Diaphragm is major muscle. Innervated by two phrenic nerves.(C3-C5)

Other Muscles:

-external intercostal muscles

-scalene muscles

-sternocleidomastoids

None

Passive process due to elastic recoil

Inspirtory muscle contract

↓

Thoracic cavity expands

↓

Pleural pressure becomes more negative

↓

Transpulmonary pressure increases

↓

Lungs inflate

↓

Aveolar pressure becomes subatmospheric

↓

Air flows into lungs into until aveolar pressure equals atmospheric pressure

Pressure inside wall minus the pressure outside.

• Transpulmonary Pressure
• Transairway Pressure

The pressure difference across the lung wall. If it ever reaches 0 the lung will collapse (Pneumothorax)

P_L=P_A-P_Pl

P_A:alveolar pressure

P_Pl:pleural pressure

-Always NEGATIVE. At rest it is around (-5) when breathing it is around (-8).

The pressure difference across the airway.

P_ta=P_aw-P_pl

P_aw:airway pressure

P_pl:pleural pressure

Compliance= ΔV/ΔP 

1. Elastic recoil

2. Surface tension of Aveoli

Does not depend on air or tissue movement.

• During inspiration the lung is working against surface tension. At lower volume the surface tension is higher.
• During expiration there is higher volume and less surface tension.
• Hysteresis: what is used to describe the inflation and deflation curves being different.

• When saline is used to inflate the lung there is no surface tension and the lung is more compliant. Inflation and Deflation curves overlap.
• 2/3 of the work of inflating the lung is used in overcoming surface tension. 1/3 is used overcoming elastic recoil.

Lung: at FRC the transpulmonary pressure is (+).

Chest Wall: at FRC pressure is (-). Above FRC pressure crosses over to (+/callapsing force) and compliance increases with volume.

Lung and Chest Wall: at FRC it is 0. Compliance is less than the two individual ones.

Emphysema: lose of elastic tissue. Easy to inflate/more compliant. Recoil is decreased. Tend to have trapped air. Higher FRC. Chest area becomes enlarged(front to back)

Fibrosis: Less compliant. Lower FRC than normal.

• Pulmonary fibrosis
• Pulmonary Vascular Congestion
• Pneumonia
• Pleural effusion
• Decreased surfactant
• Spine Deformity
• Obesity

Open:

-Transmural pressure gradient

-Pulmonary surfactant(which apposes surface tension)

-Alveolar interdependence

Close:

-Elasticity of stretched pulmonary connective fibers.

-Alveolar surface tension

The smaller the radius the more pressure it has. This makes the air want to leave the smaller aveoli and go to the larger ones.

P= (2T)/r

Pulmonary surfactant reduces surface tension to:

1. Promote stability of the lung. (prevent small aveoli from emptying into large aveoli→ prevent collapse or atelectasis.)
2. Reduces inflation pressure and work of breathing
3. Help keep lungs dry

1. Neonatal respitory distress syndrome(hyaline membrane disease) Premature babies. Surfactant usually appears around 34 weeks of gestation.
2. Adult respitory distress syndrome
3. Post cardio-pulmonary bypass
4. Pulmonary embolus
5. Oxygen toxicity and other toxic agents.

If one aveolus starts to collapse than the surrounding alveoli will pull it back open.

Turbulent: Large airways e.g. trachea and bronchi

Laminar: Small peripheral airways

R_aw=(P_mouth-P_A)/V

same as R=ΔP/Q(flow)

R_aw:total airway resistance

V:airflow

What is the relationship between airflow resistance and the radius of the airway?

Airway resistance is INVERSELY proportional to r⁴

If r decreases by 1/2 Resistance increases by 16.

If r doubles Resistance decreases by 1/16

The small airways are arranged in parrallel so that the total resistance is lower than any individual resistance.

Pathological factors:

-Allergy induced spasm of the airways caused by:

--Slow-reactive substance of anaphylaxis

--Histamine

-Physical blockage of airway caused by:

--Excess mucus

--Edema of walls

--Airway callapse

Physiological control factors:

-Neural control: Parasympathetic stimulation.

-Local Chemical control: ↓CO₂

Pathological factors: none

Physiological control factors:

-Neural control: Sympathetic stimulation (minimal defect)

-Local chemical control: ↑CO₂

Increasing lung volume reduces resistance by opening airway.

When is the only time that the plueral pressure is positive?

P_aw=P_pl

Transairway pressure=0 (collaspe)

EPP divides the airway into:

1. Upstream segment→ from alveoli to EPP

2. Downstream segment→ from mouth to EPP→ Negative transairway pressure→ collapsed segment.

In normal conditions the elastic recoil causes the EPP to take place in the large airways. These airways have cartilage and have minimal collapse.

When there is loss of elastic recoil the EPP takes place earlier in a smaller airway and the airway can collapse.

Supportive method to prevent atelectasis(aveoli collaspe)

Prevents aveolar pressure from returning to 0. Apparently the lung will be kept at a larger volume. Not sure what this is really talking about??!!

- when I talked to him he said it didn't really matter.

1. Partial pressure gradient

2. Pulmonary capillary blood flow

3. Diffusion properties of aveolar-capillary membrane

The Atmospheric/Barometric pressure (P_B) decreases with altitude.

The Fr_O2 remains at 21%(.21)

V_gas= (As x D x ΔP)/T

V_gas:volume of gas diffusing per minute

As:membrane surface area

D:diffusion coefficient

ΔP:partial pressure difference across membrane

T:membrane thickness

The time required for the red cells to move through the capillary.

Things that do not bind to hemeglobin. The diffuse into the blood and raise partial pressure quickly. Reaches equilibrium quickly.

• N₂O(Nitrous Oxide)
• CO₂
• O₂ under normal conditions

Things have a strong affinity for hemeglobin. Doesn't diffuse much. Equilibrium is almost never reached.

• CO
• O₂ during exercise
• Pathology: Emphysema, Fibrosis

Fibrosis increases the thickness of the membrane and results in a diffusion-limited curve.

A decrease in altitude results in a smaller gradient which takes more time for the perfusion-limited curve to reach equilibrium.

D_L= V_CO/P_ACO

D_L: lung diffusing capacity in mL/min per mmHg

V_CO:CO uptake in mL/min

P_ACO:alveolar partial pressure of CO in mmHg

CO is used because:

-it is diffusion-limited.

-not in venous blood

-affinity to Hb 210x more than Oxygen's.

1. Dissolved Oxygen= ~2% of the total O₂ content.

2. Bound to Hemoglobin= 98%

Both added together =O₂ content

• Affinity of the binding site of Hb to O₂
• PO₂

Thus, the greater the affinity of Hb site to O₂ the lower PO₂ required to keep the O₂ attached to Hb

• The loading phase(plateu region) happens in the lungs where the P_O2 is 100mmHg.
• The unloading phase(steep region) happens in the tissues where the P_O2 is 40mmHg.
• P₅₀ is the P_O2 required to saturate 50% Hb with O₂.

↑P_CO2

↑(H+)

↑Temperature

↑2,3-DPG

Exercise increases CO₂ production. That CO₂ is converted to bicarbonate and produces H+.

Increase in 2,3-DPG relates to hypoxia like in a high altitidude.

↓P_CO2

↓(H+)

↓Temperature

↓2,3-DPG

DPG decreases when the RBC enzyme that makes DPG is lacking. Without the DPG to get the oxygen to the tissues, the body responds by making more RBC's leading to erythrocytosis.

Curve shifts down(O₂ content decreases)

Curve shifts left(O₂ affinity increases)

CO binds Hb with much more affinity than Oxygen. Once CO is bond to Hb, Oxygen can no longer bind. The number of sites available decrease wich causes an increase in Oxygen affinity for Hb.  This increase in affinity makes it harder for the Hb to transfer the Oxygen to the tissues.

• Losing RBC's
• Low Hb
• Lower O₂ content (curve shifts down)
• O₂ affinity decreases (curve shifts right)

Increase RBC's

↑Hb concentration

↑O₂ content

As Bicarbonate(HCO₃-) in the plasma. In the process of converting to bicarbonate it releases a H+.

NONE of this is true in the LUNG. It is the opposite.

Higher P_O2 will shift the CO₂ equilibrium curve down and to the right.

• Blood loads more CO₂ in tissues(where P_O2 is lowest)
• Blood unloads more CO₂ in lungs(where P_O2 is highest)