indication of a persons pulmonary health

FEV1/FVC

• measure airway resistance

• volume of forced expiration in one sec (FEV1) divided by forced vital capacity (FVC)

• 3 liters/4 liters = 75%

• 70-80% is normal

• decreased with obstructive disease like asthma or COPD

disease - restrictive (R)

• low compliance or stiff lungs

• small tidal volume with high RR
  fibrosis, tuberculosis, interstitial lung disease, ARDS, pulmonary edema

disease - obstructive (O)

• high airway resistance

• must be taught to breath slowly and quietly (pursed lip breathing)

• asthma, emphysema, chronic bronchitis

commonalities between restrictive and obstructive

• both have reduced vital capacity

  • R - difficulty expanding to get air in

  • O - difficulty recoiling to get the air out

• both would have a reduced flow rate

• both would have an increased work of breathing (WOB)

local control of blood flow

• exercise dilates arterioles

  • arterioles get warmer, exposed to metabolic processes, exposed to more CO2 (local control)

  • this sends more blood flow

• capillaries are dense in alveoli

hypoxic vasodilation

• local responses in the lung are different

• low oxygen in the airways cause the blood vessels going to that part of the lung to constrict

• hypoxia in the lungs constricts arterials

branching

layers of diffusion membrane

1. alveolar type 1 cell

2. epithelial basement membrane

3. interstitial space

4. endothelial basement membrane

5. endothelial cell

6. RBC and hemoglobin binding

diffusion is influenced by

• temperature - incoming air is warmed to body temp

• distance - barrier is very thin

• surface area - alveolar system increases surface area

• gradients - large stable gradients (FRC is about 3L - alveolar gas concentrations are fairly stable)

*human lungs are adapted and structured for diffusion

how do we measure concentration in the pulmonary system

• partial pressure in mmHg

• atmospheric pressure X fractional concentration of a gas

• ex. at sea level, the atmospheric pressure is 760mmHg, and the air is 20% O2

  • 760mmHg x 0.20 = 160mmHg is the PO2 in the atmosphere

partial pressure diffusion gradients

1. very small concentration of CO2 in the atmosphere

2. tidal volume mixes with the air already in the lungs (CO2 comes from you!!!)

3. at the cells, O2 is consumed, and CO2 is produced PO2 must be at least 3 mmHg to make ATP (less than 5 mmHg)

alveolar gases

• in the mitochondria, PO2 must be at least 3 mmHg to make ATP via oxidative phosphorylation

• changes in ventilation change the partial pressure of oxygen and carbon dioxide in the alveoli

hyperventilation

hyperventilation is an alveolar ventilation that is higher than required for metabolism *hyperventilation is not a pattern of breathing

• PO2 increases above 100mmHg

• PCO2 decreases below 40mmHg

• PCO2 is linked to pH

• hyperventilation causes alkalosis (pH over 7.4)

hypoventilation

hypoventilation is an alveolar ventilation that is less than required for metabolism

• PO2 decreases

• PCO2 increases

• CO2 is linked to pH

• hypoventilation causes acidosis (pH under 7.4)

why might a person hypoventilate

head injury, lung disease, COVID, drug overdose

if hypoventilation decreases PO2 in the alveoli, what happens to the diffusion gradient for O2 across the alveolar barrier?

the diffusion gradient will decrease

• lowers partial pressure of oxygen (PO2)

how do we transport O2 and CO2 in the blood?

• we transport most of the oxygen bound to hemoglobin

• we convert most of the CO2 into bicarbonate

lung volumes in mL (spring 2012)

O2 diffusion gradients

• What are the gradients that permit O2 to diffuse into the blood from the alveoli?

  • PAO2 = 100 mmHg > PvO2 = 40 mmHg

• What are the gradients that permit O2 to diffusion from the blood to the tissues?

  • PaO2 = 100 mmHg > Pmito 3 mmHg

O2 transport

blood is 1/3 of the way through the capillary when it is fully loaded with O2

how is oxygen carried in blood?

1. dissolved content

2. bound content (to hemoglobin)

*hemoglobin bound content is more important

bound content

• hemoglobin molecule can bind 4 molecules of oxygen

  • relies on iron

• when oxygen binds to hemoglobin it is not oxygen anymore!!!

• PP ends equal again

• this is what happens in capillaries

how does O2 diffuse?

O2 diffuses from alveoli into the plasma, binds to hemoglobin, oxygen is no longer oxygen

saturation and coopertivity

• saturation is a percent

• cooperativity - when a molecule behaves in a cooperative way

  • when oxygen binds, the easier it is for other oxygen to bind

  • when oxygen lets go, the easier it is for other oxygen to release

  • when PO2 is high it favors binding

• he dissolved oxygen is exerting PO2; the oxygen has to dissolve and diffuse into the RBC before it can bind to hemoglobin

• at the tissues, the oxygen has to unbind, dissolve and diffuse into the tissue cell so it can participate in oxidative phosphorylation in the mitochondria

content and saturation

• mary has a 12 gm% of hemoglobin and frank has 13 gm%

• at PO2 of 100 mmHg of mercury

• who is more saturated?

  • equal - their PO2 is equal, so their saturation is equal

• who has higher dissolved content?

  • equal - their PO2 is equal, so their dissolved content is qual

• who has a higher bound content?

  • frank - he has more hemoglobin and spots to bind

saturation and content review

• saturation is a percentage

  • depends on PO2 alone

  • independent of the hemoglobin concentration

• content is an amount

  • mL O2/100 mL blood

  • depends on both PO2 and hemoglobin concentration

bohr effect (right shift)

right shift (release)

• high temp, CO2, H+

• promotes O2 release

*50% saturation is farther because oxygen is being released more rapidly

bohr effect (left shift)

left shift (latch)

• low temp, CO2, H+

• promotes O2 binding

carbon monoxide

• 240 times the affinity for hemoglobin than oxygen

• decreases content with normal PO2 and PCO2

• NO SHORTNESS OF BREATH

• left shift

  • carbon monoxide hogs binding sites and prevents oxygen from releasing - causes left shift

carbon dioxide transport

• some dissolves in blood 

• some binds to hemoglobin

• MOST is converted to HCO3-

CO2 + H2O → H2CO3 → H+ + HCO3-

*a build up of CO2 causes a build up of acid

pacemakers of respiration

• the pacemakers that drive the system of breathing are in the brain

• respiratory centers are in the medulla; some areas in the pons regulate centers in the medulla

• CO2 + H20 → Carbonic Anhydrase → HCO3- + H+

*the hydrogen ion stimulates the chemo receptors

receptors

central receptors and peripheral receptors

• all regulate arterial blood

• are in aortic arch and internal carotids

• include baroreceptors and ???

central receptors

respond to and monitor CSF H+ from arterial PCO2

peripheral receptors

respond to CO2, H+, and O2

• innervated by afferent 

• oxygen response is ONLY at the peripheral chemo receptors

low oxygen stimulates ventilation at…

PO2 levels of 60mmHg or below

*small changes in oxygen wont change breathing, need dramatic drop to cause change

arterial PO2 less than 60mmHg

signals sent to brainstem/medullan - ecourages muscles to contract - encourages contraction - PO2 goes up

*a person in this condition may not feel short of breath (SOB) if both O2 and CO2 were low

most important regulator of ventilation

arterial PCO2 is the MOST important regulator of ventilation especially at rest

• normal arterial PCO2 is about 40 mmHg, minute arterial ventilation is 5 L/min

• PCO2 is tightly regulated, small changes in PCO2 causes big changes in minute ventilation

• PCO2 is intimately related to pH - maintain PCO2 = regulating pH

acidosis

acidosis stimulates ventilation at peripheral chemoreceptors

• acidosis can be unrelated to breathing (ex. diabetes)

• pH should be 7.4

arterial PCO2 is major stimulus of ventilation

• stimulates BOTH central and peripheral chemoreeptors

• CO2 can be converted to H+ in blood and peripheral chemoreceptors. CO2 can cross blood brain barrier and be converted to H+ in CSF

• PCO2 levels have an important impact on dyspnea (shortness of breath)

how do pacemakers and regulators in pons/medulla regulate how fast we breath

• decrease in PO2, increase in PCO2, increase in H+ increases breathing

• increased temperature increases breathing

• increased epinephrine and plasma increases breathing

• we can control increase breathing in motor cortex

• joint receptors anticipate increased breathing (feedfoward control)