The amount of oxygen consumed per minute

The amount of CO2 produced per minute

95-100mmHg

40mmHg

40mmHg

46mmHg

ARTERIAL OXYGEN CONTENT

 (mL O2/100mL blood)

~20mL O2/100mL blood

VENOUS OXYGEN CONTENT

(mL O2/100mL blood

~15mL O2/100mL blood

ARTERIAL CARBON DIOXIDE CONTENT

(mL CO2/100mL blood)

49 mL CO2/100mL blood

VENOUS CARBON DIOXIDE CONTENT

(mL CO2/100mL blood)

53mL CO2/100mL blood

Breaths/minute

The volume inspired or expired with each normal breath

1. Nose

2. Mouth

3. Nasopharynx

4. Oropharynx

5. Larynx

1. Conducts air

2. Warms air

3. Humidifies air

4. Filters air

1. Cilia propel mucus mouthward at 15-22mm/min

2. The rate of beatig of the cilia responds to a variety of stimuli

1. Mobile

2. Chemoattractant

3. Phagocytotic

4. Migrates out of alveolus, up bronchus, trachea, on mucociliary escalator to be expelled

The first 16 generations where no gas exchange occurs and blood flow is from systemic circulation

1. Trachea

2. Bronchi

3. Bronchioles

4. Terminal bronchioles

The 17th-23rd generations where gas exchange occurs and blood flow is from pulmonary circulation.  

1. Respiratory bronchioles

2. Alveolar ducts

3. Alveolar sacs

Diameter and length decreases, while surface area and total-cross sectional area increases from conducting zone to respiratory zone

1. The major site of gas exchange

2. Surface of alveolus composed of type I and type II cells

1. Located on the surface of the alveolus

2. Thin layer of squamous epithelial cells that promote gas exchange

1. Located on surface of alveolus, interspersed with type I

2. Simple cuboidal cells

3. Synthesize and secrete surfactant

1. Consists of the rib cage, intercostal muscles, and the diaphragm

2. Coated by parietal pleura

1. Diaphragm

2. External intercostals

3. Accessory muscles (sternocleidomastoid, scalene)

1. Dome-shaped muscle

2. Innervated by two phrenic nerves

3. When diaphragm contracts during normal breathing, its dome descends 1-2cm and as much as 10cm during deep inspiration

4. Contraction of diaphragm increases the volume of the thoracic cavity

1. Raise and enlarge the rib cage

2. Their action increases the anterior and posterior dimension of the chest as the ribs rotate upwards

Not involved in normal breathing, but play a role during exercise

Expiration is passive during normal breathing. As the inspiratory muscles relax, the recoil of the distended alveoli is enough to decrease volume. During exercise and forced maneuvers, there is an active muscular component to expiration

1. Abdominal muscles

2. Internal intercostals

1. When the abdominal muscles contract, they force the diaphragm upward into the thoracic cavity

2. They also depress the lower ribs and pull down the anterior part of the chest

Contraction depresses the rib cage, decreasing thoracic volume

1. Alveolar pressure=0cm H2O

2. Atmospheric pressure=0cm H2O

3. Inward recoil of alveoli

4. Transmural pressure=0cm H2O-(-5cm H2O)=+5cm H2O

4. Intrapleural pressure= -5cm H2O

5. No air flow: atmospheric pressure=alveolar pressure

1. Atmospheric pressure= 0cm H2O

2. Alveolar pressure= -1cm H2O

3. Air flows in: atmospheric pressure > alveolar pressure

3. Outward force generated by inspiratory muscle

4. Intrapleural pressure: -8cm H2O

5. Transmural pressure= -1cmH2O-(-8cm H2O)= +7cm H2O

6. Inward recoil of alveoli

7. Outward recoil of chest wall

1. Alveolar pressure=atmospheric pressure

-Because lung pressures are expressed relative to atmospheric pressure, alveolar pressure is said to be zero

2. Intrapleural pressure is negative

-The opposing forces of lungs trying to collapse and chest wall trying to expand creates a negative pressure in the intrapleural space between them

3. Lung volume is Functional Residual Capacity (FRC)

-The volume remaining in the lungs after tidal volume is expired (ERV+RV)

1. Inspiratory muscles contract and cause volume of the thorax to increase

-As lung volume increases, alveolar pressure decreases to less than atmospheric pressure (becomes negative)

2. The pressure gradient between the atmosphere and alveoli now causes air to flow into lungs; airflow will continue until pressure gradient dissipates

3. Intrapleural pressure becomes more negative

-Because lung volume increases during inspiration, the elastic recoil strength of the lungs also increases; as a result, the intrapleural pressure becomes more negative

4. Lung volume increases by one tidal volume (VT)

-At peak inspiration, lung volume is FRC+VT

1. Alveolar pressure becomes greater than atmospheric pressure

-Alveolar pressure becomes greater (positive) because alveolar gas is compressed by elastic forces of the lung, thus alveolar pressure is now higher than atmospheric pressure, pressure gradient reverses and air flows out of lung

2. Intrapleural pressure returns to its resting value during passive expiration

-However, during forced expiration, intrapleural pressure becomes positive, compressing airways and making expiration more difficult

3. Lung volume returns to FRC

The property by virtue of which an object resists and recovers from deformation produced by force

For lungs:

E=change in pressure/change in volume=

cm H2O/L

The reciprocal of elasticity and is the deformation per unit force applied

For lungs:

C= change in volume/change in pressure= L/cm H20

1. Lung compliance is decreased

2. Tendency for lungs to collapse is increased

3. At the original FRC, the tendency for the lugns to collapse is greater than the tendency of the chest wall to expand

4. The lung-chest wall system will seek a new, lower FRC so that the two opposing forces can be balanced

1. Lung compliance is increased

2. Tendency of lungs to collapse is decreased

3. Therefore, at the original FRC, the tendency of lungs to collapse is less than the tendency of the chest wall to expand

4. The lung-chest wall system will seek a new, higher FRC so that the two opposing forces can be balanced

5. Patient's chest becomes barrel-shaped, reflecting this higher volume

1. As transpulmonary pressure increases, the lung volume increases in a non-linear fashio to what appears to be a maximal volume

2. Slope=Compliance

3. Compliance changes at different volumes

4. Hysteresis (different pressure-volume curve for inspiration than expiration)

5. Pressure-volume relationship reflects many alveoli, which may not all be the same

1. Tissue elasticity

2. Surface tension

The lung tissue contains elastin, collagen, and other components which stretch and recoil when released

Surface forces exist at any gas-liquid interface (like in the alveolus)

1. Lines alveoli

2. Reduces surface tension by disrupting intermolecular forces between liquid molecules

3. Secreted by Type II alveolar cells

If air is introduced into the intrapleural space (pneumothorax), the intrapleural pressure becomes equal to the atmospheric pressure and the lungs will collapse and the chest wall will spring out

The sum of the tidal volume and IRV

1. The sum of ERV and RV

2. The volume remaining in the lungs after tidal volume is expired

1. VC=IRV+TV+ERV

2. The volume of air that can be forcibly expired after maximal inspiration

1. TLC=VC +RV

2. The volume in the lungs after maximal inspiration

1.  The volume that can be inspired over and above the tidal volume

2. Used during exercise

The volume that can be expired after the expiration of the tidal volume

The volume that remains in the lungs after a maximal expiration

1. The volume of conducting airways

2. Approximately 150mL

1. A functional measurement

2. The volume of the lugns that does not participate in gas exchange

3. Approximately equal to the anatomic dead space in normal lungs

4. May be greater than the anatomic dead space in lung diseases in which there are ventilation/perfusion (V/Q) defects

5. VD= VT[(PCO2 of alveolar/arterial blood-PCO2 of expired air)/PCO2 of alveolar/arterial blood)]

-This fraction represents the dilution of alveolar PCO2  by dead-space air, which does not participate in gas exchange and does not therefore contribute CO2 to expired air

R=Pressure Difference/Flow

R=8(gas viscosity)(airway length)/(pi)(radius^4)

* If radius of a tube is reduced by 1/2, the resistance increases 16-fold

1. Lung volume

2. Smooth muscle tone

3. Intraluminal material

1. As lung volume increases, airways resistance decreases

2. Alters airway resistance because of radial traction exterted on the airways by surrounding lung tissue

1. The airway wall contains smooth muscle cells which can change the radius of the tube

2. Parasympathetic and sympathetic stimulation

Increased mucous secretion or a foreign object will increase resistance

1. Tidal Volume(TV)=500mL

2. Inspiratory Reserve Volume (IRV)=3100mL

3. Expiratory Reserve Volume (ERV)=1200mL

4. Residual Volume (RV)=1200mL

1. Total Lung Capacity (TLC)=6000mL

2. Inspiratory Capacity (IC)=3600mL

3. Vital Capacity (VC)=4800mL

4. Functional Residual Capacity (FRC)=2400mL

1. The process by which air enters and leaves the lung

2. Normally we take 12-15 breaths/min

3.This rate must be enough to provide the oxygen needed by the cells and to remove the carbon dioxide being produced

A measure of the total volume leaving the lung each minute

VE=VT x f

VE=(500mL/breath)(15breaths/min)=7500mL/min

* Increases in minute ventilation (VE) can be achieved by increasing frequency (f) and/or tidal volume (VT)

The volume of fresh gas which reaches the gas exchanging areas per unit time (this is different from minute ventilation)

VA=f(VT-VD)

1. In the respiratory system, gas exchange occurs in the respiratory bronchioles and alveoli, while the remaining airways serve as conducting tubes

2. The volume contained in the conducting areas is known as the dead space and is generally equal (in mls) to person's ideal body weight in pounds

1. Barometric pressure (PB)= 760mmHg

2. Gas concentration= 21% oxygen

When air is inspired, it is warmed to 37 degrees C and 100% humidified with water, so the calculation is modified to correct for the partial pressure of water (47mmHg)

PIO2= FIO2 x (PB-PH2O)= 0.209 x (760mmHg-47mmHg)=149mmHg

2000-3000mL

(continuously being replaced by fresh gas during ventilation)

Alveolar PO2= 100mmHg and Alveolar PCO2=40mmHg

1. Volume of gas in lungs=2000-3000mL

2. Oxygen being removed from alveolus by blood, and carbon dioxide added in its place

3. The balance between the alveolar ventilation (VA) and the relative consumption of oxygen (VO) and production of carbon dioxide (VCO2) that determines the alveolar partial pressures of oxygen and carbon dioxide

4. The level of PCO2 in alveolar gas or arterial blood is inversely related to alveolar ventilation (VA): If VA is doubled, alveolar PCO2 is halved; the partial pressure of oxygen in the alveolus will increase as VA increases and approaches inspired PO2

 Abnormally high VA associated with a below-normal arterial PCO2

1. Reduced alveolar ventilation (VA)

2. Associated with a rise in arterial PCO2

Passive diffusion

Ventilation of gas=(Area/Thickness) x D(P1-P2)

* The greater the molecular weight of the gas, the smaller the diffusion constant (D), and thus less ventilation

1. Depends on the properties of the tissue and the solubility of the gas in medium and molecular weight

2. The solubility of CO2 in water is 20x that of O2

1. The thickness of the alveolar-capillary barrier is 0.2-0.5 microns

2. The barrier can thicken in interstitial fibrosis or interstitial edema

1. Represents the area of functional alveoli in contact with blood

2. This area is estimated to be ~70M^2

3. If more capillaries are recruited, as in exercise, the surface area for diffusion increases