RS

• 1. Provide O2 for oxidative phosphorylation to gereate ATP & CO2
• 2. Regulate the bodyy's H+ concentration (pH) and CO2 levels
• 3. Defence mechanism: mucous that is present and cilia beating in such a way that bacteria get trapped and pushed back out

• 1. Respiratory muscles (skeletal muscles attaching to ribs and diaphragm - voluntary); lungs
• 2. CNS centers which control respiration - rhythmic breathing patter
• - Can ocerride by holding breath, or breathing really fast
• - When just wall expands we are pushing lungs out
• - The basic breathing rhythm is generated by CNS neurons in the medulla respiratory center

150ml = extends from the top of the trachea to the beginning of the respiratory bronchioles; contains no alveoli and has no gas exchange with blood.

3L = extends from the respiratory bronchioles down to the alveolar sacs; it contains alveoli and is the region where gases exchange between alveoli and capillaries.

Gas Exchange - diffusion of O2 and CO2 between the atmosphere and the capillary bed in the lungs and then between the blood in systemic capillaries and surrounding cells.

• Stem cells that create surfactant
• -Makes sufactant (detergent - like)
• -Also stem cells for this epithelium -> able to differentiate into Type I or Type II

• 1. Ventilation - Exchange of air between atmosphere and alveoli by BULK FLOR
• 2. Exchange - of O2 and CO2 between alveolar air and blood in lung capillaries by DIFFUSION
• 3. Transport - of O2 and CO2 through pulmonary and systemic circulation by BULK FLOW
• 4. Exchange - of O2 and CO2 between blood in tissue capillaries and cells in tissues by DIFFUSION

Is the exchange of air between atmosphere and alveoli

• Skeletal muscles contract to expand the chest cavity. Alveoli expand passively, alveolar air pressure drops and air enters.\
• Patm > Palv

• Is Passive, as the thoracic cavity and lung return to normal dimensions due to elastic recoil, pressure rises and air is forced out. (Ptp decreases)
• Patm < Palv

• difference in pressure between the inside and outside of the lungs.
• Ptp = Palv - Pip

One inspiration and one expiration. Ventilation is in the range of 10 - 18 breaths per min.

• approximately .5 L / breath. Ventilation in 1 minute = .5L/breath x 10 breaths/min = 5L/min
• Ventilation = tidal volume x frequency = minute ventilation

is the total volume of air moved per minute.

volume of air entering the lung (inspiration) equals the volume of air leaving the lung (expiration) Approximately .5L but depends on body size. Your ripped out husband is like .67L

= maximal amount of air that can be increased above tidal voume during deepest inspiration. Approximately 3L

That volume expired with maximal active expiration. Approximately 1.5L

The amount of air that must remain in the lungs after maximal expiration. (1L) To prevent alveolar collapse. Cannot be measued with a spirometer.

• TC = RV + ERV + TV + IRV = 1L + 1.5L + .5L + 3L = 6L
• Total lung capacity comprises several columes and overallping capacities. All can be measured by a spirometer except residuale colme (RV), functional reserve capacity (FRC) and total lung capacity.

The maximal amount of air that a person can expire after maximal inspiration. VC = TV+IRV+ERV

volume remaining in the lung after a normal expiration. At FRC, lung recoild = chest wall recoild, if respiratory muscles are relaxed. FRC = ERV + RV

is a change in lung volume for change in transpulmonary pressure.

• - Tissue Elastic Forces
• - Surface Tension (the amount of attractive pressure between the water molecules) If have small alveoli they actually get pulled into the big one and wouldn't be used
• SURFACTANT: (detergent - Inserts into water layer and reduces surface tensions Made from the Type II cells constantly.
• - Surface Tension - reduced
• - stabalizes alveoli
• - Defense function.

= maximal volume of air that a person can expire after a maximal inspiration.

individual takes a maximal inspiration and then exhales as fast as possible. the important value is the fraction of the total forced vital capacity expired in 1 second. Normal individuals expire approx 80% of their vital capacity in this time.

FEV1 < FVC<80% because it is difficult for them to expire air rapidly through the narrowed airways, but normal vital capacity (FVC)

normal FEV1/FVC=80% normal airway resistance byt impaired respiratory movements becayse of abnormalities in the lung tissue, the pleura, the chest wall, or the neuromuscular machinery. But reduced vital capacity (FVC) hard to fill the lung.

is the volume of fresh air that reaches the alveoli per minute.

Elena.

Volume in conducting airways (approx 150 mL) no exchange of gas with blood.

• Co2 production > alveolar ventilation (increased PCO2 in arterial blood).
• - CO2 increases on alveolar side
• - PaCO2 > 40mmHg
• - O2 is falling from alveolar space into alveolar blood; CO2 levels rise
• - PaO2 < 100mmHg

CO2 production < alveolar ventilation (decreased PCO2 in arterial blood) PaCO2 < 40 mmHg

• 1. bicarbonate ion (HCo3 - ) = 60%
• 2. Bound to Hb in RBC (ie carbmino Hb) = 30%
• 3. Dissolved gas in plasma (PCO2) = 10%

• when ventilation falls and PaCO2 > 40mmHg (H+ concentration increases)
• - if lung not working correctly - pH going down because we are retaining CO2 because the lung is not functioning correctly. So problem is respiratory.

• When ventilation increases and PaCO2 < 40 mmHg. (H+ decreasing)
• - If bloign off to much CO2, then pH is increasing.

• - As excercising muscles produce more CO2, only systemic venous blood increases (not arterial)
• 1. Alveolar PCO2 sets arterial PCO2
• 2. Alveolar PCO2 is determined by the ration of CO2 production to alveolar ventilation
• - During moderate excercise -> alceolar ventilation increases in proportion to increased CO2 production.
• - Strenous excercise -> alveolar ventilation increases more than CO2 production. Person may hyperventilate -> causing alveolar and systemic arterial PCO2 to decrease

Although systemic venous Po2 decreases during excercise (due to an increase in O2 consumption in the tissues) -> alveolar PO2 and systemic arterial PO2 remain unchanged due to cellular O2 consumeption and alveolar ventilation increasing in exact proopotion to each other.

• - During moderate excercise -> no accumulation of H+ resulting from CO2
• - During strenuous excercise-> there is an increased in H+ generating a lot of lactic acid and in order to get rid of the pH protons we breathe faster to blow them off
• - Not respiratory alkalosis but can stimulate hyperventilation accompanying the decreased in Co2

In order to maintain O2 level and CO2. The major clinical problems are disorders that either impair gas exchange or increase the work of breathing.

arterial PO2 decreased PaO2 < 60mmHg (arterial side)

• total blood O2 content decreased PaO2 can be 100
• - Decreased in RBC's and decreased in Hb
• -Because not enough of the carrier to deliver the O2

blood flow to tissues is low, perfusion is low - possible clot

poisoned cell metabolism (example cyanide) so can't do oxidative metabolism/