Pulmonary Physiology Flashcards
Muscles contract and the volume of the thorax increases
Intrapleural pressure becomes more negative
Alveolar pressure decreases
Pressure gradient causes air to flow into the lung
Inspiration
Alveolar pressure becomes greater than atmospheric pressure
Elastic forces of the lung compress gas
Air flows out
Expiration
the total volume expired from maximum inspiration to maximum expiration
reduced in obstructive and restrictive disease
Forced Vital Capacity (FVC)
the maximum volume that can be expired in 1 second (not measured directly from flow volume loop)
reduced in restrictive disease
greatly reduced in obstructive disease
Forced Expiratory Volume in 1 second (FEV1)
the ratio of FEV1 to FVC expressed as a percentage
reduced in obstructive disease
no change in restrictive disease
FEV1/FVC
forced expiratory flow over the middle half of FVC
Thought to be influence more by diseases affecting the smaller airways
reduced in obstructive disease, no change in restrictive disease
Maximum mid-expiratory flow rate (MMEFR)
Forced Expiratory Flow 25-75 (FEF25-75)
highest expiratory flow achieved (only measured directly from flow/volume loop)
Peak expiratory flow rate (PEFR)
FEF max
vital capacity + residual volume
no change or increase in obstructive disease
decrease in restrictive disease
total lung capcity
inspiratory reserve volume + tidal volume + expiratory reserve volume
vital capacity
expiratory reserve volume + residual volume
functional residual capcity
tidal volume + inspiratory reserve volume
inspiratory capacity
Helium (inert) of a known concentration is added to a spirometer, the patient breathes until the He is dispersed throughout the air in the lungs and spirometer (equilibration)
Nitrogen washout: 100% O2 is added to a spirometer, the patient breathes until the nitrogen found in the RV is washed into the spirometer
C1 x V1 = C2 x (V1 + V2)
C1 = concentration of He in the spirometer at the start
V1 = volume of the spirometer
C2 = concentration of He in the spirometer after equilibration
V2 = FRC
Gas dilution method of measuring FRC
Patient lays in an airtight box and tries to inhale against a closed mouthpiece, this results in the expansion of the lungs, lung volume increases and the box pressure rises because gas volume decreases
P1V1 = P2 (V1-deltaV), solve for deltaV P1 = pressure in the box before inhalation P2 = pressure in the box after inhalation V1 = volume in the box before inhalation deltaV = change in the volume of the box with inhalation
P3V2 = P4(V2 + deltaV), solve for V2 P3 = mouth pressure before inhalation P4 = mouth pressure after inhalation deltaV = change in the volume of the box with inhalation V2 = FRC
Body plethysmography to measure FRC
change in volume divided by the change in pressure
compliance
measure of diffusion across the membrane
reduced by increased thickness and surface area, disease at the alveolar capillary membrane, V/Q mismatch, anemia, poor perfusion of the membrane and very low lung volumes
Diffusing capacity of the lung for carbon monoxide (DLCO)
PAO2 = FiO2 x (Patm - Pwater) - PaCO2/0.8
FiO2 = 0.21
Patm at sea level = 760 mmHg
P water = 47 mmHg
normal PaCO2 = 40 mmHg
Alveolar Gas Equation
DLO2 = rate of O2 uptake/(PAO2 - PaO2)
Diffusion across the alveolar membrane
Aa = PAO2 - PaO2
abnormal if > 30 mmHg
normal value = 10 mmHg
A-a gradient
AV = RR x (TV - dead space)
Alveolar ventilation
most superior portion of the lung V/Q >> 1 PA>Pa>Pv no flow does not normally exist
Zone 1
middle portion of the lung
V/Q > 1
Pa>PA>Pv
flow is proportional to Pa-PA
Zone 2
inferior portion of the lung
V/Q = 1
Pa>Pv>PA
flow is proportional to Pa-Pv
Zone 3
O2 delivery = CO x arterial O2 content
oxygen delivery
CaO2 = 1.39(Hb)(SO2) + 0.003(PO2)
oxygen bound to hemoglobin + oxygen dissolved in plasma
arterial O2 content
medullary respiratory center
Innervates inspiratory and expiratory muscles
Abdominal muscles, internal intercostal muscles, accessory muscles of inspiration
Involved in regulation of inspiratory force and voluntary expiration (active on forced expiration)
Active during heavy exercise and stress, no output during passive breathing
Nucleus ambiguous: inspiratory, upper airways
Nucleus retroambigualis
Rostral part: inspiratory, diaphragm and external intercostal muscles
Caudal part: expiratory, abdominal and internal intercostal muscles
Botzinger’s complex: expiratory, inhibits inspiratory neurons
Ventral respiratory group
medullary respiratory center
within the nucleus tractus solitarius
Active with each breath
Referred to as the pacesetting center or the inspiratory center
Output signals 12-15/minute; output for 1-2 seconds, pause for 2-3 seconds to allow expiration
Output signals diaphragm and external intercostal muscles
Dorsal Respiratory Group
pontine area that sends input to medulla
regulates rate and depth of respiration by cyclical inhibition of inspiration
Receives input from the cerebral cortex
Coordinates speed of inhalation and expiration
Sends inhibitory signals to the DRG
Involved in fine tuning of respiration rate
Pneumotactic center
pontine area that sends input to medulla
stimulates inspiration and is antagonized by the pneumotactic center
Promotes inspiration and controls depth of breathing
Signals to the DRG
Sends stimulatory impulses to the inspiratory area, inhibited by stretch receptors
Apneustic center
located at the ventrolateral surface of the medulla and respond indirectly to changes in PaCO2 allowing acute regulation of PaCO2
The most powerful stimulus known to influence the respiratory components of the medulla (DRG, VRG) is H+ in the CSF, an indirect measure of PaCO2
BBB is impermeable to HCO3- and H+ but CO2 diffuses readily into the CSF
Increased PaCO2 –> decrease CSF pH –> detection by central chemoreceptors –> increased RR
Decreased PaCO2 –> increased CSF pH –> detection by central chemoreceptors –> decreased ventilation
Central chemoreceptors
located in the carotid bodies and convey information to the respiratory center thereby affecting ventilation
Respond directly to changes in PaO2, PaCO2, and pH
Decreased PaO2, increased PaCO2, decreased pH –> increased ventilation
Changes in ventilation due to changes in PaO2 are small when PaO2 is above 60mmHg, very responsive if PaO2 falls below 60 mmHg
Once PaO2 falls below 30 mmHg, receptors become less effective
respond directly to PaCO2 but less responsive to changes
Affected by changes of H+ concentration in arterial blood independent of PaCO2 - Lactic acid, ketones
respond to hypoperfusion, nicotine, increased temperature, PaCO2
sensitive to PaO2 not total O2 content - PaO2 might be normal, represents the O2 free in the blood, but the O2 content might be low when hemoglobin is absent or nonfunctional as in chronic anemia, carbon monoxide poisoning, methemoglobinemia
activation –> increased ventilation, peripheral vasoconstriction, increased pulmonary vascular resistance, systemic arterial hypertension, tachycardia, increase in left ventricular performance
Peripheral chemoreceptors
respond to inflation of the lung and result in termination of inspiration
Afferent signals from receptors in airway smooth muscle (bronchi/bronchioles) and visceral pleura are transmitted through the vagus to the medulla where they inhibit the apneustic center terminating inspiration
Hering-Breuer reflex
More active in newborns than adults
pulmonary mechanoreceptors
in the large airways, respond to noxious gases and particular matter
Activation results in afferent signals to the CNS through the vagus causing reflexive bronchoconstriction and coughing
irritant receptors
in the alveoli, stimulated by hyperinflation of the lungs and various chemical stimuli and signaling results in reflexive, rapid, shallow breathing.
Small C fibers located in the small conducting airways, blood vessels, and interstitial tissue between the capillaries and the alveolar walls
Respond to alveolar inflammation, pulmonary capillary congestion/edema, serotonin/bradykinin, pulmonary emboli
Juxtacapillary receptors
stimulated during movement of joints and muscles, producing an increased respiratory rate.
Proprioreceptors play an important role in initiating and maintaining increased ventilation during exercise
Sudden pain causes apnea, prolonged pain causes hyperventilation
joint and muscle mechanoreceptors
deoxygenation of the blood increases the ability of Hb to carry CO2
O2 shifts the CO2 dissociation curve to the right
low PaO2 in tissues faciliates CO2 loading, high PaO2 in the lungs facilitates CO2 unloading
The Haldane Effect
oxygen consumption (VO2) / oxygen delivery (DO2)
at rest = 20%, may increase to 80% with exertion
extraction ratio
oxygen bound to Hb + oxygen dissolved in plasma
CaO2 = 1.39(Hb)(SaO2) + 0.003(PaO2)
arterial O2 content
