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Manual Hyper-Inflation (MHI)

20 min read

Description #

This unit is designed to help students and clinically registered physiotherapists develop a better understanding of the skills involved in performing the technique of MHI. It also covers the precautions/contraindications and safety aspect of performing MHI. After completion of this unit participants will be able to clinically reason when it is appropriate to use MHI as a treatment option and perform the technique safely and effectively. Prerequisites to this course are CCBSP 001-004, CCBSP 101-102. Prior to starting each module in the CCBSP-100 series the participant will be required to complete a Knowledge and Clinical Scenario Pre-Test. Once the CCBSP 100 course is finished the participant will write a Knowledge and Clinical Scenario Post-test and then complete a practical session.

Learning Objectives #

Understand the theory and pathophysiological rationale behind the application of MHI.

Know the precautions/contraindications to using MHI as a treatment technique.

Be able to safely perform MHI on patients with an artificial airway.

Understand the limitations of MHI as a treatment technique.

Clinically reason when MHI is an appropriate treatment option.

Understand how to combine MHI with other Physiotherapeutic treatment techniques.

What is Manual Hyperinflation? #

Manual Hyperinflation (MHI), also known as ‘bagging’, is a technique used by Physiotherapists and other Health Professionals to maintain or improve the respiratory status of a patient. It is usually performed on intubated/ventilated patients (or those with a tracheostomy) by using a resuscitation circuit to assist the patient in taking a larger than normal breath. Manual Hyperinflation is defined by a slow inspiration phase, an inspiratory pause, and then quickly releasing the air thus simulating a ‘huff’ or ‘cough’ (1)­, and is usually performed in conjunction with other Physiotherapeutic techniques such as positioning, vibrations or assisted coughs. 

The MHI technique performed by Physiotherapist’s is different from that of other Health Professionals as it simulates deep breathing and airway clearance rather than baseline tidal volume breathing.

The first description of MHI in Physiotherapy was by Clement and Hubsch in 1968 (2). Together they described the then ‘new’ technique and elaborated on its effectiveness in the critically ill patient. Shortly after in 1972, Windsor and colleagues (3) continued to describe the effectiveness of MHI, mostly through case studies. However, in the early days MHI was performed with an Anaesthetist ‘bagging’ the patient and a Physiotherapist performing chest vibrations during the expiratory phase of each breath (4). Since this initial description in 1968 not much has changed. Manual Hyperinflation itself is now, and has been for some time, performed without an Anaesthetist. It became a routine treatment in ICU’s around the world for intubated patients (4).

There has been little meaningful research about the effects, both positive and negative, on the lungs; cardiovascular system; or the patient in general (5), until the late 80’s and early 90’s. Since then Physiotherapists and other Health Professionals around the world have begun questioning the validity of MHI as a routine treatment (6), and its effect on patients in greater detail. There have been multiple small specific studies (5) (7) (8) (9) (10) (11) (12) (13) (14) (15) supporting the use of MHI and investigating its effect of patient populations, the evidence of which suggests it is beneficial. Since its inception there has not been an official standardised technique with which to apply MHI to patients. The result of this makes it hard to cohort smaller studies into an effective meta-analysis, as each study has subtle differences in the application of MHI, the use of Positive End Expiratory Pressure (PEEP), FiO2 and type of circuit used.

As a result of the questioning of MHI both within and outside of the Physiotherapy Profession, it is no longer a routine treatment, and requires critical evaluation of each individual patient as to the possible positive and negative impact MHI may have. As more evidence based research becomes available we are slowly getting a picture of appropriate parameters for MHI; medical conditions MHI is beneficial in; the most effective technique and circuit; and most importantly the positive and negative effect on the patients that we treat. 

Theory of Manual Hyperinflation #

Since the early 1960’s it has been known that larger than baseline tidal volumes helps to re-expand atelectasis, improve oxygenation, improve lung compliance and aid in clearance of secretions. 

The slow inspiration phase of MHI facilitates collateral ventilation.  By using a slow inspiratory air flow rate we also ensure that we are not forcing sputum peripherally toward the smaller airways (16) (17).  Collateral ventilation is further increased with an inspiratory hold, which allows the pressure within the lung to redistribute and open up areas of atelectasis and deflated alveoli due to mucus plugs (via the Channels of Martin (inter-bronchiolar), Channels of Lambert (Bronchiole-Alveolar) and Pores of Kohn (inter-alveolar) (1)). The inspiratory hold also allows alveoli with slower time constants to open up. As a result alveoli are re-inflated and atelectasis is reversed. When pressure is released, simulating a cough, the shear forces of air rushing past mucous shifts it centrally to assist in sputum clearance (16) (17). 

When a person is spontaneously breathing every now and then they take a larger than normal breath, a ‘sigh’.  This ‘sigh’ helps to realign surfactant by allowing it to re-enter alveoli, reducing surface tension and improving Lung Compliance (CL) (18).   When a Mechanically Ventilated person receives MHI it artificially performs this ‘sigh’.  These ‘sighs’ or hyperinflations also serve to improve lung compliance and decrease airway resistance (6) (7) (8) (9) (15), however it is unclear if this improved compliance and reduced resistance is due to the re-expansion of atelectic areas, or other factors. 

Manual Hyperinflation is usually performed in conjunction with other physiotherapeutic techniques, such as positioning, assisted coughing or expiratory vibrations.  This helps to maximise the potential benefits of therapy.

Effects of Manual Hyperinflation #

 This next section of the module will discuss both the Positive and Negative effects in detail.

Positive Effects of Manual Hyperinflation #

As more evidence based research is completed we are beginning to get a picture increasingly supportive of the initial theory behind MHI.  Outlined in the following pages are the positive/beneficial effects that research has confirmed when MHI is included into Physiotherapy Treatment regimes. 

Reversing Atelectasis #

MHI has been shown to reverse acute atelectasis in the intubated patient by recruiting collapsed alveoli (1), however to be effective Peak Airway Pressure (Paw) needs to be close to 40cmH20 (19).  Resolution of acute atelectasis can be enhanced with a combination of positioning and chest vibrations in conjunction with MHI (13).

Mobilisation of Pulmonary Secretions #

There has been numerous studies looking into the efficacy of physiotherapy techniques (Mobilization, Positioning, Percussion, Vibrations, Chest Shaking, Postural Drainage, et cetera) on sputum clearance. Recently a study by Hodgson et al (7) compared a treatment regime of MHI, side lying and suction with just side lying and suction for sputum production. The inclusion of MHI into the treatment improved sputum production by 58.6% compared to just positioning in side lying alone.

Another study looking into the most effective MHI circuit found that for clearance of secretions using a Mapleson C type circuit is significantly more effective than a Laerdal resuscitation circuit (15) which is similar to the Ambu-Spur II circuit that VGH uses.

Increasing Lung Volume/Decreased Paw/Improved Lung Compliance #

Improvements in Lung Compliance (CL) from MHI have been shown as far back as 1959 (20).

More recent studies have looked at the changes in CL with respect to Physiotherapeutic treatments, and found significant evidence for improvements of up to 30% in CL with MHI as part of the treatment (4) (7) (8) (9), along with decreases in Peak Airway Pressure (PAW) and increased lung volumes (9). These improvements were maintained for varying lengths of times ranging from 20-120 minutes. However, it is unclear if the reduction in PAW or CL is due to the increased lung volume (from resolution of atelectasis, therefore reducing airway resistance and improving CL) or the realignment of surfactant (4) (7) (9).

Reversing Hypoxaemia #

Unfortunately there is little data available on the effects of MHI on improving PaO2. A few studies that have reported improvements have been using an FiO2 of 1.0 (2) (3) (5) (9) (13) (20), therefore any improvement in PaO2 immediately post treatment is most likely attributable to the fact that patients were breathing 100% oxygen.  To determine whether the 100% Oxygen or MHI improved PaO2 Oxygen would be somewhat difficult.

Some studies have taken this factor into account and used the same FiO2 as the ventilator and found that, whilst there wasn’t really improvements in PaO2, there were no significant deteriorations post MHI when included into physiotherapy treatment regimes (7) (8) (12).

Negative Effects #

There have been a lot of reported negative effects of MHI and these have been looked at in detail in various studies.  The main concerns and detrimental effects are outlined in the following pages.

Barotrauma/Volutrauma #

From the description of the technique used in the late ‘60’s, early ‘70’s it is possible that Barotrauma/Volutrauma may have been caused, due to the use of a 4L capacity resuscitation bag (2) (3). Since then these effects have been studied in depth and measures put in place to minimise the risk.

Barotrauma/Volutrauma causes changes in the lung micro vascular permeability resulting in air, protein and fluid leakage along with an increased risk of Pneumothorax (PTx) (21) (22). The effect of this trauma causes a decrease in Lung Compliance (CL), decrease in oxygenation and pulmonary oedema. There have been no reports to speak of describing Barotrauma/Volutrauma from MHI.

Safe limits have been proposed (22) and to date research seems to concur with these limits. Rothen et al (19) conducted a study which looked at the resolution of atelectasis with MHI via CT and concluded that Peak Inspiratory Pressures (PIP) of 40cmH2O is required to completely resolve areas of atelectasis in the supine patient. They also reported no deleterious effects and recommended, a PIP of 30-40 cmH2O should be used to help resolve ventilator induced atelectasis. An interesting discovery from the Rothen study was that an inspiratory volume of 200% the baseline tidal volume (VT) (the suggested volume for a ‘sigh’) only equated to a PIP of 20cmH2O and did not significantly reduce the amount of atelectasis. They found that a PIP of 40cmH2O was equivalent to a Vital Capacity breath, which coincided with complete resolution of atelectasis.

The PIP delivered by Physiotherapist’s and other health professionals during MHI has been studied in great detail. It has been found that with appropriate training Physiotherapist’s are consistent with appropriate MHI parameters in the ICU (10) (12).

Even when practitioners have vast experience in performing MHI, studies have also shown no Health Professional is able to accurately judge the Paw without using a manometer, therefore it is recommended that one be included to ensure that a PIP of 40cmH2O is not exceeded (4) (5) (6) (9) (10) (20) (23) (24).

CardioVascular Depression #

Changes in intra-thoracic pressures can affect the Cardiovascular System (CVS) especially if care is not taken during MHI. Potential effects of MHI on the CVS are altered blood pressures (Mean Arterial, Pulse, Pulmonary Artery, Preload/Afterload both sides of the Heart), stroke volumes, cardiac outputs, systemic vascular resistance (14).

Exactly how MHI causes these changes has been described well by Anning et al (14), however they do suggest that the changes they saw in their animal model were likely exaggerated compared to Human subjects due to the difference in vascular structure and size. Other studies looking into the CVS changes associated with MHI have failed to find significant changes with any Cardiac or Vascular parameters in critically ill patients (5) (7) (8) (12) (13) (15). It is also suggested that healthy lungs are more prone to CVS changes than diseased, stiffer lungs with lower Lung Compliance (CL) which display a protective effect as the stiffer airways provide more resistance and changes in airway pressures are not as readily transmitted to lung vasculature (14).

The effects of MHI on Intracranial (ICP) and Cerebral Perfusion Pressures (CPP) have not been extensively researched. However we do know that as CO2 is a potent vasodilator (18), allowing levels to increase during MHI increases ICP and thus decreases CPP. The converse is also true for lowering CO2 levels which in turn reduces ICP and raises the CPP.

Equipment and Circuits #

There are a variety of Anesthetic circuits used throughout the world. In 1954, Dr Mapleson described 5 different anesthesia circuits/bags (A, B, C, D, E). More modern bags have been derived from these different circuits. Physiotherapists and other Health Professionals most commonly use the Mapleson A (Macgills circuit), Mapleson C, the Laerdal resuscitator, or like here in VGH, the Ambu Spur II resuscitator.

The more modern Laerdal and Ambu Spur II systems have safety blow off valves built in set between 35-40cmH2O. The downside to this safety valve is that the therapist is unable maintain and inspiratory hold during MHI. The Mapleson circuits conversely do not contain safety valves.

Few studies have compared the types of bags for effectiveness. Hodgson et al (15) found the Mapleson C circuit more effective than the Laerdal circuit for clearing secretions, and the ability of the Physiotherapist to achieve appropriate Peak Inspiratory Pressure (PIP). Patman et al (24) found that the Mapleson B circuit was able to maintain an element of Positive End Expiratory Pressure (PEEP) (up to 10cmH2O) without using a PEEP valve. Patman et al also identified a potential for high Peak Airway Pressure (PAW) and tidal volumes to be generated from the Mapleson B circuit if not monitored. McCarren and Chow (23) concluded that Physiotherapist’s need to take into account the advantages/disadvantages of each type of circuit and the desired effect of MHI treatment.

The ability of Physiotherapist’s to alter the technique in varying situations with different types of bags has been well demonstrated also (15) (23) (24). However, it seems that for the most effective treatment a circuit able to maintain a PIP near 40cmH2O would be advantageous.

Safety Aspects of Manual Hyperinflation #

The lungs are made of sensitive tissue that is easily damaged if care is not taken. If the delivered volume of air or pressure is too large then damage will occur (Volutrauma/Barotrauma) (22). If not enough air is delivered or the rate is to slow the patient will hypo-ventilate (24). If too much air is delivered or the rate too fast, hyperventilation or gas trapping may occur (8). If PEEP is not maintained during MHI then unstable Alveoli will collapse at end expiration increasing the potential shearing forces on the smaller airways (6). Conversely, if a large amount of PEEP is required to ventilate a patient (>10 cmH2O) then it may not be possible to safely perform MHI (4) (6). With respect to these issues, prior to performing MHI as a treatment technique it is vital that there be sound clinical reasoning. 

Physiotherapist’s must take into account the patients Respiratory Rate (RR), Peak Airway Pressure (PAW), Positive End Expiratory Pressure (PEEP), Fraction of Inspired Oxygen (FiO2), Lung Compliance (CL), mode of Ventilation and cardiovascular stability (also ICP/CPP if being monitored) to determine if they are able to safely match the ventilator settings or the spontaneously breathing patient whilst performing MHI. Failure to do so could end in harming the patient, therefore delaying recovery and prolonging mechanical ventilation. 

It would be considered dangerous to mechanically ventilate without appropriate monitoring, so we should not perform MHI without adequate monitoring. It is also clearly evident from the literature that certain measurements need to be monitored during MHI (4) (7) (9) (20) (23) (24). These measurements include PAW, Peripheral Oxygen Saturation (SPO2), Mean Arterial Pressure (MAP), Heart Rate (HR), and watching the patient for signs of distress. Therefore it should be mandatory to use a Manometer (to measure PAW), SPO2 monitor (to monitor Oxygen levels), and position yourself to be able to easily watch the patients vitals on the bedside monitor, thus getting an idea as to the patients CVS stability during treatment. 

A PEEP valve should be included in the circuit and set to the same level as the mechanical ventilator. Preferably an Oxygen concentrator should be used to match the delivered FiO2 of the Ventilator. A flow rate of 10-15l/min into the circuit is required to prevent re-breathing of CO2, however the exact flow rate varies between types of circuits (The Ambu-Sur II requires a minimum of 14 l/min). To further assist ventilation and prevent re-breathing an ideal Inspiration to Expiration ratio (I:E ratio) of <0.9 should be the goal. This will facilitate opening of alveoli with different time constants (5), and facilitate secretion removal via the two-phase gas-liquid flow model (16) (17). This may, however, not be achievable in a patient who is spontaneously breathing who may require assistance with every second or third breath to improve coordination between patient and therapist. If the above measurements are made during MHI then the risks of adverse effects are minimised and treatment potential is maximised.

Technique of Manual Hyperinflation #

To improve effectiveness of MHI the patient should be positioned appropriately (affected lung uppermost) and the application of Expiratory Vibrations or if needed an abdominal thrust by another Physiotherapist can be applied to facilitate secretion removal.  If possible the patients should be left with their affected lung uppermost to benefit from the effects of positioning (allowing re-expansion of atelectasis, or postural drainage of secretions) and Ventilation/Perfusion matching after treatment.

It should be noted that MHI as part of a Physiotherapy treatment is vastly different in aims and technique from the manual ventilation or ’bagging’ that other health professionals use to ventilate patients during anaesthesia, resuscitation or transport.  This difference should be recognised principally among Physiotherapists and, through education, the other health professionals that we work with.

Recommended Guideline for Equipment Setup #

  1.  Physiotherapists should have adequate training prior to using MHI as a treatment technique.
  2. Mandatory use of a manometer when administering MHI.
  3. PEEP valve incorporated into the MHI circuit and set to the ventilator setting.
  4. Minimum flow rate of 10-15l/min for the MHI circuit.
  5. FiO2 ideally set to the same as the ventilator (this will be limited by the amount of concentrators available).
  6. Position equipment so the patients’ vitals monitor can easily be seen and monitored during application of MHI.
  7. If able to, attach MHI circuit so that closed system suction remains in place.

Please follow the link below to watch a video demonstration on how to set up your circuit and perform the technique of MHI.

 Recommended Guideline for Manual Hyperinflation 

Recommended Guideline for Manual Hyperinflation #

  1. Slow inspiratory phase (at least 3 seconds, this ensures and I:E ratio <0.9)
  2. Inspiratory Pause of at least 2 seconds (can incorporated into the end of the slow inspiratory phase)
  3. Aim for a Peak Inspiratory Pressure (PIP) of 30-40cmH2O (may need to reduce PIP if treating diseased lungs)
  4. Quick release of pressure and allow minimum of 4-6 seconds for complete evacuation of air in lungs between breaths (this will vary if patient is spontaneously ventilating).
  5. If secretions are mobilised they should be suctioned prior to continuing.
  6. The number of sets and breaths per set will vary patient to patient, however a guideline of 2-3 sets of 8-10 breaths, depending on patient response to treatment.
  7. If any adverse effects of MHI are noted treatment should cease immediately (i.e. altered BP/HR, altered ICP/CPP, decreased SpO2, and increased RR).

Donning Basic Personal Protective Equipment (PPE) #

Please watch the video for a demonstration on how to Don your Basic Personal Protective Equipment or PPE

References #

1. Pryor, J and Webber, B. Physiotherapy for Respiratory and Cardiac Problems. Sydney : Churchill Livingstone, 1998.

2. Chest physiotherapy by the ‘bag squeezing’ method: A guide to Technique. Clement, A and Hubsch, S. 1968, Physiotherapy, Vol. 54, pp. 355-9.

3. “Bag Squeezing”: A Physiotherapeutic technique. Windsor, H, Harrison, G and Nicholson, T. 1972, Medical Journal of Australia, Vol. 2, pp. 829-33.

4. The use of manyal hyperinflation in airway clearance. Denehy, L. 1999, European Respiratory Journal, Vol. 14, pp. 958-65.

5. Pattern of ventilation during manyal hyperinflation performed by physiotherapists. Maxwell, LJ and Ellis, ER. 2007, Anaesthesia, Vol. 62, pp. 27-33.

6. To bag or not to bag? Manual hyperinflation in intensive care. Robson, WP. 1998, Intensive and Critical Care Nursing, Vol. 14, pp. 239-43.

7. An investigation of the early effects of manual lung hyperinflation in critically ill patients. Hodgson, C, et al. 3, 2000, Anaesthesia and Intensive Care, Vol. 28, pp. 255-61.

8. A comparison of the effects of manual and ventilator hyperinflation on static lung compliance and sputum production in intubated and ventilated intensive care patients. Berney, S and Denehy, L. 2, 2002, Physiotherapy Research International, Vol. 7, pp. 100-108.

9. Effects of manual hyperinflation and suctioning on respiratory mechanics in mechanically ventilated patients with ventilator-associated pneumonia. Choi, J and Jones, A. 2005, Australian Journal of Physiotherapy, Vol. 51, pp. 25-30.

10. Description of manual hyperinflation in intubated patients with atelectasis. McCarren, B and Chow, C. 1998, Physiotherapy Theory and Practice, Vol. 14, pp. 199-210.

11. The effect of manual lung hyperinflation and postural drainage on pulmonary complications in mechanically ventilated trauma patients. Ntoumenopoulos, G., Gild, A. and Cooper, DJ. 5, Oct 1998, Anaesthesia and Intensive Care, Vol. 26, pp. 492-6.

12. Cardiovascular responses to manual hyperinflation in post-operative coronary artery surgery patients. Patman, S, et al. 1998, Physiotherapy Theory and Practice, Vol. 14, pp. 5-12.

13. Acute lobar atelectasis: A comparison of two chest physiotherapy regimens. Stiller, K, et al. 6, 1990, Vol. 98, pp. 1336-1340.

14. Effect of manual hyperinflation on haemodynamics in an animal model. Anning, L, et al. 3, 2003, Physiotherapy Research International, Vol. 8, pp. 155-163.

15. The Mapleson C circuit clears more secretions than the Leardal circuit during manual hyperinflation in mechanically-ventilated patients: a randomised cross-over trial. Hodgson, C, et al. 2007, Australian Journal of Physiotherapy, Vol. 53, pp. 33-8.

16. Mucus Clearance by two-phase gas-liquid flow mechanism: asymmetric periodic flow model. Kim, C., Iglesias, A. and Sackner, M. 3, 1987, Journal of Applied Physiology, Vol. 62, pp. 959-71.

17. Removal of Bronchial Secretions by Two-Phase Gas-Liquid Transport. Benjamin, R., et al. 3, 1989, Chest, Vol. 95, pp. 658-63.

18. Vander, A, Sherman, J and Luciano, D. Human Physiology. 7th Edition. s.l. : McGraw-Hill, 1996.

19. Re-expansion of atelectasis during general anaesthesia: A computed tomography study. Rothen, HU, et al. 6, 1993, Vol. 71, pp. 788-795.

20. The use of a pressure manometer enhances student physiotherapists’ performance during manual hyperinflation. Redfern, J, Ellis, E and Holmes, W. 2001, Australian Journal of Physiotherapy, Vol. 47, pp. 121-31.

21. Barotrauma is volutrauma, but which volume is the one responsible? Dreyfuss, D and Saumon, G. 3, 1992, Intensive Care Medicine, Vol. 18, pp. 139-41.

22. Barotrauma in human research. Leith, D. 1976, Critical Care Medicine, Vol. 4, pp. 159-61.

23. Manual hyperinflation: a description of the technique. McCarren, B and Chow, C. 3, 1996, Australian Physiotherapy, Vol. 42, pp. 203-208.

24. Manual hyperinflation: consistency and modification of the technique by physiotherapists. Patman, S, Jenkins, S and Smith, K. 2, 2001, Physiotehrapy Research International, Vol. 6, pp. 106-117.

25. A survey on Manual Hyperinflation as a Physiotherapy technique in intensive car units. King, D and Morrell, A. 10, 1992, Physiotherapy, Vol. 78, pp. 747-50.

Additional resources: #

Manual Hyperinflation Video: