Pulmonary Mechanics I Flashcards Preview

Physiology > Pulmonary Mechanics I > Flashcards

Flashcards in Pulmonary Mechanics I Deck (33)
Loading flashcards...

what kind of pump is the lung and what does this mean in terms of inflation and deflation?

negative pressure pump
-the lung inflates due to a drop in intrapleural pressure outside the lung, but inside the chest wall
-the lung deflates from the passive elastic recoil of the lung (increase in intrapleural pressure)


what is the intrapleural pressure if respiratory muscles are relaxed?

pressure in the intrapleural space is less than atmospheric pressure, thus said to be -5 cm H2O


what happens to intrapleural pressure in pneumothorax

intrapleural pressure rises up to atmospheric pressure, so the lung collapses


eupnea (normal ventilation value)

normal (quiet) breathing (7.5 L/min)
-inspiration active (only diaphragm), but expiration passive (recoil of lung and chest wall w/o muscles)


muscles of inspiration

diaphragm (primary muscle)
external intercostals (lifts ribs up and forward, increases anterior-posterior dimension of chest cavity to add tone to chest wall)
accessory (sternomastoid lifts sternum, scalene lifts upper ribs, etc.)


muscles of expiration

internal intercostals (lower ribs)
4 abdominal muscles (depresses lower ribs, compresses abdominal cavity, pushes up diaphragm and other chest muscles)
only used in strenuous exercise (active breathing)


hyperpnea (and normal ventilation value)

deeper and faster breathing than normal (like in exercise, up to 120 L/min)
-inspiration and expiration are both active
-inspiration uses external intercostals
-expiration uses internal intercostals



more rapid breathing than normal (hyperventilation)


hyperventilation and what it causes

breathing faster than required for O2ation leads to alveolar hypocapnia (too little CO2 in blood)
-respiratory alkalosis (increases pH b/c decreased H+)


hypoventilation and what it causes

happens in muscular dystrophy or respiratory muscle paralysis, and it leads to alveolar hypoxia and hypercapnea
-respiratory acidemia (H+ high in blood, so low pH)


lung compliance in terms of pressure

Cl = dV/dPl


chest wall compliance in terms of pressure

Cc = dV/dPc


total compliance in terms of pressure

consists of 2 compliances in series (lung and chest wall)
Ct = dV/dPt = dV/dPalv


what does contraction of the diaphargm do on the intrapleural space?

it exerts an expansive force (increase volume), decreasing the intrapleural pressure, making it more negative, and acting to inflate the lung


when is external pressure not equal to atmospheric pressure?

if a weight is placed on the chest, then external pressure > atm, and is called the body surface pressure


what are the transmural pressures, and what do they set?

1. chest wall pressure = interpleural pressure - atmospheric pressure (sets degree of inflation of chest wall)
2. lung pressure = alveolar pressure - interpleural pressure (sets degree of inflation of lung)
3. total transmural pressure = relaxation pressure = alveolar pressure - atmospheric pressure = transmural chest pressure + transmural lung pressure (since in series; sets degree of inflation of entire system of bag w/in a bag)


what happens if all respiratory muscles are relaxed? what things are balanced?

the system is at mechanical equilibrium
-total transmural rpessure = 0
-transmural lung pressure = - transmural chest pressure
-positive outward lung pressure is balanced by inward passive elastic recoil pressure of lung, and negative inward chest wall pressure is balanced by passive outward elastic recoil pressure of chest


how is pulmonary compliance measured with a spirometer? (in terms of ressure and volume)

patient inspires and holds breath with glottis open, then relaxes chest muscles against weighted spirometer
-since lung PV = spirometer PV, when lung V increases, the interpleural P decreases, so spirometer V decreases and the P of spirometer (equated to alveoli) increases

the respiratory muscles must be relaxed, since it's passive elastic recoil pressure we want to measure


static compliance

determines what particular volume the lung and chest wall will assume for a given transmural pressure when the elastic vessels are at mechanical equilibrium with no air moving


how do you normalize compliance for lung volume?

specific compliance (Csp) = dV/(V * dP)


what happens in barrel-chest coal miners?

decreased total compliance (Ct)
-could be due to properties of lung or chest wall (Cl or Cc) so need to measure each separately
-fibrosis of lung, chest wall physique


static compliance curves for lung, chest wall, and total system (y axis = vital capacity, x axis = pressure)

the curves are all nonlinear, so the compliance (slope) depends on degree of inflation, so is usually measured at FRC
-from left to right is Pc - Pl - Pt if P > 0 (and past end inspiratory volume), but Pc - Pt if P < 0


functional residual capacity (FRC)

lung volume when Pt = 0, at end-expiratory position
-occurs at about 36% vital capacity, when Pc = - Pl


what happens during forced expiration (at volumes below FRC?)

the expansive force of the chest wall provides dominant driving force for return of lung to FRC


what happens to Pc if lung is resting or expanded?

resting: Pc = 0, only elastic force of lung opposes inspiration
expanding: Pc > 0, and elastic recoil of lungs AND chest provide passive driving force for expiration


lung compliance in fibrotic lung disease VS emphysema

fibrosis: compliance decreases (dV decreases), so it's harder to inhale
emphysema: compliance increases (dP, or recoil pressure decreases) so it's harder to exhale



related lung diseases induced by inhalation of dust asbestos, coal, silica, etc.
-form granulomatous and fibrous tissue in lungs, decreasing compliance (as in fibrosis) to cause "stiffer" lung
-inspiration hard, work of breathing increased


what happens to FRC and TLC if compliance of lung increases?

they will both increase too (positive relationship)


how does smoke cause emphysema?

neutrophils accumulate in lung to remove inhaled smoke particles, and release proteases
-alpha-antitrypsin in plasma usually inhibits proteases to protect lung, but smoke inhibits aa1
-lung CT is digested by proteases, which increases Cl


effect of surfactant on lung compliance
-what happens if saline-filled lung?
-what happens if air-filled with surfactant?
-what happens if air-filled w/o surfactant?

compliance increases by decreasing surface tension
-increased compliance b/c surface tension eliminated
-normal compliance
-decreased compliance (very high surface tension)

Decks in Physiology Class (60):