Show the model answerAttempt it first — that is what makes it stick
2 marks
Define end-tidal carbon dioxide. How is it measured?
What earns the marks2 marks
| A precise definition | Two marks — keep it short |
|---|---|
| Name the method | Infrared absorption; do not describe sampling here |
Measurement: infrared absorption spectroscopy
Carbon dioxide has a dipole moment and therefore absorbs infrared radiation, with a peak at 4.26 µm. Clinical analysers use a narrow band of 4.2 to 4.3 µm. Infrared light of that wavelength is passed through a sample chamber of fixed path length and the transmitted intensity is measured.
Beer's law: absorption is proportional to the concentration of the absorbing substance. Lambert's law: absorption is proportional to the path length. Combined, the energy absorbed by carbon dioxide from the narrow infrared band passing through the chamber is proportional to the concentration of absorbing molecules, and that concentration is determined by comparing the absorbance with a known standard.
2 marks
Draw and label a capnogram
What earns the marks2 marks · a drawing
| Draw it first | Large, before writing anything else — 90 seconds for a fifth of the question |
|---|---|
| y-axis labelled | PCO₂ in mmHg or kPa, or concentration as a percentage |
| x-axis labelled | Time in seconds |
| Baseline on zero | It must start at zero |
| All four phases | Numbered on the trace |
| The end-tidal point | Marked, at the end of phase III |
| Expiration and inspiration | Indicated; α and β angles labelled if there is room |
| Phase | What it represents | Shape |
|---|---|---|
| Phase I | Exhalation of carbon dioxide-free gas from the airways — the anatomical dead space | Flat, on a zero baseline |
| Phase II | Rapid S-shaped upward swing as dead-space gas mixes with alveolar gas | Steep, S-shaped |
| Phase III | Alveolar plateau — carbon dioxide-rich gas from the alveolar units | Near-horizontal with a slight upslope; ETCO₂ is the value at its end |
| Phase IV | The inspiratory phase | Descending limb making almost a right-angle turn, falling rapidly to baseline |
Commonly lost: The commonest way to lose this question is to write an essay on carbon dioxide transport for parts (a) and (b), then run out of time for (c) and (d), which carry 6 of the 10 marks.
The α angle sits between phases II and III and is normally about 100 to 110 degrees; it widens with obstruction to expiratory flow. The β angle sits between phase III and the inspiratory downstroke and is normally about 90 degrees; it widens with rebreathing. Neither is required by the question, but naming them demonstrates that the drawing is understood rather than memorised.
3 marks
List the causes of increased ETCO₂
What earns the marks3 marks
| Group by mechanism | Increased production, reduced elimination, equipment |
|---|---|
| Breadth over depth | It says list — cover the groups |
| Mechanism | Causes |
|---|---|
| Increased endogenous production | Malignant hyperthermia · thyroid storm · phaeochromocytoma · sepsis · fever · shivering · seizures · light anaesthesia · release of a limb tourniquet or reperfusion of an ischaemic bed · a rise in cardiac output delivering more carbon dioxide to the lungs |
| Exogenous carbon dioxide | Carbon dioxide administered during laparoscopy · sodium bicarbonate administration · administration of stored blood |
| Reduced removal from the blood | Hypoventilation · reduced alveolar ventilation from increased physiological dead space · increased equipment dead space · exhaustion of the carbon dioxide absorber · airway obstruction and bronchospasm · chronic obstructive pulmonary disease |
| Artefact | Collision broadening by nitrous oxide · an uncalibrated or unzeroed analyser |
3 marks
What are the physiological effects of hypercarbia?
What earns the marks3 marks
| By system | Respiratory, cardiovascular, cerebral, metabolic/renal |
|---|---|
| Breadth again | Three marks for range, not for one system in detail |
Carbon dioxide raises hydrogen ion concentration by spontaneous and carbonic anhydrase-catalysed combination with water to form carbonic acid. It also reacts with free amine groups in proteins to form carbamate compounds. At cellular level it diffuses readily across cell membranes and generates hydrogen ions intracellularly, but intracellular buffering is rapid, reaching about 90% completion within three hours of the onset of hypercarbia.
| System | Effect |
|---|---|
| Cardiovascular | Increased sympathetic discharge with raised plasma adrenaline and noradrenaline, leading to increased myocardial contractility and cardiac output, and an increased risk of arrhythmias. Systemic vasodilatation with warm peripheries. At severe tensions the direct depressant effect on the myocardium and vascular smooth muscle takes over and cardiac output falls. |
| Central nervous | Cerebral vasodilatation, increased cerebral blood flow and intracranial pressure, and lowering of the seizure threshold. Progressive depression of consciousness towards carbon dioxide narcosis at high tensions. |
| Respiratory | Stimulation of central and peripheral chemoreceptors with increased minute ventilation. Enhanced hypoxic pulmonary vasoconstriction with improved ventilation–perfusion matching. Bronchodilatation and increased pulmonary vascular resistance. |
| Oxygen transport | Rightward shift of the oxyhaemoglobin dissociation curve (Bohr effect), favouring tissue unloading; the Haldane effect assists carbon dioxide offloading in the lung. Alveolar PO₂ falls if the inspired oxygen fraction is fixed. |
| Metabolic and renal | Hyperkalaemia through hydrogen ion and potassium exchange; increased ionised calcium; renal compensation with increased hydrogen ion excretion and bicarbonate reabsorption over two to three days. |
| Immunological | Immunomodulatory and protective effects of hypercapnic acidosis, dampening neutrophil and cytokine-mediated injury. |
Taking it further
Viva prompts
Why can infrared absorption not be used to measure oxygen? What would you use instead?
Answer
Oxygen is an elementary, symmetrical molecule with no dipole moment, so it does not absorb infrared radiation. The same is true of nitrogen and the noble gases.
Oxygen is measured instead by paramagnetic analysis, exploiting the two unpaired electrons in its outer shell, or electrochemically by a fuel cell or a polarographic (Clark) electrode.
What is the normal arterial to end-tidal carbon dioxide gradient, why does it exist, and what widens it?
Answer
Normally 2 to 5 mmHg (0.3–0.7 kPa), with PaCO₂ 35–45 mmHg and PETCO₂ 30–40 mmHg.
It exists because alveolar dead space — ventilated but unperfused alveoli — contributes carbon dioxide-free gas that dilutes the alveolar sample.
It widens with hypovolaemia, reduced cardiac output, pulmonary embolism, high airway pressures or excessive positive end-expiratory pressure, chronic lung disease, increasing age and the upright posture.
End-tidal carbon dioxide falls from 38 to 15 mmHg over three breaths. What is your differential, and what do you do first?
Answer
A fall to a low but non-zero value with a preserved waveform points at the circulation: pulmonary or gas embolism, a sudden fall in cardiac output, severe hypotension or major haemorrhage. A fall to absolute zero with no waveform points at the circuit or the airway: disconnection, extubation, complete obstruction or sampling-line failure.
Look at the patient and the chest first, then the circuit and the tube, then feel for a pulse and check the blood pressure and rhythm. Treat a lost waveform as an emergency until it is proven to be a monitoring fault.
Your capnograph reads higher after nitrous oxide is introduced. What has happened?
Answer
Collision or pressure broadening. Nitrous oxide molecules colliding with carbon dioxide molecules broaden its absorption peak, so more infrared is absorbed at the analyser's wavelength than the carbon dioxide alone accounts for, and the reading is too high. Nitrous oxide also absorbs close to the carbon dioxide band, adding spectral overlap. Modern analysers correct for this automatically once the gas mixture is entered or measured.
The trace no longer returns to zero between breaths. What does that mean, and what do you do?
Answer
Inspired gas contains carbon dioxide — rebreathing. The causes are an exhausted absorber, an incompetent unidirectional valve, fresh gas flow too low for the breathing system in use, or channelling within the canister. Increase the fresh gas flow immediately, then change the absorbent and check the valves. Consider a self-inflating bag if the circuit is suspect.
End-tidal carbon dioxide climbs steadily despite increasing minute ventilation. What is the concern?
Answer
A progressive rise that is resistant to increased ventilation indicates increased production rather than reduced elimination, and malignant hyperthermia must be considered — a rising end-tidal carbon dioxide is its earliest and most sensitive sign. Stop the trigger, call for help and dantrolene, and change to a vapour-free breathing system. Other causes of increased production are thyroid storm, phaeochromocytoma, sepsis and prolonged tourniquet release.
During cardiopulmonary resuscitation, end-tidal carbon dioxide rises from 11 to 30 mmHg. What has happened?
Answer
Return of spontaneous circulation. During compressions, end-tidal carbon dioxide is limited by pulmonary blood flow rather than by ventilation, so it reflects the cardiac output compressions generate. A sudden sustained rise without any change in ventilation means pulmonary blood flow has increased. Use it as a prompt to check for a pulse at the next rhythm check rather than interrupting compressions.
What is permissive hypercapnia, and when would you avoid it?
Answer
Accepting a raised PaCO₂ rather than increasing tidal volume or airway pressure to normalise it. It is tolerated in acute respiratory distress syndrome and severe asthma because lung-protective ventilation matters more than a normal number, and because hypercapnic acidosis appears to be anti-inflammatory. Avoid it where raised intracranial pressure makes cerebral vasodilatation dangerous, and where pulmonary hypertension or right ventricular failure makes a further rise in pulmonary vascular resistance unsafe.