Chapter 22

Marieb & Hoehn (2019), p. 8181

We won’t do much anatomy here (left column; 22.1-22.3). Main issues (in lecture and

lab): mechanics and measurement of breathing (22.4-22.5), chemoreceptor control of ventilation (22.8), and a few respiratory disorders (22.10). *** Sections 22.6-22.7 were briefly covered in Chapter 17.

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Ch. 22: Test Question Templates

• Q1. If given an appropriate graph of volume of air in lung vs. time, estimate or calculate FEV₁/FVC ratio, FVC, residual volume, TLC, tidal volume, and/or minute ventilation.

• Example (from Winter 2019 exam):

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Q1. There are multiple ways to do this. The key is to choose a respiratory rate (breaths per minute) and a tidal volume (milliliters of air per breath) that, when multiplied together, give you 4000 mL air/minute. For example, I can draw a curve to show a tidal volume of 400 mL and a respiratory rate of 10 breaths/minute. Minute ventilation = (tidal volume)*(respiratory rate) = (400 mL air/breath)*(10 breaths/min) = 4000 mL

air/min.

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• Q2. If given two of the three values, calculate the third one: minute ventilation, respiratory rate, and tidal volume.

• Example: Lola takes 10 breaths per minute, and her minute ventilation is 6000 mL air per minute. What is her tidal volume?

• Q3. If given spirometry data and reference values,

determine whether the data are consistent with obstructive pulmonary disease, restrictive pulmonary disease, both, or neither.

• Example [from Fall 2019 test]: Rik is put through various pulmonary function tests. At time 0 in the table below, he begins deflating his fully inflated lungs as forcefully and rapidly as he can. You can assume that by the time of 4 seconds, he has reached his residual volume (RV). Based on these data, is he likely to have an obstructive lung disease? Explain your reasoning, citing any relevant math.

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Q2. MV = TV*RR. Here, 6000 mL/min = TV*(10 breaths/min). TV = 600 mL/breath. Q3. A FEV₁/FVC ratio of less than 0.8 (or 80%) suggests possible obstructive disease. Here FEV₁ = 4.5 minus 3.0 = 1.5 Liters, and FVC = 4.5 minus 1.5 = 3.0 Liters, so FEV₁/FVC = 1.5/3.0 = 0.5, or 50%. This low ratio is consistent with obstructive pulmonary disease.

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• Q4. Given changes to components of Fick’s Law of

Diffusion, say whether the diffusion rate will increase or decrease, or whether the information given is insufficient to determine this.

• Example: The conditions in a patient’s lungs change such that

the O₂ concentration gradient from lungs to pulmonary capillary blood increases, and the diffusion barrier thickness also

increases. What will be the net effect of these two changes on O₂ diffusion rate into the blood? Explain the direction of change

(increase or decrease), or explain why you can’t tell from the

information given.

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Q4. Example. According to Fick’s Law, a higher concentration gradient will increase the

diffusion rate, but a thicker diffusion barrier will decrease the diffusion rate. Since these

two changes have opposite effects on the diffusion rate, and since we don’t know the magnitude of either change (and thus whether one would “dominate” the other), the

information given is not enough to establish whether diffusion rate will increase or

decrease or neither.

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Functions of the Respiratory System

• 2 main ones

• Bulk flow in and out of lungs (Poiseuille) • Diffusion of O₂ and CO₂ (Fick)

S. Freeman et al. (2014), Figure 45.1 (like Marieb & Hoehn, Figure 22.1)

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2 functions (bulk flow and diffusion, both of which reflect flow down a gradient

(pressure and concentration, respectively). We’ll spend more time here on bulk flow.

You already understand that bulk flow depends on a pressure gradient, but understanding how that works in the lungs is not trivial. *** A common misconception:

if CO₂ leaves the lungs, that “leaves more room” for O₂ and vice versa. The term “gas

exchange” is partly to blame. Each gas actually diffuses according to its own

concentration gradient. *** Additional respiratory system functions: communication

(voice), olfaction, innate immunity/protection from environment….

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The most important muscles for breathing

Q1. What are they? Q2. Do they contract during

inhalation or exhalation?

Q3. How does their contraction change the thoracic cavity?

Q4. How does their relaxation change the thoracic cavity?

Marieb & Hoehn (2019), Figure 22.16

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Respiratory muscles (just the most important ones). *** Q1. Diaphragm and external

intercostal (“between-the-ribs”) muscles. Q2. Inhalation. Q3. When these muscles

contract, the thoracic cavity increases in volume. Q4. When these muscles relax, the thoracic cavity decreases in volume. *** External intercostals are more lateral, internal intercostals are more medial. Both are pictured here. Internal intercostals can contribute

to forced exhalation.

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Why does air move in and out of the lungs?

A simple description of breathing is this: The contraction of your

diaphragm and external intercostal muscles expands your thorax. Since your lungs are tethered to the thorax walls, they expand too,

and additional air enters the now-enlarged lungs.   Then your

inspiratory muscles relax and the process reverses.

This description is true, but incomplete. It doesn’t explain scenarios such as pneumothorax, when a hole in the chest wall impairs breathing even if the lungs themselves are still intact. The thorax can

still expand and shrink – so why don’t the lungs follow along any

more? Clearly, the pressures in the different compartments must be important.

For a fluid (air) to flow in bulk, there must be a pressure gradient. Our respiratory system manipulates volumes to create the desired pressure gradients and thus the desired flow (see following slides).

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Changing a compartment’s pressure by changing its volume

Boyle’s Law states that for a given quantity of gas molecules, the pressure and

volume are inversely proportional -- as one goes up, the other goes down. Thus, to decrease the pressure of a compartment, increase its volume. To increase the pressure of a compartment, decrease its volume.

Martini et al. (2015),
Figure 23.12

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This may sound like obscure chemistry, but we’ve actually encountered the general

concept during our CV chapters! Heart chamber contracts => pressure in that chamber increases; chamber relaxes, pressure falls. Similarly, vessel vasoconstriction increases pressure and vasodilation decreases pressure.

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The lungs are often represented as a balloon in a jar. Balloon = lungs, jar = thorax wall, space between them = pleural cavity.

Contract inspiratory muscles, ↑ pleural cavity volume, ↓ pleural cavity pressure,

↑ transpulmonary pressure gradient,

lung inflates

Relax inspiratory muscles, ↓ pleural cavity volume, ↑ pleural cavity pressure,

↓transpulmonary pressure gradient,

Freeman et al. (2017), Figure 44.12

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lung deflates

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Questions regarding the previous slide…

Q1. Would the balloon still inflate if there was a hole in it? Q2. Would the balloon still inflate if there was a hole in the side of the jar?

One more point…. Why doesn’t the balloon ever expand all the way

to the sides of the jar? There must be an opposing force! Thus, the actual volume of normal lungs at any given time reflects the

balance of 2 opposing forces…

Finally, note differences between the balloon model and actual lungs.

1. The two lungs are in separate pleural cavities. 2. Our actual pleural cavity volume is TINY. 3. Diaphragm shapes/changes are different.

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Q1-Q2. No. A (reasonably large) hole in either place would make it impossible to have a pressure difference between the inside of the balloon/lung and the outside of the

balloon/lung. *** Opposing force: elastic recoil of balloon material (doesn’t “like” to be

overstretched – just like the actual lungs). Thus, 2 opposing forces are: pressure gradient (drives lungs toward inflation) and elastic recoil (drives lungs toward deflation).

Expansions of the lungs are opposed by their tendency to recoil elastically, so the lungs

will never expand enough to eliminate the pressure gradient between the inside and outside of the lungs. *** Similarities of balloon model to actual lungs: basic principle of expand the volume around the lungs => decrease the pressure around the lungs => lungs inflate based on increased pressure gradient overcoming elastic recoil. Also, inhaling is the active process (requires muscle contraction).

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Pneumothorax

Q1. What does the word

“pneumothorax” mean,

based on its roots?

Q2. A knife blade goes through the skin into the left pleural cavity, but does not touch the lungs. Which lungs will collapse, if any?

youtube.com/watch?v=0vZ9gVyWreo

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Q1. Pneumothorax means air in the thorax – specifically the pleural cavity. Q2. The left lung will collapse because the transpulmonary pressure gradient has collapsed. The right lung will not collapse because it resides in its own separate pleural cavity. *** X-ray of

pneumothorax…. Note that the right side is “cloudy” while most of the left side is clear and dark. The “cloudiness” reflects the blood vessels, which do not stretch out across

the thorax if the lung is collapsed. So the left lung is collapsed here.

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Quantifying ventilation

Q1. Definition of tidal volume? Q2. Definition of residual volume?

Q3. Definition of Vital Capacity (VC or FVC)? What is it in this particular example?

Marieb & Hoehn (2019), Figure 22.19

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So far, we’ve focused on explaining why air moves in and out of lungs. NOW, let’s consider HOW MUCH air is moving in and out. Can make a graph… And name/label lots

of quantities, of which we will focus on a few. *** Q1. Tidal volume = how much air goes

in and out during one breath. Q2. Residual volume is the air that you can’t get out of

your pulmonary system (lungs + conducting airways), no matter how hard you try. (1200

mL seems like a lot, yet is normal.) Q3. FVC is total lung capacity minus residual volume,

i.e., the maximum amount of air that you can get out of your lungs if you start with them fully inflated. In this example, FVC is 6000 mL minus 1200 mL, which equals 4800 mL. *** Residual volume vs. dead space. Dead space is way less – only about 150 mL.

It’s the air that can’t do gas exchange because it’s in the conducting airways, not the

lungs themselves.
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Minute ventilation: just like cardiac output!

• Stroke Volume x Heart Rate
• = Cardiac Output

• mL/beat x beats/min
• = mL/min

Tidal Volume x Respiration Rate = Minute Ventilation

• mL/breath
• x breaths/min
• = mL/min

Two Equations in One!

• Volume moved per beat
• Volume moved per breath

Times number of breaths per minute Is volume of air per minute;
Times number of beats per minute Is volume of blood per minute;

• That’s all this equation has in it!
• That’s all this equation has in it!

faculty.washington.edu/crowther/Misc/Songs/2equations.shtml

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Just as SV = EDV minus ESV, TV has an equivalent formula… Tidal Volume equals end-

inspiratory volume minus end-expiratory volume. (TV = EIV – EEV.)
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Q1. What is the minute ventilation based on the data below?

(Hint: this should remind you of CO calculations!)

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Note parallel with cardiac output questions. *** Q1. Tidal volume times respiration rate equals minute ventilation. TV = 2000 mL minus 1500 mL equals 500 mL. Respiration rate = 10 breaths per minute. (Just count the number of respiratory cycles in the 1-minute period.) Then MV = TV*RR = (500 mL/breath)*(10 breaths/min) = 5000 mL/min.

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To our previous spirometry terms we now add one more: FEV₁.

Time (sec)

• 1
• 5
• 6
• 7

FEV₁ stands for Forced Expiratory Volu²me³in 1⁴second. To measure FEV₁, the patient is instructed to inflate maximally and then exhale as quickly and as fully as possible. How much air leaves in that first second? Q1. What is the approximate FEV₁ in this example?

Marieb & Hoehn (2019), Figure 22.19a

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FEV₁ is the amount of air you started with at the start of the second minus the air left at the end of the second. *** Q1. In this figure, FEV₁ is 6000 mL minus 2400 mL, which

equals 3600 mL. (It’s hard to judge exactly when that second ends, though, so it’s OK if

you got a different number as long as you understand what to do.)
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FEV₁ could be low for different reasons:

• Maybe the patient can’t get air out quickly. • Or maybe there isn’t much air in the lungs at the start of

exhalation, so FEV₁ will be small regardless of how quickly the air leaves.

To distinguish between these options, FEV₁ is often

expressed as a percentage of the FVC. In other words, “Out

of all the air that COULD come out of your lungs, how much

of it can you get out in 1 second?”

Rule of thumb: less than 80% is bad; 80% or above is fine.

Q1. Does the previous slide represent a FEV₁/FVC ratio that

is normal, or low?

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We measure things like FEV₁ to figure out whether patients’ respiratory systems are healthy. If FEV₁ is lower than normal, that is a potential warning sign. But now let’s think

through what it might mean to have a low FEV₁… *** Q1. Based on the numbers from the previous slides, I get 3600 mL/4800 mL x 100% = 75% -- slightly lower than normal, but not too bad.

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Two general types of lung disease…

• NORMAL
• OBSTRUCTIVE
• RESTRICTIVE

Problem Example
FVC

For each box:

Normal, or Low?

FEV₁
FEV₁/FVC

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Many pulmonary problems fall into one of two general categories, shown here. ***

Problem: small airways (O), lungs that don’t inflate well (R). Example: allergies, bronchoconstriction, chronic inflammation (O); preemies’ lack of surfactant, pulmonary

fibrosis, weak respiratory muscles (R). FVC: normal (O), low (R). FEV₁: low (O), low (R). FEV₁/FVC: low (O), normal (R).

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Case study:

“I can’t stop coughing!”

Marya moved from Southern California to play soccer at Northern Minnesota University (NMU) as a highly recruited player. All was well until she got sick with a miserable cold. She soon recovered, but now she finds herself with a lingering dry cough and difficulty catching her breath any time she exerts herself, which is every day! She also notices it has gotten worse as the weather has become colder. You guessed it – Marya has asthma.

Q1. Is this an obstructive problem or a restrictive problem? Q2. This disorder is often treated with an inhaler that mimics the autonomic nervous system. How does that work?

Marieb & Hoehn (2016) instructor materials;
Image from www.chkd.org

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Q1. Obstructive (narrowed airways). Q2. Albuterol or similar drugs (short-acting beta-2 agonists) can bind to beta-2 adrenergic receptors and cause bronchodilation. You can use an inhaler with such a drug shortly before exercising in the cold. Ahhhh! *** Albuterol = salbutamol. Another common one: salmeterol.

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Neural control of breathing

Q1. Which part of the brain is the most important controller of breathing, according to this figure?

Note the spinal cord levels involved.

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www.nataliescasebook.com/tag/neural-control-of-breathing

Neural control of breathing. There’s a basic pattern of breathing which can be modified according to the body’s current status and needs. *** Q1. Medulla oblongata. (The pons

assists, but is less important.) *** Green/yellow areas of medulla: Ventral Respiratory Group (VRG) and Dorsal Respiratory Group (DRG) nuclei, respectively. VRG generates the basic rhythm/pattern, which the DRG adjusts in response to sensory info. *** Spinal

levels for intercostals? The thoracic ones (T₁-T₁₁). Picture is potentially misleading in that

it only shows output to one pair of muscles, not the whole bunch. *** In the future, consider this figure: http://www.nataliescasebook.com/tag/neural-control-of-breathing (shows intercostal innervation better)

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Chemoreceptors & negative feedback

Q1. These chemoreceptors are called

“central” or “peripheral.”

WHY? Q2. Why do hypoventilation and hyperventilation usually resolve spontaneously?

Marieb & Hoehn (2019), Fig. 22.27

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This slide shows the sensory information that the medulla uses to adjust the breathing pattern (frequency and depth of breathing). *** 1^st key point: chemoreceptors (here, sensing O₂, CO₂, H⁺). 2^nd key point: homeostasis & negative feedback. What is being regulated by homeostasis here? O₂, CO₂, H⁺ (the chemicals being monitored). 3^rd key point: additional regulation by non-chemoreceptor regulation (on right). *** Q1. Central

and peripheral refer to the central nervous system and peripheral nervous system,

respectively. The central chemoreceptors are in the brainstem, which is part of the CNS; the peripheral chemoreceptors are in the aortic arch and carotid arteries, which are outside the CNS. Q2. Hypoventilation and hyperventilation alter the levels of CO₂, H⁺, and O₂ in the blood, which then alter the respiratory drive to bring the levels back to normal. Example: hyperventilate => CO₂ and H⁺ levels drop => lower stimulus to breathe => stop hyperventilating. Classic negative feedback! *** Receptors in muscles and joints? Proprioceptors (p. 845). Help account for sudden increase in breathing upon initiation of exercise.

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