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Lung Physiology (Lung Volumes (Ventilation Rates (Minute ventilation = VT…

- - - - VD = VT x (PACO2 - PECO2)/PACO2
      - PACO2 = P CO2 of alveolar gas = P CO2 of arterial blood
      - PECO2 = P CO2 of expired gas
- - - - Most impt
      - Contracts, abdominal contents pushed down, ribs lifted up and out, increasing vol of thoracic cavity
    - - not used normally in quiet breathing
      - During exercise and respiratory distress
      - Extrernal IC more for support
  - - - Abdominal muscles to compress abdominal cavity, push diaphragm up
      - Internal IC: pull ribs down and in
  - - - Inflation of lungs (due to negative pressure outside of lungs, ie. intrapleural pressure) follows a different curve from deflation of lungs (expiration)
        
        called hysteresis, due to need to overcome surface tension forces when inflating the lungs
      - In mid-range of P, compliance is greatest, lungs most distensible
      - High P, compliance lowest
    - - Compliance of combined system is less than lungs or chest wall alone (slope)
      - At rest, where airway pressure in the combined system is same as atmospheric pressure (airway P = 0), corresponds to FRC (volume left aft passive expiration)
        
        At this pt, both push and pulling forces are equal and opposite, neither wants to collapse nore expand
      - Changes in lung compliance
        
        Could be due to disease (e.g. emphysema, where compliance increased and tendency for lung to collapse decreased -> seek new, higher FRC so two opposing forces can be balanced -> patient's chest become barrel shaped
        
        In Fibrosis, compliance decreased, tendency of lungs to collapse increase -> find new, lower FRC to balance opposing forces
  - - - T = surface tension
      - R = radius of alveolus
      - High collapsing P > harder to keep open > no surfactant, small alveoli have tendency to collapse
    - - Acts to reduce surface tension by disrupting intermolecular forces
      - Prevents alveoli from collapsing and increases compliance
      - Synthesized by type 2 alveolar cells, produce primarily phospholipid dipalmitoylphosphatidylcholine (DPPC)
      - Neonatal RDS: lack of surfactant, atelectasis, hypoxemia
  - - - major site of airway resitancec: medium-sized bronchi
      - Para (irritants, asthma): constrict airways, decrease radius, increase resistance
      - Symp: dilate airways via beta 2 receptors, increase radius, decrease R
      - Lung vol
        
        High lung vol: Decrease resistance due to greater traction on airways
        
        Low lung vol: less traction, increased airway R
        
        Hyperinflated lungs: press on vasculature, cause increased pulmonary vascular reistance
      - Viscosity
  - - - alveolar P = atmospheric P > Alveolar P said to be 0
      - Intrapleural P is negative (due to opposing forces of lungs trying to collapse and chest wall trying to expand)
      - Lung Vol is FRC
    - - Alveolar P decreases due to expansion
      - Intrapleural P more negative as lungs expansion causes an increase in elastic recoil strength
      - Lung Vol increase by VT
    - - Alveolar P greater than Atmospheric P (+ve)
      - Intrapleural reutrns to resting value
        (but during forced expiration, could become positive, and this positive pressure could block airways, making expiration more difficult:
        
        Dynamic compression, higher intrapleural pressure than alveolar pressure, compressing airway)
      - COPD use pursed liips to increase P in airways and prevent in from collapsing due to higher intrapleural P
- - - - Alveolar P > arterial > venous
      - High alveolar P may compress most capillaries, reduce blood flow
      - Can also occur if arterial BP decrease due to hemorrhage
    - - Arerial > alveolar > venous
      - Blood flow driven by difference between arterial P and alveolar P
    - - arterial > venous > alveolar
      - blood flow driven by difference between arterial and venous P
    - - e.g. during pulmonary embolism, more anatomical deadspace, higher proportion of zone 1 (more dead space area) than zone 3 (more perfused areas)
  - - - tetralogy of fallot
      - decrease in arterial PO2 due to mixture of venous blood with arterial blood
    - - more common
      - Usually congenital abnormalities (e.g. PDA)
      - Do not decrease arterial PO2, but increases PO2 in right side of heart
- - - - proportional to diffusion coefficient and surface area of gasesous exchange, inversely proportional to thickness
      - Measured with CO
      - Increases during exercise as there are more capillaries (increase surface are)
      - Decreases in emphysema (decrease surface area due to damage of tissues) and in fibrosis and pulmonary edema (increase thickness)
    - - Alveolar air: 100
      - Dry inspired air: 160
      - Humidified air: 150
      - Systemic arterial blood: 100
        
        Mixed Venous blood: 40
    - - Dry inspired air and humidified tracheal air: 0
      - Alveolar air: 40
      - Systemic arterial blood: 40
      - Mixed venous blood: 46
  - - - fast diffusion of gas over capillaries, such that only flow of blood will affect the speed of intake of gas into blood stream
      - N2O and O2 under normal conditions
    - - Gas does not equilibriate through the whole pulmonary capillary, partial pressure difference maintained, and is thus limited only by rate of diffusion
      - CO and O2 during strenuous exercise, or in fibrosis or emphysema, where diffusion of O2 is limited
- - - - Adults: a2b2
      - Fetal: a2y2
      - each subunit has one heme moiety (Fe2+) that binds to O2
      - Hemoglobin S: sickle cell, beta subunits affected
        
        In deoxygenated form, forms sickle shaped rods
      - O2 binding capacity of hemoglobin: maximym amt of O2 that can be bound, measured at 100% saturation
      - O2 content of blood = ([hemoglbin] x O2 binding capacity x % saturation) + dissolved O2
        
        Both bound and dissolved
        
        Depends on hemoglobin conc., O2 binding capacity of hemoglobin, PO2 and P50 of hemogobin
    - - S shaped (result of affinity and positive cooperativity)
      - Po@ of 100 mm Hg: 100% saturation
      - PO2 of 40 mm Hg: 75%
      - PO2 of 25 mm Hg: 50 % saturated (pressure at this level is the P50)
      - Changes in curve
        
        Shift to right
        
        Affinity decreased, increase unloading of O2 to tissues
        
        P50 increased
        
        Due to increase in PCO2 or decrease in pH, increase in temp, increase in 2,3-DPG conc. (adaptation to chronic hypoxemia)
        
        Shifts to left
        
        Affinity increased, P50 decreased, unloading of O2 to tissues more difficult
        
        Decrease PCO2, icnreased pH, decreased temp and decreased 2,3-DPG conc,
        
        HBF does not bind as strongly to 2,3-DPG, and thus has a higher affinity of O2
        
        CO poisoning: shifts curve to left as it increases affiniity for O2, but limits total saturation (decreases plateau) as some parts are taken by CO
  - - - Decrease in arterial PO2
        
        Caused by decrease in PAO2, diffusion defect, V/Q defects and right to left shunts
        
        A-a gradient = PAO2 (alveolar) - PaO2(arterial)
        
        Normal: 0-10 mmHg
        
        Increased (>10 mm Hg) does not equilibrate between alveolar gas and arterial blood (diffusion defect, V/Q defect and right to left shunt), making PAO2 > PaO2
        
        PAO2 =PIO2 - (PACO2/R)
        
        PIO2 = inspired PO2
        
        PACO2 = alveolar PCO2 = arterial PCO2 (measured in arterial blood)
        
        R = respiratory exchange ratio (CO2 production/O2 consumption)
    - - Decreased O2 delivery to tissues
        
        O2 delivery = cardiac output x O2 content of blood
      - Due to
        
        Decrease cardiac output
        
        Hypoxemia
        
        Anemia
        
        CO poisoning
        
        Cyanide poisoning (decrease O2 utilization by tissues)
      - Erhthropoietin (EPO)
        
        growth factor synthesized in kidneys in response to hypoxia
        
        Promotes development of RBC
- - - - Dorsal
        
        For inspiration, generate basic rhythm for breathing
        
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        vagus (peripheral chemoreceptors and mechanoreceptors in lung)
        
        glossopharyngeal: peripheral chemoreceptors
        
        Output: phrenic nerve to diaphragm
      - Ventral
        
        Primarily expiration
        
        Not active during normal quiet breathing, when it is passive
        
        activated during exercse
    - - lower pons
      - Stimulates inspiration (deep prolonged inspiratory gasp, apneusis)
    - - Upper pons
        
        Inhibits inspiration
    - - Voluntary control
      - Hypoventilation ( holding breath) is limited by increase in PCO2 and decrease in PO2
  - - - sensitive to pH
        
        CO2 can go through BBB as sit is lipid soluble
        
        Combines with H2O in CSF to increase [H+]
        
        Increase in [H+] acts directly on receptors, and stimulate breathing to decrease [H+] and thus PCO2
    - - Carotid at bifurcation of common carotid arteries
      - Aortic above and below arch
      - Decrease in arterial PO2
        
        increase breathing rate
      - Increase in arterial PCO2
        
        increase breathing rate
      - Increase in arterial [H+}
        
        stimulate carotid body peripheral chemoreceptors direclty
        
        Metabolic acidosis, breathing rate increased to increase CO2 release
    - - Lung stretch
        
        Located in smooth muscle of airways
        
        Lungs distended: decrease in breathing freq
      - Irritant receptors
        
        Between airway epithelial cells
        
        Stimulate by noxious substances
        
        Reflex
      - Juxtacapillary receptors
        
        In alveolar walls, close to capillaries
        
        Engorgement of pulmonary capillaries stimulates, cause rapid and shallow breathing
      - Joint and muscle receptors
        
        activated during movement of limbs
        
        Involved in early stimulation of breathing during exercise