Case 25: Chronic Obstructive Pulmonary Disease (COPD)
Bernice Betweiler is a stupid old spinster, I mean seamstress, who won't stop smoking even tho no one likes her for it. So her lungs are as useless as she is.
1. Chronic bronchitis is associated w/ inflammation of airways & mucus hypersecretion, which ↑airway resistance. How does this explain her pulmonary function tests?
- ↑airway resistance → ↓airflow, esp. in expiration → expiratory phase compromised → air is trapped in lungs, so ↑residual volume (RV) & FRC → ↓vital capacity, b/c RV encroaches on it (greater fraction of TLC)
1. Her emphysema is associated w/ loss of alveolar-capillary units & ↓lung elasticity. How does this explain her pulmonary function tests?
- ↓elastance = ↑compliance → ↓elastic recoil force that drives air out of lungs, so expiration impaired - also, airways us. kept open in expiration by radial traction by elastic recoil forces → airways may collapse in expiration, trapping air in lungs → ↑RV, ↑FRC, ↓VC
2. How is her ↑anteroposterior (AP) chest diameter explained by the results of her pulmonary function tests?
- compromised expiratory functions → air trapping, ↑RV, ↑FRC → barrel-shaped chests to breathe at higher lung volumes, b/c need more volume to compromise that left to residual volume
3. Why does she have a decrease in arterial P(O₂) (Pa(O₂))?
- Pa(O₂) was 48 mmHg (instead of 100) - normal oxygenation of blood in lungs needs ventilation-perfusion matching - she had impaired ventilation, so ↓V/↑Q → part of pulm. blood flow not ventilated (oxygenated), mixed w/ oxygenated blood to ↓P(O₂) overall
4. Why is her % O₂ saturation decreased, & what are the implications for O₂ delivery to the tissues?
- ↓P(O₂) causes ↓saturation, according to O₂-Hb dissociation curve - O₂ content in blood largely depends on Hb binding (very little free O₂)
5. Her hemoglobin concentration is normal. If it had been decreased, would that have altered her Pa(O₂)? In what direction?
- ↓Hb → ↓O₂ content of blood (total amount decreased) - BUT Pa(O₂) is determined by *free*, unbound O₂, so NOT directly affected by Hb conc.
6. Why does she have an increase in arterial P(CO₂)?
= hypercapnia - b/c she could not eliminate all the CO₂ that her tissues made → unable to maintain alveolar ventilation, so retained CO₂
7. What acid-base disorder does she have, and what is the cause? Why is her HCO₃⁻ concentration increased?
- respiratory acidosis, secondary to CO₂ retention - pH = 6.1 + log ([HCO₃⁻]/(P(CO₂)x.03)) = 6.1 + log(34/(69x.03)) = 7.32 < 7.4 - ↑[HCO₃⁻] b/c chronic resp. acidosis → renal compensation (HCO₃⁻ reabsorption), so only small ↓pH even tho ↑CO₂ (H₂CO₃)
8. How does respiratory acidosis alter the delivery of O₂ to the tissues?
- ↑P(CO₂) & ↓pH → right shift in O₂-dissociation curve (Bohr effect) → for given P(O₂), ↓% Hb saturation, so unloads easier in tissue, BUT loads worse in lungs to begin with
Case 24?: Asthma attack
Mary is a hottie with a body. A body that can't breathe. She wheezes and can't exhale so well.
1. Is this primarily a restrictive or obstructive disorder? Why?
- obstructive disease: - airways narrow → ↑resistance to airflow into & out of lungs
2. Why is exhalation more difficult than inspiration in this person?
- ↑airway resistance → harder to expire - esp. in forced expiration, when intrapleural pressure is pos. & compresses airways → airways close prematurely in expiration → air trapping, air stays in lungs
3. Why is wheezing more prominent on exhalation?
- wheezes are sounds made when air is forced thru narrowed airways - In expiration, airways compress & close prematurely, instead of inspiration, so further narrowed and forced flow → more prominent sounds made on exhalation
4. Why is it easier to breathe at higher lung volume? Was she breathing at higher lung volume? Explain youself.
- ↑volume (↑radius) → ↓airflow resistance → ↑airflow, inspiration, breathing - she had ↑residual volume, which would try to compensate for ↓resistance from inflammation
5. Why does the bronchodilator (epinephrine) exaggerate the tachycardia?
- even tho she already showed tachycardia, heart rate ↑ more b/c β₂-AR's on heart pacemaker cells respond to epinephrine
6. An anticholinergic agent was also suggested as a possible nebulizer agent. How might this help the breathing problem?
- anticholinergic → ↓parasymp. pathways: → bronchodilation → ↓inflammation, ↓hyper-responsiveness to NO → does *not* induce tachycardia (lowers parasymp, doesn't activate symp)
7. How does breathing in an oxygen-helium gas mixture help patients who have an asthma attack?
- He:O₂ mixture has ρ/η = 0.31 (density over viscosity), much lower than pure O₂ (1.00) → low ρ/η → ↓turbulence → ↓airflow resistance → ↑airflow rate → delivers O₂ in same conc. as atmosphere
8. What is the residual volume before & after treatment with a bronchial smooth muscle dilator? Explain the changes.
TLC = VC + RV: → RV(before) = 6.82 - 2.5 = 4.32 L → RV(after) = 5.96 - 4.15 = 1.81 L - RV ↓ after bronchodilator b/c airways stay open, don't close early & trap air → more air expired, so ↓RV
9. Draw a normal flow-volume curve. How would it change with restrictive lung disease? Obstructive lung disease?