Respiratory Function & Physiology (8/19-26) Flashcards
Transmural pressure is a measure of what property of the lung?
elastic recoil of the lung aka distending pressure Ptm = Palv-Ppl
Pressure gradient for air flow is generated by these three factors:
1) contraction of inspiratory muscles 2) lung elastic recoil 3) contraction of expiratory muscles
Elastic recoil of the lung is determined by:
1) intrinsic elasticity of lung fibrous networks 2) tension generated at the air:liquid interface
How is elastic recoil different in lungs with emphysema vs lungs with interstitial lung disease?
Emphysema: decreased elastic recoil - causes flow to cease sooner, which increases residual volume ILD: increase
How is tension different in lungs with respiratory distress vs lungs filled with saline?
RDS: increase tension due to surfactant deficiency Saline: decrease
How does compliance change with volume? How does compliance change if the surfactant was removed?
reciprocal relationship - as lung volume increases, compliance decreases remove surfactant: lung compliance decreases
Define FRC
point at which the + elastic recoil of the lung = - elastic recoil of the rib cage. in other words: the NET elastic recoil = 0
Why does resistance decrease as lung volume increases?
Resistance is a function of the TOTAL cross sectional area available for flow. Thus, the resistance decreases because the total cross-sectional area available for flow increases distally.
What is the difference between passive vs forced expiration?
passive = occurs at the end of normal inspiration, driven by (+) alveolar pressure (elastic recoil) forced = occurs when alveolar pressure + pleural pressure increase by equal amounts
What is flow limitation?
point at which increases in expiratory effort does NOT equal increases in expiratory flow.
What is Pcrit? What happens when: Pcrit 0?
critical transmural pressure at which the airway collapses Pcrit 0 = inherent TENDENCY to collapse
What are some factors that will decrease airway flow (Vdot)?
decreased elastic recoil (ex: emphysema) increased Pcrit (ex: asthma) increase upstream resistance (ex: swelling/mucus)
What is air trapping? What happens to RV when there is air trapping?
occurs when air can’t get out of the lungs despite maximal expiratory effort. Results in an increase in residual volume
Draw a respirogram and label IRV, ERV, FRC, VT, RV, VC, and TLC
see image
How is maximal expiratory effort measured? (2) What are some of the dependent factors of these two measurements?
FEV1 = VOLUME of air produced in the first second; depends on airway resistance, recoil, and volume of lung FEF25-75 = average flow rate measured over the middle half of vital capacity; depends on how fully the lungs are inflated and whether the lung has fully deflated prior to the next inspiration
What is the FEV1/FVC ratio a measure of?
proportion of a person’s vital capacity that they are able to expire in the FIRST second of a MAXIMAL expiratory effort. used to diagnose obstructive vs restrictive defects
The rate at which the lungs deflate depends on:
resistance and elastic recoil (which depends on the properties of the lungs and volume of inflation)
What are examples in which FEF25/75 increase? decrease?
increase FEF25/75: - increase stiffness of the airway (fibrosis) results in a FASTER collapsing decrease FEF25/75: - decrease elastic recoil (emphysema) - decrease lung volume (lung disease) - increase airway resistance (bronchitis, asthma, tumor)
What are examples in which FEV1 increase? decrease?
Increase FEV1: - scarring/fibrosis of the lungs increases elastic recoil pressure (but actually, it decreases it because the inspiratory muscles can’t inflate the lung properly, so actually get decrease in FEV1)
Decrease FEV1: - scarring/stiffening of the lungs makes it so that the inspiratory muscles cannot inflate the lungs as well - obstructive defect
How does pulmonary fibrosis affect FEV1?
with pulmonary fibrosis, there is an increased stiffening of the lungs and therefore the lung can’t inflate to its normal value, which decreases FEV1, but the stiffening of the lung increases the elastic recoil pressure, which increases FEV1. Since volume predominates, the FEV1 decreases.
What is an OBSTRUCTIVE defect?
What causes it?
What are some examples?
What characterizes an obstructive defect?
lungs can’t empty properly (decrease in expiratory flow rate). caused by pathologies that increase RESISTANCE (airway narrowing), which causes less air to come out, thus may lead to air trapping (increase RV)
Examples: COPD, asthma, Cystic fibrosis
Characterized by DECREASED FEV1/FVC ratio
What is a RESTRICTIVE defect?
What causes it?
What are some examples?
What characterizes an restrictive defect?
lungs can’t fill properly caused by WEAK inspiratory muscles or FIBROSIS (results in decreased air intake, thus decrease VC)
examples: Interstitial lung disease, Pleural Effusions
Characterized by decreased TLC and normal/increased FEV1/FVC ratio
What is a COMBINED defect? What are some examples? What characterizes an obstructive defect?
lungs can’t fill properly and can’t empty properly..shit. examples: COPD or pneumoectomy characterized by a decrease in FEV1, FVC, FEV1/FVC ratio
How does TLC change with: 1) neuromuscular dz? 2) emphysema? 3) increased inspiratory muscle function?
1) neuromuscular dz - decrease TLC 2) emphysema - increase TLC (due to increase lung compliance, and less elastic recoil) 3) increased inspiratory muscle function - decrease CHANGE in TLC because at higher lung volumes, there is decrease compliance (a larger pressure change results in little volume change)
How does FRC change with: 1) pulmonary fibrosis? 2) emphysema?
1) pulmonary fibrosis - decrease FRC due to decreased lung compliance (more CW component) 2) emphysema - increase FRC due to increased lung compliance (more lung component) see image
How does RV change with: 1) asthma? 2) COPD? 3) emphysema? 4) neuromuscular disease? 5) Interstitial Lung Disease (ILD)
1) asthma - increase RV due to weak expiratory m. 2) COPD - increase RV due to weak expiratory m. 3) emphysema - increase RV (increased compliance 4) neuromuscular disease - increase RV 5) ILD - decrease RV (decreased compliance)
What is a restrictive ventilatory defect? What are some examples that cause restrictive ventilatory defects?
pathology in which EXPANSION of the lung is restricted/limited (results in decreased TLC) due to neuromuscular disease, chest wall problems, pleural disease, loss of lung, interstitial lung disease
What is DLCO?
measure of CO transferred across the lung from the inspired gas to the blood stream.
During inspiration, inspired air mixes with alveolar air via these two processes:
convection + diffusion
Alveolar O2 (PAO2) is determined by these two factors: What two factors alter the efficacy of alveolar ventilation?
Alveolar PO2 = alveolar ventilation + metabolic rate Efficacy = VQ mismatch + Shunting
Failure or reduced gas equilibration between alveolus (A) and arterial blood (a) is due to: Both of these result in:
NO contact time (SHUNT) or DECREASED contact time (VQ mismatch) between air and blood. This can be due to - increased CO/exercise - thickened alveolar membrane Both of these result in HYPOXEMIA
T/F Shunts may be corrected by increasing FiO2 T/F VQ mismatch may be corrected by increasing FiO2
SHUNTS: False dude. True shunts may not be completely corrected by raising inspired PO2 since the shunted blood does not come into contact with the high alveolar PO2 VQ MISMATCH: True dat. Increasing FiO2 will increase PO2 of blood in regions of low ventilation
Which gas (O2 or CO2) is most affected by shunts?
O2 is drastically decreased by shunting. CO2 is not really affected by shunting - get only a minor increase with a large shunt
How do you calculate the Aa difference? What is the normal Aa difference in adults? elderly? How do you calculate PiO2?
Aa = (PiO2 - 1.2PaCO2) - PaO2 Adults normal Aa = 5-10mmHg Elderly normal Aa = higher PiO2 = 0.21 x (760-47) 0.21 = fraction of inspired air at RT 47 = VP of H2O at 37C, sea level
What are some of the mechanistic causes of hypoxemia? (4 biggies)
1) alveolar HYPOventilation 2) low PiO2 (altitude) 3) impaired pulmonary diffusion (reduced contact time) 4) shunt
In what situations do Aa difference increase?
1) normal aging 2) collapsed lung parenchyma (atelectasis) 3) shunt 4) pathology that decreases diffusion between capillary and alveolar air
What is the response of these factors to hypoventilation? Hyperventilation? CO2 H+ pH
Hypoventilation: CO2 = increase H+ = increase pH = decrease Hyperventilation: CO2 = decrease H+ = decrease pH = increase
What are normal values for: alveolar O2? arterial O2? CO2? HCO3?
alveolar O2 = 150 arterial O2 = 100 CO2 = 40 HCO3 = 24
How is respiratory alkalosis and acidosis compensated for? How is metabolic alkalosis and acidosis compensated for?
Respiratory alkalosis/acidosis = compensated for by RENAL excretion or retention of HCO3 (thus, an increase PCO2 -> Increase HCO3 retention and H+ excretion) Metabolic alkalosis/acidosis = compensated for by changes in VENTILATION (see 8/23 lecture for flow diagram)
T/F compensatory mechanisms returns the initial pH back to normal (7.4)
False - it returns it to a pH that is close to normal, but not exactly normal
How does temperature affect pH? A hypothermic person should have a higher or lower pH?
pH is inversely proportional to the temperature (increased temperature increases dissociation of H2O -> H+ OH-, thus decreases pH) Thus, a hypothermic person should have a higher pH
The respiratory system is comprised of the voluntary and reflex systems. What two neural tracts govern these systems? What do they form?
voluntary system - corticalspinal tract descends from the brain reflex system - reticulospinal tract descends from the CPG in medulla both systems emerge form the spinal cord to form the phrenic nerve (C3-5) and the intercostal-abdominal nerves (via thoracolumbar cord)
Lesion to the CST will result in what respiratory syndrome? Lesion to the CPG/medulla will result in what respiratory syndrome?
CST lesion: Locked-in syndrome - voluntary control is diminished, but reflex control is intact CPG/medulla lesion: Ondine’s curse - voluntary control is intact, but reflex control is impaired (most problematic during sleep, and results in profound hypoventilation)
Respiratory muscle energy consumption is determined by these two factors:
1) tension produced (increase tension = increase O2 consumption) 2) velocity of shortening of inspiratory muscles (increased velocity = increase O2 consumption)
What is the difference between active and resting tension?
Active tension: tension that develops in the PRESENCE of contractile function (length is proportional to force generated, but only up to a certain length) Resting tension: tension that develops in the ABSENCE of contractile function (length is proportional to force generated)
How does fatigue of respiratory muscles occur? What increases the energy requirements of respiratory muscles?
supply << demand Increased energy requirements during - increased ventilation - stiff lungs (require more tension to be generated to inflate lungs) - airway obstruction - hyperinflation of the lungs
How does the radius of curvature (roc) of the diaphragm affect the amount of pressure that can be generated?
Small roc = small change in tension can generate a large pressure change Large roc = larger change in tension can only generate a small pressure change Flat (infinite) roc = changes in tension does not result in changes in pressure change (law of laplace: Pressure = tension/radius)
What are the two mechanistic forces that govern how diaphragm and ribs moves during inspiration/expiration?
1) insertional forces: costal fibers contraction lifts the lower portion of the diaphragm (insertion points) upwards, thus elevating the ribs in response 2) zone of apposition force: diaphragm fibers that are directly opposed to the ribcage contract and cause the diaphragm to descend into the abdomen, thus the rib cage pushes outwards Both serve to increase the thorax size, resulting in NEGATIVE pleural pressure, and air flow into the lungs.
How does the diaphragm of a COPD patient look like? What is this indicative of in terms of how much pressure it can generate?
COPD patients tend to have a flattened diaphragm. Since the radius of curvature is infinite, any changes in muscle tension would not result in change intrathoracic/abdominal pressure. As the flattened diaphragm contracts, the lower costal margins are pulled INwards, resulting in a Hoover’s sign.
What is Hoover’s sign? In what patients would you normally see a Hoover’s sign?
As the flattened diaphragm contracts, the lower costal margins are pulled INwards, resulting in a Hoover’s sign. This is normally observed in patients with hyper-inflated lungs.
What happens when there is unilateral/bilateral paralysis of the diaphragm? What causes it? When is this most problematic? How do you treat this?
intercostal + accessory muscles are recruited to help with inspiration; the flaccid diaphragm + abdominal contents move upwards upon inspiration (though the problem is minimized because of gravity). Cause: Unilateral: trauma, tumor, idiopathic Bilateral: neuromuscular disease (ALS, polio, Guillain-Barre) Problematic: supine position, swimming pool (compression) Treatments: 1) ventilatory support 2) plication - useful for unilateral paralysis of the diaphragm. Procedure pulls the diaphragm downwards and allows for diaphragm to move so that it can expand better and improve ventilation
Which 3 muscles are important for inspiration? (3) What other muscles of respiration aka “accessory muscles”?
impt: 1) diaphragm 2,3) intercostal + scalene muscles = both expand and stabilize rib cage to prevent inward displacement that would otherwise occur with the reduced pleural pressure.
What other muscles of respiration aka “accessory muscles”? How do they function in inspiration and expiration?
Accessory muscles 1) SCM 2) Pectoralis 3) Serratus 4) Trapezius Inspiration - inactive/minimally active during normal respiration; recruited only when there is an INCREASED demand for ventilation Expiration - only when there is an INCREASED demand for ventilation; contraction of these muscles: 1) pull the lower ribcage down and inward 2) increase abdominal pressure, which forces the diaphragm upwards these two factors help to increase alveolar pressure, leading to greater expiratory flow.
What is quadriplegia inspiration?
malfunctioning/paralysis of the inspiratory muscles (intercostal + scalene muscles), which results in the rib cage moving INWARD during inspiration
Muscles of the upper airway help to maintain patency of the airway at points that are vulnerable to collapse. What happens if these muscles malfunction?
sleep apnea
What is MEP? MIP?
MIP reflects the strength of the diaphragm and other inspiratory muscles. MEP reflects the strength of the abdominal muscles and other expiratory muscles.
Describe how the following factors are affected in a patient with COPD/hyperinflation of the lungs: 1) length of inspiratory muscles 2) zone of apposition 3) diaphragm radius of curvature 4) threshold load
1) length of inspiratory muscles - shortened; generates less pressure with same amount of tension 2) zone of apposition - decreases 3) diaphragm radius of curvature - increases, so it is able to generate less pressure 4) threshold load - pt must overcome elastic recoil to initiate next breath
Describe how the following factors are affected in a patient with neuromuscular disease of the lungs: 1) respiratory muscle strength 2) vital capacity 3) TLC 4) residual volume 5) ventilation 6) cough
1) respiratory muscle strength - decreases 2) vital capacity - decreases 3) TLC - decreases 4) residual volume - increases due to air trapping 5) ventilation = HYPO due to weak respiratory muscles 6) cough - decreased due to weak respiratory muscles #2 and #3 = decreases = RESTRICTIVE DEFECT (can’t get air in properly) #5 and #6 = may lead to mucus retention, atelectasis and pneumonia
What are some examples of OBSTRUCTIVE lung disease? What are some examples of RESTRICTIVE lung disease?
OBSTRUCTIVE: Asthma, COPD (airway is narrowed, causing less air to come out) RESTRICTIVE Weak respiratory muscles fibrosis (restriction causes decreased air intake, which causes less air to come out)
