Pulse oximetry and capnography: a nursing guide

Pulse oximetry and capnography are the two most widely used continuous monitoring modalities in acute care nursing. Together they give the nurse a real-time window into two distinct but inseparable physiological processes: oxygenation and ventilation. SpO2 tells you whether the blood is carrying enough oxygen; end-tidal CO2 (EtCO2) tells you whether the patient is ventilating effectively enough to eliminate carbon dioxide. Understanding what each measurement reflects – and crucially, what it does not – is what separates competent monitoring from safe monitoring.

This guide covers the physiology behind both modalities, how to interpret values and waveforms, where common errors occur, and how to apply both tools across the clinical scenarios you will encounter most often: post-intubation confirmation, procedural sedation, CPR, and ventilated ICU patients. Twenty NCLEX high-yield tips close the article.

Pulse oximetry: how it works and what it measures

The physics of SpO2

A pulse oximeter probe contains two light-emitting diodes that transmit light at 660 nm (red) and 940 nm (infrared) through a vascular tissue bed to a photodetector. Oxyhemoglobin and deoxyhemoglobin absorb these two wavelengths at different ratios. By comparing the pulsatile (arterial) component of absorbance at both wavelengths, the device calculates the percentage of hemoglobin that is bound to oxygen – the functional arterial oxygen saturation (SpO2).

The key distinction nurses must understand is functional vs fractional saturation. Functional saturation is the percentage of hemoglobin capable of carrying oxygen that is saturated. Fractional saturation is the percentage of total hemoglobin that is saturated – and total hemoglobin includes dyshemoglobins like carboxyhemoglobin (COHb) and methemoglobin (MetHb). Standard two-wavelength pulse oximeters measure functional saturation only, which is why carbon monoxide poisoning produces a falsely normal SpO2 (see Limitations below).

The oxyhemoglobin dissociation curve

The relationship between SpO2 and the partial pressure of oxygen (PaO2) is not linear – it follows the S-shaped oxyhemoglobin dissociation curve. Three inflection points are clinically essential:

• PaO2 ~100 mmHg → SpO2 ~98–99%: Normal healthy adult at rest. Increasing PaO2 above 100 mmHg adds very little additional saturation – the curve has plateaued. This is the “flat” upper portion.
• PaO2 ~60 mmHg → SpO2 ~90%: This is the critical inflection point at the “shoulder” of the curve. Above this point, large drops in PaO2 cause only small drops in SpO2. Below it, the curve steepens sharply – small further drops in PaO2 cause disproportionately large drops in saturation. A patient at SpO2 90% is at the cliff edge, not in a stable zone.
• PaO2 ~40 mmHg → SpO2 ~75%: Normal mixed venous oxygen level – the saturation at which tissues return deoxygenated blood to the right heart.

The curve shifts right (reduced hemoglobin affinity for O2, promotes offloading) with acidosis, hyperthermia, hypercapnia, and increased 2,3-DPG. It shifts left (increased affinity, impairs offloading at tissues) with alkalosis, hypothermia, hypocapnia, fetal hemoglobin, and carbon monoxide poisoning. In clinical practice, the right-shift is a compensatory adaptation during hypoxia; the left-shift in CO poisoning is one reason why tissue hypoxia is so severe despite a normal-appearing SpO2.

For a full discussion of the arterial blood gas values that quantify PaO2 and SaO2 directly, see the guide to ABG interpretation.

Probe placement

The finger is the default site – well-perfused, simple to apply, and comfortable. Place the probe so the light source sits over the nail bed and the emitter and detector face each other directly; follow the manufacturer’s site guidance.

Earlobe: Ear probes respond to a change in saturation more quickly than finger probes (Jubran 2015). Useful during rapid clinical deterioration when you need the most current value, and as an alternative site when the fingers are cold or poorly perfused.

Forehead (reflectance probe): Measures SpO2 via reflection rather than transmission. It reads from the supraorbital artery, which is less affected by vasoconstriction than the digits. In one study of apneic anesthetized patients, the forehead probe detected desaturation to 90% at 94 seconds and the finger probe at 100 seconds (Jubran 2015). Useful in patients with cold, poorly perfused extremities.

Nasal alar / nose: Reflectance probe; used when other sites are inaccessible.

Toe / foot: Used in neonates and infants, or when upper extremity sites are unavailable. Note that toe response time is slower than finger and earlobe.

Plethysmographic waveform quality

Most monitoring systems display a plethysmographic (pleth) waveform alongside the numeric SpO2 value. This waveform represents the pulsatile variation in blood volume as detected by the photodetector. A good signal shows a regular, tall, rounded waveform with a clear dicrotic notch – the small notch on the downstroke that represents aortic valve closure. A poor signal is flat, irregular, or noisy with no identifiable dicrotic notch. Never trust a SpO2 numeric value accompanied by a poor pleth waveform – it is the device reporting noise, not physiology.

When the waveform is poor, reposition the probe, try the earlobe, warm the extremity, or dry the probe site before documenting the reading.

Interpreting SpO2 values

Normal ranges and clinical thresholds

Population-specific targets: COPD and chronic hypercapnia

Some patients with COPD and other chronic lung, chest wall, or neuromuscular conditions develop a rising PaCO2 and respiratory acidosis when given too much oxygen. The traditional explanation is loss of “hypoxic drive”, but the British Thoracic Society guideline (BTS 2017, section 6.3.1) ranks the mechanisms differently. Worsening ventilation-perfusion mismatch, as oxygen releases hypoxic vasoconstriction in poorly ventilated lung, is the main cause. Reduced hypoxic drive comes second and contributes only a small part, followed by the Haldane effect, absorption atelectasis, gas density, and rebreathing.

The practical rule is the same either way. For patients at risk of hypercapnic respiratory failure, BTS recommends a target SpO2 of 88–92% pending blood gas results, titrating oxygen to stay within that range. In a prehospital trial of patients with COPD exacerbations, high-flow oxygen carried a mortality of 9% versus 2% with oxygen titrated to 88–92% (Austin 2010). An SpO2 of 97–100% in an at-risk patient on supplemental oxygen should prompt the nurse to reduce the flow rate per the prescription, not feel reassured. Never withhold oxygen from a hypoxemic patient because of hypercapnia concerns: titrate to the target range instead, and if a blood gas shows a normal PaCO2, the target can be reset to 94–98%. A full discussion of oxygen delivery devices and titration is in the guide to oxygen therapy nursing.

Limitations and sources of error

Understanding where pulse oximetry fails is as important as knowing normal values. A falsely normal SpO2 in a deteriorating patient is dangerous; a falsely low reading in a stable patient triggers unnecessary interventions. The table below covers the most clinically significant sources of error.

Continuous vs spot-check monitoring

Continuous monitoring is indicated for any patient at risk of sudden respiratory deterioration: post-operatively, during and after procedural sedation, on opioid infusions or patient-controlled analgesia, receiving supplemental oxygen for acute illness, or with known cardiorespiratory instability.

Spot-check monitoring (periodic measurement, typically q4h with vital signs) is appropriate for stable patients without active respiratory conditions and not on therapies that suppress ventilation.

The monitoring frequency should escalate with clinical acuity, and the decision to upgrade from spot-check to continuous must be individualized to the patient’s risk profile – it cannot be driven solely by the current SpO2 value.

Capnography: waveform analysis and clinical use

What EtCO2 measures

Capnography measures the concentration of carbon dioxide in exhaled gas, expressed as a partial pressure (mmHg) or percentage. End-tidal CO2 (EtCO2) is the CO2 concentration at the end of a complete exhalation – the point at which exhaled gas most closely approximates alveolar CO2 and, by extension, arterial CO2 (PaCO2).

In a patient with normal lung physiology and normal cardiac output, EtCO2 runs approximately 2–5 mmHg below PaCO2. This gradient exists because exhaled gas is diluted by dead-space ventilation (gas from airways that never participates in gas exchange). Normal EtCO2 is 35–45 mmHg. When pulmonary dead space increases – as in pulmonary embolism, severe COPD, or low cardiac output – the EtCO2-PaCO2 gradient widens. In these patients, EtCO2 underestimates PaCO2 more significantly, and the absolute EtCO2 value alone is less useful than the trend.

Two types of capnography are in clinical use:

• Mainstream capnography: Sensor sits directly in the airway circuit. Fast response, no sample lag. Used on intubated patients.
• Sidestream capnography: Gas is aspirated from the circuit or nasal cannula sampling line to an external sensor. Slightly slower response; works on non-intubated patients via nasal cannula or nasal-oral sampling cannula.

Normal capnogram waveform: four phases

A normal capnogram is rectangular with sloped transitions and has four distinct phases. Every nurse monitoring ventilated patients or patients under sedation should be able to identify these on sight.

Phase I (baseline / anatomical dead space): EtCO2 = 0 (or near 0). This is the early part of exhalation – CO2-free gas from the anatomical dead space (trachea, bronchi) exits before alveolar gas reaches the sensor. Normally flat at zero.

Phase II (expiratory upstroke): EtCO2 rises rapidly as alveolar gas displaces dead-space gas at the sensor. Should be steep and linear on a normal capnogram.

Phase III (alveolar plateau): EtCO2 reaches its maximum and forms a near-horizontal plateau as alveolar gas – relatively uniform in CO2 concentration – is continuously exhaled. The plateau should be flat or only slightly upward-sloping. The value at the end of Phase III is the EtCO2 reading. The slight upward slope normally seen reflects heterogeneity in alveolar emptying times.

Inspiratory downstroke (labeled phase 0 in Kodali’s nomenclature; some texts call it phase IV): CO2 rapidly drops back to zero as fresh inspired gas flushes the sensor. Should be steep and return to baseline (zero). The angle between Phase II and Phase III is the alpha angle, which widens in airway obstruction; the near-90° angle between Phase III and the inspiratory downstroke is the beta angle (Kodali 2013).

Abnormal capnogram patterns

Clinical applications of capnography

Post-intubation confirmation

Continuous waveform capnography is the gold standard for confirming endotracheal tube (ETT) placement in the trachea. When the ETT is correctly placed in the trachea, CO2 is exhaled with each breath and a normal rectangular waveform appears immediately. When the tube is in the esophagus, no CO2 waveform is detected – the EtCO2 reads zero (or falls to near zero within the first few breaths, as any CO2 from carbonated beverages or gastric gas is rapidly washed out).

Do not rely on chest rise, epigastric auscultation, or misting in the tube alone to confirm placement – these are adjuncts, not confirmatory tests. Chest X-ray confirms tip position relative to the carina but cannot be obtained fast enough to serve as the primary confirmation method. The capnogram waveform is immediate, continuous, and unambiguous. Full protocols for ETT placement confirmation are covered in airway management nursing.

Procedural sedation monitoring

Capnography detects hypoventilation and apnea before SpO2 drops, and the lead is longest in a patient breathing supplemental oxygen (Krauss 2007). This detection lag is the most clinically critical reason to use capnography during procedural sedation.

When a sedated patient begins to hypoventilate or becomes apneic, oxygen stored in the lungs keeps the saturation up for a time. In a well-preoxygenated healthy adult, SpO2 can stay above 90% for several minutes of apnea, and the window is much shorter in obese, critically ill, or pediatric patients (Weingart 2012). During this window, capnography has already detected the problem: EtCO2 has stopped cycling (no waveform = apnea) or the value is rising (hypoventilation with CO2 accumulation). Waiting for SpO2 to drop before intervening means the apnea has already gone undetected for some time.

For moderate procedural sedation, the 2018 American Society of Anesthesiologists guideline recommends monitoring ventilation with capnography in addition to clinical observation, unless it is precluded or invalidated by the patient, procedure, or equipment. Assess and document EtCO2 waveform and value at the same intervals as SpO2, heart rate, and blood pressure (ASA 2018 suggests checking responsiveness and blood pressure at 5-minute intervals once moderate sedation is established). See conscious sedation nursing for the full monitoring framework.

CPR and cardiac arrest

During cardiac arrest, cardiac output falls to zero or near zero, and pulmonary blood flow ceases. Without blood flow through the pulmonary vasculature, CO2 cannot be transported to the lungs for exhalation – EtCO2 drops precipitously, typically to less than 10 mmHg or absent waveform.

EtCO2 serves two distinct functions during resuscitation:

1. Compression quality feedback: EtCO2 correlates with cardiac output during CPR. The 2025 AHA adult ALS guideline suggests aiming for an EtCO2 of at least 10 mmHg, and ideally 20 mmHg or higher, as a sign of mechanically adequate compressions. A persistently low value should prompt a check of compression depth, rate, and recoil, although a very low EtCO2 also reflects the underlying arrest and carries a poor prognosis (Sanders 1989).

2. ROSC detection: When spontaneous circulation returns, cardiac output is restored, CO2 is rapidly transported to the lungs, and EtCO2 rises sharply (Falk 1988). AHA 2025 notes that an abrupt rise predicts ROSC but that no absolute cutoff has been identified; a sudden increase of more than about 10 mmHg may indicate ROSC. Confirm with a pulse check at the next planned pause rather than stopping compressions on the EtCO2 change alone.

In intubated adults, an EtCO2 of 10 mmHg or less after 20 minutes of advanced life support may be considered as one part of a multimodal decision to stop resuscitation, never as a stand-alone rule (AHA 2025).

For a full discussion of defibrillation and post-ROSC care, see cardioversion and defibrillation nursing. Capnography protocols in code situations are covered in rapid response and code blue nursing.

Ventilated ICU patients

In mechanically ventilated patients, EtCO2 provides a continuous, non-invasive approximation of PaCO2 and enables real-time ventilator management without requiring serial ABGs for every adjustment. The key clinical uses include:

• Trending PaCO2: Once the EtCO2-PaCO2 gradient is established from an ABG (normal: 2–5 mmHg), EtCO2 trends reliably track PaCO2 changes. A rising EtCO2 in a ventilated patient indicates CO2 retention – increase respiratory rate or tidal volume per order.
• Detecting circuit leaks and disconnections: A sudden drop in EtCO2 to zero or near zero in a ventilated patient is a circuit disconnection or accidental extubation until proven otherwise.
• PEEP adjustment guidance: Changes in EtCO2 following PEEP adjustments can reflect changes in dead-space ventilation and alveolar recruitment.
• Detecting acute changes in pulmonary perfusion: A sudden decrease in EtCO2 in a ventilated patient (without ventilator changes) can indicate a new pulmonary embolism or acute decrease in cardiac output – both reduce CO2 delivery to the lungs.

Ventilated patient management, weaning criteria, and ventilator settings are covered in depth in mechanical ventilation nursing.

Non-intubated patients via nasal sampling cannula

Nasal capnography cannulas deliver supplemental O2 from one port while aspirating exhaled gas samples from nasal prongs for EtCO2 analysis. This enables combined O2 delivery and capnography monitoring in spontaneously breathing patients without an artificial airway. Signal quality is generally good for patients breathing through their nose; mouth-breathing patients require an oral-nasal sampling cannula.

Indications include: procedural sedation, post-operative monitoring in PACU, patients on opioid infusions, any spontaneously breathing patient in whom ventilation adequacy cannot be assumed from SpO2 alone.

Monitoring during patient transfer

Portable capnography is essential for any high-acuity patient transfer – whether inter-unit (floor to ICU) or inter-facility. During transport, SpO2 and EtCO2 should both be monitored continuously, with waveform display confirmed prior to leaving the originating unit. Intubated patients are at particular risk during transport for inadvertent extubation, and a flat EtCO2 waveform on a transport monitor is the earliest detectable sign. Document both values and waveform quality on the transfer handoff record.

When using bag-valve-mask ventilation during transport, capnography confirms each ventilation is reaching the lungs. For BVM technique and circuit management, see bag-valve-mask nursing.

Using SpO2 and EtCO2 together

Pulse oximetry and capnography monitor two independent physiological processes. SpO2 measures oxygenation – whether hemoglobin is carrying oxygen. EtCO2 measures ventilation – whether CO2 is being eliminated. Each has blind spots that the other covers.

What SpO2 detects that capnography misses: Hypoxemia in patients with adequate ventilation – hypoxia from diffusion impairment, V/Q mismatch, or low FiO2 in a patient breathing adequately. Capnography can be completely normal while the patient is severely hypoxemic.

What capnography detects that SpO2 misses: Hypoventilation and apnea in patients on supplemental oxygen, rising CO2 (hypercarbia) before it causes SpO2 change, esophageal intubation, circuit disconnection, ROSC during CPR, inadequate chest compressions. A patient who is apneic for 90 seconds and well pre-oxygenated may still show SpO2 of 97–98%; their capnogram will be flat.

Scenario-based interpretation

Post-operative patient on 3 L/min nasal cannula, SpO2 97%, EtCO2 rising from 40 to 55 mmHg, respiratory rate dropping from 14 to 8 breaths/min: This patient is hypoventilating. SpO2 is reassuringly normal and will remain so for another minute or more – the supplemental O2 is masking the problem. Capnography has caught it. Stimulate the patient, reduce opioid if ordered, notify provider, prepare for reversal agent if respiratory depression is opioid-induced.

Sedated patient undergoing colonoscopy, SpO2 95%, EtCO2 flat waveform for 30 seconds: The patient is apneic. SpO2 has not yet dropped. Capnography has detected the apnea. Stimulate the patient verbally and physically, apply jaw thrust, prepare for BVM ventilation if no response, alert the proceduralist.

Intubated ICU patient, SpO2 88%, EtCO2 48 mmHg: Both oxygenation and ventilation are impaired. SpO2 below target indicates hypoxemia (increase FiO2 or PEEP); elevated EtCO2 indicates CO2 retention (increase respiratory rate or tidal volume per order). This is a combined oxygenation and ventilation problem – both parameters must be addressed. ABG ordered to confirm and guide adjustments.

CPR in progress, SpO2 unobtainable (no perfusion), EtCO2 rises abruptly from 8 to 42 mmHg: Probable ROSC. Check for a pulse and blood pressure at the next pause in compressions. Do not delay pulse check waiting for SpO2 to read – there will not be a SpO2 value until perfusion is restored.

Nursing monitoring protocol

Documentation requirements

Document the following at every monitoring interval:

• SpO2 value and probe location
• Supplemental oxygen in use (device type, flow rate or FiO2)
• EtCO2 value and waveform quality (if capnography in use)
• Respiratory rate
• Patient’s subjective respiratory effort and comfort
• Any alarms triggered and nursing response

For capnography, document whether the waveform is present, morphology (normal rectangular vs abnormal pattern), and any trend changes since the previous documentation point.

Monitoring frequency

Minimum documentation frequencies by context:

• Procedural sedation: Continuous monitoring throughout procedure; document q5 minutes and at baseline, during procedure, and post-procedure recovery intervals per facility policy
• Post-operative (PACU): Continuous monitoring; document per Aldrete/PADSS score intervals (typically q15 min until discharge-ready)
• ICU / mechanically ventilated: Continuous monitoring; document q1h or per unit protocol
• Ward patient on supplemental O2: Minimum q4h; q1–2h if unstable
• Spot-check for stable ward patient: With routine vital signs (typically q4–8h)

Provider notification thresholds

Contact the provider or activate rapid response for:

• SpO2 below the prescribed target range (94–98% for most patients, 88–92% if at risk of hypercapnia) that does not correct with position change and oxygen titration, or a rising oxygen requirement to stay in range
• A new EtCO2 below about 30 mmHg (hyperventilation, possible alkalosis or reduced perfusion) or above about 50 mmHg (significant hypoventilation or CO2 retention); these are common protocol values, so use your facility’s thresholds
• Sudden waveform change – particularly absent waveform in a previously intubated patient
• Any upward trend in EtCO2 with concurrent decrease in respiratory rate (evolving hypoventilation)
• SpO2 drop that is occurring rapidly rather than gradually, regardless of absolute value

Facility protocols may specify tighter thresholds for specific patient populations (post-cardiac surgery, neurological monitoring). Always follow the more conservative threshold – facility protocol or clinical judgment – whichever requires earlier escalation.

Patient and family education

Explaining the monitor

Patients and families frequently become anxious about monitoring equipment, particularly when alarms sound. A brief, clear explanation at the start of monitoring reduces anxiety and improves cooperation.

For the pulse oximeter: “This small clip on your finger measures the oxygen level in your blood. It shines a light through your skin – it doesn’t hurt and doesn’t draw blood. We’ll see a number on the screen showing your oxygen percentage. If the number drops too low or the signal is lost, an alarm sounds so we can check on you.”

For capnography via nasal cannula: “This is a special nasal cannula that both delivers oxygen and samples the air you breathe out. It measures the carbon dioxide you exhale, which tells us how well you’re breathing. It doesn’t go into your airway – it just sits at your nose.”

Managing alarm anxiety

Reassure patients that alarms are precautionary – most are triggered by movement, probe position, or a brief interruption and do not indicate a clinical problem. However, explicitly tell the patient: “If the alarm sounds and it bothers you, press your call button – do not remove the probe yourself, because we need to see the signal to know everything is fine.”

For families: explain that a monitoring alarm does not automatically mean something is wrong. Staff will assess and determine whether it represents a true clinical change or a technical artifact. Encourage them to notify the nurse rather than attempt to adjust or silence equipment themselves.

NCLEX review: 20 high-yield tips

Summary

Pulse oximetry and capnography are complementary monitoring modalities that provide real-time assessment of two separate and essential respiratory functions. SpO2 is the nurse’s window into oxygenation – whether hemoglobin is carrying sufficient oxygen to meet metabolic demand. EtCO2 is the window into ventilation – whether CO2 is being eliminated effectively and the airway is patent.

Competent use of these tools requires more than reading the numeric values. It requires understanding where each modality can mislead – from nail polish and poor perfusion affecting SpO2, to the EtCO2-PaCO2 gradient widening in disease states – and recognizing the waveform patterns that carry the most clinical urgency: the absent waveform of esophageal intubation, the shark fin of bronchospasm, the rising EtCO2 that heralds ROSC. Used together and interpreted in context, they form one of the most powerful surveillance systems available to the bedside nurse.

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