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1. Chronic Obstructive Pulmonary Disease 2. Asthma Attack

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?

A: normal
B: restrictive lung disease: ↓VC, ↓TLC, ↓RV, ↑FEV₁/FVC
C: obstructive lung disease: ↓VC, ↑TLC, ↑RV, ↓FEV₁/FVC, ↓FEF₂₅-₇₅

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