Respiratory Physiology &
Oxygen Therapy

• Interpret SpO₂ in context and state the correct oxygen target for general vs at-risk (COPD / CO₂-retainer) patients
• Explain the oxyhaemoglobin dissociation curve and why a falling SpO₂ below 90% signals a steep drop in PaO₂
• Titrate oxygen to target — up, down, or hold — using the Oxygen Target Interpreter
• Differentiate type 1 from type 2 respiratory failure and adjust the oxygen plan accordingly
• Read a basic ABG: pH, PaCO₂, PaO₂, HCO₃ — acute vs chronic compensation
• Recognise impending respiratory failure from the work of breathing and the whole-patient picture
• Distinguish a COPD exacerbation from an asthma exacerbation and select a first-line approach

This module was developed from bedside workflow analysis across North American emergency and acute-care settings — not from a flow-rate chart taped to a wall. Oxygen is the single most administered drug in the hospital, yet it is the one most often given without a target, without a prescription, and without anyone deciding when to turn it down.

Module 09 is not against oxygen. It is against thoughtless oxygen — the reflex that reads a number, opens a flow meter, and walks away; that mistakes 100% for “safe”; that never asks what the saturation is costing the patient in work of breathing, and never asks whether this is a person who will stop breathing if you over-oxygenate them.

On most wards, oxygen is treated as harmless comfort — something you give because the patient “looks like they could use it.” But oxygen is a pharmacological agent with indications, a dose, a target, and real toxicity. Given without a target, it routinely overshoots. Hyperoxia is not benign: it causes vasoconstriction (including coronary and cerebral), absorption atelectasis, oxidative injury, and — in the CO₂ retainer — a rise in arterial CO₂ that can progress to narcosis and arrest.

Pulse oximetry estimates the percentage of haemoglobin saturated with oxygen. It is fast, non-invasive, and indispensable — but it is an estimate, and it has blind spots. Knowing where it lies is part of reading it honestly.

The relationship between SpO₂ and the partial pressure of oxygen in the blood (PaO₂) is not a straight line — it is a sigmoid curve.^[5] This single shape explains why the 90% mark matters so much and why oxygen behaves the way it does at the bedside.

The central skill of oxygen therapy is matching the dose to a target range and then adjusting — up, down, or hold — to keep the patient inside it. For most acutely unwell adults the target is 94–98%.^[1] But for patients at risk of hypercapnic (type 2) respiratory failure — established COPD, obesity hypoventilation, neuromuscular disease, chest-wall disease, prior CO₂ retention — the target is the lower 88–92%, because over-oxygenation can suppress their respiratory drive and let CO₂ rise.

Respiratory failure is the lungs failing at one of two jobs: getting oxygen in, or getting carbon dioxide out. Telling the two apart changes everything about how you give oxygen.

An arterial blood gas tells you what the pulse oximeter cannot: the CO₂, the pH, and whether the kidneys have had time to compensate. A simple, repeatable reading order keeps you out of trouble.

The most important respiratory assessment costs nothing and takes ten seconds: watch the patient breathe. A normal saturation bought with enormous effort is a patient about to crash. The work of breathing is the early-warning system the monitor doesn’t have.

Breathlessness is frightening, and fear makes breathing worse — anxiety raises the respiratory rate, tightens the chest, and burns oxygen. A calm, present clinician is part of the treatment. Keep words short (a breathless patient cannot follow long sentences), stay at eye level, and tell them what you are doing and why.

The patient who arrests from a respiratory cause almost always announces it first — in signs that precede the saturation drop. Knowing the pre-arrest pattern buys you the minutes that matter.

A saturation of 100% feels like success. On a CO₂ retainer flooded with oxygen, it can be the opposite: the SpO₂ looks flawless while the CO₂ quietly climbs toward narcosis and the patient slides toward arrest — with the monitor reassuring everyone the whole way down. The default reflex chases the highest number; WestNet keeps the patient inside their target and watches the whole picture. The best saturation is the right one, not the highest one.

The following patterns recur across North American acute admissions. This section presents composite, anonymous cases drawn from recurring systemic habits — not any single patient, clinician, or institution. The lesson is about the reflex, not the person.

These beliefs are common, well-intentioned, and once taught as standard — the point is not that anyone was careless, but that the evidence has moved. The root issue is a single idea: that more oxygen is always better. It usually is not. The aim is to treat the patient and the cause of their breathlessness — and the person, not the label on the chart.

The device is part of the dose. Some deliver a low, variable oxygen concentration; others a high, precise one. Choosing the wrong device for the patient type is one of the commonest ways oxygen therapy goes wrong. Tap through the main devices — what they deliver, where they go wrong, and who they suit.

The thoughts that come most naturally at the bedside are often the ones that lead to over-oxygenation. Tap any card to flip the reflexive instinct into the physiologically sound one — and see why it matters.

Both present as a breathless, wheezy patient — but the oxygen target, the CO₂ risk, and the first-line plan differ. Mark what you actually observe; the tool weighs the picture, indicates the likely lean, and flags the first-line approach. It supports clinical judgement — it never replaces it.

A pulse oximeter and an ABG describe the blood. They do not describe the lungs. A structured hands-on examination — inspect, palpate, percuss, auscultate — localises the problem and often names it before any number returns. The discipline is to do the same sequence every time so nothing is skipped under pressure.

§07 gave you the five-step order. This section puts it to work. Set a pH, a PaCO₂, and a bicarbonate, and the interpreter names the primary acid–base disturbance and whether compensation looks acute or chronic. It applies the same logic every time — pH first, then the respiratory component, then the metabolic one — so you can rehearse the pattern until it is automatic.

Pulse oximetry tells you about oxygenation, and it lags. End-tidal CO₂ (EtCO₂) tells you about ventilation, breath by breath, in real time. Where SpO₂ can stay reassuring for minutes after a patient stops breathing on oxygen, the capnograph flattens almost immediately. It is the earliest non-invasive warning of a ventilatory problem.

Oxygen cannot reach the lungs through a blocked airway. Before any saturation can be fixed, the airway must be open. The approach is a ladder: start with the simplest manoeuvre that works, escalate only as far as you need, and call for skilled airway help early. Most airway emergencies are rescued by basic manoeuvres, not by advanced equipment.

When the problem is that air is not moving — not that oxygen is missing — the answer is ventilation, not a higher FiO₂. This is the single most important reframe in type 2 failure: you can flood a tiring COPD patient with oxygen and watch them die of CO₂ narcosis, because oxygen does not move air. Ventilation does.

Asthma is reversible airway narrowing — which is exactly why it can be fatal: it looks recoverable right up until the patient exhausts. The clinical task is to grade severity accurately, treat early and aggressively, and recognise the life-threatening features that mean “call critical care now.” This is a framework for recognition — all drug choices and doses follow your local protocol and GINA.

A COPD exacerbation is a sustained worsening beyond normal day-to-day variation — more breathlessness, more cough, more sputum, often a change in sputum colour. It is the setting where every lesson in this module converges: controlled oxygen, a low target, an early ABG, and a low threshold for NIV. Confirm all management against GOLD and your local protocol.

Wheeze is not the only cause of breathlessness, and treating every dyspnoeic patient as “asthma or COPD” misses the ones who are drowning in fluid, throwing clots, or bleeding out their oxygen-carrying capacity. Oxygen corrects the saturation; it never corrects the cause. Select a presentation below to see the pattern that points to it and the direction of management.

Pneumonia is infection of the lung tissue itself: alveoli fill with inflammatory fluid, gas exchange fails, and the patient becomes hypoxaemic (a type 1 picture). It is common, it is treatable, and it is still a leading cause of death — because severity is under-recognised at the bedside.

A pulmonary embolism is a clot lodged in the pulmonary circulation, blocking blood flow to part of the lung. It is dangerous precisely because it hides: the chest can sound clear, the chest film can look normal, and the patient can be breathless and hypoxaemic with no obvious cause. PE is missed when clinicians wait for a sign that never comes.

A pneumothorax is air trapped in the pleural space, between lung and chest wall, collapsing the lung beneath it. Most are not immediately life-threatening — but one form, the tension pneumothorax, kills within minutes and is treated on clinical suspicion alone, before any imaging.

Not every breathless, crackly chest is a chest problem. In cardiogenic pulmonary oedema the lungs are flooding because the left heart is failing to clear blood forward — pressure backs up into the lungs and fluid leaks into the alveoli. The lungs are the victim; the heart is the culprit. Oxygen alone treats neither.

Acute respiratory distress syndrome (ARDS) is the lung’s severe inflammatory response to an insult — severe pneumonia, sepsis, aspiration, major trauma, pancreatitis. The alveoli flood with protein-rich fluid, the lung stiffens, and oxygen will not cross. It is the extreme end of type 1 failure, and it is defined by hypoxaemia that resists oxygen.

An increasing number of patients on general wards have a tracheostomy — an artificial airway through the front of the neck. They breathe differently, they are oxygenated differently, and when they deteriorate the usual reflexes can fail or even harm. A few principles prevent the commonest disasters.

Spirometry is how chronic airway disease is objectively defined, rather than guessed. It measures how much air a patient can blow out and how fast — and the shape of that limitation separates obstruction from restriction. Understanding the two key numbers makes the COPD-versus-asthma distinction (§15) concrete.

Breathing does not stop being clinically important when the patient falls asleep. Obstructive sleep apnoea and obesity hypoventilation are common, frequently undiagnosed, and directly relevant to oxygen therapy — because the obesity-hypoventilation patient is exactly the kind of CO₂ retainer who can be harmed by uncontrolled oxygen.

This module has spent thirty sections on the consequences of failing lungs. The single most powerful intervention against the commonest cause — COPD — is not an oxygen device or a ventilator. It is helping the patient stop smoking. Treating the exacerbation and ignoring the cigarette is treating the symptom and feeding the disease.

The clinical positions in this module are drawn from peer-reviewed literature indexed by the U.S. National Library of Medicine (PubMed / PMC) and from the published guidelines of major clinical-guideline bodies.

Sixteen short-answer questions plus an interactive self-check below. Pass threshold: 11/16 for CE credit (upon accreditation approval).

Course Director: WestNet Medical Clinical Education Division
Publication: WestNet Medical Publications • WestNet Catalog 731985456635 • ISBN 978-0-XXXXX-XXX-X (Pending)
Platform: WestNet Unified Health Platform / HealthOS v3.6