Details of respiratory system monitoring of patient under anesthesia

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ASA Standards for Basic Anesthetic Monitoring ventilation oxygenation capnography current

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Respiratory system monitoring during anesthesia

Respiratory monitoring aims to ensure adequate oxygenation, ventilation, airway patency, and mechanical ventilation throughout anesthesia. It is required because anesthetic drugs, opioids, neuromuscular blockers, and airway devices can cause hypoventilation, apnea, airway obstruction, bronchospasm, aspiration, and accidental disconnection.

Respiratory monitoring assesses gas movement through the airways, alveolar gas exchange, and systemic oxygenation. Routine clinical monitors mainly reflect pulmonary mechanics and global gas exchange. Miller's Anesthesia, 10e, p. 5440.

1. Clinical observation

Continuous direct observation remains essential, even with electronic monitors.

Assess:

Chest and abdominal movement
Respiratory rate, rhythm, and depth
Movement of the reservoir bag
Airway sounds by auscultation
Position, patency, and security of face mask, supraglottic airway, or endotracheal tube
Signs of upper-airway obstruction, such as paradoxical chest movement, stridor, snoring, or absent airflow
Cyanosis, although it is a late and unreliable sign, especially under operating-room lighting
Condensation in the endotracheal tube, which is only a rough indicator of expired gas

Clinical assessment can identify obstruction, apnea, bronchospasm, circuit disconnection, or inadequate tidal volume, but it cannot reliably detect hypoxemia or hypercapnia early.

2. Pulse oximetry - monitoring oxygenation

Pulse oximetry (SpO₂) continuously estimates arterial hemoglobin oxygen saturation.

What it detects

Hypoxemia
Falling oxygen saturation due to apnea, hypoventilation, airway obstruction, bronchospasm, atelectasis, accidental extubation, or low inspired oxygen
Quality of peripheral perfusion through the displayed plethysmographic waveform

Key points

A variable-pitch pulse tone and low SpO₂ alarm should be audible.
It is mandatory during anesthesia as a quantitative measure of oxygenation.
Normal SpO₂ is usually 95% or greater in a healthy patient breathing room air, but values must be interpreted in clinical context.
During supplemental oxygen administration, saturation may remain normal for several minutes despite complete apnea. Therefore, pulse oximetry is a relatively late indicator of hypoventilation.

Limitations

Poor peripheral perfusion, vasoconstriction, shock, hypothermia
Motion artifact
Nail polish or pigmented dyes
Dyshemoglobinemia, especially carboxyhemoglobin and methemoglobin
It does not measure PaO₂, PaCO₂, tidal volume, or adequacy of ventilation.

The ASA requires a quantitative method of oxygenation assessment, such as pulse oximetry, during all anesthetics. The ASA monitoring standard also requires the low-alarm limit and pulse tone to be audible.

3. Inspired oxygen concentration - FiO₂ monitoring

During general anesthesia with an anesthesia machine, an oxygen analyzer measures oxygen concentration in the breathing system.

Purpose

Confirms delivery of an adequate inspired oxygen concentration
Detects hypoxic gas mixtures caused by pipeline failure, empty oxygen supply, wrong gas delivery, machine malfunction, or misconnections

A low FiO₂ alarm must be enabled. This monitor checks what oxygen is delivered to the circuit, whereas pulse oximetry checks the patient's resulting oxygenation.

4. Capnography - monitoring ventilation

Capnography continuously measures and displays expired carbon dioxide against time. It provides both a waveform, called a capnogram, and a numerical end-tidal carbon dioxide value (EtCO₂).

It is the most useful routine monitor of ventilation and airway integrity.

Uses

Confirms tracheal intubation
Detects apnea, hypoventilation, airway obstruction, bronchospasm, rebreathing, and circuit disconnection
Assesses adequacy of ventilation
Helps assess the effectiveness of chest compressions during cardiac arrest
Detects return of spontaneous circulation by a sudden sustained rise in EtCO₂
Helps identify reduced pulmonary perfusion, such as severe hypotension, pulmonary embolism, or cardiac arrest

Normal capnogram phases

Phase	Description
Phase I	Dead-space gas, normally near-zero CO₂
Phase II	Rapid upstroke as alveolar gas mixes with dead-space gas
Phase III	Alveolar plateau
EtCO₂	Highest CO₂ concentration at the end of expiration
Phase 0	Inspiratory downstroke back to baseline

EtCO₂ is often about 35-45 mmHg in a normally ventilated adult, but the clinical target depends on the case and patient. PaCO₂ is generally a few mmHg higher than EtCO₂ because of alveolar dead space.

Important capnogram abnormalities

Finding	Likely causes
No trace or sudden loss of trace	Apnea, esophageal intubation, extubation, disconnection, complete airway obstruction, depleted CO₂ absorber, cardiac arrest
Gradually rising EtCO₂	Hypoventilation, reduced minute ventilation, rebreathing, increased CO₂ production
Low EtCO₂	Hyperventilation, low cardiac output, pulmonary embolism, major hemorrhage, circuit leak
Sloping “shark-fin” expiratory upstroke	Bronchospasm, COPD, partial airway obstruction, kinked endotracheal tube
Baseline fails to return to zero	Rebreathing due to exhausted CO₂ absorbent, incompetent expiratory valve, inadequate fresh-gas flow
Sudden rise in EtCO₂	Hypoventilation, release of tourniquet, bicarbonate administration, malignant hyperthermia, return of spontaneous circulation

For an endotracheal tube or supraglottic airway, its correct position must be confirmed clinically and by detection of exhaled CO₂. Continuous quantitative EtCO₂ monitoring should continue from insertion until extubation or transfer to postoperative care. This is specified in the ASA standard.

5. Respiratory rate and apnea monitoring

Respiratory rate may be obtained from:

Capnography
Impedance pneumography
Ventilator measurements
Observation of chest movement

A respiratory-rate value alone can be misleading. A patient may have a normal rate but very low tidal volume, producing inadequate alveolar ventilation. Capnography and clinical observation are therefore more informative.

6. Airway pressure monitoring

In patients receiving positive-pressure ventilation, airway-pressure monitoring helps identify airway, lung, circuit, and ventilator problems.

Peak inspiratory pressure (PIP) rises in:

Bronchospasm
Secretions or mucus plug
Kinked tube
Patient biting the tube
Decreased lung compliance
Pneumoperitoneum or surgical retraction
Pulmonary edema
Tension pneumothorax
Excessive tidal volume

Plateau pressure is measured during an inspiratory hold and reflects alveolar pressure more closely. A high plateau pressure suggests reduced lung or chest-wall compliance.

Interpretation

High peak pressure with normal plateau pressure suggests increased airway resistance, for example bronchospasm or tube obstruction.
Both high peak and high plateau pressure suggest reduced compliance, for example atelectasis, pulmonary edema, pneumoperitoneum, or pneumothorax.

Low-pressure alarms can detect circuit disconnection, leak, accidental extubation, or inadequate gas delivery.

7. Exhaled tidal volume and minute ventilation

Modern anesthesia workstations display:

Inspired and expired tidal volumes
Respiratory rate
Minute ventilation
Leak volume
Pressure-volume and flow-volume loops

These parameters help confirm that the set tidal volume is actually delivered and exhaled. A discrepancy between inspired and expired volumes suggests a circuit leak, cuff leak, bronchopleural fistula, or leak around a supraglottic airway.

For mechanically ventilated patients, an audible alarm capable of detecting breathing-system disconnection is required by the ASA ventilation standard.

8. Spirometry and flow-volume loops

Spirometry measures airflow, volumes, and pressures in the anesthesia circuit.

It can assist in detecting:

Bronchospasm
Air trapping and auto-PEEP
Small tidal volumes
Incomplete expiration
Circuit obstruction
Leaks
Altered respiratory mechanics

A flow-volume loop that does not return to baseline before the next breath indicates incomplete expiration and possible air trapping.

9. Arterial blood gas analysis

An arterial blood gas (ABG) is not required routinely but is valuable in high-risk patients, prolonged procedures, major surgery, severe lung disease, major blood loss, or unexplained abnormalities.

It directly measures:

PaO₂
PaCO₂
pH
Bicarbonate
Base excess
Lactate, if included
Electrolytes and hemoglobin, depending on analyzer

ABG is the reference test when EtCO₂ may not accurately reflect PaCO₂, such as during severe lung disease, major V/Q mismatch, low cardiac output, obesity, one-lung ventilation, or pulmonary embolism.

10. Neuromuscular monitoring and recovery of respiration

Residual neuromuscular blockade can cause upper-airway obstruction, impaired cough, reduced tidal volume, hypoventilation, and aspiration after extubation.

Quantitative train-of-four monitoring should guide reversal and extubation. A train-of-four ratio of at least 0.9 is generally used to indicate adequate recovery from neuromuscular blockade, alongside clinical assessment of ventilation and airway protection.

11. Additional or advanced respiratory monitoring

Used selectively according to patient condition and procedure:

Transcutaneous CO₂ monitoring: useful when continuous noninvasive CO₂ monitoring is needed, especially in prolonged cases or when capnography is unreliable.
Lung ultrasound: can rapidly identify pneumothorax, pleural effusion, atelectasis, pulmonary edema, and consolidation.
Electrical impedance tomography: assesses regional ventilation distribution and lung recruitment, mainly in specialized settings.
Continuous arterial pressure monitoring and ABG sampling: useful in major thoracic, vascular, or critically ill cases.
Near-infrared spectroscopy: assesses regional tissue oxygenation, not ventilation directly.

Lung ultrasound and electrical impedance tomography are increasingly used for perioperative assessment of pneumothorax, edema, consolidation, pleural fluid, aeration, and recruitment. Miller's Anesthesia, 10e, p. 5440.

Monitoring requirements by anesthetic technique

Situation	Essential respiratory monitoring
General anesthesia with airway device	Clinical observation, SpO₂, inspired O₂ analyzer, continuous capnography, airway-pressure alarms, tidal volume and minute ventilation monitoring
Controlled mechanical ventilation	All above plus continuous disconnect alarm and airway pressure monitoring
Moderate or deep sedation / monitored anesthesia care	Clinical observation, SpO₂, and continuous exhaled CO₂ monitoring whenever feasible
Regional anesthesia with minimal/no sedation	Continuous clinical assessment of ventilation and oxygenation monitoring as appropriate
Recovery room / PACU	SpO₂, respiratory rate and clinical observation; capnography for patients at increased risk of hypoventilation, especially opioid-treated, OSA, obese, or deeply sedated patients

Summary

The core respiratory monitors during anesthesia are:

Clinical observation and auscultation
Pulse oximetry for oxygenation
FiO₂ analyzer for inspired oxygen delivery
Capnography for ventilation, airway patency, and confirmation of tracheal intubation
Airway pressure, tidal volume, minute ventilation, and disconnect alarms during mechanical ventilation
ABG and advanced techniques when clinically indicated

The key principle is: pulse oximetry detects oxygenation, while capnography detects ventilation and airway problems earlier. Both are needed for safe anesthetic care.

Principle and working of pulse oximeter and effect of abnormal hemoglobin on pulse oximeter

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Pulse oximeter: principle and working

A pulse oximeter is a noninvasive monitor that estimates arterial hemoglobin oxygen saturation (SpO₂) and pulse rate. It measures functional saturation:

[ \text{SpO₂} \approx \frac{\text{Oxyhemoglobin (HbO₂)}}{\text{Oxyhemoglobin (HbO₂) + deoxyhemoglobin (HHb)}} \times 100 ]

It does not directly measure PaO₂, oxygen content, ventilation, or the amount of oxygen dissolved in plasma. Costanzo Physiology, 7e, p. 226.

Basic principle

Pulse oximetry combines:

Spectrophotometry: different hemoglobin species absorb different wavelengths of light.
Photoplethysmography: arterial blood volume changes with each heartbeat.

It follows the Beer-Lambert law, where light absorption depends on the concentration of a substance and the distance travelled by light through it.

Probe components

A conventional transmission probe, commonly placed on a finger, toe, or earlobe, has:

Two light-emitting diodes:
- Red light: approximately 660 nm
- Infrared light: approximately 940 nm
A photodetector on the opposite side of the tissue.

Deoxyhemoglobin (HHb) absorbs relatively more red light at 660 nm.
Oxyhemoglobin (HbO₂) absorbs relatively more infrared light at 940 nm.

How it distinguishes arterial blood

The sensor receives light after it has passed through:

Skin, bone, connective tissue
Venous blood
Capillary blood
Arterial blood

Most of these produce a constant, non-pulsatile absorption signal. Arterial blood volume alone increases and decreases with each cardiac pulse, producing the pulsatile component.

The monitor:

Separates the pulsatile arterial component from constant background absorption.
Calculates the ratio of pulsatile absorption at red and infrared wavelengths.
Compares this ratio with calibration curves derived from healthy volunteers.
Displays the estimated arterial oxygen saturation as SpO₂ and the pulse waveform/rate.

Thus, pulse oximetry selectively estimates arterial saturation because arterial blood is pulsatile, whereas venous and tissue absorption are largely constant. Costanzo Physiology, 7e, p. 226. Conventional probes use red light at about 660 nm and infrared light around 900-940 nm. Roberts and Hedges' Clinical Procedures in Emergency Medicine, pp. 63-64.

Important distinction: functional versus fractional saturation

Measurement	Formula	Meaning
Functional saturation	HbO₂ / (HbO₂ + HHb)	What a standard two-wavelength pulse oximeter estimates
Fractional oxyhemoglobin saturation	HbO₂ / total Hb species	Includes HbO₂, HHb, COHb, MetHb, and other hemoglobin species

A standard pulse oximeter assumes only two major hemoglobin forms, oxyhemoglobin and deoxyhemoglobin. Therefore, it can give misleading results when abnormal hemoglobin species are present.

A co-oximeter, usually performed on an arterial or venous blood sample, uses four or more wavelengths and can directly measure oxyhemoglobin, deoxyhemoglobin, carboxyhemoglobin, and methemoglobin.

Effect of abnormal hemoglobin on pulse oximetry

1. Carboxyhemoglobin - COHb

Cause

Carbon monoxide poisoning, smoke inhalation, faulty heaters, vehicle exhaust exposure, or heavy smoking.

Effect on SpO₂

Falsely high or normal SpO₂ reading.

Carboxyhemoglobin absorbs light at wavelengths that standard pulse oximeters may interpret as oxyhemoglobin. Therefore, a patient with significant carbon monoxide poisoning may have a displayed SpO₂ of 98%-100% despite severe tissue hypoxia.

Clinical implication

Standard pulse oximetry is unreliable in carbon monoxide poisoning.
PaO₂ on an ABG may also be normal because PaO₂ measures dissolved oxygen, not hemoglobin-bound oxygen.
Confirm with co-oximetry, which gives the COHb percentage.

A normal pulse oximeter reading does not exclude carbon monoxide poisoning.

2. Methemoglobin - MetHb

Cause

Oxidant drugs or chemicals, for example:

Benzocaine or prilocaine local anesthetic sprays
Dapsone
Nitrates/nitrites
Nitroglycerin in some settings
Aniline dyes
Certain antimalarials

Effect on SpO₂

Methemoglobin absorbs both red and infrared light relatively similarly. With rising MetHb concentration, the standard two-wavelength oximeter tends to show a reading near 85%, regardless of the true arterial oxygen saturation.

At low MetHb levels, the SpO₂ may be mildly underestimated.
With substantial MetHb, often greater than 10%, the reading may remain around 85% even if the true SaO₂ is much lower or higher.

Clinical implication

Suspect methemoglobinemia if there is:

Cyanosis that does not improve as expected with oxygen
SpO₂ around 85% that is resistant to change
A discrepancy between a normal/high PaO₂ and a low SpO₂, called a saturation gap
Chocolate-brown blood

Confirm using co-oximetry. Roberts and Hedges' Clinical Procedures in Emergency Medicine, pp. 63-64.

3. Sulfhemoglobin - SulfHb

Cause

Uncommon. It may occur after exposure to sulfur-containing drugs, for example some sulfonamides, and certain oxidant medications.

Effect on SpO₂

Sulfhemoglobin can cause low or unreliable SpO₂ measurements and may be confused with methemoglobin by some co-oximeters. It can also produce cyanosis with relatively preserved PaO₂.

Clinical implication

Routine pulse oximetry cannot identify or quantify sulfhemoglobin. Specialized laboratory assessment may be necessary.

4. Fetal hemoglobin - HbF

Effect on SpO₂

Minimal clinically important effect. Conventional pulse oximeters are generally accurate in neonates despite high HbF levels.

However, newborns can deteriorate rapidly because of their limited oxygen reserve, so trend monitoring and clinical assessment remain important.

5. Hemoglobin variants - hemoglobinopathies

Examples include HbS, HbC, HbE, and rare unstable hemoglobins.

Effect on SpO₂

Most common variants do not significantly affect pulse oximetry when the hemoglobin is normally oxygenated. However:

Rare variants with altered light-absorption spectra can cause falsely low or falsely high SpO₂.
Variants with altered oxygen affinity may produce a mismatch between SpO₂ and PaO₂.
In sickle cell disease, standard SpO₂ is usually usable, but confirmation with co-oximetry or ABG is appropriate when results conflict with the clinical picture.

6. Severe anemia

Anemia usually does not substantially change the percentage saturation if the monitor has an adequate pulsatile signal. However, it markedly reduces arterial oxygen content, despite a normal SpO₂.

[ \text{Oxygen content} = (1.34 \times Hb \times SaO₂) + (0.003 \times PaO₂) ]

Therefore, a severely anemic patient may have SpO₂ 100% but inadequate oxygen delivery to tissues.

Summary table

Hemoglobin form/condition	Effect on standard SpO₂	Best confirmatory test
Carboxyhemoglobin	Falsely high or normal	Co-oximetry for COHb
Methemoglobin	Trends toward about 85%	Co-oximetry for MetHb
Sulfhemoglobin	Unreliable, often low	Specialized co-oximetry/laboratory testing
Fetal hemoglobin	Usually little effect	Routine monitoring generally reliable
Rare Hb variants	Variable false high/low values	Co-oximetry, ABG, hemoglobin analysis if needed
Severe anemia	SpO₂ may be normal despite low O₂ content	Hemoglobin measurement and clinical assessment

Key examination points

Pulse oximeter uses two wavelengths, red 660 nm and infrared 940 nm.
It measures pulsatile arterial absorption and removes non-pulsatile tissue and venous absorption.
It estimates functional saturation, not PaO₂ or total oxygen content.
It cannot reliably detect COHb, MetHb, or sulfhemoglobin.
COHb causes falsely high SpO₂.
MetHb drives SpO₂ toward approximately 85%.
When dyshemoglobinemia is suspected, obtain a blood sample for multiwavelength co-oximetry.

What is PI reading on pulse oximeter

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PI on a pulse oximeter means Perfusion Index.

It indicates the strength of the pulsatile arterial blood flow at the site of the probe, usually a finger, toe, or ear lobe.

[ \text{PI} = \frac{\text{pulsatile (arterial) light absorption}}{\text{non-pulsatile light absorption from tissue, venous blood, etc.}} \times 100 ]

In the plethysmographic waveform, it is commonly expressed as:

[ \text{PI} = \frac{AC}{DC} \times 100 ]

AC component: changing absorption produced by each arterial pulse
DC component: constant absorption from tissues, venous blood, and non-pulsatile arterial blood

Interpretation

Higher PI: stronger peripheral pulse and better signal/peripheral perfusion at the sensor site.
Low PI: weak pulsatile flow at the probe site, often due to peripheral vasoconstriction or poor perfusion.

A low PI can occur with:

Cold extremities or hypothermia
Shock or low cardiac output
Hypovolemia
Peripheral vasoconstriction, anxiety, pain, or vasopressor use
Peripheral arterial disease
Incorrect or poorly placed probe

Important cautions

PI is not the same as SpO₂. It does not measure oxygen saturation.
It is not a direct measurement of cardiac output or whole-body tissue perfusion.
The actual numerical range and any cutoff differ between device brands and clinical settings. The trend in an individual patient is usually more useful than a single reading.
A low PI means the SpO₂ reading may be less reliable if the monitor has difficulty detecting a stable pulsatile signal.

PI is a pulse-oximeter-derived ratio of the pulsatile arterial signal to the non-pulsatile signal and reflects local peripheral perfusion, as described in a recent review.

Abnormal patterns of EtCO2 with different pathologies

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