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27 Cards in this Set
- Front
- Back
Compliance
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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 |
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Elastance
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- E = ΔP/ΔV = 1/compliance
- Opposition of an object to deformation (like arteries) - Reflects low changes in volume to high changes in pressure |
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Transpulmonary (Translung) pressure
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- Difference between alveolar and pleural pressure
- Driving force for expansion of lungs - determines degree of inflation |
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Hysteresis
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- 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 |
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Compliance measurement technique
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Take 2 points of expiratory side of cycle from patient
- Slope = compliance |
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Compliance factors
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- Lung volume/size
- Elastic/fibrous tissue in lungs - Alveolar surface tension |
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Decreasing compliance factors
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- 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 |
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Increasing compliance factor
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- Destruction of elastic tissue (emphysema)
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Chest wall + Lung compliance/PV loop
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- 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 |
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Surface tension and lung recoil
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- At alveolus - interface between air and watery surface - surface tension
- Size of alveoli determined by balance of translung pressure and air-liquid interaction |
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Surface tension - Laplace's Law
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- Pressure in alveolus = 2x wall tension/r
- If r = twice as big, pressure is twice as low! - Bigger sacs easier to stay open |
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Air-water surface tension effect
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- 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! |
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Surfactant
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- 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 |
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4 advantages of surfactant
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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 |
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Respiratory distress syndrome
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- 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 |
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Exercise, rest vs. static pressure curve
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- Curve establishes max values
- You can work within the curve, but cannot exceed those values |
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Airway resistance factors - Ohm's Law
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- 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 |
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Bronchiole smooth mm. dilation factors
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- Sympathetic stimulation
- Epinephrine (β2 adrenergic receptors) - NO - relaxes mm - Increased PCO2 in small airways - Decreased PO2 in small airways |
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Bronchiole smooth mm. Constriction factors
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- Parasympathetic stimulation (+ mucus secretion)
- Acetylcholine - Leukotriene - Histamine - Thromboxane A2 - α-adrenergic agonists - Decreased PCO2 in small airways |
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Parasympathetic vs. sympathetic influence strength
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-Trachea -> alveoli under control of autonomics
- Parasympathetic tends to be stronger! |
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Dynamic airway compression
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- 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 |
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Emphysema dynamic compression complication
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- 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 |
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Flow volume relationship curve
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- 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! |
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Obstructive emphysema/COPD flow-volume relationship
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- 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 |
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Restrictive Fibrotic disease flow-volume relationship
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- 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 |
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Work of breathing (area of PV-loops)
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- Sum of resistive work + elastic work
- Mostly related to muscle flexing and inherent elastic recoil |
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Efficiency of breathing
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- 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 |