Flashcards in Mechanics of Breathing, Pulmonary Circulation Deck (35):
Cause structures to snap back to equilibrium position after stretched or compressed. Due to collagen/elastin.
Distensibility of a system. The inverse of compliance. Change in volume/change in pressure.
Pressure across alveolar wall. Intraalveolar pressure - intrapleural pressure.
Compliance of lung is different exhaling and inhaling. Exhaling, the lung is more compliant. This is due to the fact that surface tension in alveoli must be overcome during inhalation.
How to calculate surface tension of alveoli?
Collapsing Pressure = 2T/r. This shows that a large alveolus experiences a weaker collapsing force than a smaller alveolus.
How is surface tension in alveoli weakened?
Surfactant. A phospholipid. Important at birth.
How does compliance of lung and chest wall system compare to their respective compliances.
Less, think of a balloon in a balloon.
What is the volume present in lungs after a normal breath called?
Functional Residual Capacity.
Is intrapleural pressure positive or negative?
Negative, created by elastic recoil lungs pulling in and elastic recoil chest wall bowing out.
What does emphysema do to lung compliance?
Loss of collagen, so it increases compliance.
What does fibrosis do to lung compliance?
Decreases compliance due to an increase in elastic tissue.
How to decrease airway resistance without altering airways?
Decrease viscosity of the air.
Active muscles of inspiration?
External intercostals, accessories
Active muscles of expiration?
Internal intercostals, abdominals
Positive transmural pressure
Expanding pressure, keeps airways open.
Negative transmural pressure
In people with emphysema, airway narrows with forced expiration.
Resistance and pressure in pulmonary vessels?
Very low because walls are very thing and distensible. Also very low pressure.
Pulmonary Systolic and Diastolic pressures?
25/10, due to low pressure from RV
How to calculate pulmonary vascular resistance?
How is pulmonary blood flow regulated?
Arteriolar smooth muscle constriction.
Most important mediator of pulmonary vasoconstriction?
Partial pressure of O2 in alveolar gas. If low PAO2, vasoconstrict, so blood can go to ventilated alveoli.
Low PAO2 causes vasoconstriction to better match V/Q.
Mechanism of Pulmonary Vasoconstriction
Low PAO2, leads to inhibition of K channels in smooth muscles, leading to depolarization, leading to Ca influx and contraction.
Role of NO
Role of Endothelin?
Constriction via endothelin receptors
Role of PGI2 and TXA2
Vasodilation by increasing cAMP.
Causes and consequences of increased PVR.
Cause: high altidude, reduced barometric pressure, reduced partial pressure of O2.
Consequence. RV pressure overload and hypertrophy.
Zone 1 Perfusion
PA>Pa>Pv. Pa is very low because of gravity, so it's compressed. Physiologic dead space.
Zone 2 Perfusion
Pa>PA>Pv. Pa is higher than PA, which is higher than Pv. Compresses end of capillary. Blood flow driven by Pa and PA difference.
Zone 3 Perfusion
Pa>Pv>PA. Blood flow is highest, driven by Pa and Pv gradient.
Blood from coronary arteries and bronchial arteries bypasses the lungs. This causes PaO2 to always be slightly less than PAO2. This accounts for 2% of blood.
Right to left shunt
Blood passes the lungs without being oxygenated. Hypoxemia occurs that cannot be corrected with inspired oxygen.
Does a right to left shunt cause great increase in PaCO2?
No, because chemoreceptors will increase ventilatory drive to rid the body of CO2. Chemoreceptors for O2 are not as sensitive.