17 CHAPTER 1.7 IPPV \200\224weaning techniques Stage 3 involves assessment for extubation or self-ventila- tion in the case of a patient w ith a tracheostomy. It usually employs a trial of SB. Clinical stability over 30 \200\22360 min in the absence of signs of fatigue or distress is required before proceeding to extubat ion. Whilst the SBT is valuable, 10% of patients will fail post-extubation usually due to an inabil- ity to clear secretions, CNS factors or unexpected upper airways obstruction due to glottic oedema. The SBT is a conservative indicator. Many COPD patients will wean despi te a respiratory rate during the SBT of >35 breaths/ min. delayed re-intubation, its value in post-extubation respira- tory failure in the general IC U population is uncertain. Further reading Baudouin SV, Davidson AC et al. National Patients Access Team Critical Care Program: weaning and long term ventilation, London: Department of Health. 2002. www.modern .nhs.uk/ critical care Ely EW, Meade M, Haponik EF, et al. Mechanical ventilation weaning protocols driven by non- physician health care professionals: evidence based clinical practice guidelines. Chest 200 1; 120: 454 \200\223635. Esterban A, Frutos-Vivar F, Ferguson ND, et al. Non invasive posi- tive pressure ventilatio n for respiratory failure after extubation. N Eng J Med 2004; 350: 2452 \200\22360. Inclusion criteria for spontaneous breathing trial: \200 Cooperative patient requiring no sedation (score \211 \200\2232), adequate analgesia Pre ssure support \211 5cm H2O PEEP \211 5, FiO2 \211 40%, Minute volume <15l/min No or low dose inotropes Adequate cough; secretions not excessive Ferrer M, Esquinhas A, Arancibia F, et al. Non invasive ventilation during persistent weani ng failure: a randomized controlled trial. Am J Resp Crit Care Med 2003; 168: 5 \200\2236. \200 \200 \200 \200 Laghi F, Tobin MJ. Disorders of the respiratory muscles. Am J Resp Crit Care Med 2003; 168 : 10 \200\22348. Lellouche F, Mancebo J, Jolliet P, et al. A multicentre randomized trial of computer driven protocolised weaning from mechanical ventilation. Am J Resp Crit Care Med 2006; 174: 894 \200\223900. Weaning protocols Some patients are capable of proceeding quickly and are held back inappro priately. Weaning protocols are effective by the earlier detection of such patients. \200 \230Smart \200\231 ventilators capable of adjusting the degree of pressure support to the a rterial carbon dioxide tension and tidal volume targets may be more effective than simple p rotocols. Pilcher DV, Bailey MJ, Treacher DF, et al. Outcomes, cost and long- term survival of patien ts referred to a regional weaning center. Thorax 2005; 60: 187 \200\22392. Non-invasive ventilation (NIV) NIV speeds weaning by acting as a bridge to spontaneous brea thing in COPD and is probably effective in neuro- muscular causes of respiratory failure. A s NIV may lead to 18 C DAVIDSON High-frequency ventilation De \201 nition High-frequency ventilation (HFV) encompasses a family of modes of mechanica l ventilation that deliver small tidal vol- umes (near to or less than the anatomical dead space) at respiratory rates in excess of normal physiological rates (60 \200\2233000 breath s/min). HFOV has the added advantage that oxygenation and carbon dioxide elimination are decoupled. Physiology of high-frequency ventilation Gas transportation Conventional mechanical ventila tion aims to duplicate the normal bulk \202 ow gas exchange pattern. For effective alveo- lar ventilation (VA), tidal volume must exceed dead space (VD). VA = f x (VT \200\223 VD) . As the tidal volumes (VT) are near to or less than the anatomical dead space (VD) during HFV, alternative mech- anisms of gas transportation are required: \200 Background In 1915, Henderson and colleagues described their obser- vation that suf \201 c ient ventilation occurred in panting dogs with tidal volumes less than the anatomical dead space. In the 1980s, the \201 rst commercial high-frequency oscillatory ventilator was pr oduced for use in neonates. Convection \200\224a small amount of bulk \202 ow occurs in the proximal airways/alveoli. Molecular diffusion \200\224this is the principle mechanism of gas transportation in the t erminal airways. Streaming (asymmetric velocity pro \201 les) \200\224during lami- nar \202 ow, a central current delivers gas distally whereas a peripheral current returns gas p roximally. Taylor dispersion \200\224the interplay between convective forces and molecular diffusion causes laminar and radial gas dispersion. Pendelluft \200\224this is the exchange of gas between adjacent lung units due to their differing time constants. Gas \202 ows f rom fast to slow \201 lling units at end inspiration. The reverse occurs at end expiratio n. Cardiogenic mixing \200\224agitation of lung units near to the heart increases molecular diffusion along concentration gradients by up to 5-fold. Types of high-frequency ventilation High-frequency jet ventilation (HFJV) and high-frequenc y oscillatory ventilation (HFOV) are the modes most com- monly used in clinical practice. H igh-frequency jet ventilators are time-cycled \202 ow genera- tors, delivering a high-pre ssure jet (10 \200\22350psi) into the air- way via a small bore cannula. Air is entrained a nd exhalation occurs passively High-frequency oscillators use a piston or reciprocating dia phragm to push gas actively into and subsequently draw gas out of the airway. High-frequenc y ventilation can be classi \201 ed according to its expiratory phase as passive or active . Passive Active Gas exchange Oxygenation Oxygenation is directly proportional to lung volume. The sigmoid s hape of the oxygen dissociation curve means that no amount of hyperventilation can compensa te directly for shunt. The important focus is to limit ventilation \200\223perfusion mis- m atch by recruitment of the maximum number of gas exchange units and then to keep them open and available for gas exchange. High-frequency jet ventilation (HFJV) High-frequency positive pressure ventilation (HFPPV) High-frequency percussive ventilation (HFPV) High-frequency \202 ow interruption (HFFI) High-frequency oscillatory ventilation (HFOV) High-frequency chest wall oscillation (HFCWO) Theory of high-frequency ventilation HFV, especially HFOV, is theoretically suited to lung pro- tective mechanical ventilation: \200 Carbon dioxide elimination PaCO2 is inversely proportional to fa x VTb, where a is 1 and b is 2. Although tidal volumes are much smaller in HFV than in conventional mechanical vent ilation (CMV), the product of tidal volume (VT) and frequency (f) is much higher. The linea r shape of the carbon dioxide dissociation curve throughout the physiological range makes i t possible to achieve normocapnia through regional hyperventilation, even with a substantia l proportion of the alveoli remaining under- or non-ventilated. Small tidal volumes limit cyclic overdistension (volutrauma) Intrinsic/extrinsic PEEP preve nts shear stress from repetitive opening and closing of atelectatic lung units (atelectraum a) and increases functional residual capacity. Mean airway pressure is maintained, correlat ing well with oxygenation for a given FiO2. Peak airway pressures are reduced, minimizing p otential for barotrauma. The lung is maintained on its de \202 ation limb on the static pr essure \200\223volume curve, thereby improving lung compli- ance and increasing the number of aerated alveoli. 19 CHAPTER 1.8 High-frequency ventilation \200 Practical aspects of high-frequency ventilation Fessler et al. describe guidelines for the use of HFV in adults with ARDS, including initial settings and weaning strategies. As yet t here is no grade A evidence available to determine optimal parameters. Inhalational anesthesia impractical Contamination of operating room air if anesthetic gasse s are used* Pressure measurements may be unrepresentative High gas \202 ow required Poten tial for lower airway soiling in ENT surgery2 Contamination of expired gas \202 ow by sur gical debris2 \200 \200 \200 2Associated with HFJV, not HFOV. CNS \200 CMV HFJV HFOV f VT PEEP manipulated by mPaw manipulated by 2 \200\22360 >VD Extrinsic PEEP valve Pinsp PEEP f x (VT \200\223 VD) <600 <VD or >VD <VD Extrinsic PEEP valve P PEEP P 300 \200\2233000 Increased sedation requirement Bias \202 ow Miscellaneous \200 Training \200 Familiarity \200 Cost \200 Ventilators not portabl e so cannot transfer patients on HFV Bias \202 ow \210\206P CO2 elimination manipulated Oxygenation manipulated by f x (VT \200\223 VD) P mPaw Complications of high-frequency ventilation All complications associated with HFV can occur in any mode of positive pressure mechanical ventilation that uses high airway pressures or a low I:E ratio that does not allow suf \201 cient time for expiration. PEEP FiO2 PEEP FiO2 FiO2 CMV, conventional mechanical ventilation; HFJV, high-frequency jet ventilation; HFOV, high- frequency oscillatory ventilation; f, frequency/tidal volume; VT, tidal volume; VD, anatomi cal dead space; VA, alveolar ventilation; PEEP, positive end-expiratory pressure; FiO2, fra ctional inspired oxygen; \210\206P, amplitude of oscillations (determines VT); Pinsp, peak airway pressure; mPaw, mean airway pressure; P, driving pressure (determines VT). Cardiovascular \200 \200 \200 \200 \200 Increased vagal activity Decreased venous return Decreased cardiac output Increased pulmona ry vascular resistance Dysrrhythmias Indications for high-frequency ventilation \200 Acute respiratory distress syndrome (ARDS )1 \200 Low resistance large volume airway leak, e.g. bronchop- ulmonary \201 stula Upp er airway surgery Optimizing blood volume and myocardial function before the HFV treatment may limit these pr oblems. 1There are signi \201 cant data to support the use of HFOV in infants and children, albeit few, if any, studies comparing it with CMV using a low tidal volume strategy. There is cur rently no evidence supporting the use of HFV in adults with ARDS over low tidal volume conv entional ventilation. Animal studies demonstrate advantages of HFOV com- pared with CMV pro vided an open-lung technique is used. Respiratory \200 \200 Pulmonary overin \202 ation (gas-trapping) Barotrauma (pneumothorax, pneumomediastinum, pn eumoperitoneum, pneumopericardium) Shearing at the interface of different lung regions with differing impedances Necrotizing tracheobronchitis3 Increased secretions3 Air embolism \200 \200 3More likely in HFJV where humidi \201 cation of the fresh gas \202 ow is dif \201 cult. Advantages and disadvantages of high-frequency ventilation Advantages Respiratory \200 \200 Miscellaneous \200 \200 \200 Minimal vocal cord/surgical \201 eld movement Improved visibility and surgical access Intracranial hemorrhages in neonates Necrotizng enterocolitis in neonates Malposition of ca theters (gastric distension, gastric rupture) Cardiovascular \200 Cardiac output may be augmented using ECG synchroni- zation Adjunctive strategies The following strategies are advocated in conjunction with HFV: \200 \200 Renal \200 Reduced antidiuretic hormone production and \202 uid retention Permissive hypercapnoea Prone ventilation to recruit lung and improve dis- tribution of ven tilation (may also improve removal of secretions) Nitric oxide to improve oxygenation and r educe vascular stress Positioning \200\224lateral rotation therapy Extracorporeal carbon di oxide removal Disadvantages Respiratory \200 \200 \200 \200 \200 Suctioning causes loss of mean airway pressure Cannot meaure end-tidal carbon dioxide2 Inac curate measurement of FiO22 Inaccurate measurement of tidal volume Cooling and drying of in spiratory gasses2 \200 20 C DAVIDSON Future developments \200 Further reading High-frequency ventilation. Resp Care Clin North Am 2001; 7: 523 \200\223 A multi-center randomized controlled trial (RCT) (i.e. the OSCAR trial) comparing the use o f HFOV with CMV using a low tidal volume strategy commenced in 2007. The Canadian Critical Care Trials Group (CCCTG) is funding a national pilot study of HFOV. The National Heart, Lu ng and Blood Institute (USA) has funded a phase II study of HFOV as a prelude to a full cli nical trial. 695 (compilation of 10 review articles). Fessler HE, Derdak S, Ferguson ND, et al. A protocol for high-fre- quency oscillatory venti lation in adults: Results from a roundtable discussion Crit Care Med 2007; 35: 1649 \200 \22354. Stachow R. High frequency ventilation basics and practical applica- tion. Draeger; 1995 This page intentionally left blank 22 L MASCIA, M ZANIERATO, & M RANIERI Positive end-respiratory pressure Decrease in compliance indicates lung over distension and risk of barotrauma Positive end-expiratory pressure (PEEP) is the positive pressure applied at the end of expi ration during mechani- cal ventilation. When PEEP is applied to a spontaneous breathing cyc le it is named \200\230continuous positive airway pressure \200\231 (CPAP). Physiological consequences of the appli- cation of PEEP depend on its effects on gas exchange, pul- monar y compliance and systemic haemodynamics. The interpretation of the effects of PEEP requires assess- ment of both lung and chest wall mechanics. In patients with a stiff chest wall due to increased intra-abdominal pressure, underestimation of LIP is expected and conse- quently relatively higher levels of PEEP shou ld be applied. Conversely, in the presence of a stiff chest wall, the pres- sure required t o expand the lung may exceed the limit of 30cm H2O without risk of alveolar overdistension. Effects of PEEP on gas exchange Hypoxaemic acute respiratory failure (ARF) is character- iz ed by an acute reduction of lung volume due to pulmo- nary oedema, atelectasis and pneumoni a; alveolar units tend to collapse at the end of expiration particularly in gravitationally dependent regions. The use of PEEP improves gas exchange by recruiting functionally closed alveoli, redistributing lung water and therefore reducing ventilation \200\223perfusion (V /Q) mismatch. Alveolar recruitment, defined as the amount of non- in \202 ated tissue that is re-expanded by a given level of PEEP, results in a more homogeneous distribution of tid al vol- ume and in an increased functional residual capacity (FRC). Moreover, application o f PEEP leads to the redistribution of lung water from the alveolar space to the perivascula r interstitial space and improves V/Q mismatch by diverting blood \202 ow from shunt regi ons to normal V/Q regions. All these effects are strongly conditioned by whether or not PEE P recruits previously collapsed alveoli. If PEEP induces alveolar recruitment, a reduction in shunt with improvement in oxygenation and reduction in dead space is expected. If hyperi n \202 ation of normal alveoli is the pre- dominant effect, a rise in PaCO2 due to the inc rease in dead space is expected, while PaO2 will slightly change according to the variation s in cardiac output. Effects of PEEP on systemic haemodynamics Application of PEEP increases intrathoracic press ure diminishing venous return to the right heart and increasing the right ventricular after load. These haemodynamic consequences depend on previous ventricular loading con- ditions a nd function, and respiratory system compliance. An adequate circulating blood volume is req uired before application of PEEP to prevent this depression of right ventricular output. Ap plication of PEEP decreases left ventricular stroke volume, while heart rate does not chang e signi \201 cantly. The reduction in stroke volume is mainly due to a decrease in left ve ntricular preload. This effect may be explained by different mechanisms: decreased venous r eturn to the right heart; increased right ventricular afterload; decreased ventricular comp liance; and decreased ventricular contractility. In patients with normal cardiac function, the main conse- quence of increased intrathoracic pressure is the reduction of venous retur n; in patients with poor left ventricular function or congestive heart failure, the increas e in intra- thoracic pressure reduces the left ventricular transmural pressure leading to a reduction in left ventricular afterload and improving left ventricular function. In these patients, cardiac output is relatively insensitive to reduction in venous return because di astolic volume is elevated. Effects of PEEP on respiratory mechanics The analysis of volume \200\223pressure curves (V/ P) of the respi- ratory system is a key point to understand the physiologi- cal effects of PEEP on respiratory mechanics. In patients with ARF, reduced compliance of the respiratory system corresponds to small variations in volume occurring for unit of change in pressure. The in \202 ation limb of the V/P curve shows: (1) a \200\230lower in \202 ection point \200\231 (LIP) where compliance suddenly improves and (2) an \200\230upper in \202 ection point \200\231 (UIP) corresponding to the pressure where compliance starts to deteriorate. In normal subjects, the LIP occurs below the volume at FRC and the UIP occurs at a volume close to total lung capacity. In patients with ARDS, both occur within tidal ventilation an d indicate the pressure at which recruitment of col- lapsed alveoli and at which hyperin \202 ation start to occur, respectively. Ventilation using levels of PEEP lower than the LI P may exacerbate lung injury by shear forces applied dur- ing repeated opening and closing alveoli; therefore, tidal excursion during mechanical ventilation should occur between LIP and UIP. Compliance of the respiratory system (i.e. tidal volume divided by plateau pressur e minus PEEP) represents a good estimate of the elastic properties of the respiratory syste m. PEEP in the clinical setting ALI/ARDS The application of PEEP in ALI/ARDS is aimed at preve nt- ing the end-expiratory collapse of the lung in order to reverse severe hypoxaemia resul ting from pulmonary shunting. Moreover, since mechanical ventilation with a high tidal volu me and a low level of PEEP is associated with pulmonary injury (VILI) indistinguishable fro m ARDS, the use of PEEP may reduce VILI by preventing the cyclical opening and closing of t he alveoli. The potential bene \201 t of the \200\230open lung approach \200\231 lies in the avoidance of recruit- ment \200\223derecruitment of partially consolidated areas, avoid ing their exposure to shear stress and miminizing the local in \202 ammatory reaction. A p rotective ventilatory strategy, limiting the Vt to 6ml/kg and the plateau pressure to <30cm H2O, is the gold standard of ventilatory strategy in patient with ALI/ARDS. Titration of t he optimal level of PEEP has been a compro- mise between the minimal PEEP providing maximum oxygen delivery at the lowest airway pressure, and high PEEP keeping the lung fully recrui ted at end expiration. Effects of PEEP on compliance \200 \200 Chronic obstructive pulmonary disease (COPD) In patients with an exacerbation of COPD, the rate of lung emptying is impaired because of increased respiratory Increase in compliance suggests recruitment No change in compliance indicates that ventilat ion is occurring on the linear portion of the V/P curve 23 CHAPTER 1.9 Positive end-respiratory pressure resistance and expiratory \202 ow limitation. End-expiratory lung volume is expected to b e higher than resting volume: a condition named dynamic hyperin \202 ation. As a conse- qu ence a positive pressure named intrinsic PEEP (PEEPi) is present at the end of expiration. PEEPi represents an inspiratory threshold load to be counterbalanced by the patient \200 \231s inspiratory muscles in order to initiate inspiration or to trigger the ventilator. In the presence of PEEPi due to expiratory \202 ow limitation, externally applied PEEP belo w measured PEEPi (85% of total PEEP) does not cause hyper- in \202 ation or an increase in intrathoracic pressure and does not affect respiratory mechanics and haemodynamics. During the assisted mode of ventilation, application of PEEP reduces inspiratory muscle effort an d improves patient \200\223ventilator interaction. Cerebral perfusion The application of PEEP may affect the cerebral circulation by haemodyna mic and CO2-mediated mechanisms. The haemodynamic mechanism may alter cerebral circulation both on the arterial side, reducing arterial pressure, and on the venous side, reducing cer ebral venous drainage. According to the concept of the vasodilatory cascade, the decrease i n arterial pressure caused by PEEP may diminish cerebral blood flow in patients whose cereb ral auto- regulation is impaired, while may cause a compensatory vaso-dilation if auto-regu lation is preserved. In the latter case, vasodilation will lead to an increase in cerebral blood volume and intracranial pressure (ICP), given a reduced intracranial compliance. Howe ver, application of PEEP does not induce a signi \201 cant reduction in arterial and cereb ral perfusion pressure if euvolaemia is ensured. Reduced oxygen delivery (DO2) Application of PEEP may worsen global oxygen delivery through three mechanisms: decreased cardiac outpu t, increase venous admixture and increased intracranial shunt. Acute severe asthma The main cause of dynamic hyperin \202 ation and PEEPi during acute ex acerbation of asthma is the increased expiratory resistance in the absence of \202 ow lim itation. Consequently \202 ow continues to the very end of expiration, driven by the diff erence in pressure between the alveoli and the airway opening. In this situation, use of ex ternal PEEP provides a back pressure to respiratory airflow, causing parallel increases in lung volume and airway, alveolar and thoracic pressure. In these patients undergoing mechan ical ventila- tion, the use of external PEEP is often detrimental and should be eventually used only if expiratory \202 ow limitation is proved. Further reading Brower RG, Lanken PN, MacIntyre N, et al. Higher versus lower positive end- expiratory pressures in patients with acute respirat- iry distress syndrome. N Engl J Med 2 004; 351: 327 \200\22336. Pinsky MR. The hemodynamic consequences of mechanical ventila- tion: an evolving story. Int ensive Care Med 1997; 23: 493 \200\223503. Ranieri VM, Giuliani R, Fiore T, et al. Volume \200\223pressure curve of the respiratory sy stem predicts effects of PEEP in ARDS: \200\230occlusion \200\231 versus \200\230constant \202 ow \200\231 tecnhique. Am J Respir Crit Care 1994; 149: 19 \200\22327. Adverse effects of PEEP Hepatic and renal perfusion PEEP decreases splanchnic blood \202 ow and may compro- mise hepatic perfusion and portal venous drainage. This effect may be ex plained by a reduction in cardiac output, coupled with elevation of central venous pressure (CVP) and an increased out \202 ow resistance due to a direct com- pressive effect of the diaphragm on the liver. The resulting passive hepatic congestion can cause moderate elevat ion of bilirubin and hepatic enzymes. PEEP may also interfere with renal function, even whe n cardiac output is preserved, by reducing renal blood \202 ow depending on the volaemic state and the amount of applied pressure. Suter PM, Fairlay B, Isemberg MD. Optimum end-expiratory pres- sure in patients with acute pulmonary failure. N Engl J Med 1975; 292: 284 \200\2239. The Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes as co mpared with traditional tidal volumes for acute lung injury and the acute respiratory distr ess syndrome. N Engl J Med 2000; 342: 1301 \200\2238. 24 S SINGH Continuous positive airway pressure ventilation (CPAP) Introduction Continuous positive airway pressure ventilation (CPAP) is the application of a positive pressure throughout the respi- ratory cycle, non-invasively, in spontaneously bre athing patients. It is applied by generating a constant \202 ow of an oxygen/air mixture, with a resistance applied in the circuit to create PEEP. It is primarily used to improve o xygenation in patients with distal airways collapse for a variety of rea- sons, thereby imp roving oxygen exchange in selected patients whose hypoxaemia does not respond to merely inc reasing fractional inspired oxygen concentration (FiO2). There may also be a bene \201 cia l reduction in the work of breathing, and an increase in minute ventilation through lung ex pansion and a small inspiratory positive pressure support effect. Thus, it may even correct acute respiratory hypercapnia associated with cardiorespiratory insuf \201 ciency in sele cted patients with cardiogenic pulmonary oedema. Alternatively, CPAP is also effective for maintaining patency of the collapsible upper airway in obstructive sleep apnoea hypopnoea s yndrome (OSAHS), and related sleep disor- dered breathing (SDB). CPAP increases intrathorac ic pressure, which may reduce venous return and preload to the heart. However, this may als o be bene \201 cial in of \202 oading the left atrium/ventricle in cardiogenic pulmonary oedema associated with acute left ventricular failure. Conversely, in patients with relativ e intravascular depletion, the application of CPAP may cause a further reduction in ventric ular preload, stroke volume, cardiac output and blood pressure. 5 Head/facial trauma. 6 High risk of aspiration \200\224including patients with gastroin- t estinal bleeding. A nasogastric tube reduces the risk. 7 Mechanical bowel obstruction 8 Recent upper gastrointestinal surgery 9 Copious secretions \200\224risk of inability to clear with tight- \201 tting mask. Equipment CPAP machine, circuit, PEEP valves, heated membrane exchange (HME) \201 lter, h eated humidi \201 er, full facial mask, straps, Oxygen analyzer and alarm, power supply an d oxygen source (Fig. 1.10.1). NON HUMIDIFIED e v l a V p e e P e p a c s E P A P C r e t l i e v l a v k s a M F Heater wire T piece Humidifier HUMIDIFIED CPAP Generator with intergrated oxygen sensor CPAP Whisper flow 2 Fig. 1.10.1 CPAP set-up. Indications 1 Acute respiratory failure (ARF) (usually normocapnic but even in acute hyperc apnic ARF if due to reversible basal atelectasis/collapse). a Post-operative \200\224for as sisted ventilation as an adjunct to lung expansion maneuvers and analgesia (i.e. phys- ioth erapy, incentive spirometry, intermittent positive pressure breathing) Venturi devices (i.e. WhisperFlow 2 \204 or Vital Signs \204 CPAP systems, Figs 1.10.2 an d 1.10.3) use an oxygen supply in conjunction with entrained air to generate an output. It can generate \202 ows >140l/min with a minimal FiO2 of 28%. These systems have internal p ressure relief safety valves for pressures >28cm H2O. The use of pressure and oxygen monito rs ensures measured pressures approxi- mate to the speci \201 ed PEEP and FiO2. b Acute respiratory insuf \201 ciency (e.g. pneumonia, in \202 am- matory lung diseases, acute lobar collapse) \200\224when simply increasing FiO2 is insufficient to maintain adequ ate oxygenation. Screen keys Press/oxygen E E c Inadequate oxygenation but adequate ventilatory drive. d Chest wall trauma with persistent hypoxaemia, despite high FiO2 and analgesia (care with potential pneumothorax). Up key Down key Confirm Cancel Alarm F F G G Cancel Reset 2 Cardiogenic pulmonary oedema \200\224unresponsive to initial medical management (i.e. inc reased FiO2, nitrate containing venodilators, diuretics). 3 Obstructive sleep apnoea/hypopnoea syndrome (OSAHS) and related conditions of SDB. D D Patient interface 4 Weaning from mechanical ventilation \200\224prior to extubation /tracheostomy decannulati on or prior to step down to oxygenation only. AA A C C B B On/Off Oxygen Flow generator Contraindications 1 Coma/impaired consciousness 2 Inability to maintain/protect own airway 3 Fixed upper airway obstruction 4 Haemodynamic instability/severe co-morbidity (relative) Fig. 1.10.2 WhisperFlow 2 \204 CPAP with Cardyne \200\231s Criterion Monior \204 \200\224 front view. A, on \200\223off; B, \202 owmeter; C, oxygen \202 owmeter; D, patient inte rface-tubing-PEEP valve; E, monitor; F, settings; G, alarm. 25 CHAPTER 1.10 Continuous positive airway pressure ventilation (CPAP) Weaning from mechanical ventilation The time spent on weaning as a percentage of total vent ila- tor time remains the same, and can vary from one to several days. CPAP has been used a s part of spontaneous breath- ing trials (SBTs) prior to extubation. Flow-based CPAP is dee med superior to ventilator-delivered CPAP, although both provide a degree of inspiratory su pport to compen- sate for tube-related airway resistance during SBT (how- ever, it may be a rgued that this reduces the sensitivity of the SBT). There is no published robust evidence demon- strating an outcome bene \201 t of CPAP used pre-emptively in post-operative patien ts. Nevertheless, intuitively and anecdotally, successes and reassurance are apparent, so t he adage \200\230absence of evidence does not mean evidence of absence \200\231 is applica ble in this setting. On/Off A O2 dial Flow generator B BB C C Air intake CPAP as an adjunct to physiotherapy There are a number of techniques used to support the ac tive cycle of breathing by physiotherapists; to promote lung expansion maneuvers. These inc lude IPPV, CPAP, positive expiratory pressure (PEP) devices (e.g. \202 utter valve) and c ough in-exsuf \202 ators. The literature would sug- gest there is little to choose between them, and personal preference/patient comfort are their determinants. D D Patient interface Fig. 1.10.3 Vital Signs \204 CPAPA. A, on \200\223off; B, \202 owmeter; C, oxygen \202 owmeter; D, patient interface-tubing-PEEP valve. Portable CPAP \202 ow generators used in the treatment of OSAHS produce lower \202 ow r ates (i.e. 30l/min). CPAP in OSAHS OSAHS is the periodic reduction (hypopnea) or cessation (apnoea) of air \202 ow through repetitive closure of the upper airway during sleep. CPAP, delivered by a porta ble \202 ow generator and mask, overcomes this periodic obstruction, thereby reducing epi sodic hypoxia and fragmented sleep. Since its \201 rst use in this setting in 1981, it ha s become the standard of care for domiciliary management of labora- tory-diagnosed OSAHS. T here is compelling evidence emerging of its short- and mid-term bene \201 ts, in those wit h moderate to severe OSAHS, in improving daily function and cardiovascular/cerebrovascular/ metabolic risk pro \201 les. The evidence in mild OSAHS is less apparent, although a trial of treatment is suggested if clinical symptoms persist in spite of a low apneoa/hypopnoea index. Patients \200\231 toler- ability of mask interfaces is sometimes problematic. This h as driven the technical development of newer machines and masks for ease of increased noctu rnal use. Masks and headgear In the acute hospital/ICU setting, full face masks are preferred to main tain a closed system. In contrast, the outpatient population with OSAHS generally prefer na sal interfaces with mouth closure. Careful daily inspection is required to prevent skin sor es. Use of a sponge or grani- \202 ex is advised. Dentures are maintained in situ if poss ible. Special attention should be paid to leaks into the eyes, and around the mouth. Pressu re monitoring is advisable to check the delivered PEEP. Checklist prior to commencement \200 Refractory hypoxaemia? No hypercapnia? \200 Contra indications? \200 Optimization of standard management \200 Reversible component?/Need f or further step-up care \200 Correct setting for CPAP delivery, i.e. High Dependecny Unit (HDU)/ICU Check and set up equipment Initial settings, e.g. PEEP 5 cmH2O, FiO2 maximum Nas ogastric tube necessary? Explanation to patient Monitoring clinical/physiological parameter s. Further reading Delclaux C, L \200\231Her E, Alberti C, et al. Treatment of acute hypoxemic nonhypercapnic respiratory insuf \201 ciency with continuous posi- tive airway pressure d elivered by a face mask: a randomized con- trolled trial. JAMA 2000; 284: 2352 \200\22360. \200 \200 \200 \200 Giles TL, Lasserson TJ, Smith BJ, et al Continuous positive airways pressure for obstructiv e sleep apnoea in adults. Cochrane Database Syst Rev 2006; (1): CD001106. Application of CPAP in clinical settings Acute respiratory insuf \201 ciency \200\224as a bridge to recovery. Early clinico-physiological improvement, based upon sub- jective parame ters, respiratory rate and oxygenation improve, as compared with face mask oxygen alone. Ho wever, CPAP may not reduce intubation rates in acute lung injury. There remains some debate as to the minimum effective PEEP level to produce a CPAP effect on oxygena- tion that is n ot merely a high \202 ow phenomenon. This is particularly so with the availability of hig h= \202 ow humidi \201 ed oxygen systems through nasal cannulae. Placidi G, Cornacchia M, Polese G, et al. Chest physiotherapy with positive airway pressure : a pilot study of short-term effects on sputum clearance in patients with cystic \201 br osis and severe air- way obstruction. Respir Care 2006; 51: 1145 \200\22353. Richardson A, Killen A. How long do patients spend weaning from CPAP in critical care? Intens Crit Care Nurs 2006; 22: 206 \200\22313. Sullivan CE, Issa FG, Berthon-Jones M, et al. Reversal of obstructive sleep apnoea by conti nuous positive airway pressure applied through the nares. Lancet 1981;1: 862 \200\2235. 26 L MASCIA, M ZANIERATO, & M RANIERI Recruitment maneuvers If gas exchange and lung mechanics do not improve sub- stantially with recruitment maneuver s, the patients are considered to have a \200\230low potential for recruitment \200\231, a nd the use of higher level of PEEP may provide little bene \201 t and actually be harmful since application of PEEP may cause overdistention. Data suggest that patients with \200 \230high potential for recruit- ment \200\231 are those ventilated for not more than 48 \200\22372h, while patients with \200\230low potential for recruitment \200\231 are those ventilated for >3 days; the underlying disease responsible for ARDS (primary vs secondary A RDS) seems not to have a role in identifying responders or non-responders to recruitment ma neuvers. The mechanism underlying hypoxaemia in acute lung injury is intrapulmonary shunt due to non -ventilated but per- fused alveoli. Any maneuver that recruits lung volume and increases th e amount of aerated lung can be expected to improve gas exchange. However, the challenge is to recruit atelectatic alveoli without overdistending normal lung units. Although PEEP is the most commonly used method to achieve or maintain recruitment, others techniques have be en evaluated: volume recruitment maneuvers, prone position and HFOV. Volume recruitment man euvers, peri- odic in \202 ations to airways pressures of 35 \200\22345cm H2O sus- tained for 5 \200\22330s, are used to reverse alveolar derecruitment and to improve gas exchange w hile allowing acceptable ventilator pressure. In ALI/ARDS, inadequate levels of PEEP may ca use tidal recruitment/derecruitment of part of the consolidated lung and may expose these r egions to shear stress. The combined use of low tidal volume and PEEP may minimize VILI. Re cruitment maneuvers are procedures speci \201 cally designed to reach an opening pressure suf \201 cient to open the collapsed lung regions that, in association with an increased l evel of PEEP post- recruitment maneuver, may improve gas exchange, reducing intrapulmonary shunt. However, the effectiveness of recruiting maneuvers to improve oxygenation is also in \202 uenced by elastic proper- ties of the chest wall since part of the pressure applied to the respiratory system during the recruiting maneuvers can be dissipated against a stiff chest wall. Moreover, the response to recruitment maneuvers is a function of the potential for recruitment (unstable units), the phase and extent of lung injury, the level of PEEP a nd the characteris- tics of the recruiting technique. In clinical practice, RM may play a r ole in the lung-protective ventilatory strategies based on the so-called \200\230open lung approach \200\231; however, their utility has not been con \201 rmed by large clinical tr ials. Lung recruitment maneuvers have also been successfully used in patients during genera l anesthesia, to restore the decreased respiratory system compliance and oxygenation. Monitoring Clinical evaluation of the response to recruitment manoeu- vres and of its poten tial use can be evaluated at the bedside. More accurate evaluation of the percentage of pot entially recruitable lung may be obtained by analysis of CT images or of respiratory mechan ics. Clinical evaluation After performing a recruitment maneuver, its ef \201 cacy can be evalu ated at the bedside by looking at the values of plateau pressure (or tidal volume if the pa tient is ventilated in a pressure-controlled mode), PaO2 and PaCO2. If the recruitment mane uver: (1) decreases plateau pressure (or increases tidal volume if the patient is ventilate d in a pressure-controlled mode); (2) increases PaO2; and (3) decreases PaCO2 (even if only few mm Hg), the patients may be considered as a responder. CT scanning Analysis of CT \201 ndings can identify the distribution of normally aerated lung regions in the non-dependent regions, and poorly aerated lung regions distributed in t he dependent lung region. The CT analysis can assess the effects of the recruitment maneuve rs as well as its safety, and most importantly the adequate PEEP levels to keep the lungs o pened after the recruitment maneuvers. With an inspiratory and expiratory pause image acqui sition of the lung, the regional tidal volume distribution can be assessed. Techniques Several approaches have been used to perform the recruit- ment maneuvers: \200 Respiratory mechanics Pressure \200\223volume (P/V) curve Analysis of P/V curves can con \201 rm that the lower in \202 ec- tion point and upper in \202 ection point correspond t o CT scan evidence of atelectasis and overdistension. Alveolar recruitment is con \201 rme d to occur continuously and along the inspiratory limb of the P/V curve, while the critical point for lung derecruitment is identi \201 ed below the point of maximum curvature of th e de \202 ation limb. Sustained in \202 ation by application of CPAP at 30 \200\22340cm H2O for 40s. Incremental PEEP on maximum pressure: PEEP is increased in increments of 5cm H2O from a baseline PEEP to 35cm H2O, reducing tidal volume to limit peak inspiratory pressure to 35cm H2O. CPAP of 35cm H2O is maintained for 30s. Intermittent higher tidal volume in pressure-controlled ven tilation applied with escalating PEEP and constant driving pressure: peak pressure of 45cm H2O, I:E ratio of 1:2 and PEEP level of 16cm H2O for 2min. Stress index The analysis of the dynamic pressure/time (P/T) curve during constant \202 o w ventilation (stress index) is a new parameter to identify clinically the best compromise between alveolar recruitment and overdistention. The stress index is the exponent of the eq uation correlating the airway pressure pro \201 le and time during each tidal volume. A st ress index <1 is associated with recruitment, assessed by CT scan, whereas a stress index > 1 is associ- ated with hyperin \202 ation. Modern ventilators are able to