Pulmonary Mechanics II Flashcards
what does air’s low viscosity mean for pressure needed for inhalation?
since air < water in terms of viscosity, a lower pressure is needed for inhalation into the lung
how are flow, alveolar pressure, and interpleural pressure related during inspiration and expiration?
- flow and alveolar pressure are closely related (decrease to negative in inspiration, then increase to positive in expiration)
- interpleural pressure is linearly following, but will have more negative/positive curves that match flow and Palv to overcome friction and other resistances to get more air in and out
what happens to pressure (of chest and lung) at end inspiratory volume?
chest pressure is equal to zero
lung pressure is equal to total pressure, and somewhat positive
what is the dominant driving force for return of the lung to FRC during forced expiration?
expansive force of the chest wall
is intrapleural pressure positive or negative during inspiration and expiration
it’s negative during inspiration, but positive in expiration and while measuring chest wall compliance (chest muscles are resting)
- the pressures recorded during measurement of compliance are not the same as during breathing
- the values will be more positive/negative with greater inspiration/expiration
dynamic compliance (typical value) -what does it do w/ small airway disease
dV/dP at end-inspiration and end-expiration, when Palv = Patm (usually 0.1 L/cm H2O)
-falls b/c increased resistance (like if there are mucous plugs or inflammatory swelling)
what does a discrepancy in static and dynamic compliance mean?
abnormal resistance
in small airway disease, what happens to:
- intrapleural pressure changes
- total volume
- respiratory rate
- airway resistance
- dynamic compliance
- dPpl changes are constant
- TV decreases
- RR increases
- AR increases
- Cdyn decreases
eddy and orifice flow
eddy - turbulent at bifurcation, laminar once through
orifice - turbulent in smaller opening, laminar once through
components of resistance to breathing
20% due to tissue resistance (depends on the size of the chest)
80% due to airway resistance
-10% small airways
-15% trachea and bronchi (bronchioles not normally main site of resistance, but can become so in bronchitis)
-25% glottis
-50% nose or mouth
how does airway resistance increase/decrease from conduction to respiratory areas
resistance increases in the conduction area (first 3 airway generations, b/c humidifies, warms, filters, and cleanses air), then falls as X-sectional area increases
how does epinephrine decrease airway resistance in fight or flight?
- E binds with high affinity B2 receptors
- increased cAMP stimulates PRO kinase A
- PKA phosphorylates MLCK
- decreased sensitivity of MLCK for Ca-calmodulin
- inhibits binding of myosin cross-bridges to actin
- dilates bronchi and bronchioles; reduces resistance
- enhances breathing
5 factors affecting airway resistance and their receptors, if applicable
- neural innervation of bronchial smooth muscle in humans is sparse, but:
- sympathetic dilation of bronchial smooth muscle by E acting on B2 receptors
- parasympathetic constriction through vagus nerve (cholinergic) on muscarinic receptors - reflex constriction (smoke particles, noxious gases, extreme cold)
- histamine is a potent bronchoconstrictor and vasodilator (H1 receptor)
- inflammatory swelling of bronchial mucosa increases Raw in asthma
- PEEP decreases Raw in patients on respirators
typical value for airway resistance
1.2 cm H2O/l/sec
is resistance greater when breathing through the nose or mouth?
resistance is greater when breathing through the nose than through the mouth
what do isovolume pressure-flow (IVPF) curves tell you? what is this due to?
resistance to expiration increases at low lung volumes (as in, maximal effort that exhales everything out)
- this is due to dynamic compression of airways (deviates from Ohm’s laws)
- during inspiration, no plateau is reached (only slight curvature is seen in dependence of flow on pressure)
how does dynamic compression relate to quiet VS forced expiration, and what does that mean for the equal pressure point (EEP)?
in forced expiration, dynamic compression partially collapses airways and moves the EEP closer to the alveoli, which compresses more of the airway to increase resistance
-this is because the pleural pressure is -5 in quiet expiration, but +10 in forced; alveolar pressure is +5 in quiet, but +20 in forced
what does the maximal effort flow volume (MEFV) loop measure?
- peak expiratory flow
- forced vital capacity
- pulmonary compliance
what does pursed lips breathing do?
it increases pressure to keep airways open to decrease resistance
what does the MEFV curve show?
it shows the maximal flow that can be attained at each lung volume
-max flow is greater at greater lung volume b/c the airways are distended and the resistance to flow is less
what is the MEFV curve used to diagnose?
obstructive and restrictive disease
- effort-independent (depends less on patient cooperation)
- less variable than IVPF and FEV1 tests
how can MEFV curves be constructed from IVPF curves?
takie points off of the plateaus of the flow pressure curves at each lung volume, and re-plot max flow versus volume expired
what are 2 reasons why maximal expiratory flow rate would be low?
- lung elastic recoil pressure is abnormally low
2. airway dimensions are restricted abnormally
how are MEFV loops measured? what is normal vital capacity, and at what percent VC does peak expiratory flow occur? when is 100% VC exhaled?
flow and volume are recorded simultaneously with a spirometer during as forceful and rapid an expiration as possible, after a maximal inspiration
- normal VC is 4.75 L
- PEF occurs at 75-80% VC
- 100% VC exhaled slightly over 1 sec with maximal effort
how does the MEFV loop change in obstructive (emphysema VS bronchitis) VS restrictive (fibrosis) lung diseases?
emphysema: peak expiratory flow is normal
-at low lung volumes, elevated compliance causes abnormally low mid-expiratory values (quickly has low flow rates)
bronchitis: steadily decreasing flow rate, similar to normal
both obstructive have increased expiration times, but normal inspiration
fibrosis: decreased vital capacity (can’t inspire much), and expiration is likewise shortened
pediatric MEFV loops
smaller chest size, so it just looks like a smaller version of the normal MEFV
-still normal developing
respiratory muscle disease MEFV loops
the peak expiratory flow is lower and hits a plateau until it reaches max volume at the end of expiration
- inspiration is likewise affected
- curve is independent of effort b/c of dynamic compression
when is dynamic compression active; inspiration or expiration?
expiration
when do intrapleural pressure, alveolar pressure, and flow attain their most negative values?
Ppl - at end-inspiration
Palv and flow - at mid-inspiration
they reach their most positive values at end-expiration and mid-expiration, respectively
when does phrenic nerve spike frequency increase?
during inspiration
how does intrapleural pressure change in eupneic breathing?
it is always negative, but is most negative at end-inspiration, and least negative at end-expiration
what can drive intrapleural pressure positive?
during vigorous expiration, contraction of internal intercostals can drive it positive
in forced expiration, when is airway resistance larger?
airway resistance is less at the beginning than at the end of forced expiration (narrowing of diameters)
-airway resistance is treater than tissue resistance, and greater in nose and mouth than bronchioles
