Anatomy & Physiology · Chapter 22

The Respiratory System

Every cell in your body burns oxygen to make energy, and every one of them produces carbon dioxide as waste — so twelve to sixteen times a minute, without a single conscious command, your body trades one gas for the other. This chapter follows a breath from the nostril to the microscopic air sac where the exchange actually happens, then explains the physics that pulls air in, the diffusion that swaps the gases, the clever chemistry that ferries them through the blood, and the volumes a clinician measures to tell a healthy lung from a sick one. By the end you will understand not just how you breathe but why the whole elegant machine works the way it does.

By the end of this chapter you can

Trace the path of air through the conducting and respiratory zones and name each structure it passes.
Describe how the airway warms, humidifies, and filters incoming air, and explain the mucociliary escalator.
Diagram the respiratory membrane and explain why its thinness and huge surface area make it ideal for gas exchange.
Explain the job of surfactant and predict what happens when it is missing.
Use Boyle’s law to explain inspiration and expiration, and name the muscles and pressures involved in each.
Apply partial-pressure gradients to external and internal respiration, saying which way each gas moves and why.
Describe how oxygen and carbon dioxide are carried in the blood, including hemoglobin and the bicarbonate system.
Define the lung volumes and capacities and interpret how spirometry separates obstructive from restrictive disease.

Section 1The respiratory tract

The respiratory tract reference figure — **Reference.** The organs of the respiratory tract, nose to alveoli — OpenStax, CC BY 3.0 (via Wikimedia Commons)

Two zones: a highway and a destination

The respiratory system does one headline job — move oxygen in and carbon dioxide out — but it also warms and humidifies air, filters out debris, gives you the sense of smell, produces your voice, and helps regulate blood pH. To do all this, the airway is split into two functional zones. The conducting zone is plumbing: the nose, pharynx, larynx, trachea, bronchi, and bronchioles that carry air but never exchange gas. The respiratory zone — the respiratory bronchioles, alveolar ducts, and alveoli — is where the actual trade of oxygen for carbon dioxide takes place. Think of the conducting zone as the highway and the respiratory zone as the destination; air only does its real work once it arrives.

Clinicians also divide the tract by location. The upper respiratory tract is everything above the larynx (nose, nasal cavity, sinuses, pharynx), and the lower respiratory tract is the larynx on down (trachea, bronchi, lungs). This is why a "cold" (an upper-tract infection) feels so different from bronchitis or pneumonia (lower-tract problems).

The journey of a breath

Follow one inhalation. Air enters the nostrils, swirls through the nasal cavity, and passes into the three-part pharynx (throat). It slips through the larynx — the voice box, guarded by the epiglottis that flips down during swallowing so food goes to the esophagus instead of the lungs — and enters the trachea (windpipe), held permanently open by C-shaped rings of cartilage. The trachea forks into the right and left primary bronchi, which branch again and again like an upside-down tree into ever-smaller bronchi and then bronchioles, until the tubes end in clusters of alveoli. The whole branching pattern is called the bronchial tree.

Structure	Zone	Key feature
Nasal cavity	Conducting	Warms, humidifies, filters; lined by mucous membrane
Pharynx	Conducting	Shared passage for air and food (naso-, oro-, laryngo-)
Larynx	Conducting	Voice box; epiglottis guards the airway
Trachea	Conducting	C-shaped cartilage rings keep it open
Bronchi	Conducting	Branch into each lung, then lobes and segments
Bronchioles	Conducting	No cartilage; smooth muscle sets their diameter
Alveoli	Respiratory	Thin-walled air sacs where gas exchange occurs

The air that arrives is conditioned

By the time air reaches the alveoli it has been transformed: warmed to body temperature, saturated with water vapor, and scrubbed nearly clean. The nasal cavity does most of this conditioning, its rich blood supply radiating heat and its mucous lining trapping dust and microbes. Beneath that mucus sits a carpet of microscopic cilia beating in waves toward the throat — the mucociliary escalator — which sweeps trapped debris up and out to be swallowed or coughed away. It is a tireless housekeeping system that protects the delicate air sacs from the world.

Smoke stalls the escalator. Cigarette smoke paralyzes and eventually destroys the cilia, so the mucociliary escalator quits. Trapped tar and germs sit in the airway instead of being cleared, which is exactly why smokers develop the chronic "morning cough" — the lungs resort to coughing because their built-in escalator has stopped running.

Walk the whole tract, structure by structure, in the interactive below.

Interactive Follow a breath from the nose down to the tiny air sacs, tapping each structure along the way. Open full ↑

Key points

The conducting zone (nose → bronchioles) moves air; the respiratory zone (respiratory bronchioles → alveoli) exchanges gas.
Air path: nose → pharynx → larynx → trachea → bronchi → bronchioles → alveoli.
Incoming air is warmed, humidified, and filtered; the mucociliary escalator sweeps debris up and out.

Section 2The alveolus & respiratory membrane

The alveolus and respiratory membrane reference figure — **Reference.** An alveolus wrapped in a capillary, and the layers of the respiratory membrane — OpenStax, CC BY 3.0 (via Wikimedia Commons)

A surface the size of a room

The lungs hold roughly 300 million alveoli, each a hollow, bubble-like sac wrapped in a mesh of capillaries. Individually they are tiny, but together their walls unfold into an astonishing 70 square meters of surface — about the floor area of a small apartment — packed inside your chest. This enormous area is the whole point: the more membrane you spread out, the more gas can cross it at once. Structure fits function, and here the function is to make oxygen and carbon dioxide diffusion as fast and abundant as physically possible.

The respiratory membrane: three thin layers

Gas exchange happens across the respiratory membrane, the barrier separating alveolar air from capillary blood. Despite the important-sounding name, it is almost nothing at all — about 0.5 micrometers thick, thinner than a soap bubble. It has just three layers: the alveolar wall (a single flat layer of type I cells), the capillary wall (a single flat layer of endothelial cells), and their fused basement membranes glued between them. Oxygen crosses all three and enters the blood in a fraction of a second; carbon dioxide crosses the other way just as fast.

Cell / layer	What it is	Job
Type I alveolar cell	Simple squamous (flat) cell	Forms most of the wall; thin enough for gases to cross
Type II alveolar cell	Rounded cell scattered in the wall	Secretes surfactant
Alveolar macrophage	Roaming immune cell ("dust cell")	Engulfs debris and microbes that reach the sac
Capillary endothelium	Flat cells lining the capillary	The blood side of the respiratory membrane

Why does the thinness matter so much? Because diffusion slows sharply as the barrier thickens. In diseases that thicken this membrane — pulmonary edema floods it with fluid, pulmonary fibrosis stiffens it with scar — oxygen suddenly has farther to travel, and the patient becomes short of breath even though the air and the blood are both right there.

Surfactant: keeping the sacs from collapsing

A wet-walled bubble wants to collapse, because water molecules lining it pull toward one another — a force called surface tension. Left unchecked, that tension would snap the smallest alveoli shut with every exhalation. To prevent this, the type II alveolar cells secrete surfactant, a soapy mix of lipids and proteins that coats the inner surface and breaks up the water’s pull, lowering surface tension and keeping the sacs open and easy to inflate.

Why premature babies struggle to breathe. A fetus does not make enough surfactant until late in pregnancy (around 28–34 weeks). Born too early, the infant’s alveoli collapse with each breath — infant respiratory distress syndrome — which is why premature newborns may be given artificial surfactant and why steroids are given to speed a threatened baby’s lung maturity.

Zoom into a single sac and its capillary in the interactive below.

Interactive Zoom into one air sac and the capillary hugging it, and tap each part of the wafer-thin respiratory membrane. Open full ↑

Key points

~300 million alveoli give ~70 m² of surface for gas exchange.
The respiratory membrane is ~0.5 µm thick and has three layers: alveolar wall, fused basement membranes, and capillary wall.
Type II cells make surfactant, which lowers surface tension and keeps alveoli from collapsing.

Section 3Breathing mechanics

Breathing mechanics and Boyle's law reference figure — **Reference.** How the diaphragm changes chest volume and pressure to move air — OpenStax, CC BY 4.0 (via Wikimedia Commons)

You make room, and air follows (Boyle’s law)

Here is the surprise most students never expect: you do not actively suck air into your lungs. You make the chest bigger, and air rushes in on its own to fill the extra space. The physics behind this is Boyle’s law — at a fixed temperature, the pressure of a gas rises as its volume falls, and falls as its volume rises. Squeeze a container and the pressure inside climbs; enlarge it and the pressure drops. Air always flows from higher pressure to lower pressure, so all your muscles have to do is change the volume of the chest, and the pressure difference moves the air for you.

Inspiration: an active pull

Breathing in is active — it takes muscle work. The diaphragm, a dome of muscle under the lungs, contracts and flattens downward, while the external intercostal muscles lift the ribs up and out. Both actions enlarge the thoracic cavity. By Boyle’s law, that larger volume drops the pressure inside the lungs (the intrapulmonary pressure) just below atmospheric pressure, and air flows in until the two pressures equalize. The lungs themselves are not muscular; they follow the chest wall because a thin film of fluid and a permanently negative intrapleural pressure keep them stuck to it, so when the chest expands, the lungs expand with it.

Expiration: mostly letting go

Breathing out at rest is the opposite — and easier, because it is usually passive. The diaphragm and external intercostals simply relax, the stretched lungs and chest wall recoil like a released rubber band, thoracic volume shrinks, intrapulmonary pressure rises above atmospheric, and air flows out. No muscle contraction is required for a quiet exhale. Only when you need to force air out — blowing out candles, coughing, exercising hard — do the internal intercostals and abdominal muscles pitch in to actively squeeze the chest.

	Inspiration	Expiration (quiet)
Effort	Active (muscles contract)	Passive (muscles relax)
Main muscles	Diaphragm, external intercostals	None — elastic recoil
Thoracic volume	Increases	Decreases
Intrapulmonary pressure	Falls below atmospheric	Rises above atmospheric
Air movement	In	Out

A punctured seal: pneumothorax. The negative intrapleural pressure is what keeps the lung glued to the chest wall. If a wound or ruptured air sac lets air into the pleural space, that seal breaks, the pressure equalizes, and the lung collapses inward — a pneumothorax. It is a vivid reminder that the lung has no muscle of its own; it inflates only because it is held tightly against a moving chest wall.

Watch the diaphragm change the chest’s volume and pressure in the interactive below.

Interactive The diaphragm changes the chest’s volume, which changes its pressure (Boyle’s law), and air follows. Watch it breathe. Open full ↑

Key points

Boyle’s law: enlarging the chest lowers lung pressure so air flows in; shrinking it raises pressure so air flows out.
Inspiration is active (diaphragm + external intercostals); quiet expiration is passive (elastic recoil).
A negative intrapleural pressure keeps the lungs adhered to the chest wall; break the seal and the lung collapses (pneumothorax).

Section 4Gas exchange

Gas exchange partial pressures reference figure — **Reference.** Partial-pressure gradients driving external and internal respiration — NIH NIAID, CC BY 4.0 (via Wikimedia Commons)

Partial pressure: each gas pushes on its own

Air is a mixture, and in a mixture every gas exerts its own share of the total pressure — its partial pressure — as if the others were not there. Oxygen makes up about 21% of air, so at sea level its partial pressure (written P_O₂) is roughly 160 mmHg in the atmosphere and about 104 mmHg once diluted inside the alveoli. This matters because gases, like everything else in diffusion, move from where their partial pressure is high to where it is low, and they keep moving until the two sides even out. Every gas exchange in the body is just this one rule applied over and over.

External respiration: loading O₂, dumping CO₂

External respiration is the swap that happens in the lungs, between alveolar air and the blood. Blood arriving from the body is oxygen-poor (P_O₂ ≈ 40 mmHg) and carbon-dioxide-rich (P_CO₂ ≈ 45 mmHg). The alveolar air is the reverse — high in oxygen (≈ 104 mmHg) and low in carbon dioxide (≈ 40 mmHg). So oxygen diffuses down its gradient into the blood, and carbon dioxide diffuses the other way out into the alveoli to be exhaled. Blood leaves the lungs fully loaded with oxygen and having given up a small share of its carbon dioxide — just enough to bring P_CO₂ from about 45 back down to about 40 mmHg. Most of the blood’s carbon dioxide stays with it, parked in the large bicarbonate pool you will meet in Section 5; each pass through the lungs trims that pool rather than emptying it.

Internal respiration: the reverse at the tissues

Internal respiration is the same physics run backward, out in the body’s tissues. Cells constantly burn oxygen and pour out carbon dioxide, so the tissue P_O₂ is low (≈ 40 mmHg) and its P_CO₂ is high (≈ 45 mmHg). Blood arriving in the tissue capillaries is the opposite, so oxygen diffuses out of the blood into the cells and carbon dioxide diffuses into the blood to be hauled back to the lungs. Same rule, opposite direction — and the cycle repeats with every heartbeat.

Gas	Alveoli (air)	Deoxygenated blood	Tissues
P_O₂	~104 mmHg	~40 mmHg	~40 mmHg
P_CO₂	~40 mmHg	~45 mmHg	~45 mmHg
Net movement	O₂ in, CO₂ out (external)	—	O₂ out, CO₂ in (internal)

Small gradient, big mover. Notice that carbon dioxide’s partial-pressure gradient (45 vs 40 mmHg) is far smaller than oxygen’s (104 vs 40). CO₂ still keeps up because it is about 20 times more soluble than O₂ and crosses the membrane easily — a good example that solubility, not just the gradient, sets how fast a gas diffuses.

Switch between the lungs and the tissues in the interactive below.

Interactive Gases diffuse from high to low partial pressure — one way in the lungs, the opposite way in the tissues. Switch between them. Open full ↑

Key points

Each gas diffuses from high to low partial pressure and stops when the pressures equalize.
External respiration (lungs): O₂ into blood, CO₂ out to be exhaled.
Internal respiration (tissues): O₂ out to cells, CO₂ into blood — the same rule reversed.

Section 5Gas transport in the blood

Oxygen and carbon dioxide transport reference figure — **Reference.** How oxygen rides on hemoglobin and carbon dioxide travels three ways — OpenStax, CC BY 3.0 (via Wikimedia Commons)

Oxygen rides on hemoglobin

Oxygen barely dissolves in water, so blood plasma alone could never carry enough of it to keep you alive — only about 1.5% of the oxygen in blood is dissolved. The other 98.5% is bound to hemoglobin, the iron-containing protein packed inside red blood cells. Each hemoglobin molecule grips up to four oxygen molecules on its iron sites, forming oxyhemoglobin. This is the whole reason red blood cells exist: hemoglobin lets blood carry roughly seventy times more oxygen than it otherwise could.

The oxygen–hemoglobin dissociation curve

Hemoglobin has a wonderful property: it grabs oxygen tightly where oxygen is plentiful (the lungs) and releases it where oxygen is scarce (the tissues). Plot how saturated hemoglobin is against the surrounding P_O₂ and you get the S-shaped oxygen–hemoglobin dissociation curve. Better still, hemoglobin reads the tissue’s needs: in an active, hard-working tissue — warmer, more acidic, richer in carbon dioxide — hemoglobin loosens its grip and hands off more oxygen right where it is needed most. This shift, driven by low pH and high CO₂, is the Bohr effect. It is homeostasis in miniature: the busiest cells automatically get the biggest oxygen delivery.

Carbon dioxide travels three ways

Carbon dioxide is more sociable than oxygen and hitches three different rides back to the lungs. A small share (~7%) simply dissolves in plasma; about 23% binds to hemoglobin (as carbaminohemoglobin, on a different site than oxygen); and the majority — about 70% — is converted inside red blood cells into bicarbonate. The enzyme carbonic anhydrase combines CO₂ with water into carbonic acid, which splits into a hydrogen ion and a bicarbonate ion (HCO₃⁻) that slips out into the plasma. At the lungs the whole reaction runs in reverse, releasing CO₂ to be breathed out.

Gas	Form in blood	Share
Oxygen	Bound to hemoglobin (oxyhemoglobin)	~98.5%
Oxygen	Dissolved in plasma	~1.5%
Carbon dioxide	As bicarbonate (HCO₃⁻)	~70%
Carbon dioxide	Bound to hemoglobin (carbaminohemoglobin)	~23%
Carbon dioxide	Dissolved in plasma	~7%

Breathing is also pH control. Because most CO₂ rides as bicarbonate and releases a hydrogen ion when it forms, your breathing rate quietly steers your blood pH. Breathe faster and you blow off CO₂, pulling the reaction backward and raising pH; hold CO₂ in and pH falls. This is why a patient hyperventilating from anxiety can turn their blood alkaline — the respiratory and buffer systems are two sides of one coin.

Switch between oxygen and carbon dioxide transport in the interactive below.

Interactive Once gases cross into the blood they must be carried — and oxygen and carbon dioxide travel very differently. Switch between them. Open full ↑

Key points

Oxygen is carried mostly on hemoglobin (~98.5%); each molecule binds four O₂.
The Bohr effect — low pH plus high CO₂ — makes hemoglobin release more oxygen in hard-working tissues; the warmth of those tissues shifts the curve the same way by a separate route.
Carbon dioxide travels as bicarbonate (~70%), on hemoglobin (~23%), and dissolved (~7%); this links breathing to blood pH.

Section 6Lung volumes & capacities

Lung volumes and capacities spirometry reference figure — **Reference.** A spirometry trace showing the lung volumes and capacities — OpenStax, CC BY 3.0 (via Wikimedia Commons)

Four volumes

A spirometer records how much air you move as you breathe, and its trace is divided into four basic volumes. Tidal volume (TV) is the modest amount — about 500 mL — you move in a normal quiet breath. On top of that, inspiratory reserve volume (IRV, ~3000 mL) is the extra you can pull in with a maximal inhale, and expiratory reserve volume (ERV, ~1100 mL) is the extra you can force out after a normal exhale. Finally, residual volume (RV, ~1200 mL) is the air that always stays behind — you can never fully empty your lungs, and that leftover air keeps the alveoli from collapsing between breaths.

Four capacities (volumes added together)

A capacity is simply two or more volumes added together, and each one answers a practical question. Vital capacity (VC) — the total you can move from a maximal inhale to a maximal exhale (TV + IRV + ERV, ~4600 mL) — is the number clinicians care about most. Total lung capacity (TLC) adds the residual volume back in for everything the lungs can hold (~5800 mL). Inspiratory capacity (IC = TV + IRV) is all you can breathe in from rest, and functional residual capacity (FRC = ERV + RV) is what remains after a normal exhale.

Measure	Definition	Typical value
Tidal volume (TV)	Air per normal quiet breath	~500 mL
Inspiratory reserve (IRV)	Extra air forcibly inhaled	~3000 mL
Expiratory reserve (ERV)	Extra air forcibly exhaled	~1100 mL
Residual volume (RV)	Air that cannot be exhaled	~1200 mL
Vital capacity (VC)	TV + IRV + ERV	~4600 mL
Total lung capacity (TLC)	VC + RV (everything)	~5800 mL

Dead space & what spirometry reveals

Not every milliliter you inhale reaches the alveoli. About 150 mL stays in the conducting airways — the anatomical dead space — where no gas exchange happens, so of a 500 mL breath only ~350 mL is fresh air that actually does work. Spirometry becomes truly powerful when timed: the FEV₁/FVC ratio (how much of your vital capacity you can blow out in the first second) separates the two great families of lung disease. In obstructive disease (asthma, COPD) the airways are narrowed, so air comes out slowly and the ratio drops. In restrictive disease (fibrosis) the lungs are stiff and small, so volumes shrink but the air that is there comes out briskly, keeping the ratio normal or high.

You can never fully deflate. Because the residual volume never leaves the lungs, a simple spirometer — which only measures air that moves in and out — cannot capture RV, FRC, or TLC directly; those require special techniques. It is also why a lung, even after your hardest exhale, still floats in water: there is always air trapped inside.

Trace each volume on a spirometer in the interactive below.

Interactive A spirometer traces how much air you move — quiet breathing uses only a sliver of capacity. Tap each volume to see it. Open full ↑

Key points

Four volumes: tidal, inspiratory reserve, expiratory reserve, and residual; capacities are volumes summed (VC, TLC, IC, FRC).
Residual volume always stays behind and keeps alveoli open; it cannot be measured by simple spirometry.
A low FEV₁/FVC ratio signals obstructive disease; shrunken volumes with a normal ratio signal restrictive disease.

The chapter in one breath

The airway has a conducting zone that moves and conditions air and a respiratory zone where gas is actually exchanged; air travels nose → pharynx → larynx → trachea → bronchi → bronchioles → alveoli.
Gas exchange occurs across the paper-thin respiratory membrane of ~300 million alveoli; surfactant from type II cells keeps the sacs from collapsing.
Breathing obeys Boyle’s law: inspiration is active (diaphragm + external intercostals enlarge the chest), while quiet expiration is passive elastic recoil.
Gases diffuse from high to low partial pressure — O₂ in and CO₂ out at the lungs (external respiration), and the reverse at the tissues (internal respiration).
Oxygen is carried mostly on hemoglobin; carbon dioxide travels mostly as bicarbonate, tying breathing to blood pH.
The lung’s volumes and capacities quantify how much air you move; a low FEV₁/FVC ratio flags obstructive disease and shrunken volumes flag restrictive disease.

ReferenceWords worth knowing

A quick reference for the terms in this chapter — skim it now, or circle back whenever a word trips you up.

Alveolus: A microscopic, thin-walled air sac (plural: alveoli) where oxygen and carbon dioxide are exchanged with the blood.
Bicarbonate (HCO₃⁻): The ion into which most carbon dioxide is converted for transport in the blood; also a key player in acid–base balance.
Bohr effect: The fall in hemoglobin’s oxygen affinity caused by rising H⁺ (lower pH) and rising carbon dioxide, so hemoglobin releases more oxygen in active tissue. Warmth shifts the curve the same direction but by a separate mechanism, not by the Bohr effect.
Boyle’s law: At constant temperature, the pressure of a gas is inversely related to its volume; the basis of how the chest moves air.
Bronchiole: A small airway of the conducting zone with no cartilage, whose diameter is set by smooth muscle.
Conducting zone: The airways (nose through bronchioles) that carry, warm, humidify, and filter air but do not exchange gas.
Dead space (anatomical): The ~150 mL of inhaled air that stays in the conducting airways and never reaches the alveoli for exchange.
Diaphragm: The dome-shaped muscle beneath the lungs; its contraction is the main driver of inspiration.
Expiration: Breathing out; passive at rest (elastic recoil) and active when forced.
External respiration: Gas exchange in the lungs between alveolar air and blood — oxygen in, carbon dioxide out.
Hemoglobin: The iron-containing protein in red blood cells that binds and carries up to four oxygen molecules.
Inspiration: Breathing in; an active process in which the diaphragm and external intercostals enlarge the chest.
Internal respiration: Gas exchange in the tissues between blood and cells — oxygen out to cells, carbon dioxide into blood.
Intrapleural pressure: The pressure in the fluid-filled space between the lung and chest wall; kept negative so the lung stays inflated against the wall.
Partial pressure: The share of total gas pressure contributed by one gas in a mixture; gases diffuse from high to low partial pressure.
Residual volume: The air (~1200 mL) that remains in the lungs after the most forceful exhale and cannot be voluntarily expelled.
Respiratory membrane: The ~0.5 µm barrier — alveolar wall, fused basement membranes, and capillary wall — across which gases diffuse.
Spirometry: A test that measures the volumes and flow rates of air a person breathes, used to diagnose lung disease.
Surfactant: A lipid-and-protein mixture from type II alveolar cells that lowers surface tension and keeps alveoli from collapsing.
Tidal volume: The volume of air (~500 mL) moved in a single normal, quiet breath.
Vital capacity: The maximum air a person can exhale after a maximal inhale (tidal + inspiratory reserve + expiratory reserve volumes).

Check yourself

1. Put these in the order air passes through them and say which is the first structure of the respiratory (not conducting) zone: trachea, alveolus, larynx, bronchiole, pharynx.

Pharynx → larynx → trachea → bronchiole → alveolus; the alveolus is the respiratory-zone structure. Everything from the nose down through the bronchioles is the conducting zone that only moves air; gas exchange begins in the respiratory zone at the alveoli.

2. A longtime smoker develops a chronic productive morning cough. Which airway defense has failed, and why does that cause coughing?

The mucociliary escalator. Smoke paralyzes and destroys the cilia that normally sweep mucus and trapped debris up and out, so material accumulates in the airway and the lungs fall back on coughing to clear it.

3. Name the three layers of the respiratory membrane and explain why pulmonary edema causes shortness of breath.

The alveolar wall, the fused basement membranes, and the capillary wall. Edema adds a layer of fluid, thickening the barrier so oxygen must diffuse farther and more slowly — less oxygen reaches the blood, and the patient feels short of breath.

4. What do type II alveolar cells secrete, what does it do, and why are very premature babies especially at risk?

Surfactant, which lowers surface tension so alveoli stay open. A fetus makes little surfactant until late pregnancy, so a very premature infant’s alveoli tend to collapse with each breath — infant respiratory distress syndrome.

5. Using Boyle’s law, explain what happens to thoracic volume, intrapulmonary pressure, and airflow during inspiration.

Volume increases, pressure falls below atmospheric, and air flows in. The diaphragm and external intercostals enlarge the chest; by Boyle’s law the larger volume lowers the pressure inside the lungs, and air moves from higher (outside) to lower (inside) pressure.

6. Which phase of quiet breathing is passive, and what supplies the force for it?

Quiet expiration is passive. The inspiratory muscles simply relax and the stretched lungs and chest wall recoil elastically, shrinking thoracic volume and pushing air out — no muscle contraction is needed unless expiration is forced.

7. A stab wound lets air into the pleural space and the lung collapses. What normal pressure was lost, and what does this reveal about how the lung inflates?

The negative intrapleural pressure was lost, causing a pneumothorax. That negative pressure is what glues the lung to the chest wall; since the lung has no muscle of its own, it inflates only by being held against a moving chest wall, and breaking the seal lets it recoil shut.

8. In the lungs, alveolar P_O₂ is ~104 mmHg and incoming blood P_O₂ is ~40 mmHg. Which way does oxygen move, and what is this process called?

Oxygen diffuses from the alveoli into the blood (high to low partial pressure); this is external respiration. At the same time carbon dioxide moves the opposite way, out of the blood into the alveoli to be exhaled.

9. Carbon dioxide’s partial-pressure gradient across the respiratory membrane is much smaller than oxygen’s, yet it keeps pace. Why?

Carbon dioxide is about 20 times more soluble than oxygen. Diffusion depends on solubility as well as the pressure gradient, so CO₂’s high solubility lets it cross the membrane quickly despite the modest 45-vs-40 mmHg difference.

10. How is most oxygen carried in the blood, and what does the Bohr effect accomplish in an exercising muscle?

About 98.5% of oxygen is bound to hemoglobin; the Bohr effect makes hemoglobin release more of it in active tissue. Exercising muscle is warmer, more acidic, and CO₂-rich, which loosens hemoglobin’s grip so more oxygen is delivered exactly where demand is highest.

11. Name the three ways carbon dioxide travels in the blood, roughly in order of amount, and name the enzyme behind the largest one.

As bicarbonate (~70%), bound to hemoglobin (~23%), and dissolved (~7%); carbonic anhydrase drives the bicarbonate route. Inside red cells, carbonic anhydrase joins CO₂ and water into carbonic acid, which splits into a hydrogen ion and bicarbonate — a reaction reversed at the lungs.

12. Two patients have abnormal spirometry: one has a low FEV₁/FVC ratio, the other has small volumes but a normal ratio. Which pattern is obstructive and which is restrictive?

The low FEV₁/FVC ratio is obstructive; small volumes with a normal ratio is restrictive. In obstruction (asthma, COPD) narrowed airways slow airflow, so less comes out in the first second; in restriction (fibrosis) stiff lungs shrink the volumes but the air that is present still exits briskly.

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