Physiology Review Sheet
Physiology Review Sheet
Respiratory Physiology
I. Anatomy
a. Nose and mouth: warm, humidify, and filter air
b. conducting zone: trachea ( terminal bronchioles (1st 16 generations of branching)
i. aka anatomic dead space (no gas exchange occurs here)
ii. blood flow provides nutrition to smooth muscle of airways
iii. air moves by bulk flow here
c. transitional zone
i. between terminal and respiratory bronchioles
ii. thin walls, but still have smooth muscle
d. respiratory zone: respiratory bronchioles ( alveolar sacs
i. respiratory bronchioles: smooth muscle and some alveoli
ii. alveolar ducts: smooth muscle sphincters
iii. alveolar sacs
iv. gas exchange occurs here
v. velocity of air flow is low ( allows equilibration of gases, but also deposition of asbestos, dust, etc.
e. gases are exchanged by diffusion
i. very thin alveolar-capillary barrier
ii. highly soluble gases
iii. driving pressures present to move O2 and CO2
f. gas exchange interface (6 layers)
i. fluid layer of surfactant on inner surface of alveolus
ii. alveolar epithelium
iii. interstitial space (fluid-filled)
iv. capillary endothelium
v. plasma in capillaries
vi. RBC membrane
II. Lung Volumes and Capacities
a. overview
i. differ by age, gender, body type, and conditioning
ii. can be index of pulmonary function
iii. help distinguish obstructive v. restrictive lung disorders
b. total lung capacity: total volume of air in lungs when maximally inflated (TLC)
c. residual volume: volume of air in lungs after maximal expiration (RV)
i. differs with age and gender
ii. increases in elderly due to decreased elastic recoil of lung and mobility of chest wall
d. vital capacity: max volume of air that can be exhaled after maximal inspiration (VC)
e. tidal volume: volume of air inspired and expired with each normal breath (VT)
i. normally ~500 mL
ii. can increase during exercise to approach VC
f. inspiratory reserve volume: amount of air that can be inhaled after normal tidal inspiration (IRV)
g. expiratory reserve volume: amount of air that can be exhaled after normal tidal expiration (ERV)
h. functional residual capacity: volume of air in lungs at end of normal expiration (FRC = RV + ERV)
i. resting volume of lung
ii. inward elastic recoil of lung = outward elastic recoil of chest wall
iii. measure with helium dilution
i. types of lung diseases
i. restrictive
1. mechanical problems that alter elastic recoil of lung
2. e.g. pulmonary fibrosis
3. ↓ VC, TLC, FRC, & RV
ii. obstructive
1. blockage of airways
2. e.g. asthma, emphysema, and chronic bronchitis
3. ↑ FRC, RV, & TLC; ↓ VC
III. Ventilation: volume of gas inspired or expired per unit time
a. minute ventilation (VE)
i. volume of gas inspired and expired per minute
ii. VE = VT x f
b. dead space
i. anatomical: conducting zone ( no gas exchange (VD); ≈ body weight (lbs)
ii. physiologic: parts of lung that are ventilated, but not perfused; ↑ with emboli
iii. VT = VD + VA
c. alveolar ventilation (VA)
i. volume of air reaching gas exchange zone / minute
ii. VA = (VT – VD) x f
iii. regulated by . . .
1. VE
2. f (↑ with kyphoscoliosis and extreme obesity)
3. dead space (↑ with emphysema – physiologic)
IV. Gas properties
a. General gas law: PV = nRT
b. Dalton’s law: Pg = PT x fg; PT = P1 + P2 + P3 . . .
c. barometric pressure at sea level = 760 mmHg (↓ @ high altitude)
d. composition of dry room air: PATM = PN2 + PO2 + PCO2 + Pother
i. O2 = 21%
ii. N2 = 78%
iii. CO2 = 0.04%
iv. these % don’t change with barometric pressure
e. in lung
i. total pressure of gases in lung = ambient barometric pressure
ii. pressure of alveolar O2 is < barometric pressure because
1. water vapor dilutes air
a. partial pressure depends on temperature, not barometric pressure
b. normally 47 mmHg
2. CO2 dilutes air (40 mmHg)
3. PIO2 = FIO2 x (barometric pressure – 47)
4. alveolar air equation: PAO2 = (PIO2 – PACO2) / (R+F)
a. R = 0.8; respiratory exchange ratio
b. F = neglect
iii. regulation of PACO2 ( regulates PAO2 ( maintain constant alveolar and arterial blood gas levels
1. VCO2 = VA x FACO2
2. PACO2 = VCO2 / (VA x 0.863)
3. ↑ in metabolic rate ( ↑ VCO2 ( stimulate central and peripheral chemoreceptors ( ↑ VA ( constant levels of PaCO2 and PACO2
4. alveolar hypoventilation
a. PaCO2 > 45 mmHg
b. ventilation can’t cope with CO2 production ( PAO2 ↓
5. alveolar hyperventilation
a. PaCO2 < 35 mm Hg
b. ventilation exceeds CO2 production ( PAO2 ↑
c. e.g. ascent to altitude
V. Gas Exchange: Diffusion
a. diffusion limited
i. gas doesn’t equilibrate across alveolar-capillary barrier
ii. depends on physical properties of barrier
iii. e.g. CO
b. perfusion limited
i. gas equilibrates rapidly across alveolar-capillary barrier
ii. depends on blood flow
iii. e.g. NO
c. equilibration of O2
i. normally perfusion limited (equilibrates 1/3 of way through capillary)
ii. capillary transit time reduced with exercise ( still able to equilibrate normally
1. well-conditioned athletes may have even more reduced transit time ( O2 can’t equilibrate ( now diffusion limited
2. also problem if alveolar-capillary barrier thickens (e.g. interstitial fibrosis or edema) ( takes longer to equilibrate ( can’t do it with decreased transit time during exercise
d. equilibration of CO2
i. normally perfusion limited
ii. occurs at same rate as O2 (done by 1/3 of way through capillary)
iii. can become diffusion limited if alveolar-capillary membrane thickens severely
iv. note: CO2 is 24x more soluble and 20x faster at diffusing through water than O2 . . . still equilibrates at same time because
1. pressure gradient is lower for CO2 than O2
2. it takes time to convert bicarb and carbamino compounds to CO2
VI. Gas transport by blood
a. O2
i. physically dissolved
1. 0.3 mL of dissolved O2/ 100mL blood at 37°C with PO2 of 100 mmHg
2. very minor role of transport
ii. bound to Hb – 98% of O2 transported by blood
1. 4 molecules of O2 / molecule of Hb
2. combine with Fe, but leave in ferrous state (oxygenation)
iii. equations
1. O2 content: total amount of O2 carried in the blood
a. O2 dissolved + O2 on Hb
b. varies with Hb amount and PAO2
2. O2 capacity: maximum amount of O2 that can be carried by Hb
a. 1 g Hb fully loaded has 1.34 mL of O2
b. normal Hb in adults: 15g Hb/ 100 mL blood
c. O2 capacity = 1.34 mL O2/ g Hb x g Hb/100 mL blood
d. normal: 20.1 mL O2/ 100 mL blood
e. varies with Hb content
3. O2 saturation: amount of O2 actually combined with Hb / O2 capacity (x 100) = %HbO2
iv. Oxyhemoglobin dissociation curve
1. relationship between PaO2 and %HbO2
2. S shaped
a. steep in lower PaO2 range ( facilitate offloading in actively metabolizing tissues
b. flat at higher PaO2s ( allows reserve of O2 in event of ↓ PaO2 (down to ~ 60 mmHg)
3. factors affecting the curve
a. shift to R
i. ↑ temperature
ii. ↑ PCO2
iii. ↓ pH
b. shift to L
i. ↓ temp
ii. ↓ PCO2
iii. ↑ pH
c. CO2 and pH: Bohr effect (recall biochem)
d. 2,3-diphosphoglycerate (2,3-DPG or 2,3-BPG)
i. facilitates unloading of O2
ii. ↑ will shift curve to R
1. only occurs with high altitude hypoxia or exercise
2. takes a while to develop
iii. recall biochem for mechanism of action
e. anemia
i. ↓ [Hb] ( ↓ O2 carrying capacity
ii. still 97% saturated
iii. ↓ PaO2 ( R shift of curve ( unloading
iv. can produce lactic acidosis and ↑ 2,3-DPG ( help unload
f. CO
i. competes for O2 binding site on Hb (200x greater affinity)
ii. ↓ saturation of Hb
iii. L shift of curve ( CO doesn’t respond to ↓ PaO2 and stay bound ( cooperativity prevents unloading of O2 that is bound
b. CO2
i. physically dissolved
1. 24x more soluble
2. 5-10% transported like this
ii. bicarbonate
1. dissolved CO2 reacts with water ( carbonic acid ( HCO3- and H+ (plasma ( very slow)
2. dissolved CO2 + water (with carbonic anhydrase) ( carbonic acid ( HCO3- + H+ (RBC ( very fast) ( bicarb diffuses out of RBC into plasma and is transported
a. Cl- shift: Cl- in plasma move into RBC to maintain electric neutrality (aka Hamburger shift)
b. buffering of H+ on Hb ( lose intracelular negative charge ( replace with HCO3- and Cl- ( ↑ total # of ion sin cell ( ↑ osmotic pressure ( water moves into cell ( swells somewhat in venous blood (venous hct > arterial hct)
3. 60-65% transported this way
iii. carbamino compounds
1. CO2 reacts with terminal amines (esp on Hb)
2. 30% transported this way
iv. CO2 elimination by lungs
1. when CO2 is released from Hb in lungs ( H+ also dissociates ( reacts with HCO3- to reform CO2
2. CO2 dissociation curve
a. relates changes in CO2 content of whole blood to changes in blood PCO2
b. linear in physiologic PaCO2 range (40-50 mmHg)
c. ↓ O2 saturation of Hb ( L shift ( unsaturated Hb more readily binds H+ formed by dissociation of carbonic acid ( more CO2 transported as bicarbonate
VII. Pulmonary Circulation
a. low pressure, low resistance, high compliance
b. accepts entire cardiac output
c. pressures
i. pulmonary artery: 25/8 mmHg; MAP = 14 mmHg
ii. left atrium: 5 mmHg
iii. pulmonary pressure drop of 9 mmHg
iv. systemic pressure gradient is 10 x pulmonary
d. pulmonary vascular resistance
i. ~ 10 % of systemic ( very distensible
ii. intraalveolar vessels (pulmonary capillaries) – in between alveoli; due to ↑ quantity, overrides effect of extraalveolar vessel resistance changes
iii. extraalveolar vessels (larger arteries and veins) – tethered to elastic tissue of lung, exposed to intrapleural pressure
iv. lowest at FRC
v. changes are primarily passive
1. lung volume
a. low
i. intraalveolar – almost maximally open
ii. extraalveolar – constricted due to ↑ intrapleural pressure
b. high
i. intra: compressed by expanded alveoli
ii. extra: dilated due to intrapleural pressure becoming more subatmospheric and expansion of lung tissue dragging the vessels with them
2. recruitment and distension of capillaries
a. resistance ↓ as pressure in pulmonary circulation ↑
i. resting closed capillaries open (recruitment)
ii. if pressure continues to ↑, capillaries distend
b. if LA pressure ↑, ↑ pulmonary a. pressure will not help ↓ resistance because venous back pressure forces all capillaries in lungs to be open and distended
vi. active regulation of pulmonary vascular resistance
1. neural
a. sympathetic stimulation: vasoconstriction
b. parasympathetic stimulation: vasodilation
2. chemical
a. vasoconstrictors: AA, leukotrienes, TxA2, PG F2, AII, 5HT, epi, and NE
b. vasodilators: ACh, bradykinin, PGI2
3. alveolar hypoxia: ↓ PAO2 in restricted region of lung
a. vasoconstriction
b. shifts blood away from poorly ventilated area to areas of greater ventilation
e. gravity and pulmonary blood flow
i. blood flow ↓ from bottom of lung to top when upright ( due to gravity
1. gradient of vascular pressures (lowest at apex, higher at base; below inlet, arterial pressure > pulmonary artery pressure)
2. alveolar pressure is still constant
ii. top of lung
1. potential region where arterial, capillary, and venous pressure are all < alveolar pressure ( can’t occur because no blood would flow
a. pulmonary a. pressure ↓ (e.g. hemorrhage)
b. alveolar pressure ↑ (e.g. positive-pressure ventilation)
2. usually vascular pressure is > alveolar pressure ( flow occurs
3. highest lung volumes ( compress capillaries and ↑ resistance
iii. middle
1. arterial pressure >alveolar pressure > venous pressure
2. flow determined by difference between arterial and alveolar pressures (not arterial and venous)
3. recruitment can occur here
iv. bottom
1. arterial > venous > alveolar pressure
2. flow determined by difference between arterial and venous pressure
3. most capillaries open here, distention can occur, though
4. lowest lung volumes
v. when lying down – pressure gradients between top and bottom of lung disappear – blood flow is more homogeneous
VIII. Alveolar ventilation / perfusion ratio
a. mismatching VA/Q
i. normal
1. rate of ↓ of blood flow > rate of ↓ in ventilation (from base to apex)
a. top: V>Q ( ↑ VA/Q (↑ PO2 and ↓ PCO2)
b. bottom: Q>V ( ↓ VA/Q (↑ PCO2 and ↓ PO2)
c. range of 0.5 – 3+
d. contributes to A-a difference in PO2
2. physiologic shunt
a. blood enters arterial system without going through ventilated area ( supplies nutrients to airways or from coronary arteries
b. 2-5% of VR
c. causes small ↓ in PaO2
ii. hypoxemia: ↓ PaO2
1. causes
a. high altitude
i. ↓ barometric pressure ( ↓ PIO2 and PAO2
ii. equilibration: normal ( A-a: normal
iii. supplemental O2 raises PIO2 and PAO2 ( ↑ PaO2
b. hypoventilation
i. ↓ PAO2
ii. equilibration: normal ( A-a: normal
iii. supplemental O2 ( ↑ PAO2 ( ↑ PaO2
c. diffusion defect (eg fibrosis)
i. ↑ diffusion distance or ↓ surface area for diffusion
ii. equilibration impaired: PaO2 < PAO2 ( ↑ A-a
iii. supplemental O2 ( ↑ PAO2 and ↑ driving force for O2 diffusion ( ↑ PaO2
d. V/Q defect
i. dead space, ↑ V/Q, ↓ V/Q, and shunt
ii. ↑ V/Q: low Q ( contributes little to total blood flow
iii. ↓ V/Q: high Q and low V ( contributes blood that is not fully oxygenated ( dilutes fully oxygenated blood ( ↑ A-a
iv. supplemental O2 ( ↑ PO2 of low V/Q regions ( ↑ PaO2
e. shunt
i. R-L cardiac shunt, intrapulmonary
ii. blood bypasses alveoli and is not oxygenated
iii. dilutes fully oxygenated blood ( ↑ A-a
iv. supplemental O2 does NOT help because cannot change oxygenation of shunted blood which still dilutes ventilated blood
2. A-a gradient: difference between PAO2 and PaO2
a. A-a gradient = [PIO2 – (PACO2/R)] – PaO2
b. describes whether O2 has equilibrated (usually it does and A-a ≈0; ↑ with defect in equilibration)
iii. hypoxia: ↓ O2 delivery to tissues
1. causes
a. ↓ cardiac output
b. hypoxemia: PaO2 < 60 mmHg ( ↓ Hb saturation ( ↓ O2 content
c. anemia
d. CO poisoning (see above)
e. cyanide poisoning (cyanide interferes with O2 utilization in tissue)
b. effects of VA/Q inequality on blood gases
i. ↑ O2 from ↑ V/Q mixes with ↓ O2 from ↓ V/Q in blood ( lower than normal PaO2
ii. normal or subnormal PaCO2 ( linear dissociation curve
iii. disease with ↑ low V/Q units ( ↓ PaO2, ↑ PaCO2 ( stimulate chemoreceptors augments alveolar ventilation ( systemic blood is hypoxemic with ~ normal PaCO2 (cannot compensate, however, if disease is severe, and CO2 ↑
c. remember: alveolar hypoxia (and hypocapnia) cause arteriolar constriction ( helps compensate for V/Q mismatch
IX. Mechanics of respiration
a. muscles
i. inspiration:
1. diaphragm (phrenic n.) – major effector
2. external intercostals prevents chest muscles from being pulled in
3. accessory muscles elevate sternum: for exercise and hyperventilation
a. scalene
b. sternocleidomastoid
ii. expiration
1. usually passive
2. ↑ ventilation ( active
a. abdominal muscles
b. internal intercostals
b. pressures
i. atmospheric pressure: nose and mouth ( 0 cmH2O
ii. alveolar pressure: in alveoli
1. no air flow ( = atmospheric
2. inspiration: alveolar < atmospheric
3. expiration: alveolar > atmospheric
iii. intrapleural pressure: inside thoracid cavity between pleura
1. chest recoils out and lungs recoil in ( subatmospheric (-3 ( -5 cmH2O)
2. alveolar pressure always > intrapleural ( keeps lungs inflated
iv. transpulmonary pressure: difference between alveolar and intrapleural pressures( distending pressure of alveoli
v. pressure-volume relationships
1. zero air flow at end of expiration and before begin inspiration ( alveolar = atmospheric = 0 cmH2O; intrapleural = -5 cmH2O
2. inspiration begins ( ↑ thoracic volume ( intrapleural pressure becomes more negative ( lungs expand ( alveolar pressure ↓ (-1 cmH2O) ( air flows into lungs
3. when alveolar pressure again = atmospheric pressure ( air flow stops at VT
4. recoil of lungs ( intrapleural pressure becomes less negative ( lung volume ↓ until reaches FRC ( compresses alveoli ( ↑ alveolar pressure > atmospheric ( air flows out of lungs until reach 0 flow again
c. resistances to ventilation
i. elastic recoil of lung: compliance = unit change in lung volume / unit change in pressure (inverse of elasticity/recoil)
1. pressure volume curve of lungs alone is S shaped
a. low volume ( low compliance due to collapsed alveoli fluid film attraction (surface tension) that must be overcome (surfactant helps)
b. once open, lungs distend easily
c. at high volumes ( low compliance due to maximal distension ( physically can’t go further
2. altered compliance
a. emphysema: loss of lung tissue ( ↓ elasticity / ↑ compliance
b. fibrosis: CT infiltrates ( stiffer ( ↓ compliance
3. regional differences in ventilation
a. intrapleural pressure is not uniform around lungs ( full weight supported at apex ( pressure ↑ from top to bottom of lung (intrapleural pressure gradient)
b. more subatmospheric intrapleural pressure at apex ( ↑ transpulmonary pressure ( expanded alveoli ( distend less (↓ compliance)
4. specific compliance: consistent value when compliance is normalized to some lung volume (~ FRC) – across species and individuals; does change with disease affecting elasticity
5. pressure volume curve of lungs and chest wall
a. respiratory position: recoil of lungs exactly balanced by recoil of chest wall ( FRC ( relaxation pressure = 0
b. inspiration ( lungs stretch and chest wall relaxes ( relaxation pressure entirely due to lung recoil ( if keep going to max inspiration, stretch chest wall, too ( now fighting both recoil of lungs and wall
c. expiration ( lungs relax and chest wall is pulled in ( relaxation pressure due to chest wall recoil (etc.)
d. if recoil of one changes without changing the other, FRC changes and pressure curve shifts (eg emphysema, fibrosis)
6. surfactant: helps reduce surface tension (↑ compliance)
a. PL with DPPC and other lipids and proteins
b. DPPC orients perpendicularly to air-water interface so polar end is dissolved in water and fatty acids project into alveolar lumen
c. prevents alveolar collapse / preventing smaller alveoli from emptying into larger ones
d. keeps surface tension from drawing fluid into alveoli
ii. resistance to air flow in airways: most important factor
1. laminar flow v. turbulent flow
a. remember Poiselliue’s equation (forgive my spelling) and effect of change in radius
b. when flow is turbulent ( driving pressure must ↑ to keep flow constant
2. sites of resistance
a. nose and mouth
b. tracheobronchial tree: esp medium-sized segmental bronchi (↓ radius and cross-sectional area)
c. terminal bronchioles have least resistance
3. determinants of resistance
a. lung volume↑ ( ↓ resistance (esp top of lung)
i. pull airways open
ii. ↑ transmural pressure across airways ( ↑ radius
b. bronchial smooth muscle (β2 receptors)
i. adrenergic sympathetic stimulation ( relaxes
ii. cholinergic parasympathetic stimulation ( constricts
iii. irritants ( reflex constriction
1. smoke, histamine, dust, etc
2. stimulate rapidly adapting receptors
iv. emboli: constriction due to ↓ PACO2
iii. tissue resistance: sliding of lung tissues over each other ( minor
X. Components of respiratory system that control breathing
a. controllers: respiratory centers . . . functions
i. respiratory rhythmogenesis – central pattern generation
ii. neural translation of central rhythm to motor output that drives respiratory muscles
iii. adjustment of rhythm and motor function to meet metabolic demands (homeostasis)
iv. adjustment of rhythm and motor function to meet behavioral and voluntary function
v. efficiency
b. sensors: sense PCO2, PO2, pH, and lung inflation
c. effectors: diaphragm, upper airway dilators (prevent upper airways from collapsing during inspiration); use phrenic n., intercostal n, and cranial nerves
XI. Respiratory centers and neurogenesis of breathing
a. central automatic respiratory centers in brainstem
i. pneumotaxic center in rostral pons
1. parabrachialis medialis and Kolliker-Fuse nuclear complex
2. transmit information to inspiratory-off switch (IO-S): determines inspiratory time
3. receives info from pulmonary stretch receptors via vagus (also activate IO-S)
4. IO-S also activated by ↑ temp ( tachypnea ( dissipate heat
ii. apneustic center in caudal pons reticular formation: controls breathing pattern; periodically inhibited by vagal impulses and pneumotaxic impulses
iii. medullary centers (dorsal and ventral respiratory groups): spontaneous respiration
1. dorsal respiratory group: dorsomedial medulla at ventrolateral nucleus of tractus solitarii
a. inspiratory related neurons
b. project to cervical and thoracic anterior spinal motor neurons of phrenic and intercostal nerves
2. ventral respiratory group: diffusely through medulla and maybe up to cervical segment of spinal cord
a. Botzinger complex (near nucleus retrofacialis)
b. nucleus ambiguus and parambigualis
c. nucleus retroambigulais
d. inspiratory and expiratory neurons
e. expiratory neurons project to expiratory intercostal motor neurons
b. central pattern generator (location unknown)
i. magnitude: determines intensity of desire to inspire ( inspiratory flow rate
ii. duration: determines inspiratory time
iii. inspiratory air flow is a function of diaphragm and upper airway muscles
iv. inspiratory time is a function of IO-S (when on, stops inspiration)
v. also does expiration when needs to be active
c. peripheral arterial chemoreceptors
i. carotid bodies
1. between internal and external carotid arteries
2. very vascular
3. carotid sinus n. (branch of glossopharyngeal n.)
4. mediate hyperventilation in response to hypoxemia (if bodies are absent, hypoxemia can cause release of adenosine and depress the brain ( reversed partially by theophylline)
5. cells
a. type I: chemotransduction of changes in PaO2, H+, K+, and PaCO2 ( immediate response
b. type II
ii. aortic bodies: at arch of aorta
d. central chemoreceptors
i. ventrolateral medulla; at least 3 areas (M, S, and L)
ii. extracellular [H+] is main stimulus (during metabolic acidosis) ( changes ventilation to compensate
1. ↑ with acute ↑ in PaCO2 because CO2 crosses BBB and H+ dissociate from carbonic acid
2. sensitivity > peripheral chemoreceptors
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alveolar-capillary barrier
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