Respiratory Physiology Flashcards
Blood-gas interface
gas moves from high pressure to low pressure (diffusion)
oxygen moves from air to blood (PO2 in air 150 mmHg and PO2 in blood 40 mmHg)
CO2 moves from blood into air (PCO2 in air is negligible and PCO2 in blood is 46 mmHg)
Gas movement across barrier
Cross-sectional area
Inversely proportional to thickness of barrier
Capillary permeability
Conducting airways order
Trachea –> L and R bronchi –> lobar bronchi –> segmental bronchi –> terminal bronchioles
- anatomic dead space - 30% of inspiration
- not involved in gas exchange
Respiratory Zone
terminal bronchioles divide into respiratory bronchioles lined with alveoli
Airflow
initiated by expansion of thoracic cavity (diaphragm contracts and intercostals raise ribs)
- dust and particles will settle in terminal bronchioles
Compliance of lungs
lungs are VERY compliant = 500 ml/3 cm of water
LOW RESISTANCE
fibrosis of lungs impinges on expansion
Surface tension issue
alveoli should want to collapse into each other because of how small they are
SURFACTANT reduces the surface tension and prevents alveolar collapse
Inhaled particles
Nose filters
Mucous-ciliary elevator
Macrophages
Ventilation
how gas gets to alveoli
reduction in ventilation –> hypoxia (can be caused by drugs, brain damage, breathholding)
Tidal Volume
amount of air inspired and expired in routine breathing
500 mL
Total Lung Capacity
volume capacity of entire lung
7000 mL
Vital Capacity
Maximum volume of air that can be exhaled after max inspiration
6000 mL
Residual Volume
amount remaining in lungs after maximal expiration
~1500 mL
Functional Residual Capacity
amount remaining after typical exhalation
~2500 mL (measured by gas dilution technique)
Total Ventilation
amount of air entering and leaving lung each minute
about 30% is “filling” anatomic dead space
Alveolar Ventilation
actual gas amount that is exchanging in alveoli (70% of inhaled air)
Va = Vco2 / Pco2 x K
Measuring dead space volume
Breathe in 100% O2 –> expired gas plotted vs. N2 –> [N2] increases with expiration until reaching peak
- midpoint on graph is the volume of anatomic dead space
Physiologic Dead Space
Vd/Vt = (PAco2 - PEco2)/PAco2
Regional differences in ventilation
lower portions of lung are ventilated better than apex
Diffusion across blood-gas barrier
Pressure difference (driving force)
Surface area of barrier
Inversely related to thickness of barrier
Inversely related to molecular weight of molecule
Solubility of gas barrier
Diffusion capacity
volume of CO transferred/partial pressure difference
Barrier Resistance
partial pressure difference/volume of gas transferred
Diffusion limited process
CO reaction with blood (not dependent on flow, will diffuse no matter what)
RBC affinity is so great, there is little rise in blood partial pressure
Oxygen transfer can be diffusion limited in pulmonary diseases (thickening)
Perfusion limited process
Reaction of N2O with blood (doesn’t react with RBCs)
Partial pressure of N2O builds as blood goes through capillaries –> saturated 10% of way through capillary
Oxygen - perfusion limited, reaches equilibrium 1/3 of way through capillary (limited by blood flow)
Oxygen uptake in pulmonary capillaries
Blood enters with pO2 of 40 mmHg
Alveolar pO2 is 100 mmHg –> O2 moves from alveoli to capillary (saturated in .25 sec)
Measurement of diffusing capacity
use CO because its not perfusion limited
Diffusion capacity = Vco/(P1-P2)
RBC reaction rate
Takes 0.2 sec for O2 to combine with RBC
R = (P1-P2)/V
Pulmonary Circulation
pressures are relatively low (25/8 mmHg)
low resistance
pulmonary capillaries surrounded by alveoli (pressure on capillaries from alveoli)
Pulmonary artery resistance decreases with an increase in pulmonary artery pressure…..why?
Recruitment of additional capillaries
Distention of capillaries conducting blood
Expansion of lung also reduces resistance
NE, 5-HT, histamine –> increase resistance
ACh, Iso, prostacyclin –> reduce resistance
Fick Principle
O2 consumption = CO x (CAo2 - CVo2)
CO = VO2 / (CAo2 - CVo2)
Zone 1 of pulmonary blood flow
PA > Pa > Pv
doesn’t occur naturally –> but during hemorrhage or PPB
*alveoli “crushes” arteriole
Apex of lung
Zone 2 of pulmonary blood flow
Pa > PA > Pv
blood flow is determined by pressure differential between arteries and alveoli (venous doesn’t influence)
Apical regions of lungs
Zone 3 of pulmonary blood flow
Pa > Pv > PA
flow is dependent on arterial/venous pressure difference (normal situation)
occurs in midregion/base of lungs
Hypoxic pulmonary vasoconstriction
Alveolar hypoxia –> constriction of blood vessels perfusing that hypoxic region of lung
Independent of nerves
Involves inhibiting VG K+ channels –> depolarize membrane potential
Causes increase in [Ca] leading to vasoconstriction
Fluid movement out of vasculature
(Pcap – P int) – ∂ (πcap – πint)
- too much fluid movement out –> alveolar edema –> shortness of breath
Other functions of pulmonary circulation
Reservoir for blood
Filter blood -> clots (PE)
Metabolic functions of lung
Ang I –> Ang II by ACE
ACE inactivates bradykinin (side effect of ACE inhibitors in increased bradykinin and cough)
Synthesizes PGE and leukotrienes
Causes of hypoxia
hypoventilation
diffusion limitation
R –> L shunt
ventilation-perfusion mismatch
Hypoventilation
If O2 is not replenished fast enough, alveolar PO2 declines
Alveolar Gas Equation
PAo2 = PIo2 - [PAco2/R]
Hypoventilation by diffusion limitation
reducing area available for gas exchange or increasing the distance can cause hypoxia
Shunt
Occurs when not fully oxygenated blood mixes with fully oxygenated blood –> if you give 100% oxygen, it won’t correct the shunt because you will still have mixing
Ventilation-perfusion mismatch
Major cause of hypoxia in lung disease
PE = Tons of ventilation and no perfusion (V/Q = infinity) –> will equilibrate to room air
Airway obstruction = tons of perfusion but no ventilation (V/Q = 0) –> will equilibrate to blood gas
Areas of V/Q in lung
Apex = high V/Q Base = low V/Q
Oxygen in the blood
2 forms
- dissolved in blood (0.3 ml/dL at Po2 of 100 mmHg)
- Hemoglobin (20 ml/dL at Po2 of 100 mmHg)
O2 dissociation curve shifted to right by?
EXERCISE 1. Decreased pH 2. Increased O2 3. Increased temp 4. Increased 2,3-BPG O2 is released easier at the tissues
CO2 in blood
3 Forms
- Dissolved in blood (much more soluble than O2)
- Bicarbonate (involves CA) Major form
- Carbamino compounds (hemoglobin)
CO2 dissociation curve
much more linear than O2 curve, O2 curve affects CO2 curve
Inhalation
diaphragm contracts down and intercostals contract bringing ribs and sternum out –> increases intrathoracic volume
Expiration
typically passive (elastic recoil of lungs) active expiration --> abdominals and intercostals pull ribs downward
Elastic properties of lungs
inflation of lung occurs when pressure around lung becomes subatmospheric
Pressure differential is greater to inflate lung than to deflate it = hysteresis
Lung volume is never 0
Compliance of lung
Lungs are very compliant
Fibrotic disease –> reduced compliance
Emphysema –> increased compliance
Surface Tension of lungs
surfactant greatly reduces surface tension of lungs
- without it, smaller alveoli would empty into larger one and collapse
Regional Differences in Ventilation
intrapleural pressure is less at base than apex (less negative) –> weight of lung is pressing against the chest wall
Airway closure
Increased pressure associated with exhalation can result in collapse of airways –> occurs at low lung volumes
Airway disease patients –> purse lips to create back pressure to keep airways open so they don’t trap air
Lung-chest equilibrium
at functional residual capacity
Airway resistance
Smallest at large lung volumes, greatest at small lung volumes
determined by radius of airways –> resistance decreases in smaller airways because total cross-sectional area is greater than large airways
Medium-sized bronchi are main source of resistance
ACh effect on airway resistance
increases because ACh binds muscarinic receptors causing contraction
Epi effect on airway resistance
decreases because Epi binds beta-2 receptors causing dilation
Dynamic compression of airways
Rate of flow during expiration is rapid initially then falls
Drop in flow caused by compression of airway when thoracic volume is decreased to expel air
Flow determined by alveolar pressure - pleural pressure
Major feedback mechanism for control of ventilation?
central controller (pons and medulla) peripheral sensors (chemoreceptors) efferent mechanisms (nerves and muscles)
Central controller of ventilation
pons and medulla (cortex can override to increase/decrease breathing)
- respond to pH –> H+ stimulates respiration, alkalosis suppresses respiration
- H+ cannot cross BBB, so CO2 diffuses across and is converted by ca to H and HCO3
Peripheral Chemoreceptors
carotid bodies and aortic arch
sense hypoxia (increased firing rate as Po2 decreases)
carotids respond to decrease in pH
both carotid and aortic respond to hypercapnia (but not as much as central)
Most relevant controller of minute-minute ventilation?
CO2 –> each 1 mmHg increase in Pco2 causes 2-3 L increase in ventilation if O2 held constant
Response to hypoxia?
If CO2 is held constant, most individuals don’t respond to hypoxia until Po2 drops below 50 mmHg
EXCEPTIONS –> high altitude, COPD
Response to acidosis
low pH stimulates ventilation when Pco2 and Po2 are constant (sensed by carotid bodies)
Response to exercise
typically observe fall in Pco2 and rise in Po2 –> pH is stable during exercise until very intense levels
