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Clinical practice review

Non-Invasive Ventilation for Adult Acute Respiratory Failure. Part I

G. J. DUKE*, A. D. BERSTEN† *Intensive Care Department, The Northern Hospital, Epping, VICTORIA †Department of Critical Care Medicine, Flinders Medical Centre, Bedford Park, SOUTH AUSTRALIA

ABSTRACT Objective: To detail the history, modes, physiological effects, and circuit geometry of non-invasive ventilation. Data sources: A review of articles published in peer-reviewed journals from 1966 to 1998 and identified through a MEDLINE search on non-invasive ventilation. Summary of review: Non-invasive ventilation (NIV) has been used for many years as an adjunct to standard therapy in patients with acute and chronic respiratory disorders. The newer modes of NIV which include continuous (CPAP), pressure support ventilation (PSV), BiPAP (bi-level positive airway pressure) and controlled and assisted modes of intermittent non-invasive positive pressure ventilation (NIPPV) have additional advantages and are often used routinely in many respiratory diseases. These modes of ventilatory support have been found to improve arterial oxygenation, ventilation, work of , and cardiac function, in patients with respiratory failure, although in normal subjects, respiration is often impaired.. Conclusions: Non-invasive ventilation using the modes of CPAP, PSV, BiPAP and NIPPV should be considered in patients with respiratory failure who are unresponsive to conventional therapy, before considering invasive . (Critical Care and Resuscitation 1999; 1: 187-198)

Key Words: Non-invasive ventilation, work of breathing, minute ventilation, ventilation circuits

Introduction Non-invasive ventilation (NIV) is a therapeutic Management of critically ill patients often involves option for respiratory failure and has been used for a treatment of acute respiratory failure (ARF). Severe variety of acute and chronic conditions, across all age ARF may require tracheal intubation and mechanical groups. It provides respiratory support without the need ventilation (MV), both of which carry an associated for tracheal intubation, maintaining many of the morbidity. Efforts to reduce morbidity from MV have physiological advantages of spontaneous respiration, included early detection and prevention of respiratory and in some patient groups there is evidence to suggest failure, and new ventilatory modes which attempt to it has lower morbidity compared to MV. improve the safety of MV and expedite weaning. Currently published reviews of NIV1-4 are small in Despite progress in these areas, avoidance of MV where number and provide incomplete information regarding possible remains a desirable option. the physiology of NIV, its various modes, and their

Correspondence to: Dr. G. J. Duke, Intensive Care Department, The Northern Hospital, Epping, Victoria 3076 (e-mail: [email protected] )

187 G. J. DUKE, ET AL Critical Care and Resuscitation 1999; 1: 187-198 clinical role in separate models of ARF. This review is were used for decades prior to the advent of positive based on the premise that a physiological framework pressure ventilators.2 provides a clear guide to: 1) the potential benefits of The use of mask-CPAP for the treatment of ARF NIV, 2) the differences between various modes of NIV, was first advocated in the mid 1930’s.20,21 In 1936 3) the side effects of NIV and, 4) the clinical indications Poulton reported a series of 22 patients with acute and limits of each mode. The aim of this two part review pulmonary oedema, asthma, and pneumonia. In the is to discuss the physiological and technical aspects of description of his CPAP circuit - the “pulmonary plus NIV (Part I), followed by the clinical use of NIV in pressure machine” - he described many characteristics adults with ARF (Part II). of an efficient circuit.20 It provided a high inspiratory flow using a household vacuum fan, an air-tight face Disadvantages of mechanical ventilation mask, an expiratory pressure-relief valve using an Ambu Although clinical experience and research support valve which was placed close to the patient’s airway, the benefits of MV in ARF it may produce significant and the option for warming the inspired gas using a hot morbidity.4-7 These complications have been well water bottle in the dust bag chamber. described and are reviewed briefly in relation to the The early achievements of NIV in ARF were potential advantages of NIV. overshadowed by other developments. By the 1930's Laryngoscopy and endotracheal intubation carries a there was widespread use of laryngoscopy and significant risk of trauma to the upper airways.6 An intubation for anaesthesia, and the early 1950's saw the endotracheal tube (ETT) bypasses the beneficial advent of simple and reliable positive pressure physiological effects of the upper airway, such as ventilators. There was also a conceptual shift away from warming and humidification of inspired gas,6,8 addition the treatment of discrete pulmonary disorders (by the of endogenous nitric oxide to the inspired gas,9-11 and respiratory physician in the general ward setting), to the protective reflexes. Depression of laryngo-tracheal treatment of the generic pulmonary condition, ‘acute reflexes increases the risk of pulmonary aspiration6 and, respiratory failure’, in a specialised ‘intensive care’ together with depression of mucociliary function, ward, by respiratory technicians and anaesthetists. NIV increases the risk of nosocomial infections. 6,8 was relegated to a minor role as an adjunct to chest Work of breathing is increased by the presence of an physiotherapy22,23 and to the delivery of bronchodilators. ETT and a breathing circuit.12,13 Problems of ventilator In the 1960's CPAP was being successfully utilised asynchrony6,8 and impaired weaning may result. in paediatric practice for the management of post- Increased patient discomfort and the loss of verbal cardiac surgery and hyaline membrane disease communication often result in increased sedative and patients.24-27 Not long after, CPAP was described for analgesic requirements. prophylaxis for the (adult) acute respiratory distress Commonly used modes of MV alter the distribution syndrome (ARDS)28,29 and PEEP was demonstrated to of ventilation and perfusion resulting in a fall in end- be of benefit in mechanically ventilated ARDS expiratory lung volume (EELV), lung compliance, and patients.30 ventilation-perfusion (V/Q) mismatch.14 This may be The use of NIV in adults grew out of this early partially overcome by using positive end-expiratory success and the simplicity of CPAP circuit construction. pressure (PEEP) and continuous positive airway By the late 1970's there were numerous anecdotal pressure (CPAP). MV may cause lung injury through reports of the successful use of mask-CPAP for a variety ,6,8,15 volume-trauma,7,16,17 ventilator of respiratory conditions.31 associat-ed pneumonia,7 and toxicity. Pressure support ventilation (PSV)32 as a NIV mode The cardiovascular side-effects of MV relate chiefly is of more recent origin.4 It arose out of the to elevated transmural pressures14,15 and intra-thoracic technological advances in pressure and flow sensors lung volumes.18 These factors may induce a fall in (which enabled mechanical ventilators to sense venous return and cardiac output, and activation of commencement and cessation of spontaneous inspiratory compensatory sympathetic and hormonal responses. pressure or flow), and the demonstrable benefit of PSV Many of these problems may be minimised or in intubated patients. eliminated through the use of non-invasive ventilatory support modes. Modes of non-invasive ventilation There are five commonly described NIV modes: History of non-invasive ventilation Non-invasive respiratory support has been used in 1. Continuous positive airway pressure (CPAP) cardiopulmonary resuscitation for many years.19 Cuirass 2. Pressure support ventilation (PSV) and other non-invasive negative-pressure generators 3. A combination of PSV + CPAP

188 Critical Care and Resuscitation 1999; 1: 187-198 G. J. DUKE, ET AL

4. BiPAP (bilevel positive airway pressure) or Oxygenation combined positive inspiratory positive airway The arterial oxygen content (CaO2) is influenced by pressure (IPAP) and expiratory positive airway a number of factors some of which may be identified by pressure (EPAP). rearranging the pulmonary shunt equation: 5. Controlled and assisted modes of intermittent positive pressure ventilation (NIPPV). CaO2 = CcO2 - Qs/Qt (CcO2 - CvO2)

There is a need for a consensus-based definition of Where “NIV” given the number of distinct modes, its CaO2 = arterial oxygen content widespread clinical use, and ongoing NIV research. All CcO2 = end-pulmonary capillary oxygen content; the above modes have three features in common: 1) the CvO2 = mixed venous oxygen content; delivery of positive airway pressure (Pao) without airway Qs = effective pulmonary shunt flow; and intubation; 2) the respiratory cycle can be patient- Qt = cardiac output. controlled - with BiPAP and NIPPV also having the option of mechanical time-cycling, and; 3) the delivery CcO2 is itself dependent upon the alveolar partial of Pao via a nasal or naso-oral (“full face”) mask. Face- pressure of oxygen (PAO2) and diffusion into the tents and head boxes have also been used for CPAP in pulmonary capillary. Factors which influence PAO2 may paediatric practice. be identified by considering the simplified ideal alveolar There is also a need for clinical guidelines to clarify gas equation, the indications for NIV in ARF. For some conditions (e.g., cardiogenic pulmonary oedema) there is strong PAO2 = [(PB - PH2O) x FIO2 ] - PaCO2/R evidence to support its routine use, but in others NIV appears to have little benefit. Although a detailed Where discussion of cardiorespiratory physiology is beyond the PAO2 = alveolar partial pressure of oxygen scope of this review, it is worthwhile considering some PB = barometric pressure aspects of respiratory and cardiac function in relation to PH2O = saturated water vapour pressure NIV and ARF. FIO2 = inspired oxygen concentration fraction PaCO2 = arterial partial pressure of CO2; and Physiology of non-invasive ventilation (Table 1) R = respiratory quotient. The physiological effects of NIV vary greatly and depend upon: 1) the nature of the subject investigated; Using these two equations it is possible to identify 2) the pathophysiology of the acute respiratory disorder; mechanisms through which NIV may improve 3) the severity of respiratory dysfunction; 4) the mode of oxygenation: NIV and level of Pao used, and; 5) the efficiency of the breathing circuit. 1. The majority of NIV circuits provide the ability to 33-35 PEEP should be distinguished from CPAP. control FIO2 and deliver high inspired O2 PEEP refers to the application of positive Pao to an concentrations through a closed circuit. The increase intubated patient during the expiratory phase of a in PAO2 is one of the most common mechanisms by mechanical breath cycle, whereas CPAP refers to which NIV improves PaO2 and CaO2. positive Pao during a spontaneous breath cycle. The distinction is important because the physiological effects 2. In principle, diffusion may improve with the of PEEP and CPAP are not necessarily equivalent.35 application of CPAP if redistribution of extra- Furthermore, CPAP applied to an intubated patient is vascular lung water decreases the water content of not necessarily identical to mask-CPAP. In the former alveoli. At present there is no direct evidence for an situation the subject must breath via an ETT and increase in diffusing capacity independent of a ventilator circuit both of which impose additional change in lung volume or PAO2 workload. These factors should be borne in mind when interpreting research data, and in determining the 3. In hypercapnic patients breathing room air, a small clinical applications of NIV. rise in PAO2 may occur if NIV increases minute The possible benefits of NIV on respiratory function ventilation (VE) and reduces PaCO2 (e.g., a chronic are improved oxygenation and alveolar ventilation respiratory failure patient using domicillary NIV (Valv), and reduced work of breathing (WB). The without supplemental oxygen). A fall in PaCO2 will potential effects on cardiac function are alterations in also allow a rise in the CaO2 via the Bohr effect. preload, afterload, chronotropy and lusitropy.

189 G. J. DUKE, ET AL Critical Care and Resuscitation 1999; 1: 187-198

4. Qs represents the combination of absolute pulmonary alveolar pressure - extrinsic EEP. Therefore the shunt and V/Q mismatch. NIV may improve V/Q equation above may be rewritten as, 36,37 relationships and CaO2 through the recruitment of collapsed alveoli and end-expiratory lung volume Pao = V/C + V& R + EEP + Pcir, (EELV).

so that the potential benefits of NIV on WB can be more 5. Finally, oxygenation may also improve if cardiac easily identified by considering each component: output (Qt) is increased. There are a number of studies which document an increase in cardiac output 1. If the application of positive Pao results in a volume with mask-CPAP in particular patient subgroups (see (V) of gas flowing into the lungs, then the amount of below). CPAP has also been shown to increase active patient work (Wpt) required may be reduced; oxygen delivery and CvO2 in intubated patients with 38 that is, Wpt = WB - (Pao x V). Many investigators chronic cardiac disease, when compared to MV. have demonstrated that NIV reduces measured 44-47 48 Wpt and increases minute volume (VE) or Work of breathing (WB) reduces respiratory rate and PaCO2 implying an WB is the pressure-volume work performed by the increase in VE (see below.) respiratory system. In healthy subjects it may be subdivided into the work required to overcome the 2. The application of CPAP (and PEEP) may result in impedance of the elastic (Wel) and the non-elastic an upward shift of the pulmonary pressure-volume properties of the lung and chest wall. Most of the non- relationship.49 If the result is an increase in lung elastic impedance comes from airway resistance to gas compliance (C) then WB will be decreased. An flow (producing a flow-resistance load, Wres), with a increase in C may occur through redistribution of component from non-elastic tissue impedance (a non- excess alveolar water, recruitment of alveoli, an elastic work load, Wti). increase in EELV, or a more homogeneous In pathological states other forms of ventilatory work distribution of ventilation. may be encountered. In severe airways obstruction an intrinsic end-expiratory alveolar pressure (PEEP ) may i 3. Inspiratory flow ( V& i) will rise in proportion to the exist which acts as an inspiratory threshold load (ITL) pressure gradient (P - P ). For this to occur it is against which work (W ) must be performed before ao alv ITL important that the circuit is capable of delivering a gas flow can occur.39-41 In intubated subjects there is gas flow equivalent to peak V& i (PIFR). Conversely also the added circuit work (Wcir) required to overcome the impedance of the ETT, tubing, and valves, etc.42,43 the pressure gradient (Pao - Palv) may retard expiratory flow ( V& e), except possibly in conditions Therefore, WB = Wel + Wres + Wti + WITL + Wcir where there is a tendency for small airways collapse.50 In this situation the application of At any given lung volume, positive pressure applied to expiratory positive Pao (PEEP or CPAP) could assist the airway (Pao) will be distributed to the individual in minimising airway collapse and thus, components; that is, paradoxically improve V& e.

Pao = Pel + Pres + Pti + PITL + Pcir 4. There is evidence that CPAP reduces flow resistance (R) in both the upper airway51 and the lower (small) Where airways48 which is disproportional to the small rise in EELV Pel = pressure required to overcome elastic recoil; 5. An inspiratory threshold load (ITL) may occur in the Pres = pressure to overcome airway resistance; presence of PEEPi particularly in patients with 52 Pti = pressure to overcome visco-elastic forces; airflow obstruction. An elevated Pao may assist in PITL = pressure to overcome an ITL (eg. PEEPi); decreasing this threshold work (WITL) by reducing and the gradient (PEEPtot - Pao) - the threshold load. This Pcir = pressure to overcome circuit impedance. mechanism may explain why patients with PEEPi, It is also possible to mathematically redefine the such as in asthma or COPD, have a reduction in components of the above equation as, 1) Pel = spontaneous WB with mask-CPAP and that ‘optimal’ volume/dynamic compliance (V/C); 2) Pres = flow CPAP levels correlate with the measured threshold load. resistance ( V& .R), and; 3) PITL = total end expiratory

190 Critical Care and Resuscitation 1999; 1: 187-198 G. J. DUKE, ET AL

6. Finally, WB may also be reduced through a reduction congestive cardiac failure, a fall in afterload may 60,67 in work (Wcir) required to overcome circuit result in an increase in CO. impedance eg., circuit tubing, inspiratory and 4. Chronotropy expiratory valves and ETT. Thus CPAP53 and Alteration in heart rate is often secondary to changes PSV54-56 are advantageous in intubated patients in stroke volume (SV), cardiac output (CO) and weaning from MV. It should be remembered that mean arterial blood pressure (MAP). If SV should NIV circuits will also add Wcir and therefore care fall then there may be a compensatory tachycardia to must be taken in designing such circuits.57 maintain CO and MAP. Conversely, in patients experiencing a rise in cardiac output with NIV there 68,69 Minute ventilation (VE) and respiratory muscle fatigue may be a compensatory reduction in heart rate. If NIV reduces respiratory muscle effort (Wpt), this This may assist in decreasing LV work and the may allow an increase in VE without increasing the risk reduce the risk of myocardial ischaemia. of respiratory muscle insufficiency (i.e. fatigue). A 5. Lusitropy reduction in Wpt together with an increase in oxygen If NIV reverses an hypoxic state, reduces ventricular delivery (see below) will benefit the oxygen afterload, and slows the heart rate, then it may supply:demand balance of the respiratory muscles, and benefit myocardial oxygen supply-demand balance. 58,59 may also allow an increase in VE. Persistent Reversal of myocardial ischaemia will improve inspiratory muscle insufficiency and/or low VE may diastolic function - ventricular relaxation and 70,71 benefit from an increase in the level of inspiratory Pao compliance. (i.e. PSV).45,47 6. Blood volume distribution Positive intrathoracic pressure decreases thoracic Cardiac function. blood volume.72 The distribution of extra-thoracic The effect of NIV on the cardiovascular system is blood volume and flow are dependent upon the complex, although most of the changes are the result of directional change in CO and MAP. If CO falls then a rise in mean intra-thoracic pressure and a fall in there may be a reduction in renal,70,73 hepatic70,74 and transmural pressure. splanchnic blood flows.73

1. Preload Long-term benefits A fall in transmural right atrial pressure will impede A detailed discussion of the long-term effects of NIV venous return. A subsequent reduction in right is beyond the scope of this review. However, it is ventricular (RV) output will also reduce left worthwhile noting that there is evidence to suggest long- ventricular (LV) preload or end-diastolic volume term benefits in cardiac and respiratory function with (LVEDV). Thus in the preload-sensitive heart, eg. NIV. healthy or hypovolaemic states, NIV may cause in a Studies using mask-CPAP in patients with fall in cardiac output (CO).60,61 congestive cardiac failure have demonstrated that long- 2. Right ventricular (RV) afterload term use improves respiratory muscle strength75,76 and Pulmonary artery pressures rises proportionally with has short76 and long term benefits on cardiac function.77 intra-thoracic pressure. An increase in RV afterload Research into the long-term effects of NIV in COPD may cause a fall in ejection fraction.62,63 However, in patients has also demonstrated improvements in the presence of reversible acute pulmonary respiratory muscle strength and improved exercise hypertension - due to hypoxic pulmonary tolerance.78 vasoconstriction - it is possible that the delivery of a high FIO2 with NIV may actually reduce RV Classification of modes and indications afterload. Based on the physiological effects of NIV, outlined 3. Left ventricular afterload above, it is possible to classify the potential benefits of LV afterload is increased by systemic various NIV modes (Table 1), and to identify specific vasoconstriction and negative intra-thoracic clinical applications. pressure.64 Even though positive intra-thoracic pressure increases RV afterload, it tends to reduce Circuit geometry LV afterload because of a fall in transmural LV pressure.65,66 Thus in subjects with afterload- Mask-CPAP sensitive LV function, e.g. cardiomyopathy or CPAP is the most widely used and commonly described NIV mode, and implies the maintenance of

191 G. J. DUKE, ET AL Critical Care and Resuscitation 1999; 1: 187-198

Table 1. Physiological effects of non-invasive ventilation modes in respiratory diseases

Mode CPAP PSV NIPPV BiPAP Respiratory Function PAO2 ++ ++ ++ + V/Q ++ + + + Wel + + + + Wres ++ + + + WITL ++ 0 0 + Wcir + ++ + + VE + ++ ++ + Cardiac Function Preload 0/- 0 0 0/- Afterload ++ +/0 +/0 + Tachycardia + +/0 +/0 +/0 Lusitropy +/0 +/0 +/0 +/0

‘+’ = beneficial effect, ‘0’= no change, ‘-‘ = adverse effect. CPAP = continuous positive airway pressure, PSV = pressure support ventilation, NIPPV = non-invasive positive pressure ventilation, BiPAP = bilevel positive airway pressure. PAO2 = Alveolar partial pressure of oxygen, V/Q = ventilation perfusion ratio, Wel = work required to overcome elastic recoil, Wres = work required to overcome airway resistance, WITL = work required to overcome an inspiratory threshold load, Wcir = work required to overcome circuit impedance, VE = minute ventilation.

81 an above-atmospheric Pao throughout the respiratory expiratory flow. This may be a threshold resistor or cycle. Respiratory rate and are determined flow resistor.33,43 Threshold resistors require a large by the subject. The circuit required is relatively simple. valve area and a low opening pressure. The To minimise Wpt and added Wcir it is necessary to expiratory valve should be placed as close to the use a CPAP circuit which minimises fluctuations in the airway (i.e. mask) as possible.57 14,79-81 patient airway pressure (∆Pao) and thus minimise large changes in intrapleural pressure. 3. Minimal length and wide bore tubing to reduce gas There are a myriad of ‘home-made’ and commercial turbulence and flow resistance. mask-CPAP circuits,14,81-84 they all have a number of common features, but not all perform efficiently. 4. A comfortable and air-tight face or nasal mask. Although many mechanical ventilators are capable of delivering CPAP, their performance also varies 5. Ability to accurately control FIO2. 12 widely. Some have a considerable imposed Wcir associated with inspiratory-flow triggering and 6. Whilst a reservoir bag is unnecessary for a circuit expiratory valve opening,81,85 although most of the capable of delivering high flows, its presence in low- newer generation ventilators have improved flow (< 50L/min.) circuits will assist in minimising 57,89,90 considerably in this area. Data from lung models and large ∆Pao. from animal and human studies have helped to identify the important characteristics of an efficient CPAP 7. Other features such as humidification, pressure-relief circuit: safety valves, acoustic suppression and monitoring 91 of volume and Pao are desirable but not essential 1. A high gas flow capable of matching spontaneous and have little influence on the circuit performance. PIFR so that the desired Pao level can be maintained 12,86 92 and ∆Pao minimised. Whilst quiet breathing may Both humidification and effective delivery of aerosol generate a PIFR of only 30L/min., in ARF this may bronchodilators93 can be delivered through most CPAP be > l00L/min. High flows can be provided from a circuits. pressurised gas supply, a gas turbine,13 or jet venturi mechanism.87,88 In general, a continuous flow device Mask-PSV

is more efficient at reducing ∆Pao than is a demand PSV involves the delivery of a patient-triggered 85 flow device. inspiratory positive Pao above baseline. Respiratory rate is determined by the subject, but the tidal volume is 2. An expiratory resistor capable of maintaining the determined by a combination of the level of inspiratory desired Pao, yet offering a low resistance to Pao and patient factors including effort, Wel and Wres.

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CPAP may used in combination with PSV as the Nasal or full-face mask benefits of both are usually additive.94 Reports of PSV Both nasal and full-face (oro-nasal) masks can be as a NIV mode have largely been confined to the successfully used to deliver NIV.84 Desirable features of management of hypercapnic ARF patients with chronic a NIV mask include: lightweight and transparent obstructive pulmonary disease (COPD). construction, a variety of sizes, a low pressure cuff (to Much of the early PSV research has been in maximise patient comfort and compliance and minimise intubated subjects, where it has been shown to reduce pressure areas), and separate inspiratory and expiratory 12,42,56,95 the Wcir and assist weaning. Many of the ports (to minimise gas turbulence). Low dead space is principles of 'invasive PSV' also apply to its non- not necessary as the high gas flows tend to minimise invasive use. The essential circuit features are: rebreathing. A monitoring port for airway pressure and/or inspired FIO2 may be advantageous with some 1. A high gas flow capable of matching the PIFR so circuits. that the desired inspiratory Pao level can be The full-face mask tends to produce more reliable sustained. and constant Pao because it is unaffected by mouth breathing. However, it impairs the patient's ability to 2. A pressure or flow sensing device to identify early talk, eat and drink and expectorate. It has a greater spontaneous inspiratory effort and trigger inspiratory tendency to produce pressure areas, especially on the pressure. This can be achieved either by sensing a nasal bridge. Patient tolerance of the full-face mask drop in circuit pressure (pressure-trigger) or a rise in usually requires regular and more frequent 'rest' periods circuit flow (flow-triggering). than the nasal mask. Nasal masks are restricted to use with those circuits 3. A pressure or flow sensing device to identify the capable of rapidly delivering high gas flows sufficient to 84 completion of spontaneous inspiration. This is minimise the effect of an open mouth on ∆Pao. To usually achieved by sensing a fall in the circuit flow. overcome the drop in Pao with an open mouth it is necessary for the circuit to rapidly deliver high flows 4. Minimal length and wide bore tubing to reduce gas (100 - 200L/minute).12,84,94 Few mask-CPAP or turbulence and flow resistance. ventilator circuits are capable of this. In general, the benefit of a nasal mask over a full 5. A comfortable but air tight seal full-face or nasal face mask is one of greater patient comfort. They tend to mask. have a smaller surface contact pressure area, and patients often feel less 'claustrophobic', they find that 6. Ability to control FIO2. they can talk, cough more effectively, and even eat and drink. Hence nasal masks tend to be preferred for long- 7. Other desirable features include the ability to add term domicillary mask-CPAP and sleep studies. CPAP, humidification, aerosol nebulisation, and Mask discomfort is a common cause of poor monitoring of airway pressures and volumes. compliance with NIV. However many patients find the initial discomfort of a tight-fitting face-mask is Most current design mechanical ventilators fulfill these outweighed by the symptomatic improvement resulting 43 criteria. BiPAP is conceptually similar to PSV + from reduction in WB. Thus even sleep is possible. CPAP as inspiratory (IPAP) and expiratory Pao (EPAP) Some form of harness is required to seat the mask with levels may be adjusted separately. However the switch an air-tight seal. Desirable features include: comfort, from IPAP to EPAP (and vice versa) depends upon the ease of application, adjustable, and reusable. ventilator identifying a change in circuit flow. Physiological effects of CPAP in healthy subjects Mask-NIPPV By definition healthy subjects have no PEEPi, have NIPPV delivers controlled or assisted ventilation to normal airways resistance and EELV, and have a low the subject via a mask. Tidal volume and rate are WB. The primary effect of mask-CPAP on respiratory determined by the type of ventilator (e.g. pressure- or function is an increase in EELV.34,79,100-102 The volume-limited) and the cycling mode (patient initiated pulmonary pressure-volume relationship is shifted 49 79 or time-cycled). This mode of NIV has been reported in upward and WB is increased. In an attempt to the setting of chest physiotherapy, the delivery of minimise the mechanical disadvantage of the increased nebulised drugs,96,97 in the treatment of ARF in COPD EELV there is heightened expiratory (abdominal) patients22,98,99 and domicillary ventilation for chronic muscle activity103,104 together with an increase in tidal respiratory failure.99

193 G. J. DUKE, ET AL Critical Care and Resuscitation 1999; 1: 187-198 volume100,101 and minute volume. This produces 2. Hillberg RE, Johnson DC. Noninvasive ventilation. N dyspnoea105 and hypocarbia.102,103 Engl J Med 1997;337:1746-1752. Healthy subjects consciously breathing at high 3. Carroll N, Branthwaite MA. Intermittent positive EELV (simulating dynamic hyperinflation and ITL) pressure ventilation by nasal mask: technique and applications. Intens Care Med 1988;14:115-117. have an elevated WB which is reduced when CPAP is 46 4. Abou-Shala N, Meduri GU. Noninvasive mechanical applied. The cardiovascular changes are consistent ventilation in patients with acute respiratory failure. Crit with the hypothesis that the healthy heart is more Care Med 1996; 24:705-715. sensitive to changes in preload than afterload. There is a 5. Zwillich CW, Pierson DJ, Creagh CE, Sutton FD, decrease in venous return,106 stroke volume61,106 and Schatz E, Petty TL. Complications of assisted 61,66,73,74,106 61 CO proportional to the level of Pao. ventlation. Am J Med 1974;57:161-170. Echocardiographic data suggests a decrease in LVEDV 6. Pingleton SK. State of the Art: Complications of Acute and end-systolic function with mask-CPAP66,106 although Respiratory Failure. Am Rev Resp Dis 1988;137:1463- some subjects show no change.107 Most investigators 1493. 7. Parker JC, Lucrecia AH, Peevy KJ. Mechanisms of report no significant change in heart rate in healthy ventilator induced lung injury. Crit Care Med subjects. 1993;21:131-143. In a sheep model, incremental CPAP was found to 8. Tobin MJ. Mechanical Ventilation. N Engl J Med increase pulmonary artery (PA) pressure and RV work, 1994;330:1056-1061. resulting in a fall in RV stroke volume (SV) and ejection 9. Schedin U, Frostell C, Persson MG, Jakobsson J, fraction (EF).62 CO was maintained by a rise in heart Andersson G, Gustafsson LE. Contribution from upper rate. A similar study was performed in a group of and lower airways to exhaled endogenous nitric oxide in anaesthetised surgical patients, but a significant humans. Acta Anaesthesiol Scand 1995;39:327-332. deterioration in RV function was only found in the 10. Lundberg JO, Farkas-Szallasi T, Weitzberg E, et al. 63 High nitric oxide production in human paranasal subgroup with a low (< 40%) baseline EF. These sinuses. Nat Med 1995;1:370-373. cardiovascular changes are likely to be exacerbated by 11. Putensen C, Rasanen J, Lopez FA, Downs JB. hypovolaemia but this has not been studied. In a Continuous positive airway pressure modulates the hypotensive dog model (nitroprusside-induced) the effect of inhaled nitric oxide on the ventilation perfusion addition of mask-CPAP (10 cmH2O) induced a greater distributions in canine lung injury. Chest fall in cardiac output and MAP.108 1994;106:1563-1569. In healthy animal and human subjects, CPAP 12. Bersten AD, Rutten AJ, Vedig AE, Skowronski GA. reduces hepatic,73,74 renal,12,73 and muscle72 blood flow. Additional work of breathing imposed by endotracheal tubes, breathing circuits, and intensive care ventilators. There is conflicting evidence about the change in Crit Care Med 1989;17:671-677. cerebral blood flow109,110 but a rise in either cerebral 73 13. Moran JL, Homan S, O'Fathartaigh M, Jackson M, blood flow or jugular venous pressure may increase Leppard P. Inspiratory work imposed by continuous 110 intracranial pressure. Blood volume in the thorax is positive airway pressure (CPAP) machines: the effect of reduced and splanchnic volume is increased.72 Atrial CPAP level and endotracheal tube size. Intensive Care natriuretic peptide levels,111,112 glomerular filtration rate Med 1992;18:148-154. and urine output decrease.113 The swallowing reflex is 14. Hillman DR. Physiological aspects of intermittent impaired114 during the application of mask-CPAP, positive pressure ventilation. Anaesth Intensive Care although CPAP has also been shown to reduce nocturnal 1986;14:226-235. 15. Haake R, Schlichtig R, Ulstad DR, Henschen RR. gastro-oesophageal reflux in patients with obstructive 115 Barotrauma pathophysiology, risk factors and sleep apnoea. prevention. Chest 1987;91:608-613. In summary, the physiological effects of mask-CPAP 16. Carlton DP, Cummings JJ, Scheerer RG, Poulain FR, in healthy subjects are of little benefit. This stands in Bland RD. Lung overexpansion increases pulmonary contrast to the evidence of physiological benefit and microvascular protein permeability in young lambs. J clinical efficacy in critically ill patients with ARF. Appl Physiol 1990;69:577-583. 17. Tuxen DV, Lane S. The effects of ventilatory pattern on hyperinflation, airway pressures, and circulation in Received: 19 November 1998 mechanical ventilation of patients with severe airflow Accepted: 12 January 1999 obstruction. Am Rev Respir Dis 1987;136:872-879. 18. Tuxen DV. Detrimental effects of positive end- REFERENCES expiratory pressure during controlled mechanical 1. Elliot MW. Non-invasive ventilation in chronic ventilation of patients with severe airflow obstruction. obstructive pulmonary disease. N Engl J Med Am Rev Respir Dis 1989;140:5-9. 1995;333:870-871.

194 Critical Care and Resuscitation 1999; 1: 187-198 G. J. DUKE, ET AL

19. Keith A. The mechanism unleying the various methods 37. Anderes C, Anderes U, Gasser D, et al. Postoperative of artificial respiration. Lancet 1909;i:745-749. spontaneous breathing with CPAP to normalize late 20. Poulton EP. Left-sided heart failure with pulmonary post-operative oxygenation. Intensive Care Med oedema. Its treatment with the “pulmonary plus 1979;5:15-21. pressure” machine. Lancet 1936;231:981-983. 38. Chin WD, Cheung HW, Driedger AA, Cunningham DG, 21. Barach Al, Martin J, Eckman M. Positive pressure Sibbald WJ. Assisted ventialtion in patients with pre- respiration and its application to the teatment of acute existing cardiopulmonary disease. The effect on pulmonary oedema. Ann Intern Med 1938;12:754-759. systemic oxygen consumption, oxygen transport, and 22. Segal MS, Salomon A, Dulfano MA, et al. Intermittent tissue perfusio variables. Chest 1985; 88:503-511. positive pressure breathing: its use in the inspiratory 39. Marini JJ. Should PEEP be used in airflow obstruction. phase of breathing. N Engl J Med 1954;250:225-227. Am Rev Respir Dis 1989;140:1-3. 23. Graham WG, Bradley DA. Efficiency of chest 40. Tobin MJ, Lodato RF. PEEP, auto-PEEP, and physiotherapy and intermittent positive pressure waterfalls. Chest 1989;96:449-451. breathing in the resolution of pneumonia. N Engl J Med 41. Milic-Emili J. Is weaning art or science. Am Rev Respir 1978;299:624-627. Dis 1986;122:1107-1108. 24. Gregory GA, Kitterman JA, Phibbs RH, Tooley WH, 42. Bersten AD, Rutten AJ, Vedig AE. Efficacy of pressure Hamilton WK. Treatment of the idiopathic respiratory support in compensating for apparatus work. Anaesth distress syndrome with continuous positive airway Intensive Care 1993;21:67-71. pressure. N Engl J Med 1971;284:1333-1340. 43. Kacmarek RM, Mang H, Barker N, Cycyk-Chapman 25. Downes JJ. CPAP and PEEP - a perspective. MC. Effects of disposable or interchangeable positive 1976;44:1-5. end-expiratory pressure valves on work of breathing 26. Allen LP, Blake AM, Durbin GM, Ingram D, Reynolds during the application of continuous positive airway EO, Wimberley PD. Continuous positive airway pressure. Crit Care Med 1994;22:1219-1226. pressure and mechanical ventilation by facemask in 44. Lougheed MD, Webb KA, O'Donnell DE. newborn infants. Br Med J;1975;3:137-139. Breathelessness during induced lung hyperinflation in 27. Crew AD, Wall E, Varkonyi PI. Continuous positive asthma: the role ofthe inspiratory threshold load. Am J airway pressure breathing (CPAP). Apparatus for use in Respir Crit Care Med 1995;152:911-920. neonates or adults. Anaesthesia 1975;30:67-72. 45. Appendini L, Patessio A, Zanaboni S, et al. Physiologic 28. Schmidt GB, Bombeck CT, Bennett EJ, Kotb KM. effects of positive end-expiratory pressure and mask Continuous positive airway pressure in the prophylaxis pressure support during exarcebations of chronic of the adult respiratory distress syndrome. Langenbecks obstructive pulmonary disease. Am J Respir Crit Care Arch Chir 1975;S439-442. Med 1994;149:1069-1076. 29. Venus B, Jacobs K, Lim L. Treatment of the adult 46. Fessler HE, Brower RG, Permutt S. CPAP reduces respiratory distress syndrome with continuous positive inspiratory work more than dyspnea during airway pressure. Chest 1979;76:257-261. hyperinflation with intrinsic PEEP. Chest 30. Petty TL, Ashbaugh DG. The adult respiratory distress 1995;108:432-440. syndrome: clinical features, factors influencing 47. Keilty SE, Ponte J, Fleming TA, Moxham J. Effect of prognosis and principles of management. Chest inspiratory pressure support on exercise tolerance and 1971;60:233-239. breathlessness in patients with severe stable chronic 31. Hillman DR, Finucane KE. Continuous positive airway obstructive pulmonary disease. Thorax 1994;49:990- pressure: a breathing system to minimise work. Crit Care 994. Med 1985;13:38-43. 48. Martin JG, Shore S, Engel LA. Effect of continuous 32. Kacmarek RM. Inspiratory pressure support: does it positive airway pressure on respiratory mechanics and make a clinical difference? Intensive Care Med pattern of breathing in induced asthma. Am Rev Resp 1989;15:337-339. Dis 1982;126:812-817. 33. Duncan AW, Oh TE, Hillman DR. PEEP and CPAP. 49. Duggan CJ, Castle WD, Berend N. Effects of continuous Anaesth Intensive Care 1986;14:236-250. positive airway pressure breathing on lung volume and 34. Schlobohm RM, Falltrick RT, Quan SF, Katz JA. Lung distensibility. J Appl Physiol 1990;68:1121-1126. volumes, mechanics, and oxygenation during 50. Barach AL, Swenson P. Effect of breathing gases under spontaneous positive-pressure ventilation: the advantage positive pressure on lumens of small and medium sized of CPAP over EPAP. Anesthesiology 1981;55:416-422. bronchi. Arch Int Med 1939;63:946-948. 35. Smith TC, Marini JJ. Impact of PEEP on lung 51. Series F, Cormier Y, Couture J, Desmeules M. Changes mechanics and work of breathing in severe airflow in upper airway resistance with lung inflation and obstruction. J Appl Physiol 1988;65:1488-1499. positive airway pressure. J Appl Physiol 1990;68:1075- 36. Lin M, Yang YF, Chiang HT, Chang MS, Chiang BN, 1079. Cheitlin MD. Reappraisal of continuous positive airway 52. Haluszka J, Chartrand DA, Grassino AE, Milic-Emili J. pressure therapy in acute cardiogenic pulmonary Intrinsic PEEP and arterial pC02 in stable patients with oedema. Short-term results and long-term follow-up. chronic obstructive pulmonary disease. Am Rev Respir Chest 1995;107:1379-1386. Dis 1990;141:1194-1197.

195 G. J. DUKE, ET AL Critical Care and Resuscitation 1999; 1: 187-198

53. Petrof BJ, Legare M, Goldberg P, Milic-Emili J, 68. Bersten AD, Holt AW, Vedig AE, Skowronski GA, Gottfried SB. Continuous positive airway pressure Baggoley CJ. Treatment of severe cardiogenic reduces work of breathing and dyspnea during weaning pulmonary oedema with continuous positive airway from mechanical ventilation in severe chronic pressure delivered by face mask. N Engl J Med obstructive pulmonary disease. Am Rev Respir Dis 1991;325:1825-1830. 1990;141:281-289. 69. Rasanen J, Heikkila J, Downs J, Nikki P, Vaisanen I, 54. Brochard L, Rauss A, Benito S, et al. Comparison of Viitanen A. Continuous positive airway pressure by face three methods of gradual withdrawal from ventilatory mask in acute pulmonary edema. Am J Cardiol support during weaning from mechanical ventialtion. 1985;55:296-300. Am J Respir Crit Care 1994;150:896-903. 70. Bersten AD, Holt AW. Acute cardiogenic pulmonary 55. Brochard L, Pluskwa F, Lemaire F. Improved efficacy of oedema. Current Opinion in Critical Care 1995;1:410- spontaneous breathing with inspiratory pressure support. 419. Am Rev Respir Dis 1987;136:411-415. 71. Crossman W. Diastolic dysfunction in congestive heart 56. Fiastro JF, Habib MP, Quan SF. Pressure support failure. N Engl J Med 1991; 325:1557-1564. compensation for inspiratory work due to endotracheal 72. Peters J, Hecker B, Neuser D, Schaden W. Regional tubes and demand continuous positive airway pressure. blood volume distribution during positive and negative Chest 1988;93:499-505. airway pressure breathing in supine humans. J Appl 57. Bersten AD, Rutten AJ, Vedig AE. Optimizing fresh gas Physiol 1993;75:1740-1747. flow and circuit design for the delivery of continuous 73. Furzan JA, Gabriele G, Wheeler JM, Fixler DE, positive airway pressure. Crit Care Med 1991;19:266- Rosenfeld CR. Regional blood flows in newborn lambs 270. during endotracheal continuous airway pressure and 58. Kanak R. Fahey PJ, Vanderwarf C. Oxygen cost of continuous negative pressure breathing. Pediatr Res breathing. Changes dependent upon mode of mechanical 1981;15:874-878. ventilation. Chest 1985;87:126-127. 74. Perkins MW, Dasta JF, DeHaven B, Halpern P, Downs 59. Field S. Kelly SM, Macklem PT. The oxygen cost of JB. A model to decrease hepatic blood flow and cardiac breathing in patients with cardiorespiratory disease. Am output with pressure breathing. Clin Pharmacol Ther Rev Respir Dis 1982;126:9-13. 1989;45:548-552. 60. Bradley TD, Holloway RM, McLaughlin PR, Ross BL, 75. Granton JT, Naughton MT, Benard DC, Liu PP, Walters J, Liu PP. Cardiac output response to Goldstein RS, Bradley TD. CPAP improves respiratory continuous positive airway pressure in congestive heart muscle strength in patients with heart failure and central failure. Am Rev Resp Dis 1992;145:377-382. sleep apnoea. Am J Resp Crit Care Med 1996;153:277- 61. Montner PK, Greene ER, Murata GH, Stark DM, Timms 287. M, Chick TW. Hemodynamic effects of nasal and face 76. Naughton MT, Liu PP, Bernard DC, Goldstein RS, mask continuous positive airway pressure. Am J Respir Bradley TD. Treatment of congestive heart failure and Crit Care Med 1994;149:1614-1618. Cheyne-Stokes respiration during sleep by continuous 62. Raper RF, Sibbald WJ. Increased right ventricular positive pressure ventilation. Am J Resp Crit Care Med compliance in response to continuous positive airway 1995;151:92-97. pressure. Am Rev Resp Dis 1992;145:771-775. 77. Baratz DM, Westbrook PR, Shah PK, et al. Effect of 63. Imai T, Uchiyama M, Maruyama N, Yoshikawa D, nasal continuous positive airway pressure on cardiac Fujita T. Influence of constant sustained positive airway function and oxygen delivery in patients with congestive pressure on right ventricular performance. Intens Care heart failure. Chest 1992;102:1397-1401. Med 1993;19:8-12. 78. Mezzanotte WS, Tangel DJ, Fox AM, Ballard RD, 64. Buda AJ, Pinsky MR, Ingels NB Jr, Daughters GT 2d, White DP. Nocturnal nasal continuous positive airway Stinson EB, Alderman EL. Effect of intrathoracic pressure in patients with chronic obstructive pulmonary pressure on left ventricular performance. N Engl J Med disease. Influence on waking respiratory muscle 1979;301:453-459. function. Chest 1994;106:1100-1108. 65. Fessler HE, Brower RG, Wise RA, Permutt S. 79. Gherini S. Peters RM, Virgilio RW. Mechanical work Mechanism of reduced LV afterload by systolic and on the lungs and work of breathing with positive end- diastolic pleural pressure. J Appl Physiol 1988;65:1244- expiratory pressure and continuous positive airway 1250. pressure. Chest 1979;76:251-256. 66. Genovese J, Moskowitz M, Tarasiuk A, Graver LM, 80. Katz JA, Kraemer RW, Gjerde GE. Inspiratory work and Scharf SM. Effects of continuous positive airway airway pressure with continuous positive airway pressure on cardiac output in normal and hypervolemic pressure delivery systems. Chest 1985;88:519-526. unanesthetized pigs. Am J Respir Crit Care Med 81. Shehabi Y, Hillman KM, Nairn M, Balnave P, Torda 1994;150:752-758. TA. Tests of six continuous flow CPAP devices. 67. Naughton MT, Rahman MA, Hara K, Floras JS, Bradley Anaesth Intensive Care 1991;19:237-243. TD. Effect of continuous positive airway pressure on 82. Moran JL, Jackson MP, Cameron DM, Peisach AR, intrathoracic and left ventricular transmural pressures in Cunningham DN, O'Fathartaigh MS. A high flow patients with congestive heart failure. Circulation turbine CPAP system. Intens Care Med 1988;14:658- 1995;91:1725-1731. 660.

196 Critical Care and Resuscitation 1999; 1: 187-198 G. J. DUKE, ET AL

83. Torda TA, Roderick C. The Bird repirator modified for 100. Werchowski JL, Sanders MH, Costantino JP, Sciurba PEEP, CPAP, and IMV. Anaesth Intensive Care FC, Rogers RM. Inductance plethysmography 1978;6:149-154. measurement of CPAPinduced changes in end- 84. Thomas AN, Ryan JP, Doran B, Pollard BJ. A nasal expiratory lung volume. J Appl Physiol 1990;68:1732- CPAP system. Description and comparison with 1738. facemask CPAP. Anaesthesia 1992;47:311-315. 101. Wherry P, Sangoul F, Fox GS, MacLean LD. Oxygen 85. Gibney RT, Wilson RS, Pontopppidan H. Comparison consumption during spontaneous ventilation with of work of breathing on high gas flow and demand valve continuous positive airway pressure: assessment in continuous positive airway pressure systems. Chest normal volunteers and patients with acute respiratory 1982;82:692-695. failure. Can Anaesth Soc J 1980;27:89-95. 86. Roeseler J, Bshouty ZH, Reynaert MS. The importance 102. Ellingsen I. The influence of the breathing pattern in of circuit capacity in the administration of CPAP. man of moderate levels of continuous positive airway Intensive Care Med 1984;10:305-308. pressure and of positive end-expiratory pressure during 87. Hillman K, Huggins C. A new continuous positive air and CO2 inhalation. Acta Physiol Scand airway pressure (CPAP) device. Anaesth Intensive Care 1990;138:273-282. 1991;19:233-236. 103. Urbscheit N. Bishop B. Bachofen H. Immediate effects 88. Zamost BG, Alfery DD, Johanson I, Glazener EL, of continuous positive pressure breathing on abdominal Trousdale FR, Benumof JL. Description and clinical expiratory activity, minute ventilation and end-tidal evaluation of a new continuous positive airway pressure PCO2 of conscious man. Phys Ther 1973;53:258-265. device. Crit Care Med 1981;9:109-113. 104. Road JD, Leevers AM. Inspiratory and expiratory 89. Tamura M, Yasumoto K, Kuwasako Y, Shimada C, muscle function during continuous positive airway Hosoyamada A. Effects of the volume of the reservoir pressure in dogs. J Appl Physiol 1990;68:1092-1100. bag and the amount of fresh gas flow on FRC during 105. O'Donnell DE, Sanii R. Younes M. Improvement in CPAP. Masui 1993;42:1330-1337. exercise endurance with chronic airflow limitation using 90. Bshouty ZH, Roeseler J. Reynaert MS, Rodenstein D. continuous positive airway pressure. Am Rev Respir Dis The importance of the balloon reservoir volume of a 1988;138:1510-1514. CPAP system in reducing the work of breathing. 106. Jardin F, Farcot JC, Gueret P, Prost JF, Ozier Y, Intensive Care Med 1986;12:153-156. Bourdarias JP. Echocardiographic evaluation of 91. Geadah MW, Seed RF. A ventilation mnonitor during ventricles during continuous positive airway pressure demand flow CPAP. Anaesthesia 1977;32:41-45. breathing. J Appl Physiol 1984;56:619-627. 92. Poulton TJ, Downs, JB. Humidification of rapidly 107. Leech JA, Ascah KJ. Hemodynamic effects of nasal flowing gas. Crit Care Med 1981;9:59-63 CPAP examined by Doppler echocardoigraphy. Chest 93. Parkes SN, Bersten AD. Aerosol kinetics and 1991;99:323-326. bronchodilator efficacy during continuous positive 108. Hodges MR, Stanley TH, Johansen RK. Pulmonary airway pressure delivered by face mask. Thorax shunt and cardiovascular reponses to CPAP during 1997;52:171-175. nitroprusside-induced hypotension. Anesthesiology 94. Hormann C, Baum M, Putensen C, Mutz NJ, Benzer H. 1977;46:339-341. Biphasic positive airway pressure (BIPAP) - a new 109. Haring HP, Hormann C, Schalow S, Benzer A. mode of ventilatory support. Eur J Anesthesiol Continuous positive airway pressure breathing increases 1994;11:37-42. cerebral blood flow velocity in humans. Anesth Analg 95. MacIntyre NR. Respiratory function during pressure 1994;79:883-885 support ventilation. Chest 1986;89:677-683. 110. Hormann C, Mohsenipour I, Gottardis M, Benzer A. 96. Pollack CV, Fleisch KB, Dowsey K. Treatment of acute Response of cerbrospinal fluid pressure to continuous bronchospasm with β-adrenergic agonist aerosols positive airway pressure in volunteers. Anesth Analg delivered by nasal bilevel positive airway pressure. Ann 1994;78:54-57. Emerg Med 1995;26:552-556. 111. Frass M, Popovic R, Hartter E, Auinger C, Woloszczuk 97. The Intermittent Positive Pressure Breathing Trial W, Leithner C. Atrial natriuretic peptide decrease during Group. Intermittent positive pressure breathing therapy spontaneous breathing with continuous positive airway of chronic obstructive pulmonary disease. A clinical pressure in volume-expanded healthy volunteers. Crit trial. Ann Intern Med 1983;99:616-620. Care Med 1988;16:831-835 98. Bott J, Carroll MP, Conway JH, et al. Randomised 112. Wilkins MA, Su XL, Palayew MD, et al. The effects of controlled trial of nasal ventilation in acute ventilatory posture change and continuous positive airway failure due to chronic obstructive airways disease. pressureon cardiac natriuretic peptides in congestive Lancet 1993;341:1555-1557. heart failure. Chest. 1995;107:909-915. 99. Marino W. Intermittent volume cycled mechanical 113. Marquez JM, Douglas ME, Downs JB, et al. Renal ventilation by nasal mask in patients with respiratory function and cardiovascular responses during positive failure due to COPD. Chest 1991;99:681-684. airway pressure. Anesthesiology 1979;50:393-398.

197 G. J. DUKE, ET AL Critical Care and Resuscitation 1999; 1: 187-198

114. Nishino T, Sugimori K, Kohchi A, Hiraga K. Nasal 115. Kerr P, Shoenut JP, Steens RD, Millar T, Micflikier AB, constant airway pressure inhibits swallowing reflex. Am Kryger MH. Nasal continuous positive airway pressure. Rev Respir Dis 1989;140:1290-1293. A new treatment for nocturnal gastroesophageal reflux. J Clin Gastroenterol 1993;17:276-280.

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