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27 Cards in this Set

  • Front
  • Back
Compliance
C = ΔV/ΔP
- ΔP = trans lung pressure = PA - Ppl
- Slope of pleural PV-loop = compliance!
- Ease with which object can be deformed
- How much volume changes for a given pressure
Elastance
- E = ΔP/ΔV = 1/compliance
- Opposition of an object to deformation (like arteries)
- Reflects low changes in volume to high changes in pressure
Transpulmonary (Translung) pressure
- Difference between alveolar and pleural pressure
- Driving force for expansion of lungs - determines degree of inflation
Hysteresis
- Difference between inspiration/expiration paths on PV-loop
- Extra force required to inspire - due to changes in surface tension of lung!
- At same volume, inspiration is harder because you're trying to break up surface tension
Compliance measurement technique
Take 2 points of expiratory side of cycle from patient
- Slope = compliance
Compliance factors
- Lung volume/size
- Elastic/fibrous tissue in lungs
- Alveolar surface tension
Decreasing compliance factors
- Lungs reaching max filled volume
- Fibrotic disease - thickened alveolar-capillary membrane - wants to contract more!
- Extra recoil - requires much higher pressures to fill
- Alveolar edema = decreased surfactant
- Vascular congestion - lung can't expand against weight/force of blood when things are backed up
Increasing compliance factor
- Destruction of elastic tissue (emphysema)
Chest wall + Lung compliance/PV loop
- Total compliance of lung/chest wall combined = lower than either individually
- This is because they oppose one another and want to inherently do different things
Surface tension and lung recoil
- At alveolus - interface between air and watery surface - surface tension
- Size of alveoli determined by balance of translung pressure and air-liquid interaction
Surface tension - Laplace's Law
- Pressure in alveolus = 2x wall tension/r
- If r = twice as big, pressure is twice as low!
- Bigger sacs easier to stay open
Air-water surface tension effect
- Causes compliance to be lower - almost completely responsible for hysteresis
- When lungs filled with saline -> air-water tension disappears -> compliance shoots up -> hysteresis almost disappears!
Surfactant
- Produced by Type II pneumocytes
- Special phospholipid that decreases surface tension
- Minimizes intralung pressure necessary for inspiration
- Stabilizes alveoli of different sizes
- Ex. = smaller alveoli = smaller radius, higher pressure = easier to collapse
- BUT -> the more they collapse, surfactant groups together -> reduced air-water interface!
- Larger radius -> less grouping of surfactant - maintained tension
- Thus, pressures in alveoli of all sizes tend to be same because the more they collapse, the more surfactant mediates
4 advantages of surfactant
1) Stabilizes alveoli of different sizes
2) Lowers elastic recoil - prevents alveolar collapse
3) Decreases muscular requirement of breathing by increasing compliance
4) Host defense
Respiratory distress syndrome
- Loss of surfactant for some reason
- Premature infants don't make it, old people with edema dilute it out
- Much higher to breathe
- Alveoli collapse, require really high pressures to inflate lung
- Muscles fatigue - can't maintain workload
Exercise, rest vs. static pressure curve
- Curve establishes max values
- You can work within the curve, but cannot exceed those values
Airway resistance factors - Ohm's Law
- R = ΔP/air flow
- Airway size = the bigger, the less resistance
- Resistance falls with increase lung volume
- Smooth mm tone - contracted = smaller r, more resistance
- Gas density = more dense -> more turbulence, more force to overcome = more resistance
*** Resistance highest @ Med. size bronchi
- Lowest at alveoli - highest surface area
Bronchiole smooth mm. dilation factors
- Sympathetic stimulation
- Epinephrine (β2 adrenergic receptors)
- NO - relaxes mm
- Increased PCO2 in small airways
- Decreased PO2 in small airways
Bronchiole smooth mm. Constriction factors
- Parasympathetic stimulation (+ mucus secretion)
- Acetylcholine
- Leukotriene
- Histamine
- Thromboxane A2
- α-adrenergic agonists
- Decreased PCO2 in small airways
Parasympathetic vs. sympathetic influence strength
-Trachea -> alveoli under control of autonomics
- Parasympathetic tends to be stronger!
Dynamic airway compression
- Normal expiration = when inherent recoil force is greater than negative interlung pressure
- Forced expiration = contract diaphragm, applying positive interlung force -> push air out of lungs
- Problem = higher interlung pressure can constrict airways without cartilage
- Harder you push, the higher the pressure -> additional pressure pinches airways tighter!
- Constriction at equal pressure point - where airway pressure = interlung pressure
Emphysema dynamic compression complication
- Reduced recoil of lung due to loss of elastic fiber
- Equal pressure point moves towards alveoli
- Harder they try to exhale, more air gets trapped in alveoli
Flow volume relationship curve
- Partly Effort dependent - flow determined by effort of subject
- Partly effort independent = flow truly determined by elastic recoil of lungs
- Because of dynamic compression - effort of subject blocks expiration because collapses airways
- As you increase residual volumes -> dynamic compression occurs -> everyone ends up on effort independent curve!
Obstructive emphysema/COPD flow-volume relationship
- Higher TLC and RV
- Lower peak expiratory flow - floppy balloon with reduced recoil!
- Lower slope towards end = flow decreases, can't get air out
*** Reduced lung elastic recoil -> chest recoil wins -> larger volumes
Restrictive Fibrotic disease flow-volume relationship
- Lower TLC
- Little/no change in RV
- Expiratory curve = normal
- Overall, problems getting air in because compliance is low - higher pressures needed
*** Lung recoil much higher -> chest loses -> lower volumes
Work of breathing (area of PV-loops)
- Sum of resistive work + elastic work
- Mostly related to muscle flexing and inherent elastic recoil
Efficiency of breathing
- How much O2 does it cost you to do work of breathing
- Respiratory muscles = skeletal mm -> can FATIGUE! (hence, ventilators...)
- Higher O2 requirement of breathing -> decreased efficiency