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Nursing Field Notes / Respiratory · Oxygenation & Airway III · Fundamentals of Nursing
🫁 RESPIRATORY + LABS SET NG-092 ABG · The Method NG-138 ABG · Compensation Practice NG-173 ABG · Answer Key NG-132 Anatomy of Breathing NG-170 Key Terms & Lung Sounds

Anatomy of Breathing 🫁

Not the plumbing — the ENGINE. What actually moves the air in and out.

NG-132 RESPIRATORY · MECHANICS ADHD-friendly visual edition

Breathing is inhalation (air in) and exhalation (CO₂ out), and it only works if four things are intact: a clear airway, an intact central nervous system — specifically the brainstem that fires the impulse to breathe — an intact thoracic cavity, above all the diaphragm, and adequate pulmonary compliance and recoil. This page is the mechanics of one breath. The airway tree, the lobes and the alveolus itself are already drawn on NG-004 · Anatomy of the Lungs — start there if you want the structures, and stay here for how they move.

📄 Simple Nursing original — opens in Drive →

🫁 BIGGER BOX = AIR INMuscles change the volume → volume changes the pressure → pressure moves the air. That is the whole of breathing.
🔽 DIAPHRAGM DOWNContract = flatten = chest bigger = inhale. Relax = dome back up = exhale. Inspiration is ACTIVE, quiet expiration is PASSIVE.
🧠 C3, C4, C5The phrenic nerve keeps the diaphragm alive. Injury above that level and the diaphragm stops.
⚖️ V and QVentilation = air getting in. Q = perfusion, blood getting there. Gas exchange needs BOTH, in the same place, at the same time.
🫁

PART 1 · THE MECHANICS OF ONE BREATH

HOW AIR MOVES

Air has no legs. It moves because you change the size of the box it is sitting in.

🫁 Inspiration and expiration, side by side

ONE BREATH — what the diaphragm and ribs actually do Coronal cutaway, anterior view · read LEFT (breathe in) then RIGHT (breathe out) KEY air moving IN air moving OUT muscle · gold arrows = the direction it moves bone — ribs, sternum, thoracic spine ① INSPIRATION — breathing IN DIAPHRAGM contracts and FLATTENS ↓ ribs swing UP and OUT Chest gets BIGGER → pressure inside DROPS air is pushed IN · ACTIVE — it costs muscle work ② EXPIRATION — breathing OUT DIAPHRAGM relaxes and DOMES back up ↑ ribs drop IN and DOWN Chest gets SMALLER → pressure inside RISES air is pushed OUT · PASSIVE at rest — elastic recoil Air always moves from HIGH pressure to LOW pressure. Breathing is nothing but changing the size of the box. Muscles change the volume · the volume changes the pressure · the pressure moves the air.

Left: the diaphragm contracts downward and the ribs swing up and out, so the chest enlarges, the pressure inside falls, and air is pushed in from outside. Right: the muscles relax, the diaphragm domes back up, the chest shrinks, pressure rises, and air is pushed out.

🧠 Down and OUT to breathe IN. The diaphragm moves the opposite way to the air.

⭐ The four things breathing depends on

  • A clear airway — nothing to move air through if it is blocked.
  • An intact central nervous system, specifically the brainstem, which controls the impulse to breathe.
  • An intact thoracic cavity, above all the diaphragm, which expands the lungs to get oxygen in.
  • Adequate pulmonary compliance and recoil — the alveoli have to be able to stretch and spring back.

Take away any one of the four and ventilation fails, however good the other three are.

🧠 Pipe · Pilot · Pump · Spring. Airway, brainstem, diaphragm, compliance.

💨 Active in, passive out

  • Inspiration is always ACTIVE — muscles contract, and that costs energy.
  • Quiet expiration is PASSIVE — the muscles simply relax and the stretched lung recoils, like letting go of a balloon.
  • Forced expiration is active — coughing, sneezing, exercise and severe airflow obstruction all recruit the internal intercostals and the abdominal muscles.
  • This is why a COPD patient works so hard: for them, getting air OUT has become the effortful part.
🧠 Breathing in costs. Breathing out is usually free — until it isn't.

💪 The muscles that do the work

THE MUSCLES OF BREATHING Panel A: where they are (anterior view) · Panel B: magnified — why the two intercostal layers do opposite jobs KEY QUIET inspiration — always working ACCESSORY — only when breathing is hard FORCED expiration only nerve supply A · WHERE THEY ARE — anterior view STERNOCLEIDOMASTOID accessory · lifts the sternum SCALENES accessory · lift ribs 1 and 2 INTERCOSTALS between every rib — see panel B PHRENIC NERVE · C3, C4, C5 the diaphragm’s nerve supply DIAPHRAGM PRIMARY muscle — most of a quiet breath ABDOMINAL MUSCLES forced expiration · cough, sneeze anterior view · muscles shown superficial-to-deep B · MAGNIFIED — between two ribs The two layers run at RIGHT ANGLES to each other — that is why they pull opposite ways. EXTERNAL INTERCOSTALS Fibers run DOWN and FORWARD — “hands in your front pockets” rib rib LIFT the ribs up and out → INSPIRATION up INTERNAL INTERCOSTALS Fibers run DOWN and BACKWARD — at right angles to the layer above rib rib PULL the ribs down and in → FORCED EXPIRATION down 🧠 “Hands in your FRONT pockets” = external = the ones that lift.

Panel A shows where each muscle sits; panel B shows why the two intercostal layers, whose fibers cross at right angles, pull the ribs in opposite directions.

🧠 Diaphragm does most of a quiet breath. Everything else is help for when it gets hard.

🚨 Accessory muscle use is a clinical sign, not a curiosity

Answer first: if you can SEE someone breathing, they are working too hard.

  • Watch for neck muscles standing out (sternocleidomastoid, scalenes), intercostal and supraclavicular retractions, nasal flaring, and tripoding — leaning forward on the arms.
  • In children add grunting and head bobbing.
  • Accessory muscles are inefficient and they tire. A patient who has been using them for hours is heading toward respiratory failure.
  • A suddenly “calmer”, quieter patient with a slowing rate after prolonged hard work is not improving — they are exhausting. Escalate.
🧠 Quiet after loud is the scariest sound in respiratory nursing.

🧠 What tells you to breathe in the first place

WHAT TELLS YOU TO BREATHE Panel A: the sensors and the switchboard (left lateral view) · Panel B: the feedback loop A · THE SENSORS AND THE SWITCHBOARD cerebrum cerebellum MIDBRAIN → PONS → MEDULLA the brainstem, top to bottom MIDBRAIN a relay — not a breathing center PONS smooths the rhythm of breathing MEDULLA OBLONGATA THE respiratory center — it sets rate and depth CENTRAL CHEMORECEPTORS green dots on the medulla they sense CO₂ (as H⁺ in CSF) the MAIN everyday driver spinal cord CAROTID BODY at the fork of the carotid artery AORTIC BODIES on the arch of the aorta PERIPHERAL CHEMORECEPTORS carotid + aortic bodies together they sense a LOW O₂ — the back-up drive, waking up around PaO₂ 60 mmHg signals travel UP left lateral view · vessels of the neck shown below the brainstem B · THE LOOP, AND WHY IT MATTERS WHAT HAPPENS WHEN PaCO₂ RISES 1 PaCO₂ rises even a small rise is enough 2 Central chemoreceptors detect it they sense the H⁺ that CO₂ makes in CSF 3 The MEDULLA fires faster rate and depth are turned up 4 Diaphragm + intercostals work harder via the phrenic and intercostal nerves 5 Ventilation increases more CO₂ is blown off 6 PaCO₂ falls back to normal the stimulus switches itself off negative feedback 🚨 WHY THIS MATTERS AT THE BEDSIDE • CO₂ — not oxygen — is the normal driver of breathing. • Opioids, sedatives and anesthetics blunt the medulla: rate and depth fall, and the CO₂ climbs. • A brainstem stroke or head injury can wipe out the drive to breathe altogether. • A high cervical cord injury spares the medulla but cuts the phrenic nerve’s route to the diaphragm. 🧠 CENTRAL = CO₂ · PERIPHERAL = O₂ The CENTRAL sensors sit on the medulla, watch carbon dioxide, and run everyday breathing. The PERIPHERAL ones (carotid and aortic bodies) are the back-up — they wake up when oxygen falls low.

The medulla is the switchboard, the pons smooths the rhythm, and two sets of chemoreceptors feed it information: central ones watching CO₂, peripheral ones watching O₂.

🧠 CENTRAL = CO₂ · PERIPHERAL = O₂. Carbon dioxide runs the show day to day.

🫀 The diaphragm is not the only thing it does

  • When the diaphragm descends it also raises abdominal pressure — which is why breathing, coughing, vomiting, straining and childbirth all use the same muscle.
  • A full stomach, obesity, ascites, pregnancy or abdominal distension all splint the diaphragm and reduce how far it can drop.
  • That is the reason we sit patients upright — gravity pulls the abdominal contents away and lets the diaphragm move.
  • Post-operative abdominal or chest pain makes people splint and breathe shallowly, which is a direct route to atelectasis.
🧠 Sitting up is a respiratory intervention, not just a comfort measure.
📉

PART 2 · PRESSURE, COMPLIANCE & RECOIL

WHY IT WORKS

Numbers make this concrete: how much air, how much pressure, and what happens when the lung stops behaving like elastic.

📉 One breath, by the numbers

THE NUMBERS BEHIND ONE BREATH Three graphs, one shared time axis · typical textbook adult values at rest — they vary with body size and technique 0 250 500 LUNG VOLUME mL above resting volume peak ≈ 500 mL — one tidal volume −1.5 0 +1.5 ALVEOLAR PRESSURE cmH₂O · 0 = atmospheric dips to about −1, then rises to about +1 −9 −7 −5 −3 INTRAPLEURAL PRESSURE cmH₂O · the pressure in the pleural space about −5 at rest → about −8 at full inspiration · NEVER reaches 0 INSPIRATION EXPIRATION end of inspiration start end of expiration TIME — one quiet breath (about 4–5 seconds at a rate of 12–16 per minute)

Volume rises by about 500 mL. Alveolar pressure dips about 1 cmH₂O below atmospheric to draw air in, then rises about 1 cmH₂O above it to push air out. Intrapleural pressure goes from roughly −5 to −8 cmH₂O — and never reaches zero. Typical textbook adult values; they vary with body size and technique.

🧠 Small numbers, big consequences. One centimeter of water moves half a liter of air.

🧲 Why the lungs don't just collapse

Answer first: the pleural space holds them open.

  • The visceral pleura hugs the lung; the parietal pleura lines the chest wall; between them is a thin film of fluid.
  • That film creates surface tension — like two wet glass slides stuck together. The lung is dragged outward with the chest wall.
  • The pressure in that space stays negative throughout the whole breath. That negative pressure is the only thing stopping the elastic lung from balling up.
  • Let air into that space and the seal is lost — the lung collapses. That is a pneumothorax.
SEE ALSO The pleural layers themselves are drawn on NG-004 Anatomy of the Lungs.
🧠 Two wet slides. Slide them, and they glide. Pull them apart, and they resist.

🧴 Surfactant — the reason small alveoli survive

  • Alveoli are wet inside, and water's surface tension tries to collapse them — the smaller the sac, the stronger the pull.
  • Surfactant is a detergent-like fluid made by type II alveolar cells. It lowers surface tension and keeps small alveoli open.
  • Without it, alveoli collapse and it takes enormous pressure to re-open them — the problem in neonatal respiratory distress syndrome and part of the problem in ARDS.
  • This is also why deep breaths and sighs matter: stretching the lung stimulates surfactant release.
🧠 Surfactant is washing-up liquid for your lungs. It stops the bubbles sticking shut.

🧪 The volumes, in plain words

  • Tidal volume — the air moved in one quiet breath. About 500 mL in a resting adult.
  • Vital capacity — the most you can breathe out after the deepest breath in. It falls with age, weakness, stiff lungs and a splinted diaphragm.
  • Residual volume — the air that always stays behind. You can never empty the lungs completely, and that is what stops them collapsing.
  • Minute ventilation = tidal volume × respiratory rate. Fast and shallow can move the same “minute” number as slow and deep, but far less of it reaches the alveoli.
🧠 Depth beats rate. Deep breaths fill alveoli; fast shallow breaths fill pipes.

🎈 Compliance and recoil — the two properties that decide the work of breathing

COMPLIANCE & RECOIL How easily the lung stretches, and how well it springs back · magnified alveolar clusters, same scale in all three panels COMPLIANCE = how easily it STRETCHES RECOIL = how well it SPRINGS BACK the two are opposites — you can’t max both NORMAL compliance normal · recoil normal capillary ▲ alveolar sacs, magnified Thin, springy walls. Inflates easily on a small effort, and empties by itself when the muscles relax. 🎈 like a well-used party balloon work of breathing: normal STIFF LUNG — LOW compliance hard to inflate · recoil often high capillary pink dashes = normal sac size ▲ alveolar sacs, magnified Thickened, scarred walls; small sacs. Every breath costs extra muscle work. Pulmonary fibrosis, ARDS, pulmonary edema, loss of surfactant. 🎈 like a brand-new balloon you can’t blow it up work of breathing: HIGH FLOPPY LUNG — HIGH compliance fills easily · recoil LOST capillary orange dashes = broken walls ▲ alveolar sacs, magnified Walls destroyed, sacs merged into big floppy spaces. Air goes in but will not come out — air trapping. Emphysema / COPD. 🎈 like a balloon blown up so often that it stays baggy work of breathing: HIGH

Compliance is how easily the lung stretches. Recoil is how well it springs back. A stiff lung is hard to fill; a floppy lung fills easily and will not empty. Either way the work of breathing goes up.

🧠 “Compliance and recoil” = fancy words for stretch and spring.

🚬 The source's warning: what smoking does to compliance

If the alveoli are damaged by years of cigarettes, the sacs won't allow gas exchange — no oxygen exchange. Be precise about which property is lost: in emphysema the walls break down, so recoil is lost and compliance actually rises — the lung fills easily but will not empty. (Where smoke drives scarring and fibrosis instead, compliance falls.) Either way the work of breathing climbs and gas exchange suffers.

  • Smoke destroys alveolar walls, so small sacs merge into big floppy ones with a much smaller total surface area.
  • It also paralyzes the cilia, so mucus is not swept out — more infection, more scarring.
  • The result is air trapping: the patient can get air in but cannot get it out, and the chest becomes barrel-shaped.
  • Smoking cessation is the single most effective respiratory intervention there is. Ciliary function begins to recover within months.
🧠 Air goes in and stays in. That is emphysema in five words.

✅ Nursing actions that directly protect lung mechanics

  • Incentive spirometry — slow, deep inhalation with a hold. The single best post-operative tool.
  • Turn, cough and deep breathe; reposition at least every 2 hours; ambulate early.
  • Sit upright — high Fowler's for anyone short of breath, so the diaphragm can descend.
  • Control pain. A splinting patient cannot take a deep breath, and pain relief is therefore a respiratory intervention.
  • Hydrate (unless fluid-restricted) to keep secretions thin enough to move.
🧠 Deep breaths pop collapsed alveoli back open. Atelectasis is genuinely nurse-preventable.
🔄

PART 3 · EXCHANGE — AND V/Q

AIR MEETING BLOOD

Moving air is only half of it. The air has to meet blood, in the same place, at the same time.

🔄 External and internal respiration

EXTERNAL vs INTERNAL RESPIRATION Two trades, one bloodstream · magnified · read LEFT (in the lung) then RIGHT (in the tissues) KEY O₂ CO₂ low O₂ blood oxygen-rich blood · arrows = which way a gas moves ① EXTERNAL RESPIRATION in the LUNGS — between the alveolus and the blood ② INTERNAL RESPIRATION in the TISSUES — between the blood and the body cells ALVEOLUS air sac from the RIGHT heart pulmonary artery — low O₂ to the LEFT heart pulmonary vein — high O₂ CO₂ out O₂ in the respiratory membrane is thinner than tissue paper DEFINITION External respiration = the exchange of oxygen and carbon dioxide between the ALVEOLI and the PULMONARY BLOOD. nucleus BODY CELL orange ovals = mitochondria — where the oxygen is actually used arrives high in O₂ leaves low in O₂ O₂ in CO₂ out DEFINITION Internal respiration = the exchange of oxygen and carbon dioxide between the BLOOD and the CELLS of the body. same blood, traveling 🧠 EX = EXIT the body EXternal respiration happens where gas EXits the body — at the alveolus. INternal respiration happens INside the tissues. Both are just diffusion: gases roll downhill, from where there is more of them to where there is less. No pump required.

External respiration is the exchange of oxygen and carbon dioxide between the alveoli and the pulmonary blood. Internal respiration is the exchange between the blood and the cells of the body. Same gases, same physics — two different addresses.

🧠 EX = where gas EXits the body. IN = INside the tissues.

➡️ Ventilation is not the same as respiration

  • Ventilation = moving air in and out. It is mechanical — muscles, pressure, volume.
  • Respiration = the actual exchange of gases across a membrane. It is chemistry.
  • You can ventilate beautifully and still not exchange — that is what happens in pulmonary embolism or in a lung full of fluid.
  • And you can have perfect lungs and still fail if nothing is moving the air, as with an opioid overdose.
🧠 Ventilation moves it. Respiration trades it. Two different failures, two different fixes.

⬇️ Why gases move at all — diffusion

  • Gases move from high concentration to low concentration. No pump involved.
  • Alveolar air is high in O₂ → oxygen moves into the blood. Returning blood is high in CO₂ → carbon dioxide moves into the alveolus and is exhaled.
  • Speed depends on surface area, membrane thickness, and the pressure gradient.
  • Every respiratory disease attacks one of those three: it shrinks the field (emphysema, atelectasis), thickens the wall (edema, pneumonia, fibrosis), or flattens the gradient (low FiO₂, altitude).
🧠 Gases roll downhill. Disease either shrinks the field, thickens the wall, or flattens the hill.

⚖️ V/Q — the three units you have to be able to picture

V/Q — VENTILATION vs PERFUSION V = air getting in · Q = blood getting there · you need BOTH, in the same place KEY airflow (V) blood flow (Q) red ✗ = the step that is blocked in that unit NORMAL UNIT air in air alveolus blood flowing O₂ in, CO₂ out — the trade works Air arrives. Blood arrives. Gas exchange happens. V and Q MATCHED SHUNT — no VENTILATION blocked collapsed alveolus blood flowing NO gas exchange in this unit Blood arrives but air does NOT. Blood leaves still deoxygenated. Pneumonia, atelectasis, pulmonary edema, mucus plug. WASTED BLOOD DEAD SPACE — no PERFUSION air in air alveolus clot no blood flow past this alveolus NO gas exchange in this unit Air arrives but blood does NOT. The breath is wasted. Pulmonary embolism, very low cardiac output. WASTED AIR

A normal unit gets both air and blood. A shunt gets blood but no air — wasted blood. Dead space gets air but no blood — wasted air. Both end in hypoxemia, for opposite reasons.

🧠 Shunt = wasted blood. Dead space = wasted air. Say it every time you see V/Q.

🧪 Anatomic dead space — the air that never trades

  • Everything from the nose down to the terminal bronchioles is a pipe. It moves air but exchanges nothing — that volume is the anatomic dead space.
  • Only the alveoli exchange gas. If a question asks where gas exchange happens, the answer is always the alveolus.
  • This is why rapid, shallow breathing is inefficient: if most of each small breath only fills the pipes, very little reaches the alveoli, even though the rate looks impressive.
  • It is also why a deep, slower breath moves far more useful air than a fast, shallow one.
🧠 Pipes don't trade — only the grapes trade.

⚠️ Why a shunt does not respond well to oxygen

Answer first: extra oxygen cannot reach an alveolus that no air is entering.

  • Turning the FiO₂ up enriches the air in ventilated alveoli. In a shunt, the affected units are not ventilated at all — so the blood going past them stays deoxygenated whatever you do.
  • The fix for a shunt is to re-open the units: treat the pneumonia, drain the fluid, re-expand the atelectasis, apply positive pressure.
  • Dead space behaves differently — there the problem is blood flow, so the answer is treating the embolism or the low cardiac output.
🧠 Oxygen fixes a gradient, not a blockage.
🌍

PART 4 · WHAT CHANGES BREATHING

ENVIRONMENT · LIFESTYLE · DRUGS · AGE

The factors the source lists — and what each one actually does to the mechanics.

🌍 Environment

  • Pollution — irritates the airways, damages cilia, worsens asthma and COPD.
  • Elevation / altitude — the air still contains 21% oxygen, but the pressure is lower, so fewer oxygen molecules arrive with each breath. The body responds by hyperventilating, which is why respiratory alkalosis is common at altitude.
  • Temperature — very cold air can trigger bronchospasm; heat and humidity increase the work of breathing.
🧠 At altitude the percentage is the same — the pressure is not.

🚬 Lifestyle

  • Smoking — destroys alveolar walls, paralyzes cilia, reduces compliance and recoil, and leads to decreased lung capacity.
  • Stress — raises the rate and makes breathing shallow and upper-chest; sustained, it can tip into hyperventilation and respiratory alkalosis.
  • A sedentary lifestyle — deconditions the respiratory muscles and reduces lung capacity, so less reserve is available when illness arrives.
  • Obesity — extra weight on the chest wall and abdomen splints the diaphragm and raises the work of breathing, especially lying flat.
🧠 Anything that stiffens the chest wall or weakens the muscles costs you reserve.

🚨 Medications

Some medications decrease lung capacity. The classic example is opioids.

  • Opioids relax the body and blunt the brainstem, so breathing becomes slower and more shallow. Sedatives, benzodiazepines and anesthetics do the same.
  • The source's rule is worth keeping: opioids make the vitals low and slow.
  • Assess the rate and depth, not just the number — a rate of 12 that is barely moving any air is worse than a rate of 10 that is deep.
  • Watch sedation level: increasing drowsiness usually comes before the respiratory rate falls.
  • Never leave a newly opioid-sedated patient unmonitored because “their rate is fine”.
🧠 Sedation score first, respiratory rate second. Sleepiness is the early warning.

👵 Ageing — “from a plump round grape to a shrivelled raisin”

THE AGEING LUNG — grape to raisin Side (sagittal) view of the chest · same scale in both panels · alveolar insets magnified ×the same amount YOUNGER ADULT spine sternum front-to-back (A–P) diameter normal alveoli ×400 plump grapes • Elastic, springy tissue • Strong respiratory muscles • Effective cough reflex • Normal lung capacity OLDER ADULT spine sternum front-to-back (A–P) diameter INCREASED — “barrel chest” alveoli ×400 shrivelled raisins • ↓ lung capacity + ↓ elasticity • Weaker respiratory muscles • ↑ WORK of breathing • ↓ cough reflex → trapped mucus • ↑ risk of pneumonia • Abnormal sleep breathing WHAT IT MEANS FOR CARE 🫁 Older patients tire faster Less reserve. A chest infection uses it up fast. 🧪 Their “normal” may be lower Compare with THEIR baseline, not the textbook. 💧 Keep secretions thin Hydration and humidification — a weak cough cannot shift thick mucus. 🚶 Move them Early ambulation, repositioning, sitting upright. 🎯 Incentive spirometry The best post-op tool for keeping alveoli open. 💊 Care with sedatives They blunt the drive to breathe — reserve is already small. 😴 Ask about sleep Snoring and daytime sleepiness suggest sleep apnea.

With age: decreased lung capacity and elasticity combined with weaker respiratory muscles, leading to increased work of breathing; an increased anterior–posterior chest diameter (the round, barrel-shaped chest); a decreased cough reflex, so foreign material and mucus are harder to expel and the risk of pneumonia rises; and abnormal breathing patterns that can affect sleep, such as sleep apnea.

🧠 Grape → raisin. Less spring, less muscle, weaker cough, rounder chest.

🛋️ Positions that make breathing easier

  • High Fowler's (sitting up ~60–90°) — the default for anyone short of breath. Gravity pulls the abdominal contents down and lets the diaphragm descend.
  • Orthopneic position — sitting up and leaning forward onto a bedside table with the arms supported. It fixes the shoulder girdle so the accessory muscles can pull on the ribs.
  • Tripod — the same idea, done standing or on the edge of the bed. Patients adopt it instinctively; it is a sign of distress, not a preference.
  • Lying flat is the worst position for almost every breathless patient — and the reason orthopnea exists.
🧠 Up and forward. If they have chosen that position, believe them.

⚔️ Ventilation failure vs oxygenation failure — tell them apart

Ventilation failureOxygenation failure
The pump has failed — air is not movingThe exchange has failed — air moves but gas doesn't cross
CO₂ rises (respiratory acidosis)PaO₂ falls; CO₂ may be normal or even low
Opioid overdose, neuromuscular weakness, exhaustion, airway obstruction Pneumonia, pulmonary edema, ARDS, pulmonary embolism
Fix: move air — reverse sedation, support ventilation Fix: fix the membrane or the blood flow — oxygen helps some, but not a shunt

Oxygen treats hypoxemia. It does not treat a patient who is not breathing.

SEE ALSO How CO₂ and HCO₃⁻ read on an arterial gas is worked through on NG-092 ABG Answers.
🧠 Pump problem = CO₂ problem. Membrane problem = O₂ problem.

✅ Assessing the mechanics at the bedside — in order

1
Look before you touch: rate, depth, symmetry, effort, position, color, ability to speak in full sentences.
2
Count for a full minute without telling them you are counting. A typical adult resting rate is 12–20 breaths per minute — children breathe faster, and the normal range is age-specific, so use your pediatric reference.
3
Listen — in the intercostal spaces, on bare skin, comparing side to side, apex to base, front and back.
4
Measure — oxygen saturation, and note what oxygen they are on.
5
Ask — “is this normal for you?” A baseline beats a textbook range every time.
SEE ALSO Auscultation landmarks, the adventitious sounds and the respiratory vocabulary are on NG-170 Key Terms & Lung Sound Locations.
🧠 Look · count · listen · measure · ask.

🎯 Cover & check — eight questions on the mechanics

Q1 · Which way does the diaphragm move to breathe IN, and why? It contracts and flattens downward. That makes the chest cavity bigger, so the pressure inside drops below atmospheric, and air is pushed in from outside.
Q2 · Which part of a quiet breath is passive? Expiration. The muscles simply relax and the stretched lung recoils. Inspiration is always active.
Q3 · Name the four things breathing depends on. A clear airway; an intact CNS, specifically the brainstem; an intact thoracic cavity, especially the diaphragm; and adequate pulmonary compliance and recoil.
Q4 · What do “compliance” and “recoil” mean in plain words? Compliance = how easily the lung stretches. Recoil = how well it springs back. Scarred, hardened alveoli have poor compliance and recoil, and gas exchange suffers.
Q5 · Define external and internal respiration. External = exchange of O₂ and CO₂ between the alveoli and pulmonary blood. Internal = exchange between the blood and the body's cells.
Q6 · Which nerve roots supply the diaphragm, and why does it matter? The phrenic nerve, C3–C5. A cervical cord injury above that level takes out the diaphragm and the patient cannot breathe independently.
Q7 · What is the difference between shunt and dead space? Shunt = blood arrives, air doesn't (pneumonia, atelectasis, pulmonary edema) — wasted blood. Dead space = air arrives, blood doesn't (pulmonary embolism) — wasted air.
Q8 · Give four ageing changes that increase the work of breathing. Decreased lung capacity and elasticity; weaker respiratory muscles; increased anterior–posterior chest diameter; a decreased cough reflex with more trapped mucus (and therefore more pneumonia). Abnormal sleep breathing patterns are common too.
🫁 VOLUME → PRESSURE → AIRMuscles change the volume of the chest; the volume change makes a pressure difference; air flows down that difference. Nothing else.
🔽 DIAPHRAGM DOWN = INContract and flatten to inhale. Relax and dome up to exhale. Inspiration active · quiet expiration passive.
🧠 C3, C4, C5Phrenic nerve. Injury above it and the diaphragm stops. Brainstem = the impulse to breathe.
🎈 STRETCH & SPRINGCompliance = stretch. Recoil = spring back. Scarred, smoke-damaged alveoli lose both — and gas exchange with them.
⚖️ SHUNT vs DEAD SPACEShunt = blood, no air (wasted blood). Dead space = air, no blood (wasted air). Both cause hypoxemia.
👵 GRAPE → RAISINAgeing: ↓ capacity, ↓ elasticity, weaker muscles, barrel chest, ↓ cough reflex, more pneumonia, sleep apnea.