Respiratory Physiology

04/11/2015

1. Conducting zone: airways, Respiratory zone: alveoli (ONLY THE ALVEOLI

EXCHANGES GASES WITH THE BLOOD. ALVEOLI SACS= FILLED WITH
AIR)
Internal respiration: Cell respiration, Using O2 in the blood to produce
ATP and CO2
External respiration: Exchange of gases between the atmosphere
O2 is highest in the lungs where it is just brought in, lowest where it is
being used in the cells. CO2 highest in the cells where it is just produced,
and CO2 lowest in the lungs where it is leaving the body into the
atmosphere.
2. Ventilation Works by changing the size of the chest (thoracic) cavity.
Pleura= a membrane. One surrounds the lungs, another lines the chest
cavity.
Visceral Pleura= outer layer of lung, inner layer of pleura. Parietal lines
inside of chest cavity, outer layer.
Visceral and Parietal pleura are separated by a fluid called the intrapleural
fluid.
Pleurisy= pleuritis, inflamation of the pleura causing friction.
3. Tiny changes in the space can change the pressure: Tiny INCREASE IN
VOLUME causes DECREASE IN PRESSURE
Intrapleural pressure is always less than alveolar pressure
Transpulmonary pressure= Pressure in the alveoli- Pressure in the
intrapleural fluid
Chest Wall moves away from lung surface, causing increase in intrapleural
space and DECREASE in pressure= -4 mmHg
TRANSPULMONARY pressure causes lungs to not collapse.
When lungs folllows chest Wall, intrapleural pressure DECREASES AGAIN
DOWN TO -7 mmHg.
4. Alveoli have surface tensin liquid inside, causing collapse of alveoli.
Pneumothrorax= when air enters the intrapleural space= loss of
transpulmonary pressure= lung collapses.
Traumatic pneumotrorax= Rupture of PARIETAL pleural, caused by
stabbing the chest Wall.
Spontaneous pneumotrorax= rupture of VISCERAL pleural
Why do lungs collapse: elastic recoil, surface tensin in alveoli.

5. Surface tensin in the alveoli: alveoli WANT TO COLLAPSE AND RESIST

STRETCH.
Surfactant: REDUCES SURFACE TENSION, acts like detergent: breaks up
wter molecules
Type I alveolar cells: flattened cells in alveolus wall
Type II alveolar cells: fatter cells, stimulates secretion of surfactant
SURFACTANT MAKES IT EASIER FOR LUNGS TO EXPAND= INCREASES
LUNG COMPLIANCE
By taking a deep breath, you stretch the type II alveolar cells to make
more surfactant.
Lung compliance= lung elasticity, ability for lung to stretch
What decreases lung compliance?
1) Fibrosis= scarring of lung tissue reduces elasticity
2) Surface tensin in alveoli affects lung compliance greatly
3) COMPLIANCE= CHANGE IN VOLUME / CHANGE IN PRESSURE
4) Surfactant INCREASES lung compliance
Respiratory Distress Syndrome of the Newborn= not producing enough
surfactant because Type II cells are not mature at 26-28 weeks inside
mothers tummy.
Its harder to blow up a new balloon each time rather than blowing up a
balloon already partially filled with air. The sndrome can cause
difficulty of inspiration and death.
Solution: pump surfactant into trachea (exogenous, external therapy)
6. Airway resistance is normally very low because airways are sufficiently
large, so small pressure is needed for air to get in and out of lungs.
Pressure of 1 mmHg.
In Asthma, increased resistance because decrease in radius of airways
BULK FLOW IN AIRWAYS, CHANGE IN PRESSURE = PRESSURE OF
ATMOSPHERE- PRESSURE OF ALVEOLI
7. Why does inspiration (inhalation) occur?
1) Chest cavity expands = pressure drops
2) Alveolar pressure drops below atmospheric pressure

3)
Why is a small change in pressure needed= 1 mmHg below atmospheric
pressure for normal, sitting around breathing. High change in pressure
causes a lot of air to be sucked into lungs (caused by weight of
atmospheric pressure and low pressure in lungs)
Air moves into lungs until Patm = Palv when that happens air stops
coming in.
Chest cavity is enlarged by contracting the diaphragm and elevating the
rib cage. During forced inspiration, neck muscles and accessory
inspiratory muscles further enlarge chest cavity.
1)
2)
3)
4)
5)
6)

Steps of inspiration:
Diaphragm contracts, intercostal muscles contract
Thorax rises
Intrapleural pressure decreases
Alveoli get bigger
Alveolar pressure goes down
Air flows into lungs until Patm = Palv

10. Respiratory volumes:

1) Tidal Volume: 500 ml (breathing in and out normally)
2) Inspiratory Reserve Volume: 3000 mls
3) Expiratory Reserve Volume: 1500 mls
4) Vital Capacity: 5000 (Adding up all the volumes)
5) Residual Volume (never leaves lungs): 1000mls
Total Lung Capacity: Vital Capacity (5000 mls) + Residual volumen (1000) =
6000 mls
Anatomic dead space: 150 ml, space within the air passageways or the
airways, NOT FRESH ATMOSPHERIC AIR
PARTIAL PRESSURE NOT THE SAME IN ATMOSPHERIC AND ALVEOLAR AIR.

1) AIR IS HUMIDIFIED WHEN IT PASSES THROUGH NOSE

2) DECREASE PO2 AND INCREASE PCO2LARGE AMOUNTS OF AIR ARE
LEFT IN LUNGS IN A NORMAL RESPIRATORY CYCLE
O2 and co2 exchange
1) In Alveoli and pulmonary vein(leaving lungs) po2= 100, pco2= 40
2) In Tissues and pulmonary artery (to heart) po2 less than 40, pco2
greater than 46