Review article

Kenney B, et al: Newer techniques of humidification and secretion clearance

Newer techniques of humidification and secretion clearance

Brent Kenney*, Felix Khusid, Emma Fisher
Email: pilot215@gmail.com

Abstract
This paper begins with a review of airway anatomy, physiology of airway secretions, alterations in disease, and the importance of the mucociliary escalator, especially in airway disease states (asthma, COPD, cystic fibrosis, bronchiectasis etc). Alternatives to treating mild to moderate hypoxemia with high flow nasal cannula oxygen (HFNCO) such as Vapotherm are mentioned. A relatively new technique called Intrapulmonary Percussive Ventilation (IPV) seems very effective in secretion removal. A newer device called CoughAssist assists cough by mechanical insufflation-exsufflation and is very useful in neurological disease. The review then focuses on High Frequency Percussive Ventilation (HFPV), otherwise known as Volumetric Diffusive Ventilation (VDR). Lastly, the use of biphasic cuirass ventilation for secretion removal has been described. Keywords: High flow nasal cannula, humidification, intrapulmonary percussive ventilation, secretion clearance.

Introduction A normal healthy human takes for granted the ability to humidify inspired air and remove irritant particles from the lung. This is, in reality, a complex process involving the nose, nasopharynx, oropharynx, hypopharynx, larynx, trachea, bronchi, bronchioles and airway epithelium. Humidification of inspired gases is one of the major functions of the respiratory tract apart from gas exchange, metabolic, defense, conservation and speech.1 The focus of this paper is to review the important considerations related to humidification of inspired gases, the role of the mucociliary escalator or mucociliary transport mechanism in health and disease and secretion removal in disease that impairs the efficient functioning of this mechanism.
Brent Kenney, BS, RRT, FAARC
Supervisor, Respiratory Care, Mercy Hospital, Sprinfield, 1235 E, Cherokee J 4702, Springfield, Missouri 65804

Conducting airway tissue The epithelial lining of the conducting airways is primarily pseudostratified ciliated columnar epithelium. Mucus secreting cells called the goblet cells are situated between these cells. In the submucosal layer are the submucosal glands that secret mucus. Airway mucus is a dilute aqueous solution containing lipids, glycoconjugates and proteins.2 Airway mucus forms a bi-layer with an upper gel layer and a lower watery or sol layer. It is thought that there is a surfactant layer in between these two levels.3 Each epithelial cell has 200 cilia, each approximately 6-7 mm long that beat 20 times/second in a metachronal wave that propels the mucousin cephalad direction.4 Tips of the cilia engage the gel layer and propel it cephalad returning for the next stroke through the sol layer. Effects of gas temperature and humidity In a healthy state, the human at rest inspires air at room temperature and relative humidity. However, by the time this inspired air reaches the mainstem bronchi, it will be almost 37 C and will have 100%

Felix Khusid, BS, RRT-ACCS, NPS, RPFT, FAARC Emma Fisher, MS, RRT-NPS

New York Methodist Hospital, Brooklyn, New York New York Methodist Hospital, Brooklyn, New York

How to cite this article: Kenney B, Khusid F, Fisher E. Newer techniques of humidification and secretion clearance. Ind J Resp Care 2013; 2:262-76. 262 Indian Journal of Respiratory Care|July 2013|Volume 2|Issue 2

Kenney B, et al: Newer techniques of humidification and secretion clearance

relative humidity (RH).5 The location at which this happens is referred to as the isothermic saturation boundary (ISB). ISB will vary in its location in relation to the changes in temperature and relative humidity of the ambient environment, temperature of the inspired air, the minute ventilation of the subject and individual anatomic variations in the subject.6 The ISBs location tends to move out deeper into the lung periphery as minute ventilation increases and gas temperature decreases.7 This has important implications for mechanically ventilated patients. Recent expert panel guidelines from the American Association for Respiratory Care recommend that invasively ventilated patients should receive a humidity level of 33 - 44 mg H2O/L, with a gas temperature between 34C and 41C at the Y piece of the circuit, with a relative humidity of 100% to prevent drying out airway secretions.8 The defense function of the mucociliary escalator is largely bypassed in intubated patients. Delivering suboptimal humidity can affect mucociliary function and thus transport which can potentially lessen the airway surface liquid (ASL) depth resulting in decreased mucociliary transport velocity.1 If the ASL level is reduced enough the cilia may stop beating. After a period of time, the cilia may not start beating with rehumidification, with inflammation and sloughing of the airway mucosa.9 Sub-optimal delivery of humidification may be associated with reduced endotracheal tube (ETT) diameter, increased airflow resistance, thick secretions, mucous plugging and atelectasis.10 Effects of disease on the airway Some of the more common disease processes to be considered with regard to mucociliary function would be chronic obstructive pulmonary disease (COPD), asthma and cystic fibrosis (CF). Chronic lower respiratory disease (CLRD) is now the third leading cause of death in the United States, surpassing cerebrovascular disease according to the Centers for Disease Control and Prevention behind heart disease and cancer.11 This classification includes chronic bronchitis, emphysema and asthma. COPD is a progressive inflammatory disease succinctly characterised by chronic bronchitis, airway thickening and emphysema in variable

proportions.12 Known risk factors include genes, exposure to particles, outdoor air pollution, female gender, age and low socioeconomic status.12 Exposure to particles includes smoking, exposure to biomass fuels and occupational dusts (organic and inorganic). The overlap of chronic bronchitis (CB), chronic bronchiolitis, emphysema and asthma is often debated and hard to define.13 CB is defined as chronic cough and recurrent increases in bronchial secretions sufficient to cause expectoration.13 The secretions are present for three months a year for at least two successive years, not attributable to other pulmonary or cardiac causes.13 Exposure to tobacco smoke is regarded as the most important risk factor, with 50% of smokers developing COPD.12 Other authors have declared 15% as the number of smokers who will develop COPD. In smokers, secretory cells in the airway epithelium undergo changes with increase in the size and number of mucous glands along with increase in the goblet cell population also resulting in excessive sputum production.13 This alters the flow/adhesive properties of the mucociliary escalator, leading to pooling of secretions, which supports growth of bacteria resulting in release of products that damage the cilia and the epithelial cells. This allows the bacteria to adhere to the surface.13 The internal calibre of the larger airways are affected with airflow obstruction and limitation.2 Chronic bronchiolitis affects the smaller airways located beyond the first six generations. These airways are 2 mm diameter. The main secretory cell in the bronchioli is the Clara cell. In smokers, mucus cells replace the Clara cells. This mucus is retained in the small narrow airways which is difficult to clear with directed coughing. The Clara cells produce antielastase which prevents proteolytic digestion. Without this protection, the bronchioli may be vulnerable to development of emphysema.13 Emphysema is the destruction of airspaces distal to terminal bronchioles without obvious fibrosis. Smoking and exposure to particulate matter leads to inflammatory changes in the lung in those who develop COPD. Neutrophils, macrophages and lymphocytes are involved. The release of neutrophilic enzymes can lead to damage of elastic
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Kenney B, et al: Newer techniques of humidification and secretion clearance

lung tissue.12 The lymphocytes are primarily T lymphocytes, which are mostly CD8+ T cells.14 The CD4+ lymphocytes release destructive enzymes that induce an autoimmune response on lung tissue. As the attack on the alveolar walls and elastin fibres continue, emphysema begins to form.13 The loss of elastic recoil leads to air trapping with increases in functional residual capacity (FRC), residual volume (RV), reduction in forced vital capacity (VC), forced expiratory volume in one second (FEV1) and FEV1/FVC ratio. The destruction of alveolar walls worsens ventilation/perfusion (V/Q) matching, leading to decreased diffusion (DLCO) and hypoxaemia. Destruction of the elastic fibres supporting the airways leads to severe airflow obstruction and reduced cough effectiveness. Emphysema can also have a genetic cause. The SERPINA1 gene which codes for the protease inhibitor, alpha-1-antitrypsin (AAT) may be defective. The resulting deficiency of AAT allows uninhibited action of proteases with destruction of lung tissue leading to emphysema. The percentage of people exhibiting AAT deficiency is estimated to be only 1-2%.12 Asthma is also part of the obstructive lung disease family. Asthma is a chronic inflammatory disorder of the airways in which many cells and cellular elements play a role: in particular, mast cells, eosinophils, neutrophils (especially in sudden onset, fatal exacerbations, occupational asthma and patients who smoke), T lymphocytes, macrophages and epithelial cells.15 These episodes are usually associated with widespread but variable airflow obstruction that is often reversible either spontaneously or with treatment.15 Reversibility of airflow limitation may be incomplete in some patients. Persistent changes in airway structure occur, including subbasement fibrosis, mucous hypersecretion, injury to epithelial cells, smooth muscle hypertrophy and angiogenesis.15 Mucous obstruction of the airways is common in asthma.2 Complete mucous obstruction of the airways is seen in patients who die of status asthmaticus.16 Asthma has been shown to have more CD4+ cells and eosinophils.13 Luminal obstruction and severe bronchospasm are seen in fatal asthma attacks.
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Cystic fibrosis (CF) is an autosomal recessive genetic disorder affecting the bodys exocrine glands.17 CF subjects exhibit pulmonary symptoms consisting of endobronchial infections, exaggerated inflammatory response, airways obstruction and bronchiectasis.18 The CF gene defect produces an absent or malfunctioning cystic fibrosis transmembrane regulator, resulting in abnormal chloride conductance on the epithelial cell, with airway surface liquid depletion.19 Depletion of airway surface liquid possibly leads to ciliary collapse and loss of mucociliary clearance. A cycle of phlegm retention, infection and inflammation is common in CF patients.19 In the past, CF was thought of a disease of childhood, due to lack of diagnosis, effective treatments and use of antibiotics to prevent chronic or repeated infections. In the United States, 45% of the 30,000 subjects with CF are older than 18 years of age with median survival reported to be 37.4 years of age.20 There are many therapeutic devices and modalities available to treat and support patients with diseases (COPD, asthma, cystic fibrosis, bronchiectasis) that alter normal airway physiology producing airflow obstruction, mucociliary escalator dysfunction, secretion retention, V/Q matching and alterations in gas exchange. This article highlights the therapeutic devices and modalities that are newer and unknown or unavailable in some areas of the world. High flow nasal cannula Historically, discovery of oxygen (O2) has been credited to Antoine Lavoisier, while in fact, the initial discovery was made by Carl Wilhelm Scheele in 1771.21 It was not until 1907 that rubber tubing was devised to be used as a nasal catheter for oxygen administration.21 Today medical environment sees O2 used in ambulances, emergency rooms, operating rooms, intensive care units, general patient wards and even patients homes. Previous research on the oxygen cannula revealed that it was more comfortable than face masks, face tents and catheters but not as comfortable as an oxygen tent.22 They studied flows from 1-6 L/minute using nasal cannula and nasal catheter with the mouth open and closed. The effect of open or close mouth was deemed negligible.22

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Research on fraction of inspired oxygen (FIO2) from nasal cannula has demonstrated that measurement is not very practical, variability exists between normal subjects, textbook predictions are often not based on data and FIO2 decreases considerably in dyspnoeic patients.23 Traditional textbooks on respiratory care note that flows of 0.5 L/min to 8 L/min in adult patients provide an FIO2 range of 22%-45%.24A high flow system for delivering O2 should provide at least 60 L/minute of total flow to the patient. The average adult inspiratory flow is approximately three times the patients minute volume. Twenty litres/ minute is approximately the flow that is sustainable for persons who are ill (20 x 3 = 60 L/min). In rare occasions flow must reach or exceed 100 L/minute.24 Based on earlier textbook recommendations most clinicians are cautioned not to exceed 6 L/min.25,26 Physical irritation and drying of the nasal mucosa, frontal sinus pain and general patient discomfort are reasons given for limiting flows to 6 L/minute. Humidification complicates the issue. O2 bubbler devices provide some humidity but fall short of published recommendations.27 The search has been ongoing for a device that is comfortable for the patient to wear, delivers adequate inspiratory FIO2 and provides adequate humidification. The first abstracts to appear describing the use of high flow nasal cannula (HFNC) with flows unheard of before, reaching 40 L/minute, surfaced in 2002.28,29 Complex physical structure and physiology makes it difficult to apply bench study findings of mannikin models to human patients. Various manufacturers including Vapotherm, Pari, Fisher and Paykel, and Teleflex have equipment and nasal cannulas for HFNCO2 delivery. Given the evidence of discomfort associated with higher flows of oxygen with nasal cannula, the question should be addressed as to why patients are able to tolerate 40-60 L/minute of O2 at varying inspired oxygen concentration with the devices shown above. A bench study published in 2004 revealed that the potential reason for toleration of the higher flows may be due to the relative humidity of the HFNC. The Salter Labs high flow nasal cannula set up delivered 72.5% - 78.7% relative humidity

at flows of 5- 15 L/minute. The Vapotherm 2000i (Figure 1), delivered 99.9% relative humidity at flows of 5 40 L/minute.

Figure 1: Vapotherm

Most authors have concluded that the comfort of the higher relative humidity flows is the reason patients tolerate HFNC.23 The devices shown above when matched with a separate or built in oxygen blender or venturi provide the clinician the ability to control the FIO2 in addition to flow. Control of the FIO2 allows one to provide adequate oxygenation, while control of the flow serves to decrease the work of breathing.30 There is a tendency to think that a patient on O2 by a nasal cannula, even if HFNC is not very ill. This may not be true as some of these patients are acutely ill. Roca et al studied 20 patients who had respiratory failure defined as blood oxygen saturation < 96% with FIO2 0.50 via face mask.31 O2 was first delivered via bubble humidifier and face mask for 30 minutes. Then the patients received HFNC with heated humidifier for 30 minutes. Patients evaluated the experience based on dyspnoea, mouth dryness and overall comfort. HFNC was associated with less dyspnoea, less mouth dryness and more overall comfort.31 HFNC was associated with higher PaO2 and lower respiratory rate.31 Patients donot receive benefit from O2 delivery if they do not wear it.32 Cuquemelle et al conducted a prospective, randomised trial (n=30) with a final crossover period
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to compare nasal airway calibre and respiratory comfort in patients with hypoxaemic respiratory failure.33 Upper airway calibre was not reduced in heated high flow O2 therapy (HHFO2) but there was a significantly reduced discomfort with the use of HHFO2.33 Park et al looked at 60 patients comparing effectiveness and tolerability of nasal high flow (NHF) to standard high-flow face mask (HFFM) O2 delivery.34 The rate of noninvasive ventilation (NIV) was lower in the NHF group, but not of statistical significance (p=0.10).34 More of the NHF patients succeeded in their therapy (p=0.006) and there were significantly fewer desaturations (p=0.009).34 In the adult population the following benefits are proposed: 1) HFNC offers the potential for improved oxygenation in moderate hypoxaemic failure 2) It can be used in the emergency department, intensive care unit and exercise lab and 3) Decreased respiratory rate provides a reliable guide to predict improved oxygenation.23 The use of HFNC is not limited to adults. Pediatric and neonatal patient populations have been treated with HFNC. Differences in size, nasal anatomy, respiratory rates and inspired tidal volumes in smaller pediatric and neonatal patients means delivery of lower flow rates than with adult HFNC. A 2009 review by Dani et al looking at nine studies of HFNC in preterm infants, concluded the following: 1) HFNC is associated with continuous distending pressures (CDP) in patients with closed mouth 2) The value of CDP is proportional to the flow only in smaller infants, 3) The use of heated humidified high flow nasal cannula (HHFNC) is effective in minimising nasal mucosal injuries 4) The use of HHFNC for apnoea of prematurity, respiratory distress syndrome and the prevention of extubation failure lacks a firm conclusion 5) HHFNC should be preferred to high flow nasal cannula (HFNC) 6) the use of HHFNC as an alternative to nasal constant positive airway pressure (NCPAP) should wait for the conclusion of randomised clinical trials.35Most studies of paediatric patients focus on the use of HFNC for viral bronchiolitis, with very few overall studies being done in this population.36 Spnentzas et al performed a prospective observational study with 46 patients, ranging in age from newborns
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to 12 years of age (median age 2.8 years).37 These patients were assessed after beginning with O2 hood, non-humidified low flow nasal cannula (LFNC), or O2 face mask and then being switched to HFNC with the Vapotherm. HFNC flow rates were 8-12 L/minute for infants and 20-30 L/minute for children. Analysis of tolerance and improved arterial oxygen saturation (SaO2) in the first 60-90 minutes was significant.37 Schibler et al conducted a 5 year retrospective analysis reviewing 298 infants less than 24 months in a paediatric ICU receiving HFNC. Most of the patients had viral bronchiolitis. For the patients with viral bronchiolitis, the intubation rate decreased from 37% to 7%.38 Ineffective cough and retained secretions The presence of retained secretions combined with the inability to effectively mobilise those secretions is seen in a variety of age specific patient populations and disease pathologies (spinal muscle atrophy, cerebral palsy, cystic fibrosis, COPD, postoperative patients, quadriplegia, amyotrophic lateral sclerosis and stroke). Clinicians are often faced with the task of mobilising secretions from the periphery of lung to the upper airway where the directed cough effort can generate enough airflow to expel them. This can be a daunting task. Bach et al looked at translaryngeal extubation and tracheostomy tube decannulation in 49 consecutive patients. Their data in these patients showed that when the peak cough flows fell below 160 L/minute, extubation and decannulation would fail.39 Not only is peak flow important but so is a sufficient vital capacity. When the vital capacity becomes less than 30% in the supine position, then nocturnal ventilatory support is required.40 There are many therapies available to the physician, physiotherapist, respiratory therapist and nurse to treat the patient who has retained secretions and a disease process that limits the ability to generate sufficient airflow to mobilised and expectorate those secretions. This paper will focus in Intrapulmonary Percussive Ventilation (IPV) as a means to resolve atelectasis and mobilise secretions. In addition to IPV, methods of insufflation and exsufflation for expectorating secretions in the upper airways will also be discussed.

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Intrapulmonary percussive ventilation Intrapulmonary Percussive Ventilation (IPV) describes a therapy using a device invented by Dr Forrest M. Bird MD, PhD, ScD. The device is manufactured by Percussionaire Corporation of Sandpoint, Idaho. The Impulsator, IPV-1C, IPV-2C (Figure 2) and IPV-HC are different devices that can be used for IPV therapy. IPV therapy is intended to treat atelectasis and mobilise secretions. All of these devices use a sliding venturi called a Phasitron, which was invented by Dr Bird in the early 1980s. These devices are pneumatically driven either by wall medical oxygen and/or air, or by a self-contained compressor. The units provide the pneumatic flow and pressure required to operate the Phasitron. They provide the working pressure (psig), pulse frequency rate and peak pressure needed to provide effective IPV therapy. The Phasitron (Figure 3) consists of a Phasitron body, spring, venturi body, servo diaphragm with stem and the end cap.

The IPV device is connected to the Phasitron by a colour coded harness. The harness provides the pneumatic power to ope rate the sliding venturi and the nebuliser attached to it. The IPV waveform is unique. The IPV unit sends high frequency pulsations of pressure to the sliding venturi at a frequency of 60-300 per minute. The amplitude of the high frequency pulsations is determined by working pressure, and knob selection and adjustment. The IPV - 2C has the abililty to add demand continuous positive airway pressure (CPAP). The IPV - HC has a biphasic waveform. IPV may also be superimposed in-line upon conventional mechanical ventilation utilising a special cone shaped device that replaces the ventilator circuit wye.This provides a unique waveform not commonly seen in conventional ventilation. There is considerable discussion regarding which therapeutic modalities and devices are superior in treating patients with excessive mucous secretions, retained secretions, ineffective cough and atelectasis. Is IPV effective in treating these conditions? Most studies use retrospective reviews and crossover designs rather than randomised, parallel designs. Seldom is sham therapy used and most studies look one therapy versus another. Long term outcomes are difficult to come by.41 IPV therapy has been used in the neonatal, paediatric and adult patient populations.42-45 Bougatef et al studied IPV in the neonatal patient population.42 They researched the idea that IPV would reduce the rate of postextubation atelectasis, reintubation and improve gas exchange in premature neonates in a prospective, randomised study. In sixty patients intubated for more than 72 hours, randomisation to Assisted Autogenic Drainage (AAD), or IPV was carried out. Treatments were given every six hours and at least for 15 minutes. In the AAD group, 23% developed postextubation atelectasis and 13% required reintubation. None of the IPV patients developed atelectasis or required reintubation (p<0.05). Duration of oxygen requirements after extubation was greater in the AAD group (21.4 12) than the IPV group (15.7 12) (p<0.05).42 Chest physical therapy including postural
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Figure 2: Intrapulmonary percussionator ventilator

Figure 3: Phasitron

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drainage and percussion (PD&P) is often deemed as the standard for cystic fibrosis. Homnick et al compared the effects of IPV to standard aerosol and chest physiotherapy in CF in a six month comparative parallel trial.46 No difference was found in spirometric measures, hospitalisations, use of antibiotics or anthropometric measures. Deakins et al in a study conducted in a childrens hospital, compared IPV and chest physiotherapy (CPT) in a retrospective trial of 46 subjects, ranging in age from one month to 15 years, evaluating atelectasis scores on chest x-ray.44 Atelectasis scores ranged from zero (complete resolution of collapse) to four (complete collapse of 2 segments or lobes). A significant improvement in atelectasis scores was seen (3 to 1, p <0.001). Next, they conducted a prospective, randomised controlled trial in 12 subjects. These children ranged in age from seven weeks to 14 years of age. Requirements for entry were intubation and mechanical ventilation in the paediatric intensive care unit, evidence of atelectasis on chest x-ray and minimum patient weight of three kilograms. Atelectasis was scored on chest x-ray by a paediatric radiologist blinded to the type of treatment received. The IPV group showed significant improvement in this score (2.3 to 0.9, p=0.026). The duration of treatment in the IPV group was significantly less (3.1 vs 6.2 days, p=0.018).44 Hospitalised CF patients had greater wet sputum weight (p=0.035) with IPV as compared to PD&P or High Frequency Chest Wall Compression (HFCWC) in another study.43Preference was equal among participants for the three modalities/ techniques. Duchenne muscular dystrophy patients have difficulty clearing secretions related to low vital capacity and low spontaneous peak expiratory flow. Toussaint et al looked at eight patients with this disease, all having mucous hypersecretion (>30 mL/day).47 In a randomised, crossover study they had two treatment sequences. The first sequence had: 1) Forced expiratory technique and manually assisted cough (AMCT), 2) endotracheal suctioning 3) nebuliser administration of 5 mL of 0.9% NaCl solution 4) a second AMCT session 5) endotracheal
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suctioning 6) 45 min after the nebuliser, a third AMCT session and 7) endotracheal suctioning. The comparative sequence was the same, except it included IPV during the nebuliser session. IPV had greater sputum weight (6.53 4.77 vs 4.57 3.50 g, p=0.01). IPV was deemed safe in this patient population, while improving the effectiveness of AMCT. In a group of adolescent patients with neuromuscular disease Reardon et al compared IPV to Incentive Spirometry (IS).48 This was a randomised controlled study (n=18) to compare days of antibiotic use, number of respiratory infections, hospitalisation and school days missed. Antibiotic use was significantly higher in the IS group (24/1000 days vs 0/1000 days, incident rate ratio 43; 95 CI 6-333). The IS group spent more time in the hospital (4.4/1000 patient days vs 0/1000 patient days, incident rate ratio 8.5; 95% CI 1.1-67).48 Patients with COPD experience exacerbations that require hospitalisation and may be admitted to the ICU.49 Some of these patients have mild respiratory acidosis. Vargas et al treated thirty three patients with exacerbation of COPD, respiratory rate 25 breaths/min, PaCO2 > 45 mm Hg and 7.35 pH 7.38.50 Patients were randomly assigned to standard treatment (oxygen, beta adrenergics, anticholinergics, steroids, antibiotics and heparin) or to IPV with the same treatment medications as the standard group. The IPV group had a significant decrease in respiratory rate, increase in oxygenation (PaO2) and a decrease in carbon dioxide elimination (PaCO2). IPV may prevent further deterioration in COPD patients with acute exacerbations of COPD with mild respiratory acidosis. Nava et al considered the use of IPV in 10 stable COPD patients, to look at minute ventilation, tidal volumes and pressure time product of the diaphragm per minute. The patients receiving IPV as compared to spontaneous breathing had similar minute ventilation, higher tidal volumes and lower pressure time product of the diaphragm per minute (p < 0.05). In five normal subjects, a prolonged apnoea trial with IPV produced an apnoea > 2 minutes with no deterioration of oxygen saturation (SaO2) or subjective discomfort.

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Patients with COPD exhibit increased inspiratory work of breathing and dyspnoea. Expiratory flow limitation related to dynamic hyperinflation is seen in patients with COPD.51 In a study of COPD patients postextubation, the expiratory flow limitation (EFL) was measured by the negative expiratory pressure method. This was done to measure the short term (30 minutes) physiologic effect of a session of IPV. Of thirty five patients studied, twenty five patients presented with EFL. IPV led to a significant improvement in EFL (p < 0.05), significant decrease in P0.1 (P < 0.05) and a significant increase in PaO2 and pH, with a decrease in PaCO2 and respiratory rate (p < 0.05).51 Bronchiectasis is another disease entity in which IPV has been studied.52 Paneroni et al in a randomised crossover study looked at 22 patients who on consecutive days underwent CPT, then IPV the next day. Only IPV improved the sensation of dyspnoea, with patients finding it more comfortable than CPT (p = 0.03). Short term IPV was as safe and effective as traditional CPT. Antonaglia et al studied the effect of adding IPV by mouthpiece to patients being treated for COPD exacerbation with noninvasive ventilation using a helmet as compared to standard respiratory physiotherapy.53 Physiologic variables were measured at ICU entry, before and after the first IPV session and at ICU discharge. All variables improved after IPV: 1) PaCO2 was lower 58 5.4 vs 64 5.2, p < 0.01. 2) PaO2/FIO2 ratio was higher in IPV: 274 15 vs 218 34, p < 0.01. 3) length of stay in the ICU was less: p <0.01.53 IPV was noted to affect NIV via helmet length of stay, ICU stay and gas exchange in severe COPD exacerbation. Residual pneumothoraces are common after surgical lobectomy and may remain in spite of long term drainage. Residual pneumothoraces may complicate with an additional empyema.54 Gatani et al report on four patients with long-term complicated postresectional residual air spaces persisting six months.54 The type of resection was upper lobectomy in one patient and lower lobectomy in three patients. IPV was administered in an outpatient setting, with 12 minute sessions every other day up to a total of 8-12 sessions. There was complete resolution of the

spaces within a mean of 22 days of the beginning of treatment.54 IPV is administered in line with conventional ventilation for a variety of reasons, with atelectasis being one of them.55 Tsuruta et al studied ten obese patients with acute respiratory failure due to compression atelectasis who had not improved by conventional ventilation.55 Institution of IPV improved the PaO2/FIO2 ratio from 189 63 mm Hg to 247 67 mm Hg at three hours, to 280 50 mm Hg at 24 hours (p < 0.01). Compliance improved from 30 8 mL/cmH2O at zero hours to 38 8 mL/cmH2O at 24 hours (p < 0.01). Chest tomography scan confirmed the improvement in compression atelectasis.55 Airway mucus clearance: mechanical insufflationexsufflation Cough is essential in health to promote normal airway clearance. Patients with airway disease (asthma, COPD, bronchiectasis, cystic fibrosis) and those with neurologic and related respiratory muscle disease (spinal muscle atrophy, cerebral palsy, Duchennes muscular dystrophy, amyotrophic lateral sclerosis, myasthenia gravis, stroke, spinal cord injury, post-polio) are considered high risk due to their inability to produce effective cough contributed by low lung volumes and low expiratory gas flow rates.56,57 Normal subjects can achieve peak cough flow rates as high as 720 L/minute.58 The minimum expiratory peak cough flow rate necessary for successful extubation from mechanical ventilation is 160 L/minute.39 Upper respiratory tract infections with increased secretions in Duchenne muscular dystrophy requires approximately 270 L/minute of peak expiratory cough flow to prevent respiratory failure.59 The Emerson CoughAssist device (Figure 4) was originally manufactured and marketed by JH Emerson, Cambridge, Massachusetts. Phillips Respironics, Murrysville, Pennsylvania bought the product. The device applies positive pressure to the airway and then rapidly shifts to negative pressure to produce a high peak flow from the lungs, which simulates a cough.60 Peak expiratory flows of 10 L/second (600 L/minute) can be achieved by the machine itself.61 Maximum inspiratory pressure is + 60 cm H2O and expiratory negative pressure of 60 cm H2O.61 The device can be used on an
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endotracheal tube or tracheostomy tube, but the airways will provide resistance thus reducing the flows generated for a given pressure.62 This may mean increasing the set pressures on the CoughAssist, which may have clinical considerations in the ICU.62 A general treatment session includes three to five cycles of in-exsufflation (with or without an abdominal thrust during expiration) followed by 30 seconds of rest.63 Alternatives to using the CoughAssist include: 1) Insufflation to maximum insufflation capacity (using bag and mask, a ventilator or glossopharyngeal breathing) followed by a spontaneous cough and 2) manually assisted cough with an abdominal thrust.60 A recent survey looking at the use of the insufflator-exsufflator was performed in patients with spinal cord injury.64 The study was set up to address use of the device and patient and provider satisfaction. The survey was sent to 525 members of the American Paraplegia Society, with 86 questionnaires returned (16%). The survey demonstrated that only 49% of the respondents used the device in their respective institution. The device was most used with a tracheostomy, and patient and provider satisfaction was high.64 Mastella et al published an original research article that was a retrospective chart review of 16 patients with type 1 spinal muscle cord atrophy.65 These patients were under three years of age and they were consecutively referred for respiratory decompensation resulting in continuous noninvasive ventilation (NIV) and oxyhaemoglobin desaturation. Hospitalisation was avoided by using

NIV with high span bilevel positive airway pressure and reversal of desaturation by mechanically assisted coughing in the home setting. Forty three of the forty nine acute episodes met the criteria for avoiding hospitalisation.65 The CoughAssist has proven useful in neuromuscular disease and traumatic spinal cord injury. Further investigation into obstructive lung disease in the paediatric and adult patient population is warranted.60 High frequency percussive ventilation High Frequency Percussive Ventilation (HFPV) is a term coined to represent the ventilatory breath delivery of the Percussionaire VDR-4 ventilator. The Percussionaire VDR-4 (Figure 5) was conceived by Dr Forrest M Bird MD, PhD, ScD in the late 1970s. It received FDA approval in 1989. The term VDR refers to the components and effects of the breath delivery of the VDR-4. It provides a convective or volumetric component, along with a high frequency component that is the diffusive component; hence the term Volumetric Diffusive Respiration (VDR).The resulting pressure waveform is unique in the world of mechanical ventilation (Figure 6). The VDR4 uses a sliding venturi (Phasitron) and a colour code harness similar to the IPV units described earlier, with minor modifications. The VDR-4 consists of the upper pneumatic Servolator Percussionator and the lower electronic monitor below, the Monitron. The upper pneumatic portion is where the bedside clinician adjusts the settings

Figure 4: Cough assist device 270

Figure 5: Percussionaire VDR-4 ventilator Indian Journal of Respiratory Care|July 2013|Volume 2|Issue 2

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cast formation.77 Cioffi et al studied HFPV in 54 burn patients with documented inhalation injury from March 1987 through September 1990 and compared them to a historical cohort. The incidence of pneumonia was decreased (25.9% vs 45.8%, p < 0.005).67 The importance of small airway patency is preventing the sequelae of inhalation injury. Carman et al published a prospective, randomised comparison of HFPV versus conventional ventilation (CV) in burned children.69 They studied 64 patients with 32 assigned to each arm. Patient age was 7.4 0.7 years, total burns surface area was 56 3% and 55 patients (86%) had inhalation injury. Peak pressures were significantly less with HFPV 30.9 0.8 versus 39.5 1.8 cm H2O, p < 0.05. The best PaO2/FIO2 ratio in the HFPV group was 563 15 vs 507 13, p < 0.05. No barotrauma was seen in the HFPV group, versus two in the CV group. Ventilatory length of stay was not significant. Hall et al studied a group of patients with inhalation injury (n=92) between 1997 and 2005.72 This group was compared with a group treated with CV between 1997 and 2005 (n=130). Ventilator days, days in the ICU and incidence of pneumonia did not differ between groups. 26 of 92 patients (28%) treated with HFPV and 56 of 130 patients (43%) of the patients treated with CV died. There was a significant decrease in morbidity and mortality in a subset of patients with inhalation injury treated with HFPV with 40% TBSA.72 Chung et al conducted a randomised controlled trial in burn patients treated at Brooke Army Medical Centre in San Antonio, Texas, comparing the low tidal volume strategy of the ARDSnet versus HFPV.76There were 62 patients randomised to control or intervention strategy. Low tidal volume was the control. Primary outcome of ventilator free days in the first 28 days, with 129 in HFPV vs 119 in low tidal volume, p value was not significant. The trial did allow for rescue mode for those failing the mode they were allocated to. The need for rescue mode was 29% in the low tidal volume group versus 6% of the HFPV group, p=0.02. This population of patients is difficult because of limited burn centre numbers compared to other populations.
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Figure 6: Volumetric diffusive respiration waveform

and the lower electronic monitor only monitors the resulting pressure waveform. It also displays I:E ratio of the convective breath cycle, the I:E of the pulse waveform, the convective breath rate, the inspiratory time of the convective breath, the expiratory time of the convective breath, the percussive high frequency rate, the mean airway pressure, peak pressure and the PEEP/CPAP. The positive end expiratory pressure (PEEP) provided is unique to the VDR-4. The clinician may set demand CPAP and then set Oscillatory CPAP to function on top of the demand CPAP. The clinician has the availability of using either one, or both, depending on patient need and whether they are breathing spontaneously or not. High frequency percussive ventilation (HFPV) was used only for investigational purposes in the early and mid 1980s, then with FDA approval in 1989, it entered more widespread use. HFPV has been used with literature documentation in the neonatal population, the paediatric burn population with inhalation injury, adult burn population with inhalation injury, adult acute respiratory distress syndrome (ARDS) population failing conventional ventilation, adult trauma patients with ARDS and elevated intracranial pressure, transport mechanical ventilator for neonatal and paediatric populations and transport mechanical ventilator for adult patients.66-76 HFPV was initially used primarily in burn centres, where it was thought to more effectively treat the sequelae associated with inhalation injury in burn patients.67 These patients typically have carbonaceous deposits, epithelial sloughing, bleeding, mucosal oedema and

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While few centres use HFPV for neonates, Bougatef et al first conducted a prospective randomised trial, comparing the effects of HFPV with conventional mechanical ventilation (CMV), in 52 neonates, between 1986 to 1989.73 The initial study was followed up with a retrospective analysis of 273 consecutive neonates from 1989 to 1998 ventilated exclusively with HFPV.73 The third part of the study was a study in 55 neonates on HFPV, from 1998 to 2002, of whom 22 were treated with surfactant as rescue therapy.73 In the first study HFPV had a lower incidence of pulmonary air leak (8% vs 33%, p < 0.05), intraventricular haemorrhage (IVH) (8% vs 37%, p = 0.02) and chronic lung disease (CLD) assessed at 28 days (15 vs 43%, p = NS) and 36 weeks gestational age (0% vs 29%, p < 0.02), than CMV group. Mortality was lower in HFPV (205 vs 48%, p < 0.04).73 Survival rate in the second part and third part of the study for HFPV was 85% and 89% respectively, with an incidence of air leak at 9%. The incidence of IVH (12% vs 9%) and CLD at 36 weeks gestational age (3% vs 4%) were similar in both groups. HFPV was determined to be safe and effective in preterm neonates with respiratory distress syndrome.73 Approximately 16% of deaths in patients with ARDS occur as a result of refractory hypoxaemia.75 Alternative techniques were reviewed by Esan et al surveying the literature and summarising the use of PEEP, recruitment manoeuvres, airway pressure release ventilation (APRV) and high frequency ventilation. The authors cautioned that improving oxygenation must be balanced with avoidance of further lung injury. The optimal time for rescue manoeuvres was estimated to be within the first 96 hours of mechanical ventilation, when alveolar recruitment potential is the greatest.75 Availability of equipment and clinician bias often direct the rescue therapy. The authors suggest an algorithm for approaching treatment for ARDS patients with refractory hypoxaemic failure.75 Biphasic cuirass ventilation Biphasic Cuirass Ventilation (BCV) is a method of ventilation which works using a noninvasive cuirass
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or shell, attached to a power unit which actively controls both phases of the respiratory cycle in both children and adults (Figure 7). As ventilation is biphasic, it is possible to achieve both higher tidal volumes (negative inspiratory tidal volume and positive expiratory tidal volume), higher frequencies from 6 to 1200 CPM and also for the user to have proper and real control over I:E ratio, without having to depend on passive recoil of the patient. In addition, the patented technology used for the cuirass and its disposable seal in the Hayek RTX allows for a comfortable fit and seal of the air within the cuirass. These advantages allow for a much higher minute ventilation to be created and thus making complete ventilation possible in both normal and sick lungs. The Hayek RTX is able to perform 4 modes of noninvasive operation that include Continuous Negative Pressure, Fully Controlled Ventilation with or without synchronization, High Frequency Chest Wall Oscillation and built in Assisted Cough for secretion clearance.

Figure 7: Hayek RTX chest cuirass ventilator

In Secretion Clearance mode the Hayek RTX uses both positive and negative pressure to create an oscillatory effect which reduces secretion viscosity and loosens impacted bronchial secretions.78 CPAP can be harmful for patients who have respiratory failure due to mucus retention.79 In these cases, mucus removal by irrigation could lead to complications, but the RTX respirator has been shown to be very effective for patients with sputum retention.80 The Hayek RTX also helps to thin secretions and expel sputum in patients with cystic fibrosis and it can be set to repeat the oscillatory mode and assisted cough modes for regular treatment.

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Kenney B, et al: Newer techniques of humidification and secretion clearance

Summary This paper began with a review of airway anatomy, physiology of airway secretions, alterations in disease and the importance of the mucociliary escalator, especially in airway disease states (asthma, COPD, cystic fibrosis, bronchiectasis etc). Alternatives to treating mild to moderate hypoxemia with high flow nasal cannula oxygen (HFNCO) were mentioned. There is a shortage of high level studies comparing HFNCO to NIV. There is concern about levels of CPAP, and the inability to measure and control it, especially in the neonatal and smaller paediatric population. Mobilisation of secretions is a task shared round the world by a variety of clinical disciplines. There is a dearth of high level studies comparing modalities, techniques and devices. We focused on a relatively new technique called Intrapulmonary Percussive Ventilation (IPV) looking at studies in various age groups and disease entities. Additional information was presented on the CoughAssist device and its use in the neurological disease and spinal cord injury population. More work and randomised studies are needed in this area. This review then focused on High Frequency Percussive Ventilation (HFPV), otherwise known as Volumetric Diffusive Ventilation (VDR). This modality and machine are not as well-known as other high frequency devices, but have proven themselves in neonates through adults, in infant RDS, adult ARDS, adult ARDS with elevated ICP, trauma ARDS, paediatric and adult burn patients and inhalation injuries. Much of the use is rescue except for a few prospective, randomised trials. Future trials will be needed to provide the benefit of VDR in more adequately powered studies and not just for rescue. Lastly, the use of biphasic cuirass ventilation for secretion removal has been described. References 1. Williams R, Rankin N, Smith T, et al. Relationship between the humidity and temperature of inspired gas and the function of the airway mucosa. Crit Care Med 1996; 24:1929.

2. Rogers DF. Physiology of airway mucus secretion and pathophysiology of hypersecretion. Respir Care 2007; 52:1134-46. 3. Morgenroth K, Bolz J. Morphological features of the interaction between mucus and surfactant on the bronchial mucosa. Respiration 1985; 47:225-31. 4. RuppelGl, White D. Tissues of the conducting airways. In: Egans Fundamentals of Respiratory Care, 8th ed. St. Louis: Mosby 2003:176-80. 5. Walker JEC, Wells RE, Merrill EW. Heat and water exchange in the respiratory tract. Am J Med 1961; 30:259-67. 6. McFadden ER, Denison DM, Waller JF, et al. Direct recordings of the temperatures in the tracheobronchial tree in normal man. J Clin Invest 1982; 69:700-5. 7. McFadden ER, Pichurko BM, Bowman HF, et al. Thermal mapping of the airways in humans. J Appl Physiol 1985; 58:564-70. 8. Clinical Practice Guideline. Humidification during invasive and noninvasive mechanical ventilation: 2012 Respir Care 2012; 57:782-8. 9. Hirsch JA, Tokayer JL, Robinson MJ, et al. Effects of dry air and subsequent humidification on tracheal mucus velocity in dogs. J Appl Physiol 1975; 39:242-6. 10. Stuart RN, Rankin N, Meyer E, Williams R. Energy balance in the intubated human airway is an indicator of optimal gas conditioning. Crit Care Med 2002; 30:355-61. 11. Centers for Disease Control and Prevention, FAST Stats, retrieved April 1, 2013 from CDC Home web site: http://www.cdc.gov/nchs/ fastats/deaths.htm 12. Brasher BB, Kodgule R. Risk factors and pathophysiology of chronic obstructive lung disease (COPD). JAPI 2012; 60:S17-21. 13. Jeffery, PK. Structural and inflammatory changes in COPD: a comparison with asthma. Thorax 1998; 53:129-36. 14. Barnes, PJ. Medical Progress: Chronic Obstructive Pulmonary Disease. N Engl J Med 2000; 343:269-80. 15. Program, NAEAP. Expert panel report 3 (EPR3): Guidelines for the diagnosis and management
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of asthma-summary report 2007. J Allergy Clin Immunol 2007; 120:S94S138. 16. Saeta M, Di Stefano A, Rosina C, et al. Quantitative structural analysis of peripheral airways and arteries in sudden fatal asthma. Am Rev Respir Dis 1991; 143:138-43. 17. Volsko TA. Cystic fibrosis and the respiratory therapist: A 50 year perspective. Respir Care 2009; 54:587-93. 18. Davis PB, Drumm M, Konstan MW. Cystic fibrosis: state of the art. Am Respir Crit Care Med 1996; 154:1229-56. 19. Ratjen FA. Cystic Fibrosis: Pathogenesis and future treatment strategies. Respir Care 2009; 54:595-602. 20. Cystic Fibrosis Foundation. Patient registry annual data report for 2007. Bethesda, MD: Cystic Fibrosis Foundation; 2008. 21. Heffner JE. The story of oxygen. Respir Care 2013; 58:18-30. 22. Kory RC, Bergmann JC, Sweet RD, et al. Comparative evaluation of oxygen therapy techniques. JAMA 1962; 179:123-8. 23. Ward JJ. High-Flow oxygen administration by nasal cannula for adult and perinatal patients. Respir Care 2013; 58:98-120. 24. Heuer AJ, Scanlan CL. Medical Gas Therapy: Overview of oxygen therapy systems. In Wilkins RL, Stoller JK, Scanlan CL editors: Egans fundamentals of respiratory care, 8th Ed., St. Louis, 2003, Mosby. 25. Egan DF. Fundamentals of inhalation therapy. St. Louis: Mosby; 1969. 26. American Association for Respiratory Care. AARC Clinical Practice Guideline: oxygen therapy for adults in the acute care facility: 2002 revision and update. Respir Care 2002; 47:71720. 27. American Society for Testing Materials. Annual Book of ASTM Standards: F1690-96 standard specifications for medical use. Part 1: general requirements for active humidification systems. Section 13: medical devices and services. West Conshohocken, PA: ASTM;2001:106201077. 28. Tiep B, Barnett M. High flow nasal vs high flow mask oxygen delivery: tracheal gas
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41. Hess DR. Secretion clearance techniques: Absence of proof or proof of absence? Editorial. Respir Care 2002; 47:757-8. 42. Bougatef A, Casteels A, Cools P, et al. A study of intrapulmonary percussive ventilation (IPV) compared to assisted autogenic drainage (AAD) as an adjunctive protocol to neonatal weaning, following mechanical ventilation (abstract). Respir Care 2005; 50:1517. 43. Varekojis SM, Douce FH, Flucke RL, et al. A Comparison of the therapeutic effectiveness of and preference for postural drainage and percussion, intrapulmonary percussive ventilation and high frequency chest wall compression in hospitalized cystic fibrosis patients. Respir Care 2003; 48:24-8. 44. Deakins K, Chatburn RL. A comparison of intrapulmonary percussive ventilation and conventional chest physiotherapy for the treatment of atelectasis in the pediatric patient. Respir Care 2002; 47:1162-7. 45. Nava S, Barbarito N, Piaggi G, et al. Physiological response to intrapulmonary percussive ventilation in stable COPD patients. Respir Med 2006; 100:1526-33. 46. Homnick DN, White F, deCastro C. Comparison of effects of intrapulmonary percussive ventilator to standard aerosol and chest physiotherapy in treatment of children of cystic fibrosis. Pediatr Pulmonol 1995; 20: 50-5. 47. Toussaint M, De Win H, Steens M, et al. Effect of intrapulmonary percussive ventilation on mucus clearance in duchenne muscular dystrophy patients: A preliminary report. Respir Care 2003; 48:940-7. 48. Reardon CC, Christiansen D, Barnett ED, et al. Intrapulmonary percussive ventilation vs incentive spirometry for children with neuromuscular disease. Arch Pediatr Adolesc Med 2005; 159:526-31. 49. Brochard L. Noninvasive ventilation for acute exacerbations of COPD. A new standard of care. Thorax 2000; 55:817-8. 50. Vargas F, Nam Bui H, Boyer A, et al. Intrapulmonary percussive ventilation in acute exacerbations of COPD patients with mild respiratory acidosis: a randomized controlled

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