11.8 Pulse Oximetry, Capnography and Chest Radiography
Key Takeaways
- The 90% / 60 mmHg anchor point defines the clinical cliff: above an SpO2 of 90% the oxyhemoglobin curve is flat and large PaO2 changes barely move the saturation, while below it the curve is steep and small further falls in PaO2 cause rapid desaturation.
- Carboxyhemoglobin makes the pulse oximeter read falsely normal or high while the patient is severely hypoxic, and methemoglobin drives the reading toward a fixed value near 85% regardless of the true saturation; both require co-oximetry, and pulse oximeters systematically overestimate true saturation in patients with darker skin pigmentation, tripling the rate of occult hypoxemia.
- Waveform capnography is the gold standard for confirming and continuously monitoring endotracheal tube position, the CPR target is an end-tidal CO2 of at least 10 mmHg, and an abrupt sustained rise toward 35-40 mmHg is the earliest sign of return of spontaneous circulation.
- Device landmarks on the chest film: endotracheal tube tip 3-5 cm above the carina, central venous catheter tip at the cavoatrial junction, pulmonary artery catheter tip in a proximal pulmonary artery within the mediastinal shadow, and the intra-aortic balloon pump tip 2-3 cm distal to the left subclavian artery just below the aortic knob.
- Pulmonary venous congestion progresses radiographically from cephalization at a wedge pressure of roughly 13-18 mmHg, to interstitial edema with Kerley B lines at 18-25 mmHg, to alveolar edema above 25 mmHg, and the film lags clinical improvement by 12 to 24 hours.
Pulse Oximetry (Test-Plan Item IV.B.3)
Principle and Its Limits
A pulse oximeter transmits red light at 660 nm and infrared light at 940 nm through a pulsatile vascular bed and compares absorbance at the two wavelengths. Deoxyhemoglobin absorbs more red light and oxyhemoglobin more infrared. The device isolates the pulsatile (arterial) component from the non-pulsatile background and converts the ratio into a saturation using calibration curves derived from healthy volunteers desaturated only to about 70%. Everything below 70% is extrapolation.
Typical accuracy is plus or minus 2 to 3%. An SpO2 of 90% may represent a true SaO2 anywhere from 87 to 93%, which is why titrating oxygen to a single digit is unwise.
The Curve Relationship That Must Be Memorised
| SpO2 | Approximate PaO2 |
|---|---|
| 98-100% | 100 mmHg or more |
| 95% | 80 mmHg |
| 90% | 60 mmHg |
| 80% | 45-50 mmHg |
| 70% | 40 mmHg |
Above 90% the oxyhemoglobin dissociation curve is flat: a PaO2 falling from 100 to 70 mmHg barely moves the saturation, so a reassuring SpO2 can conceal substantial deterioration. Below 90% the curve is steep, and a small further fall in PaO2 produces a rapid drop in saturation. The 90% / 60 mmHg point is the cliff edge, and it is why a patient whose saturation has started to slide needs intervention now rather than another set of vital signs in 15 minutes.
Sources of Error
| Source | Effect on the reading |
|---|---|
| Poor perfusion, vasopressor-induced vasoconstriction, hypothermia, hypotension, Raynaud phenomenon | Signal loss or an unreliable dampened value. Look at the plethysmographic waveform first — an SpO2 without a good pleth is not a number |
| Motion, shivering, tremor | Falsely low or erratic |
| Dark nail polish, artificial nails, dried blood | Falsely low; rotate the probe 90 degrees or move to the earlobe or forehead |
| Ambient or procedural lighting | Falsely high or erratic; shield the probe |
| Carboxyhemoglobin (carbon monoxide poisoning, smoke inhalation, heavy smoking) | Absorbs light almost identically to oxyhemoglobin, so the SpO2 reads falsely normal or high while the patient is profoundly hypoxic. Requires co-oximetry |
| Methemoglobin (benzocaine spray before TEE, dapsone, nitric oxide, phenazopyridine, some nitrates) | Absorbs both wavelengths nearly equally, driving the reading toward a fixed value near 85% regardless of true saturation. Classic saturation gap with a high PaO2 and chocolate-brown blood; treated with methylene blue 1-2 mg/kg IV |
| Intravenous dyes (methylene blue, indigo carmine, indocyanine green) | Transient falsely low reading |
| Severe anemia | Saturation stays normal while oxygen content and delivery are markedly reduced — saturation is a percentage, not a quantity |
| Darker skin pigmentation | Systematic overestimation of true arterial saturation. Occult hypoxemia is roughly three times more common in Black patients, and the bias worsens at lower saturations. The FDA has issued updated guidance directing that oximeter validation studies enrol across the full range of skin pigmentation. Correlate with an arterial blood gas when the number does not match the patient |
| Non-pulsatile or low-pulsatility flow — continuous-flow LVAD, VA-ECMO, deep hypothermia, an intra-aortic balloon pump in a patient with minimal native pulse pressure | Unreliable or absent reading. Use arterial blood gas co-oximetry. On peripheral VA-ECMO, monitor the right hand or ear to detect differential hypoxemia (north-south or Harlequin syndrome) |
Nursing Priorities
Use the waveform to validate every number. Never titrate FiO2 on a poor-quality signal. Escalate a normal SpO2 in a patient who is working hard to breathe rather than being reassured by it. Confirm with an arterial gas whenever the reading and the patient disagree. Set targets deliberately: avoid hyperoxia after cardiac arrest, targeting an SpO2 of about 92 to 98%, and in acute coronary syndrome give supplemental oxygen only when the saturation is below 90%, since routine oxygen in normoxemic infarction offers no benefit and may cause coronary vasoconstriction.
Capnography (Test-Plan Item IV.B.4)
Physiology and the Normal Waveform
End-tidal carbon dioxide (EtCO2) is the partial pressure of carbon dioxide at the end of exhalation, normally 35 to 45 mmHg. The PaCO2-to-EtCO2 gradient is normally only 2 to 5 mmHg, representing alveolar dead space. EtCO2 depends on three things — carbon dioxide production, pulmonary blood flow, and alveolar ventilation — and the middle term is what makes capnography a cardiac monitor rather than merely a respiratory one.
The normal capnogram has four parts: Phase I, the baseline representing anatomic dead space, which should sit at zero; Phase II, the rapid expiratory upstroke; Phase III, the alveolar plateau with a slight upslope, at the very end of which EtCO2 is read; and Phase 0, the inspiratory downstroke back to baseline.
Abnormal Waveforms
| Pattern | Meaning |
|---|---|
| Shark-fin shape — loss of the plateau with a sloped, prolonged upstroke | Obstructive expiratory flow: bronchospasm, asthma, COPD, or a kinked or partially obstructed endotracheal tube. Improves with bronchodilator therapy |
| Curare cleft — a notch cut into the alveolar plateau | Spontaneous respiratory effort against the ventilator; neuromuscular blockade wearing off |
| Elevated baseline — Phase I fails to return to zero | Rebreathing: exhausted carbon dioxide absorbent, incompetent expiratory valve, or inadequate flow on non-invasive ventilation |
| Sudden drop to zero | Extubation, disconnection, complete tube obstruction, apnea, or ventilator failure — assess the airway immediately |
| Sudden drop to a low but non-zero value | Partial obstruction or circuit leak, or an abrupt fall in pulmonary blood flow: massive pulmonary embolism, cardiac arrest, sudden severe hypotension |
| Gradual rise | Hypoventilation, or rising carbon dioxide production from fever, sepsis, shivering or malignant hyperthermia |
| Gradual fall | Falling cardiac output, hypovolemia, hyperventilation, or falling temperature and metabolic rate |
Cardiac Applications
- Endotracheal tube confirmation. Continuous waveform capnography is the gold standard for confirming and continuously monitoring tube position. An esophageal intubation produces no sustained waveform. Auscultation, chest rise, misting and the chest radiograph are adjuncts, not the standard, and a radiograph confirms depth but not that the tube is in the trachea rather than the esophagus.
- CPR quality feedback. Because pulmonary blood flow during arrest is generated almost entirely by chest compressions, EtCO2 is a real-time compression-quality monitor. Target 10 mmHg or higher. A persistently lower value means compressions are too shallow, too slow, without full recoil, or too frequently interrupted — change the compressor. Do not increase the ventilation rate to raise the number: hyperventilation washes out carbon dioxide, raises intrathoracic pressure, and reduces venous return and coronary perfusion pressure.
- Detecting return of spontaneous circulation. An abrupt, sustained rise in EtCO2, typically toward 35 to 40 mmHg, is the earliest indicator of ROSC and identifies it without interrupting compressions for a pulse check.
- Prognostication. An EtCO2 that remains below 10 mmHg after 20 minutes of high-quality advanced cardiac life support in an intubated patient is associated with an extremely low likelihood of ROSC and may contribute to a multimodal decision to stop. It is never used alone, and never in a patient who is not intubated.
- Pulmonary embolism and low cardiac output. Obstruction of pulmonary blood flow creates alveolar dead space, so the PaCO2-to-EtCO2 gradient widens. A falling EtCO2 with a stable or rising PaCO2 in a patient with sudden dyspnea points toward pulmonary vascular obstruction or a fall in cardiac output rather than a ventilation problem.
- Procedural sedation. During cardioversion, transesophageal echocardiography, ablation and catheterisation laboratory cases, capnography detects apnea and airway obstruction minutes before pulse oximetry desaturates, because a preoxygenated patient on supplemental oxygen maintains saturation long after ventilation stops. This is a heavily tested point.
- Capnography also verifies that a small-bore feeding tube has not entered the airway during placement.
Chest Radiography (Test-Plan Item IV.B.5)
A Systematic Approach
Check quality first, using RIPE: Rotation (the spinous process should sit midway between the clavicular heads), Inspiration (8 to 10 posterior or 5 to 6 anterior ribs visible above the diaphragm), Penetration (vertebral bodies faintly visible behind the cardiac silhouette), and Entire field included. Then read in a fixed order: airway and tracheal position, bones and soft tissues, cardiac silhouette and mediastinum, diaphragms and costophrenic angles, lung fields, and finally every line, tube and device.
A portable anteroposterior film magnifies the cardiac silhouette. Never diagnose cardiomegaly on a portable AP film, and never on a poor-inspiration film.
Device Position
| Device | Correct radiographic landmark | Consequence of malposition |
|---|---|---|
| Endotracheal tube | Tip 3-5 cm above the carina with the head in neutral position, roughly at the level of the aortic arch | The tip descends about 2 cm with neck flexion and rises about 2 cm with extension. Too deep gives right mainstem intubation with left lung collapse; too shallow risks vocal cord injury and extubation |
| Central venous catheter | Tip in the lower superior vena cava at the cavoatrial junction, approximately at or just below the level of the carina and lateral to the right tracheobronchial angle | A tip in the right atrium or ventricle risks arrhythmia and perforation with tamponade; a tip abutting the vessel wall at an angle, common with left-sided lines, risks perforation |
| Pulmonary artery catheter | Tip in a proximal right or left main pulmonary artery, within the mediastinal shadow and no more than about 2 cm lateral to the mediastinal border | Distal migration risks pulmonary artery rupture and pulmonary infarction; a persistently wedged tracing with the balloon deflated requires immediate action. Waveform interpretation is covered in the hemodynamic monitoring sections |
| Intra-aortic balloon pump | Radiopaque tip 2-3 cm distal to the origin of the left subclavian artery, just below the aortic knob, roughly at the level of the carina, near the second to third intercostal space | Too high occludes the left subclavian or carotid artery, causing left arm ischemia with a diminished left radial pulse, or stroke. Too low occludes the renal and mesenteric arteries, causing acute oliguria and a rising creatinine |
| Pacemaker and ICD leads | Right atrial lead in the appendage with an anteromedial J curve; right ventricular lead at the apex or septum; CRT left ventricular lead in a lateral or posterolateral coronary sinus tributary; ICD leads show the shock coils as thickened segments | Compare with the prior film for dislodgement, lead fracture, insulation break, or the coiled lead of twiddler syndrome |
| Chest tube | All side holes, marked by the interruption in the radiopaque stripe, inside the pleural space. Apical and anterior for air, basal and posterior for fluid | A side hole outside the chest wall produces a persistent air leak and subcutaneous emphysema |
| Mediastinal or pericardial drain | Retrosternal within the mediastinum | Sudden cessation of drainage with rising and equalising filling pressures suggests clotted tubing and tamponade |
| Nasogastric or feeding tube | Tip and the proximal side port below the diaphragm in the stomach | Coiling in the esophagus predisposes to aspiration; passage into a bronchus or the pleura can cause pneumothorax. Radiographic confirmation is the standard before feeding; pH testing and auscultation are not |
| Temporary epicardial pacing wires | Fine wires exiting the subxiphoid region after cardiac surgery | Retained fragments may be visible after removal and should be documented |
Cardiac and Pulmonary Findings
- Cardiothoracic ratio. On a PA film, maximum transverse cardiac width divided by maximum internal thoracic width; above 0.50 defines cardiomegaly. Invalid on AP portable and poor-inspiration films.
- Chamber enlargement. Left atrial enlargement produces a double density behind the right heart border, splaying of the carina beyond about 90 degrees, and posterior esophageal displacement on the lateral view. Left ventricular enlargement displaces the apex inferolaterally. Right ventricular enlargement fills the retrosternal clear space on the lateral view. Right atrial enlargement bulges the right heart border.
- Pulmonary venous congestion, which correlates loosely with pulmonary capillary wedge pressure:
- Cephalization / vascular redistribution at a wedge of roughly 13-18 mmHg — upper-lobe vessels equal to or larger than lower-lobe vessels on an upright film.
- Interstitial edema at roughly 18-25 mmHg — peribronchial cuffing, hazy indistinct vascular and hilar margins, thickened fissures, and Kerley B lines, the short horizontal 1-2 cm lines meeting the pleura at right angles at the lateral bases.
- Alveolar edema above roughly 25 mmHg — perihilar bat-wing airspace opacity, air bronchograms, and pleural effusions, often larger on the right. Radiographic change lags clinical change by 12 to 24 hours in both directions, so the film is not the tool for judging the response to the last dose of furosemide.
- Pleural effusion. Blunting of the posterior costophrenic angle on the lateral view detects as little as about 50 mL; lateral costophrenic blunting on the PA view requires roughly 200 mL. On a supine film fluid layers posteriorly and produces a diffuse hazy opacification of the entire hemithorax with vascular markings still visible through it — easily overlooked.
- Widened mediastinum — more than 8 cm on an AP film at the level of the aortic knob, or more than 6 cm on PA — raises concern for aortic dissection or traumatic injury, supported by an indistinct or irregular aortic knob, a left apical pleural cap, rightward displacement of the trachea or nasogastric tube, and a left pleural effusion. A normal chest film does not exclude dissection; CT angiography or transesophageal echocardiography does.
- Pneumothorax. On an upright film, a visceral pleural line with absent lung markings beyond it, best seen apically. On a supine film air collects anteriorly and basally, so look instead for the deep sulcus sign — an abnormally deep and lucent lateral costophrenic sulcus — plus a hyperlucent hemidiaphragm, an unusually sharp cardiac border or pericardial fat pad, and the double-diaphragm sign. Tension pneumothorax is a clinical diagnosis treated with immediate decompression; do not wait for a film.
- Post-sternotomy findings. Sternal wires should form an intact, aligned vertical midline row. Displaced, rotated, fractured or migrated wires, or a new midline lucency between the wire halves, suggest sternal dehiscence — correlate with a clicking or unstable sternum on palpation and new wound drainage, and escalate. Also expect left lower lobe atelectasis and a small left pleural effusion after internal mammary artery harvest, and watch for new mediastinal widening from postoperative bleeding or tamponade.
Nursing Translation
Verify device position on every post-insertion film and after any repositioning, transport or resuscitation. Document the endotracheal tube depth at the lip or teeth and compare it every shift. Correlate the film with the hemodynamics rather than reading either in isolation. And when the film and the patient disagree, re-examine the patient.
Twenty minutes after benzocaine spray was used for topical pharyngeal anesthesia before a transesophageal echocardiogram, a patient becomes dusky and dyspneic. The pulse oximeter reads 85% and will not rise on 100% oxygen by non-rebreather mask. An arterial blood gas shows a PaO2 of 240 mmHg, and the blood is described as chocolate brown. What should the nurse suspect?
During CPR for a witnessed ventricular fibrillation arrest, an intubated patient's continuous waveform capnography shows an end-tidal CO2 of 7 mmHg after six minutes of compressions. What should the team do?
A patient whose intra-aortic balloon pump was placed two hours ago has had urine output fall from 60 mL/h to 12 mL/h, with a rising creatinine. The left arm is warm with a strong radial pulse and no neurologic changes. What should the nurse suspect and verify first?