Kirby Index: Definition, Advantages, Disadvantages, Clinical Relevance, and Uses of This Measurement Ratio

It is a proportion that indirectly measures lung injury in the pediatric stage; its proven application is as a predictor of mortality.

The Kirby index refers to PaO2 / FiO2 (a measure of lung function/fraction of inspired oxygen).

The PaO2 / FiO2 ratio is the ratio between the partial pressure of arterial oxygen and fractional inspired oxygen, also known as the Carrico index and the PF ratio (PaO2 / FiO2).

Although its diagnostic utility is discussed at sea, it is a widely used clinical indicator of hypoxemia. The normal level is> 500mmHg.

For many years, clinicians have relied on it to define and characterize the severity of acute respiratory distress syndrome (ARDS). This ratio remains a central element of the new definition of ARDS (Berlin definition).

Also, doctors use this ratio to:

  • Track change in lung conditions and establish positive end-expiratory pressure (PEEP).
  • Assess response to different ventilation strategies and decide the need for advanced supportive treatment modalities (e.g., paralysis, prone position, and extracorporeal membrane oxygenation).

Despite having the merit of simplicity and availability, PaO2 / FIO2 is more complex to interpret than what is recognized and can sometimes be misleading.


This risk is particularly present if one does not understand or consider the critical determinant of each patient’s PaO2 / FIO2 ratio and why this ratio may change over time.


Quick and simple, it can be used as a rough guide to determine if there is a significant Aa gradient: PaO2 should = FiO2 x 500 (eg 0.21 x 500 = 105 mmHg).

They are used in SMART-COP (systolic blood pressure, multilobar infiltrates, albumin, respiratory rate, tachycardia, confusion, oxygen, and pH) for intensive ventilation or vasopressor support in community-acquired pneumonia (PF mmHg ratio if age <50 years or PF ratio <250mmHg if age> 50y).

It is used as part of the definition of Berlin acute respiratory distress syndrome (PF ratio <300 mmHg) and is correlated with mortality.


Depending on the barometric pressure, normal lungs (with an average Aa gradient) will have lower PF (PaO2 / FiO2) ratios at high altitude and higher PF (PaO2 / FiO2) ratios at supra-atmospheric pressures.

Hypoxemia due to alveolar hypoventilation (high partial pressure of carbon dioxide) cannot be distinguished from other causes, such as V / Q mismatch (while the Aa gradient can), which is highly dependent on the fraction of inspired oxygen, is partly due to the shape of the Hb -O2 dissociation curve.

Highly dependent on CaO2-CvO2, which tends to fluctuate markedly in sepsis, the PF ratio (PaO2 / FiO2) should only be used as a general rule of thumb to detect an Aa gradient when:

Carbon dioxide partial pressure is normal, and the shunt is not suspected.

Oxygenation index

The oxygenation index is used in intensive care medicine to measure the fraction of inspired oxygen (FiO2) and its use within the body.

A lower oxygenation index is better; this can be inferred from the equation itself. As a person’s oxygenation improves, they will be able to achieve a higher lung function measurement with a lower fraction of inspired oxygen.

This would be reflected in the formula as a decrease in the numerator or an increase in the denominator, thus reducing the oxygenation index.

Typically, an oxygenation index threshold is set for when a neonate needs to be placed on extracorporeal membrane oxygenation (ECMO), for example,> 40.

Clinical relevance of the PaO2 / FiO2 ratio

The PaO2 / FIO2 ratio is a commonly used indicator of lung function in critically ill patients.

Any index that describes pulmonary oxygenation or gas exchange should not vary with the fraction of inspired oxygen.

And that the physiological effects of the variable fraction of inspired oxygen, namely, hypoxic vasoconstriction and absorption atelectasis, are minor when the fraction of inspired oxygen is varied over range.

Although pulmonary gas exchange rates should not vary with the fraction of inspired oxygen, this is not the case for positive end-expiratory pressure (PEEP) or other airway pressure measurements.

Indeed, positive end-expiratory pressure is a therapeutic intervention, the increase of which should increase alveolar pressure, recruit alveoli, and thus improve gas exchange.

Therefore, it is difficult to see the usefulness of measuring lung function/fraction of inspired oxygen x mean airway pressure -> PaO2 / (FiO2 × MAP), which should consider the effects of changes in blood pressure. Airway pressure.


FiO2 = fractional inspired oxygen; MAP = mean arterial pressure; PaO2 = arterial oxygen tension; PEEP = positive end expiratory pressure.

Kirby index (PaO2 / FiO2) uses

In the absence of a reliable direct marker of lung injury, gas exchange is commonly used to define respiratory failure (e.g., hypoxic versus hypercapnic), as well as the degree of lung dysfunction/injury (eg, acute respiratory distress syndrome mild to severe).

For hypoxic respiratory failure in general and acute respiratory distress syndrome in particular, the PaO2 / FIO2 ratio is the most common index of impaired gas exchange. It is a central element in the definition of acute respiratory distress syndrome.

The recently revised definition (the so-called Berlin definition) has not changed its importance. The PaO2 / FIO2 ratio is still necessary to define acute respiratory distress syndrome and characterize its severity (mild, moderate, or severe).

This ratio is also used to identify the population with acute respiratory distress syndrome most likely to benefit from specific support modalities, such as prone position or paralysis.

Finally, this ratio is also usually calculated at the bedside to follow the course of acute respiratory distress syndrome or the response to specific intervention and help establish a positive end-expiratory pressure level in individual patients.

Despite its simplicity and availability, the PaO2 / FIO2 ratio can be complex to interpret and misleading at the bedside if one does not understand or consider its various physiological determinants.

Determinant of the PaO2 / FIO2 ratio in patients with acute respiratory distress syndrome

To appreciate the limitation of applying this ratio to characterize the degree of lung injury in a given patient and to understand that sometimes this ratio changes over time regardless of the degree of lung injury.

It is essential to review the critical clinical factors that determine the ratio (PaO2 / FIO2) in critically ill patients.

The primary determinant of arterial oxygen partial pressure in a healthy individual is alveolar oxygen content (PAO2).

Only a negligible shunt is present when the ventilation-to-perfusion (V / Q) ratio is close to 1 (perfusion of non-ventilated pulmonary units). The venous blood is fully oxygenated and largely content with independent mixed venous oxygen as partial pressure.

The arterial oxygen becomes identical to the partial pressure of arterial oxygen.

One of the characteristics of acute respiratory distress syndrome is the presence of a shunt.

Shunt and venous mixing are used interchangeably to express the calculated fraction of cardiac output that bypasses alveolar units and contributes to the blending of poorly oxygenated venous blood with oxygenated capillary.

In contrast to the arterial oxygen partial pressure of healthy individuals, that of patients with acute respiratory distress syndrome varies significantly with:

  1. The degree of V / Q mismatch and shunt present.
  2. The oxygen content in mixed venous blood.

As bypass increases, arterial oxygen partial pressure tends to be less and less sensitive to arterial oxygen partial pressure and inspired oxygen fraction. It is increasingly dependent on mixed venous oxygen content and saturation.

This is because arterial and venous blood oxygen content and saturation tend to become increasingly similar as the shunt fraction increases.

The degree of the shunt can be viewed as determined and modulated by factors that affect the number of alveolar units that are not ventilated (V factors) and the perfusion of those units (Q factors).

Ventilation factors (V)

In patients with acute respiratory distress syndrome, the non-aerated alveolar units that contribute to shunt physiology are primarily the result of alveolar flooding (from edema, pus, or blood) or collapse.

Although some units can be quickly recruited (e.g., collapsed alveoli) by increasing transpulmonary pressure, others resist recruitment (e.g., alveoli are filled with pus in the setting of pneumonia).

As a result, the degree of recruitable lung units varies between patients with acute respiratory distress syndrome and within the same patient throughout the disease (more lung recruitable early and less late).

This has important implications.

First, depending on the ventilation strategy used and the degree of the recruitable lung, the PaO2 / FIO2 ratio can vary greatly. This is well illustrated by the study by Grasso et al. performed on patients with acute respiratory distress syndrome.

In patients without a significant recruitable (non-recruiting) lung, the higher positive end-expiratory pressure did not affect the PaO2 / FIO2 ratio.

In contrast, in recruiters, positive end-expiratory pressure often causes this ratio to increase, leading to a decrease in acute respiratory distress syndrome severity.

Additionally, other patients may no longer meet the definition of acute respiratory distress syndrome (ratio greater than 300 in high positive end-expiratory pressure).

Second, the presence of different populations of acute respiratory distress syndrome (recruiters and non-recruiters) undermines and discredits the use of the fraction of inspired oxygen tables proposed by some to establish the positive level of pressure at the end of expiration.

Indeed, in patients with a similar large shunt but with a marked difference in the amount of lung recruited (and therefore in response to positive end-expiratory pressure).

These tables would lead clinicians to choose a high positive end-expiratory pressure (constant high fraction of inspired oxygen requirement) in non-recruiters who are less likely to benefit from positive end-expiratory pressure.

Comparatively, such tables lead to choosing a lower positive end-expiratory pressure in recruiters than in non-recruiters since the response to positive end-expiratory pressure reduces the fraction of inspired oxygen.

Adjusting the positive end-expiratory pressure based on this table puts non-recruitable patients at risk for volutrauma (highly positive end-expiratory pressure without recruitment).

And recruitable patients at risk of atelectrauma by tidal opening and collapse (positive end-expiratory pressure level too low to avoid cyclical alveolar collapse).

Such tables lack a robust physiological validation rationale and, therefore, should not be used to guide the choice of positive end-expiratory pressure.

Therefore, it is important not to infer from the definition of acute respiratory distress syndrome severity that the best strategy can be identified simply by looking at its impact on the PaO2 / FIO2 ratio, which does not appear to be a reliable surrogate for results.

Venous mixing correlates with non-inflated tissue mass and lung compliance with the size of the customarily aerated lung or “baby lung.”

There is an apparent discrepancy between the extent of pulmonary infiltrates and respiratory mechanics at one extreme and the degree of venous mixing.

For example, a severe shunt with an unexpectedly low amount of infiltrates and essentially unchanged respiratory system compliance.

It should increase the possibility that other factors could be contributing to low arterial oxygen content.

Perfusion factors (Q)

In addition to considering the number of alveolar units that do not contribute to gas exchange, the factors that regulate their perfusion must also be considered.

The reduction in blood flow through non-aerated alveoli in response to alveolar hypoxia can vary significantly due to the presence or absence of factors that have the potential to increase or decrease the hypoxic vasoconstriction response.

For example, sepsis, alkalemia, high cardiac output during positive pressure ventilation but not during spontaneous respiration, or medications such as intravenous vasodilators tend to attenuate the hypoxic response and increase the degree of venous mixing.

In contrast, inhaled vasodilators or good lung downward or prone positioning help redistribute blood flow to the aerated lung and thus reduce venous mixing.

Finally, excessive airway pressure in an aerated compatible lung (when the other is extensively consolidated and not compatible) results in compression of the alveolar vessel in the good lung in the redistribution of blood flow to the lung. Bad and in the increased shunt.

The wide range of reported correlations (r 0.5 to 0.9) between the PaO2 / FIO2 ratio and the degree of shunt towards modulating factors of the PaO2 / FIO2 ratio other than shunt alone.

Extrapulmonary factors, mixed venous oxygen content, cardiac output, and cardiac bypass

Mixed venous oxygen content along with the percentage of cardiac output that avoids aerated lung units (venous mixing) are critical determinants of:

Arterial oxygen partial pressure, arterial oxygen saturation, and content in acute respiratory distress syndrome patients.

As mixed venous oxygen content and saturation decrease, so does the arterial partial pressure of arterial oxygen in the context of shunt physiology.

Any immediate increase in tissue consumption (VO2) or reduction in tissue oxygen supply (DO2) is associated with a compensatory increase in oxygen extraction.

It can cause a drop in mixed venous oxygen partial pressure, oxygen content, saturation, and thus arterial oxygen partial pressure.

This effect is trivial for a small pulmonary shunt but significant for a large one.

In patients with acute respiratory distress syndrome, a drop in cardiac output is not an uncommon cause of decreased arterial partial pressure of oxygen.

This should be suspected in all patients who developed a decrease in oxygen saturation with mechanical mechanisms of the respiratory system that have not changed significantly if associated with hypotension.

The effect of an increase in carbon monoxide on mixed venous oxygen is more complex.

Since the resulting increase in mixed venous oxygen partial pressure, saturation, and oxygen content can be offset by the more significant shunt associated with, the higher carbon monoxide.

It is essential to consider the cardiac output and the relationship between oxygen supply and demand as a potential cause of a change in arterial partial pressure of oxygen in acute respiratory distress syndrome.

For example, if a patient meets the criteria for severe acute respiratory distress syndrome, primarily due to:

With low carbon monoxide and reduced mixed venous oxygen saturation compared to a large shunt, the priority would be to restore adequate hemodynamics and not undertake recruitment maneuvers or oxygenated extracorporeal membrane.

Failure to distinguish the different mechanisms and the cause of reaching a PaO2 / FIO2 lower than 100 can lead to a wildly inappropriate intervention (increasing positive end-expiratory pressure in a patient with low carbon monoxide due to decompensated cor pulmonale).

It’s also worth remembering that cor pulmonale (which has been reported in about 25 percent of patients with acute respiratory distress syndrome) should be systematically looked for in this setting.

Finally, it is also important to remember that approximately 15 percent of patients with acute respiratory distress syndrome may also have a right-to-left heart bypass through a patent foramen ovale.

Therefore, an echocardiogram with a bubble study should be obtained whenever a low PaO2 / FIO2 ratio cannot be clearly explained by:

  1. The extension of the non-aerated alveolar process alone.
  2. A low mixed venous oxygen saturation.
  3. Circumstances knew to be associated with impaired hypoxic vasoconstriction.

Worsening gas exchange when positive end-expiratory pressure is marked may not only be an essential clue to the presence of a right-to-left shunt through a patent foramen ovale.

But it can also be seen in decompensated cor pulmonale or hypovolemia.

These three possibilities are usually easy to differentiate from each other using a bedside echocardiogram.

Physicians and fraction of oxygen-inspired factors

The contributions of involuntary physicians to the PaO2 / FIO2 ratio are often underestimated.

This is the consequence of varying practice and recommendations regarding what arterial oxygen partial pressure should be addressed for acute respiratory distress syndrome.

In the ARDSnet trials, the explicit targets were 55-80 mmHg for arterial oxygen partial pressure and 88-95 for arterial oxygen saturation.

Consider the implication of those goals in a patient with a 30 percent lead.

If one targets an arterial oxygen partial pressure of 60 mmHg, the fraction of inspired oxygen needed to achieve that goal would be 0.5, and the corresponding PaO2 / FIO2 120 (moderate acute respiratory distress syndrome).

If one is targeting an arterial oxygen partial pressure of 80 mmHg, the required fraction of inspired oxygen would be one and the resulting PaO2 / FIO2 80 (severe acute respiratory distress syndrome).

In other words, depending on the arterial oxygen partial pressure, the severity of the apparent acute respiratory distress syndrome may change.

It is important to underline that varying the fraction of inspired oxygen has different effects on the PaO2 / FIO2 ratio depending on the:

  • Degree of intrapulmonary bypass.
  • Arteriovenous differences.
  • Carbon dioxide partial pressure.
  • Respiratory quotient.
  • Hemoglobin under conditions of constant metabolism.
  • Ventilation / perfusion abnormalities.

For example, increasing the fraction of inspired oxygen causes the PaO2 / FIO2 ratio to increase if the intrapulmonary shunt is small but decreases if the shunt is large.