page370-379 Flashcards
Total lung volume (TLV) =
IRV + TV + ERV + RV.
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Active process of inspiration
■ Requires muscular effort.
■ Mostly diaphragm at rest.
■ Intercostals used on exertion (accessory muscles).
Inspiratory effort causes:
■ ↓ intrapleural pressure.
■ ↓ alveolar pressure.
■ Pressure gradient from mouth to alveoli.
■ Gas flow down pressure gradient.
Expiration
■ Passive process (usually).
■ Due to lung recoil.
Relaxation of inspiratory muscles causes:
■ ↑ intrapleural pressure (intrapleural pressure becomes less negative).
■ ↑ alveolar pressure.
■ Pressure gradient from alveoli to mouth.
■ Gas flow down pressure gradient
FUNCTIONAL RESIDUAL CAPACITY
■ FRC = At rest.
■ Balance between inspiratory and expiratory forces.
■ Collapsing forces = Expanding forces.
■ Muscle contraction is needed to ↑ or ↓ lung volume from FRC.
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ALVEOLAR PRESSURE
■ Atmospheric pressure in resting position.
■ 760 mm Hg (at FRC). Palv = 0 mm Hg
INTRAPLEURAL PRESSURE
■ Pressure within pleural cavity between outer surface lung and inner surface
chest cavity.
■ 756 mm Hg (at FRC) (< atomospheric pressure). Ppl = −34 mm Hg
ALVEOLAR VENTILATION
■ Amount of gas that reaches the functional respiratory units (ie, alveoli) per
minute.
■ Amount of atmospheric air that can undergo gas exchange.
■ Good gauge for breathing effectiveness
VA=RR °ø (TV − dead space air volume).
RESPIRATORY RATE
■ Breaths per minute.
TIDAL VOLUME
■ TV = amount of air brought into/out of lungs with a normal breath.
■ 500 mL.
■ 350 mL used for alveolar ventilation.
■ 150 mL dead space (fixed due to conducting airways).
tidal vol
DEAD SPACE
■ VD = Volume of air not participating in gas exchange
Anatomic dead space.
■ Typically 150 mL.
■ Volume of nonventilated gas in airways.
■ No gas exchange occurs within the nasal passages, pharynx, trachea,
bronchi.
Physiologic dead space.
■ Due to alveoli that are ventilated but not perfused.
■ Usually insignificant, unless there is disease.
TV °* RR = .
VT
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Conducting zone airways contain mucous-secreting cells:
■ Goblet cells
■ Mucous cells
■ The epithelium is pseudostratified ciliated columnar.
Respiratory zone, alveolar wall has:
■ Type I epithelial cells
■ Type II epithelial cells ↓ pneumocytes
■ Produce surfactant
O2 uptake, CO2 elimination by the blood
■ O2 diffusion (alveolus → blood)
■ CO2 diffusion (alveolus ← blood)
Partial pressure gradient
■xxx difference between two sides of the membrane.
■ Diffusion occurs from high to low pressure (down the gradient).
■ PAyyy > Pzzz (alveolar > pulmonary arterial); O2 diffuses from
alveoli →aaaa
■ PaCO2 xxxx > PACO2 in xxxx; CO2 diffuses from blood →alveoli
Partial pressure gradient
■ Pressure difference between two sides of the membrane.
■ Diffusion occurs from high to low pressure (down the gradient).
■ PACO2 > PaO2 (alveolar > pulmonary arterial); O2 diffuses from
alveoli → blood.
■ PaCO2 blood > PACO2 in alveolus; CO2 diffuses from blood →alveoli
Gas solubility
■ Number of molecules dissolved in the liquid aa partial pressure of gas bb.
■ Solubility is an xxx property of the gas.
■ Solubility xx as partial pressure yy (Henry’s law). CO2 more zzz
than O2.
Gas solubility
■ Number of molecules dissolved in the liquid ↑ partial pressure of gas ↑.
■ Solubility is an intrinsic property of the gas.
■ Solubility ↑ as partial pressure ↑ (Henry’s law). CO2 more soluble
than O2.
Thickness of membrane (alveolus)
■ Rate of diffusion is xxxl to the diffusion distance.
■yy diffusion as zz alveolar thickness
Thickness of membrane (alveolus)
■ Rate of diffusion is inversely proportional to the diffusion distance.
■ ↑ diffusion as ↓ alveolar thickness
Alveolar surface area
■ Rate of diffusion is xxxx to surface area.
■ x surface area (eg, emphysema), y diffusion, z gas exchange
Alveolar surface area
■ Rate of diffusion is directly proportional to surface area.
■ ↓ surface area (eg, emphysema), ↓ diffusion, ↓ gas exchange
Hemoglobin
Carries O2 from lungs to tissues.
■ Carries CO2 from tissues to lungs.
Normally:
■xx saturated with O2 in lungs (arterial).
■ yy saturated in tissues (venous).
■ PaO2 = 40 mm Hg
■ zz million Hb molecules in each erythrocyte.
■ Synthesis begins in xxxx
hemoglbin
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Bohr Effect
Curve shifts right (→) in an acidic environment (↓pH) to help unload O2 to
the tissues.
■ Hb has decreased affinity for O2 when pH ↓.
■ H+’s ↑ as pH ↓.
■ The H+’s bond more actively to deoxygenated Hb than to oxyhemoglobin.
■ As CO2 ↑, pH ↓, curve shifts to the right (→).
Haldane Effect
■ Oxygen tension affects the affinity of Hb for CO2.
■ High oxygen tension—lungs:
■ Hb ↑ O2 binding; ↓ affinity for CO2.
■ CO2 released in the lungs (as ↑ O2–Hb).
Low oxygen tension—tissues:
■ Hb ↓ O2 binding; ↑ affinity for CO2 (binds H+, forms carbamino compounds).
■ CO2 uptake in the tissues (as ↓ O2–Hb).
Amount of O2 in Blood
■ Dissolved O2 + O2 bound to Hb.
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OXYGEN CONTENT
■ Total amount of oxygen carried in blood (PO2 + O2–Hb).
■ Determined mostly by the amount of hemoglobin and its saturation.
■ Amount of hemoglobin is affected by anemia (production, loss, or
destruction).
■ The more hemoglobin in blood, the more O2 that can be carried.
OXYGEN SATURATION
■ The amount of Hb saturated with O2.
■ Corresponds to O2–Hb curve.
■ Determined by:
■ PO2 (important; see table corresponding SaO2 : PO2).
■ O2 affinity of Hb altered by:
■ Changes in Hb molecule.
■ Intrinsic (hemoglobinopathies).
■ Extrinsic (eg, changes in pH, PCO2, temperature, etc.).
■ Competition for Hb binding (eg, CO poisoning).
O2 saturation determined by
NORMAL VALUES
■ Oxygen content (per 1 g Hb) = 1.34 mL of O2.
■ Hemoglobin concentration = ~15 g/dL.
■ Women: 12–16 g/dL.
■ Women have ↓ Hb concentrations than men
■ Men: 14–18 g/dL.
■ Infants: 14–20 g/dL.
■ Oxygen concentration = ~20 g-mL/dL (or 15 g/dL °ø 1.34 mL)—just 20.1 mL.
OXYGEN -CARRYING CAPACITY OF BLOOD
Depends on:
■ Oxygenation (from lungs).
■ FiO2.
■ PaO2 (gradient).
■ Effective gas exchange (no dead space or shunt
Hb concentration.
■ Hb avidity for oxygen.
■ CO.
■ Left shift of curve.
OXYGEN -CARRYING CAPACITY OF BLOOD
Perfusion.
■ Cardiac function.
■ Patency of vessels.
■ Adequacy of forward flow
OXYGEN -CARRYING CAPACITY OF BLOOD
Carbon Dioxide
See Figure 13–3.
■ Carbon dioxide (CO2) is carried in blood as:
■ Bicarbonate in serum (most).
■ Bicarbonate in RBC.
■ Carbaminohemoglobin.
■ CO2
+ NH2 group of Heme (not Fe2+ of Heme like O2 or CO).
■ Dissolved in blood (PCO2).
CHLORIDE SHIFT
■ Bicarbonate carried in serum is generated within the RBC.
■ It is transported to the serum in exchange for Cl−.
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Hypoxemia
■ Low oxygen level in blood (PO2 <80).
■ Causes of hypoxemia:
■ ↓ FiO2
■ Hypoventilation
■ V/Q mismatch
■ Shunt
■ Diffusion limitation
HYPOXIC VASOCONSTRICTION
■ Mechanism to minimize V/Q mismatch.
Shunt (air cannot get into alveolus).
■ Peanut occluding bronchiole (child).
■ Atelectasis.
Blood perfuses past the alveolus.
Blood perfuses past the alveolus.
■ No/minimal gas exchange occurs.
■ Response is vasoconstriction of the pulmonary vasculature in that region.
■ ↓ amount of blood going to nonventilated segment of lung.
If this vasoconstriction secondary to hypoxia exists for long enough,
If this vasoconstriction secondary to hypoxia exists for long enough,
■ Get permanent secondary changes to the pulmonary vasculature.
■ Pulmonary hypertension.
■ Only place in body to constrict, not dilate
Hypercarbia
■ ↑ CO2 in blood.
■ Occurs because of either or both of the following:
■ ↑ CO2 production.
■ ↓ VA (alveolar ventilation)—hypoventilation.
■ Compensation: hyperventilation.
■ Headache.
■ Confusion.
■ Coma.
Hyperventilation
■ ↑ rate and depth of breathing exceeding requirement for O2 delivery and
CO2 removal
■ Stimulated by:
■ ↓ PO2 in normal circumstances (non-COPD).
■ Chemoreceptor stimulation (↑CO2, ↑H+, ↓PO2).
■ Effect on brain—emotional situations, anxiety.
Hyperventilation
Results in:
■ ↓ CO2: hypocapnia (hypocarbia).
■ Respiratory alkalosis (pH ↑).
■ ↑cerebrovascular resistance.
■ ↓ cerebral blood flow.
■ ↑PO2 (and arterial oxygen concentration
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SYMPTOMS OF HYPERVENTILATION
■ Related to ↓ cerebral blood flow.
■ Example: anxiety → ↑ventilation → ↓ CO2 → ↓ cerebral blood flow →
neurologic symptoms:
■ Faintness/dizziness.
■ Blurred vision.
■ Also experience sensation of:
■ Suffocation.
■ Chest tightness.
Terminate hyperventilation attack must:.
■ ↑ PCO2.
■ Breathing in and out of a plastic bag.
■ Inhale 5% CO2 mixture
Respiratory Drive
■ Based on arterial PCO2, specifically H+.
■ The H+ (derived from CO2) that acts at central chemoreceptors (medulla).
PATHWAY
■ As ↑ PCO2 → CO2 diffuses from cerebral blood vessels into CSF → carbonic
acid (H2CO3) is formed → dissociates into bicarbonate (HCO3
−)
and protons (H+s) → these protons (H+s) stimulate the central chemoreceptors→↑
ventilation.
■ CO2 can diffuse from the blood vessels into CSF across the BBB because
it is nonpolar.
↑RESPIRATORY DRIVE
↑RESPIRATORY DRIVE
■ Central chemoreceptors (medulla)
■ ↑ PCO2 (as its byproduct, H+, in CSF or brain interstitial fluid sensed
in medulla).
■ Peripheral chemoreceptors (carotid or aortic bodies)
■ ↑ H+ (in blood or brain interstitial fluid).
■ ↓ PO2 (in blood)(<60 mm Hg
FUNCTION OF RESPIRATORY REGULATION
■ Keep alveolar PCO2 stable (prevent hypercarbia or hypocarbia).
■ Buffer acid–base changes.
■ Prevent hypoxemia (↑ PO2 when it falls).
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