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45 Cards in this Set

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Pleural Pressure
Always negative due to elastic properties. Chest wall always wants to go out & lungs want to collapse in.
Alveolar Pressure
Can be negative or positive compared to pressure outside
If - air moves in
If + air moves out
Hole in the chest wall, air in the pleural space
Lungs will collapse and chest goes out
Mechanism of normal inspiraton
Contract diaphragm-->pulls down, increased volume of chest cavity, decrease in pressure
Mechanism of increased inspiration
Contract external intercostal muscles -->pulls the chest wall up & out
Contract accessory muscles in neck
Increased volume, decrease in pressure-->Air moves IN
Mechanism of normal expiration
Diaphragm relaxes and moves back up -->decrease in volume, increase in pressure
Mechanism of increased expiration
Contract internal intercostal muscles -->pulls the chest wall down & in
Decrease in volume and increase in pressure --Air moves IN
Amount of air moved during each breath
Vital Capacity
Total amount of air that canbe moved
Typically ~ 5L
Total Lunch Capacity
Vital + Residual = 6L
Airway Constriction
Primarily an obstructive disorder
Obstructive Disorders
Emphysema, Asthma
Can't get air out due to loss of alveoli and elastic recoil
Restrictive Disorders
Can't get air in
Anatomic Dead Space
Air in the conducting zone (no gas xchange)
Total Ventilation
amount of air moved/minute
=tidal volume x frequency of breathing
Alveolar Ventilation
amount of air moved that is involved in gas exchange/minute
=(tidal volume - anatomic dead space) x frequency of breathing
Deep and Slow v. Rapid and Shallow
Deep & Slow breaths are much more efficient
Airway Resistance
Increase radius-->drastic decrease in resistance
The greatest R is @ the bronchi
The most important R is @ the bronchioles due to the amount of smooth muscle
Parasympathetic NS control of airway resistance
Para releases Ach-->muscarinic receptors-->airway constriction
Sympathetic NS control of airway resistance
Sympathetic releases NE/Epi-->B2 receptors -->airway dilation

Tx of Asthma: B2 agonist
How easy it is to inflate the lungs
Increased compliance
Large change in volume for a change in pressure
Ex. Emphysema: easy to inflate lungs but hard to get it out
Decreased compliance
Small change in volume for a change in pressure
Ex. Restrictive disorders: hard to inflate lungs
Causes a decrease in surface tension by getting b/t water molecules and decreasing surface tension which prevents alveoli from collapsing
Secreted by Type II alveolar cells
Perfusion limited Diffusion
diffusing capacity is limited by blood flow
Must increase blood flow to get more O2 in blood
Diffusion Limited
Diffusing capacity is limited by rate of diffusion
Need to increase rate of diffusion to get more O2 into the blood
*If you double the rate of diffusion for O2 you DON'T increase transfer of O2 because its limited by hemoglobin
Pulmonary circulation problem with Left Congestive Heart failure
Failure of left ventricle
Blood backs up into pulmonary circulation
Increase in pulmonary capillary pressure -->filtration
Pulmonary edema -->poor gas exchange -->DEATH!
3 Benefits of Recruitment/Distension of capillaries
Decrease in resistance-->decrease in pressure-->no edema
Decreased velocity of blood flow-->increase in gas exchange
Increased surface area for gas exchange
Effect of autonomic nervous system on regulation of pulmonary vascular resistance
Not an important regulator
Low Oxygen levels
Effect of hypoxia on surround vessels
Low O2 in blood-->vasoconstriction
Low CO2 in blood-->airway constriction
Affintity of Oxygen binding to hemoglobin
As O2 binds to Hb, it increases the affininity of Hb for more O2
O2-Hb Curve
Shift Left
In the lungs
More O2 binds to Hb
Causes: Decreased CO2, Decreased H+, Decreased temperature, Decreased DPG
O2-Hb Curve
Shift Right
More O2 leaves Hb
Causes: Increased CO2, Increased H+, Increased temperature, Increased DPG
Bohr Effect
If shift is caused by increased CO2 or Increased H+
Causes of Hypoxia
Diffusion Impairment (ie. Pulmonary Edema)
Decreased atmospheric Po2 (ie. High Altitude)
Both Result in Decreased P02 in arterial blood-->Chemoreceptors will detect this and stimulate breathing

Anemia: Less Hb, less O2 bound to Hb
CO Poisoning: CO binds to Hb with very high affinity and O2 can't bind to Hb. The same amount of O2 is dissolved in the blood-->normal PO2 so therefore NOT detected by chemoreceptors-->DEATH!
Transport of CO2
Dissolved in plasma (10%)
Bound to proteins, mainly Hb (30%)
Bicarbonate ions (60%)
Haldane Effect
Occurs in the lungs
When O2 binds to Hb, less CO2 will bind to Hb
Peripheral Chemoreceptors
Detect changes required for respiratory adjustments
Detect increased CO2 and H+ and decreased O2
Inhibitors of Inspiration
Pulmonary stretch receptors
Other brain centers
Stimulators of Inspiration
Pulmonary Irritant Receptors
Central Chemoreceptors
Stimulated by increased PCo2 and increased H+ in CSF
NOT STIMULATED by decreased P02 or increased H+ in blood
Pulmonary Receptors
Slowly adapting receptors (Pulmonary stretch receptors)
Found in lungs in the smooth muscle of the bronchioles
Hering-Breur Reflex
Stops inspiration when the lungs are being overinflated, a protective reflex
(NOT involved in stopping normal inspiration)
Pulmonary Irritant Receptors
Respond to Irritants
Produces complex effects like cough and a general stimulus to inspire