NIV settings cannot be assessed solely on the basis of IPAP and EPAP values. Key variables when titrating treatment include tidal volume, minute ventilation, respiratory rate, mask leak, adequacy of expiration, and changes in blood gases and the clinical condition. This article discusses the practical interpretation of these variables and adjustment of NIV in different types of respiratory failure.

 

Tidal Volume and Minute Ventilation

Use Predicted Body Weight

Tidal volume should be related to predicted body weight (PBW), not the patient's actual body weight.

 

Lung size is determined primarily by height and biological sex rather than the amount of adipose or muscle tissue.

 

The ARDSNet formulas are:

Male: PBW = 50 + 0.91 × (height in cm − 152.4)

 

Female: PBW = 45.5 + 0.91 × (height in cm − 152.4)

 

For example, the PBW of a 170-cm-tall woman is:

PBW = 45.5 + 0.91 × (170 − 152.4) = 61.5 kg

 

Physiological Resting Values

Approximate resting values for a healthy adult are:

• Vt approximately 6–8 mL/kg PBW

• respiratory rate approximately 12–20/min

• VE usually approximately 5–8 L/min.

 

These are not absolute target values for an acutely ill patient receiving NIV.

 

Minute ventilation requirements may be increased by, for example:

• fever

• metabolic acidosis

• increased physiological dead space

• high CO₂ production

• high respiratory drive

• hypoxemia

• pain or agitation.

 

Interpreting Device-Displayed Tidal Volume

Mask NIV involves intentional expiratory leak and often also unintentional mask leak.

 

Particularly in a single-limb circuit, the device does not measure Vt completely directly but estimates it using an algorithm.

 

As leak increases, the Vt reported by the device may differ substantially from the actual volume.

 

Therefore:

• check mask fit

• check the amount of leak

• follow the average over several breaths

• assess trends in Vte and MVe

• inspect flow and pressure waveforms

• confirm treatment response with blood gas analysis.

 

General Tidal Volume Targets

In conventional NIV for hypercapnic respiratory failure, a practical starting point is often approximately 6–8 mL/kg PBW.

 

Pressure support can be increased gradually if:

• Vt remains low

• work of breathing is high

• PaCO₂ does not decrease

• pH does not improve

• the patient does not receive adequate support.

 

In an awake patient with COPD, a useful Vt may in some protocols be 8–10 mL/kg ideal body weight if a higher Vt is required to improve alveolar ventilation and air trapping, synchrony, or hemodynamics do not worsen.

 

For example, in a patient with an ideal body weight of 50 kg:

• Vt 400 mL → approximately 8 mL/kg

• Vt 450 mL → approximately 9 mL/kg

• Vt 500 mL → approximately 10 mL/kg.

 

At a respiratory rate of 15/min:

• Vt 400 mL → VE 6.0 L/min

• Vt 450 mL → VE 6.8 L/min

• Vt 500 mL → VE 7.5 L/min.

 

A satisfactory VE may therefore be approximately 6–8 L/min if pH and PaCO₂ improve and work of breathing decreases.

 

In acute severe hypercapnic respiratory failure, VE may temporarily be 10 L/min or more. However, a high minute ventilation should not be pursued at all costs if expiratory time becomes shorter and dynamic hyperinflation worsens.

 

In severe emphysema, a large dead space may increase ventilatory requirements.

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Interpreting Minute Ventilation

If PBW is 70 kg and Vt is 7 mL/kg, Vt is 490 mL.

• RR 16/min → VE approximately 7.8 L/min

• RR 30/min → VE approximately 14.7 L/min.

 

A VE of 14–15 L/min may appear high, but ventilation may still be inadequate if a large proportion of ventilation is directed to dead space or the patient is becoming fatigued.

 

Conversely, a VE of 6 L/min is not necessarily too low for a small patient who is breathing calmly.

 

Minute ventilation is adjusted so that:

• pH increases

• PaCO₂ decreases toward the patient's usual level

• respiratory rate decreases

• work of breathing decreases

• accessory respiratory muscle use decreases

• consciousness and alertness improve

• patient–ventilator synchrony improves

• Vt does not become unnecessarily large.

 

For example:

• in pulmonary edema, a VE of 14 L/min may be acceptable initially if it decreases rapidly with treatment

• in COPD, the same VE may be excessive if expiration does not complete

• in metabolic acidosis, a VE of 15 L/min may be necessary for compensation

• in ARDS, a VE of 15 L/min together with a high Vt and marked work of breathing is concerning.

 

There is no universal safe maximum minute ventilation in liters per minute. A value of 15–20 L/min is not automatically toxic, but it may indicate an extremely high respiratory drive.

 

Tidal Volume Targets by Clinical Condition

Cardiogenic Pulmonary Edema

With CPAP, Vt is not set. The goals are alveolar recruitment, improved oxygenation, and reductions in respiratory rate and work of breathing.

 

With bilevel NIV, a practical Vte target is generally approximately 6–8 mL/kg PBW.

 

A sustained increase in Vte above 8–9 mL/kg is not a routine target. If Vte is 9–10 mL/kg and the patient is breathing vigorously, assess:

• concomitant pneumonia or ARDS

• excessive pressure support

• strong spontaneous inspiratory effort

• changes in RR and work of breathing

• response of pulmonary edema to treatment.

 

In de novo hypoxemic respiratory failure, Vte above 9.5 mL/kg has predicted NIV failure. This threshold has not been validated specifically in isolated cardiogenic pulmonary edema, so it should be regarded as a warning sign rather than an absolute threshold for discontinuation.

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COPD and Obstructive Respiratory Failure

A usual starting point is Vte 6–8 mL/kg PBW.

 

In selected patients, 8–10 mL/kg may be accepted if:

• pH increases

• PaCO₂ decreases

• work of breathing decreases

• expiratory flow approaches baseline before the next breath

• dynamic hyperinflation does not increase

• the patient does not become asynchronous

• hemodynamics remain stable.

 

A slightly higher Vt may improve CO₂ elimination in COPD because physiological dead space is often increased.

 

For example, if dead space is 150 mL:

• Vt 300 mL → alveolar component approximately 150 mL

• Vt 450 mL → alveolar component approximately 300 mL.

 

In this simplified example, increasing Vt by 150 mL doubles the effective alveolar component of each breath.

 

However, Vt should not be increased without limit. The more gas that is delivered during inspiration, the more gas must be exhaled through narrowed airways before the next breath.

 

An excessively high Vt may cause:

• dynamic hyperinflation

• auto-PEEP

• increased work of breathing

• difficulty triggering the ventilator

• asynchrony

• hemodynamic deterioration.

 

Severe Emphysema

In severe emphysema, Vte is usually kept within the range of 6–8 mL/kg PBW, often closer to the lower end of this range.

 

Even 8 mL/kg may be excessive if:

• expiration remains incomplete

• air trapping increases

• auto-PEEP increases

• blood pressure decreases

• the patient becomes asynchronous.

 

Lung compliance may be high in emphysema, but this does not mean that large tidal volumes are safe.

 

If Vt is 450 mL:

• RR 12/min → VE 5.4 L/min

• RR 30/min → VE 13.5 L/min.

 

The latter may cause severe air trapping even if Vt itself is reasonable.

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Neuromuscular Disease

A useful starting point is usually 6–8 mL/kg PBW.

 

In neuromuscular disease or a stiff chest wall, the following may be required:

• a guaranteed backup rate

• a longer inspiratory time

• adequate pressure support

• sometimes a relatively high IPAP.

 

The aim is to correct daytime or nocturnal hypoventilation, hypercapnia, and symptoms.

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Chest Wall Restriction

A useful starting point is usually 6–8 mL/kg PBW.

 

In neuromuscular disease or a stiff chest wall, the following may be required:

• a guaranteed backup rate

• a longer inspiratory time

• adequate pressure support

• sometimes a relatively high IPAP.

 

The aim is to correct daytime or nocturnal hypoventilation, hypercapnia, and symptoms.

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Obesity Hypoventilation Syndrome

Vte 6–8 mL/kg PBW is a usual starting point. In selected patients, 8–10 mL/kg may be used.

 

Vt should not be calculated according to actual body weight because this would result in unreasonably large volumes in patients with severe obesity.

 

The following are often required:

• high pressure support

• adequate EPAP to treat upper airway obstruction

• a guaranteed backup rate.

 

Pneumonia, ARDS, and De Novo Hypoxemic Respiratory Failure

The target Vte is generally close to 6 mL/kg PBW.

 

An acceptable lung-protective ventilation range is approximately 4–8 mL/kg PBW. In practice, 8 mL/kg represents the upper end of the range, not the target.

 

Vte above 9–9.5 mL/kg together with a high respiratory rate and strong inspiratory effort is a clear warning sign.

 

A high Vte may result from the patient's own strong inspiratory effort rather than solely from excessive ventilator pressure. In this situation, reducing pressure support may not solve the problem.

 

The risk of patient self-inflicted lung injury may increase even when the IPAP displayed by the device is moderate because a strongly negative pleural pressure increases transpulmonary pressure.

 

If high Vt, high RR, hypoxemia, and increased work of breathing persist, the appropriateness of NIV and the need for intubation should be assessed rapidly.

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Interstitial Lung Disease

A useful Vte may be approximately 4–6 mL/kg PBW.

 

Functional lung volume may be small, and therefore volumes above 6–8 mL/kg may overdistend the remaining functional lung.

 

A high minute ventilation should not be pursued using high pressures. The appropriateness of NIV should be reassessed readily.

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Severe Asthma

If NIV is used in severe asthma, Vte is generally approximately 6–8 mL/kg PBW.

 

Key risks include:

• air trapping

• auto-PEEP

• hypotension

• barotrauma

• pneumothorax

• delayed intubation.

 

The goals are a relatively low respiratory rate, short inspiratory time, and long expiratory time. Hypercapnia may need to be accepted.

 

High Tidal Volume and Adjustment of Pressure Support

A high Vte does not automatically mean that pressure support is too high. Tidal volume is simultaneously influenced by ventilator pressure assistance, the patient's own inspiratory effort, lung compliance, airway resistance, and mask leak.

 

Before changing settings, it should therefore be confirmed that the volume reported by the device is reliable, and Vte should be assessed together with respiratory rate, work of breathing, synchrony, expiratory flow, and trends in pH and PaCO₂.

 

Pressure support can be reduced gradually, usually by 1–2 cmH₂O at a time, if the high Vte appears to result from excessive pressure assistance and the patient's gas exchange and clinical condition have improved. After the change, determine whether adequate ventilation, patient comfort, and reduced work of breathing are maintained. Pressure support should not be reduced solely because of the Vte value displayed by the device if the patient remains acidotic, is becoming fatigued, or alveolar ventilation worsens.

 

Particularly in hypoxemic respiratory failure, a high Vte may result from the patient's own vigorous respiratory effort. In this situation, reducing pressure support may increase negative pleural pressure swings and work of breathing without significantly reducing tidal volume. Persistent high Vte together with a high respiratory rate, strong respiratory effort, or poor oxygenation may indicate inadequate NIV, in which case the need to escalate respiratory support should be assessed rapidly rather than focusing solely on pressure adjustment.

 

There is likewise no fixed safe upper limit for minute ventilation. The significance of a high VE depends on whether it results from a high tidal volume, a high respiratory rate, or both.

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Mask Leak

Interpreting Leak Values

A completely leak-free NIV mask should not be pursued at all costs.

 

Many single-limb systems require intentional expiratory leak. In contrast, unintentional leak from around the mask or circuit connections should be minimized.

 

If the device's leak value refers to unintentional patient leak, zero is technically a good result, although a small amount of leak is common in clinical practice.

 

If the value includes intentional expiratory leak, it should not be zero.

 

Approximate interpretation of unintentional leak:

• 0–10 L/min: excellent

• 10–20 L/min: generally good

• 20–30 L/min: often acceptable if treatment is effective

• 30–40 L/min: elevated; check the mask and circuit.

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Consequences of Excessive Leak

A large unintentional leak may cause:

• reduced effective IPAP and EPAP support

• lower actual Vt

• impaired CO₂ elimination

• poorer oxygenation

• incorrect or failed triggering

• unnecessary auto-triggered breaths

• delayed cycling

• excessively long inspiratory time

• unreliable volume measurements

• discomfort

• NIV intolerance.

 

Optimizing Mask Fit

The goal is a well-sealed but comfortable mask, controlled leak, and effective patient–ventilator synchrony. The mask should not be tightened so firmly that it causes pain, skin injury, or increased patient distress.

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Air Trapping and Dynamic Hyperinflation

Clinical Signs of Air Trapping

Air trapping may be suggested by:

• rapid respiratory rate

• prolonged and labored expiration

• use of accessory respiratory muscles

• a sensation that the patient does not have enough time to exhale

• breath stacking

• poor synchrony with the ventilator

• inspiratory efforts that fail to trigger the ventilator

• worsening dyspnea when pressures or respiratory rate are increased

• the chest remaining in an inspiratory position

• decreased blood pressure.

 

Wheezing alone does not indicate the severity of obstruction. In very severe obstruction, airflow may be so limited that breath sounds become diminished.

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Recognizing Air Trapping on the Flow Waveform

The key finding is that expiratory flow does not return to baseline before the next inspiration.

 

Normal:

inspiration → expiratory flow → return to baseline → new breath

 

Air trapping:

inspiration → expiratory flow → does not reach baseline → new breath

 

This means that the lungs had not finished emptying when the next inspiration began.

 

When the Patient Initiates the Next Breath Too Early

If the patient initiates the next inspiration before expiratory flow has returned to baseline, the problem is not necessarily caused by an excessively high backup rate.

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The patient's respiratory drive may be so high that they do not wait for the lungs to empty.

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Possible causes include:

• hypoxemia

• hypercapnia

• acidosis

• pulmonary edema

• bronchospasm

• pain

• panic

• fever

• metabolic acidosis

• patient–ventilator asynchrony.

 

In this situation, changing ventilator settings alone may not be sufficient; the cause of the high respiratory drive must also be treated.

 

How to Reduce Air Trapping

The basic principle is to give the lungs more time to empty.

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Measures include:

• reducing an excessively high respiratory rate

• reducing the backup rate

• shortening Ti

• earlier cycling

• prolonging expiratory time

• avoiding an excessively high Vt

• avoiding excessive pressure support

• avoiding excessive EPAP

• treating bronchospasm

• treating mucus and secretions

• correcting mask leak

• improving patient–ventilator synchrony

• treating hypoxemia, pulmonary edema, pain, and panic.

 

Inspiratory-to-Expiratory Ratio and Expiratory Time

In severe obstruction, the aim is often an I:E ratio that provides substantially more time for expiration than inspiration. In controlled ventilation, for example, a ratio of 1:3 or a longer expiratory time may be used. In COPD, a practical starting point is often approximately I:E 1:2–1:3. The more severe the expiratory flow limitation and the longer the lung emptying time, the more expiratory time is required. In severe obstruction, an I:E ratio of 1:3–1:5 or an even longer expiratory phase may be required.

 

The main goal is not a specific numerical ratio but to allow expiratory flow to return close to baseline before the next inspiration begins. If expiratory flow remains incomplete, it may be necessary to reduce respiratory rate, shorten inspiratory time, or adjust the cycling setting to cycle earlier.

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The I:E ratio should not be interpreted without considering respiratory rate. If respiratory rate is 20/min, one respiratory cycle lasts three seconds:

• I:E 1:2 → Ti 1.0 s and Te 2.0 s

• I:E 1:3 → Ti 0.75 s and Te 2.25 s

• I:E 1:4 → Ti 0.60 s and Te 2.40 s.

 

If respiratory rate is 30/min, the entire respiratory cycle lasts only two seconds. In this case, even an I:E ratio of 1:4 provides only 1.6 seconds for expiration. In severe obstruction, reducing respiratory rate may therefore prolong expiratory time more effectively than changing the I:E ratio alone.

 

Auto-PEEP and Triggering

If the patient attempts to inhale but the ventilator does not trigger, a small increase in EPAP may help overcome the threshold load caused by auto-PEEP.

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For example:

• 16/4 → pressure support 12

• 18/6 → pressure support 12.

 

EPAP increases while pressure support remains unchanged.

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If the patient triggers effectively but initiates breaths too rapidly, the problem is not necessarily an EPAP that is too low.

 

More important measures may include:

• reducing respiratory drive

• shortening Ti

• earlier cycling

• reducing Vt

• ensuring sufficiently long expiration.

 

Permissive Hypercapnia

When Hypercapnia May Be Accepted

In severe COPD or asthma, rapid normalization of PaCO₂ using high pressures, large tidal volumes, or a high respiratory rate may worsen air trapping.

 

Permissive hypercapnia means temporarily accepting an elevated PaCO₂ if rapid correction would cause:

• more severe dynamic hyperinflation

• high airway pressures

• barotrauma

• hypotension

• worse hemodynamics.

 

This does not mean that CO₂ can be ignored.

 

The principle is: CO₂ should not be corrected at all costs if doing so worsens the mechanical trapping of gas in the lungs.

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Practical Ventilatory Strategy

In obstructive respiratory failure, it may be appropriate to:

• prolong expiratory time

• use a moderate respiratory rate

• avoid excessively high tidal volumes

• avoid unnecessarily high pressures

• accept an elevated PaCO₂ if pH and the clinical condition remain acceptable

• treat bronchospasm, inflammation, mucus, infection, pulmonary edema, pain, and synchrony problems.

 

The BTS/ICS guideline for severe airflow obstruction mentions a low respiratory rate of 10–15/min, prolonged expiratory time, and, when necessary, permissive hypercapnia to avoid high pressures.

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NIV Settings in COPD

EPAP and Auto-PEEP

The purpose of EPAP is generally not to match auto-PEEP one-to-one.

 

If auto-PEEP can be measured reliably, external PEEP of approximately 60–80% of the measured auto-PEEP has been used as a physiological rule of thumb.

 

A usual starting point in COPD is:

• EPAP 4–5 cmH₂O

• IPAP 10–15 cmH₂O.

 

Excessively high EPAP prevents the lungs from emptying as far during expiration. At an appropriate level, EPAP helps keep the airways and alveoli open, but at an excessively high level the lungs may remain continuously overinflated. As a result, dynamic hyperinflation may worsen. In addition, it reduces venous return to the heart.

 

A good EPAP is the lowest level that reduces the work required to trigger the ventilator and improves synchrony and oxygenation without worsening hyperinflation.

 

A usual level in respiratory failure caused solely by COPD is 4–6 cmH₂O, and sometimes 6–8 cmH₂O. EPAP above 8 cmH₂O in isolated COPD with a tendency toward hyperinflation generally requires a clear rationale.

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IPAP and Pressure Support

IPAP increases ventilatory support if EPAP is kept unchanged.

 

In acute COPD treated with NIV:

• IPAP can be started at 10–15 cmH₂O

• titrated to 16–20 cmH₂O

• 20–25 cmH₂O is often used in severe hypercapnia

• 25–30 cmH₂O can be used selectively.

 

IPAP above 30 cmH₂O is not routine treatment without specialist assessment.

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Pressure Titration

In severe COPD, however, a relatively high IPAP does not necessarily produce an exceptionally high Vte. High airway resistance slows airflow, auto-PEEP increases the threshold for initiating inspiration, and part of the pressure delivered through the mask is used to overcome these resistive loads. Therefore, IPAP of 20–25 cmH₂O may be required to achieve adequate ventilatory support. In the Intensive Care NSW protocol for acute NIV in COPD, IPAP is increased in increments of 2 cmH₂O while targeting a Vte of 8–10 mL/kg ideal body weight; IPAP of 20–25 cmH₂O is described as fairly common.

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Signs That Ventilatory Support Is Excessive

Pressure is excessive or the breathing pattern is harmful if:

• Vt becomes unnecessarily large

• expiration remains incomplete

• RR remains high

• auto-PEEP increases

• triggering deteriorates

• the chest becomes hyperinflated

• blood pressure decreases

• mask leak becomes uncontrollable

• the patient becomes distressed or fights the ventilator

• air distends the stomach or causes nausea.

 

Practical NIV Pressure Ranges

Cardiogenic Pulmonary Edema

CPAP:

• start at 5–8 cmH₂O or directly at 8–10 cmH₂O

• usual target 8–12 cmH₂O

• above 12–15 cmH₂O is generally not a routine target.

 

Bilevel NIV:

• start with IPAP 10–15, EPAP 5–8

• usual target IPAP 15–20, EPAP 8–10

• IPAP above 20–25 or EPAP above 12 → assess for other pulmonary disease, hemodynamic effects, or inadequate NIV.

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Severe COPD

• start with IPAP 10–15 or 14 cmH₂O

• initial EPAP approximately 4 cmH₂O

• IPAP often 20–25 cmH₂O

• EPAP usually 4–6 cmH₂O

• IPAP 25–30 cmH₂O may be used under close monitoring

• IPAP above 30 or EPAP above 8 → specialist assessment.

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Severe Emphysema

• start, for example, at 10–14/4

• IPAP often 15–25 cmH₂O

• EPAP usually 4–6 cmH₂O

• use the lowest effective IPAP

• even IPAP 18–20 may be excessive if Vt becomes large

• conversely, IPAP 25–30 may be justified in severe airway resistance under close monitoring.

 

In emphysema, pay particular attention to:

• Vte relative to PBW

• return of expiratory flow to baseline

• RR

• Ti/Te ratio

• blood pressure

• signs of pneumothorax.

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Obesity Hypoventilation Syndrome

• example starting setting approximately 20/8–10

• IPAP often 20–30 cmH₂O

• high pressures are common

• leak, Vt, synchrony, and hemodynamics determine the appropriate settings.

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Neuromuscular Disease

• example starting setting approximately 8/4

• IPAP often 12–16 cmH₂O

• EPAP is usually kept low if there is no upper airway obstruction

• a backup rate and adequate Ti are often important.

 

Chest Wall Restriction

• example starting setting approximately 14/4

• IPAP may be 20–25 cmH₂O

• the required pressure depends on chest wall stiffness and the target Vt.

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Pneumonia, ARDS, and Other Hypoxemic Lung Injury

• CPAP/EPAP often 8–12 cmH₂O

• use the lowest pressure support required

• Vte 4–8 mL/kg PBW, preferably close to 6 mL/kg.

IPAP above 20–25 or CPAP/EPAP above 12–15 cmH₂O is not automatically dangerous, but it is not a routine target in hypoxemic lung injury.

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PIP and Upper Pressure Limits

There is no single physiological maximum safe PIP value in NIV.

 

An IPAP of 30 cmH₂O is used in some acute NIV protocols as a threshold for specialist assessment. However, it has not been demonstrated to represent a threshold for lung injury and is not an absolute maximum pressure. In selected situations, such as severe obesity hypoventilation, higher pressures may be required, but treatment then requires an appropriate device, close monitoring, and assessment by a physician experienced in NIV.

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Mixed Cardiogenic Pulmonary Edema and COPD

Conflicting Physiological Goals

If a patient simultaneously has cardiogenic pulmonary edema, COPD, and extensive emphysema, the physiological requirements may conflict:

• pulmonary edema may benefit from higher EPAP/CPAP

• COPD and emphysema may worsen with excessively high EPAP

• pulmonary edema increases respiratory drive

• high respiratory drive may worsen air trapping

• high intrathoracic pressure may improve left ventricular loading conditions but reduce venous return.

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Practical NIV Strategy

In practice:

• use sufficient EPAP for oxygenation and alveolar recruitment

• avoid unnecessarily high EPAP if blood pressure decreases or air trapping worsens

• keep IPAP moderate if PaCO₂ is normal and Vt is high

• increase IPAP if hypercapnia and acidosis require additional ventilatory support

• monitor RR, Vt, VE, pH, PaCO₂, blood pressure, level of consciousness, and the flow waveform.

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Recognition of NIV Failure

Clinical Signs of NIV Failure

NIV should not be continued for a prolonged period in a deteriorating patient.

 

NIV failure should be suspected if:

• dyspnea worsens

• RR does not decrease or increases

• work of breathing increases

• the patient becomes agitated or fatigued

• blood pressure decreases

• SpO₂ cannot be maintained within the target range

• pH decreases

• PaCO₂ increases

• mask leak is uncontrollable

• the patient is not synchronous with the ventilator

• expiratory flow does not return to baseline

• the chest becomes hyperinflated

• vomiting or aspiration risk increases

• copious secretions prevent effective treatment

• pneumothorax is suspected

• level of consciousness or airway safety deteriorates.

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When to Consider Intubation

Intubation should not be delayed if respiratory failure progresses despite oxygen and NIV.

 

A GCS below 8 has been used in several local protocols as a threshold at which NIV is generally not considered safe as the primary treatment because of aspiration and airway risks.