Respiratory center depression, e.g. drugs or intracranial pathology. Peripheral neuromuscul ar disease, e.g. Guillain-Barr syndrome, myasthenia gravis, or spinal cord pathology. The rapeutic muscle paralysis, e.g. as part of balanced anesthesia, for management of tetanus o r status epilepticus. Loss of chest wall integrity, e.g. chest trauma, diaphragm rupture. H igh CO2 production, e.g. burns, sepsis or severe agitation. Reduced alveolar ventilation, e .g. airways obstruction (asthma, acute bronchitis, foreign body), atelectasis, pneumonia, p ulmonary oedema (ARDS, cardiac failure), pleural pathology, \201 brotic lung disease, obe sity. Pulmonary vascular disease (e.g. pulmonary embolus, ARDS). \200 \200 To reduce intracranial pressure Reduction of PaCO2 to approximately 4kPa causes cerebral va soconstric- tion, and therefore, reduces intracranial pressure after brain injury. Studies suggest this effect is transient and may impair an already critical cerebral blood \202 o w. To reduce work of breathing Assisted ventilation 9 sedation and muscle relaxation reduces r espira- tory muscle activity and the work of breathing. In cardiac failure or non- cardioge nic pulmonary oedema, the resulting reduction in myocardial O2 demand is more easily matche d to the supply of O2. VENTILATORY SUPPORT \200\224INDICATIONS 45 Indications for ventilatory support Consider ventilatory support (invasive or non-invasive) if: \200 \200 \200 \200 \200 \200 \200 \200 \200 \200 \200 Respiratory rate >30/min. Vital capacity <10 \200\22315mL/kg. PaO2 <11kPa on FIO2 \211 0. 4. PaCO2 high with signi \201 cant respiratory acidosis (e.g. pH <7.2). Vd/VT >60%. Qs/Qt >15 \200\22320%. Exhaustion. Confusion. Severe shock. Severe LVF. Raised ICP. See also: Respiratory failure, p350; Acute weakness, p440. 46 CHAPTER 2 Respiratory therapy techniques IPPV \200\224description of ventilators Classi \201 cation of mechanical ventilators Moder n ventilators deliver a gas \202 ow with a cycling mechanism to cut \202 ow during expi ration. They may be classi \201 ed by the method of cycling from inspiration to expiration , i.e. when a preset time has elapsed (time-cycled), a preset pressure is reached (pressure -cycled), or a preset volume delivered (volume-cycled). The ventilator breath may be volume -controlled (a pre- determined tidal volume (VT) is delivered), pressure-controlled (gas \202 ow is at a pre-determined pressure), or volume controlled with a limited pres- sure (t he ventilator delivers a preset VT within a pressure limit unless the lungs are non-complia nt or airway resistance is high). The latter is useful to avoid high airway pressures. Vari ous \200\230mixed \200\231 modes are available. In volume- cycled mode with a time limit, the inspiratory \202 ow is reduced; the ventilator delivers the preset VT unless impossib le at the set respiratory rate (limiting airway pressure). In time-cycled mode with pressur e control, preset pres- sure is delivered throughout inspiration with cycling determined by time. VT is dependent on respiratory compliance and airway resistance. Setting up the mechanical ventilator Tidal volume Values of 6 \200\2237mL/kg ideal body wei ght are related to better outcomes in severe acute respiratory failure, by reducing ventila tor-associated trauma and distant in \202 ammatory effects. In severe air \202 ow limitat ion (e.g. asthma, acute bronchitis), smaller VT and minute volume may be needed to allow pr olonged expiration. Respiratory rate Usually set in accordance with VT to provide minute ventilation of 85 \200 \223100mL/kg/min. In time-cycled or time-limited modes, the set respiratory rate determines the timing of the ventilator cycles. Inspiratory \202 ow Usually set between 40 \200\22380L/min. Higher \202 ow rates are mo re comfortable for alert patients. This allows for longer expiration in patients with sever e air \202 ow limitation, but may result in higher peak airway pressures. The \202 ow pa ttern may be adjusted on most ventilators. A square waveform is often used, but deceleratin g \202 ow may reduce peak airway pressure. I:E ratio A function of respiratory rate, VT, inspiratory \202 ow, and inspiratory time. Prolonged expiration is useful in severe air \202 ow limitation while a pro- longed inspir atory time is used in ARDS to allow slow-reacting alveoli time to \201 ll. Alert patients are more comfortable with shorter inspiratory times and high inspiratory \202 ow rates. FIO2 Set according to arterial blood gasses. Usual to start at FIO2 = 0.6 \200\2231, then a djust according to arterial blood gasses and pulse oximetry. Airway pressure In pressure-controlled or -limited modes, a peak airway pressure (circuit r ather than alveolar pressure) can be set (ideally \211 30cmH2O). PEEP is often increased t o maintain FRC when compliance is low. IPPV \200\224DESCRIPTION OF VENTILATORS 47 Initial ventilator set-up \200 \200 \200 \200 \200 \200 \200 \200 Check for leaks. Check O2 is \202 owing. FIO2 VT Rate I:E ratio Peak pressure PEEP 0.6 \200\2231. 5 \200\22310mL/kg. 10 \200\22315/min. 1:2. \211 35cmH2O. 3 \200\2235cmH2O. Key paper Acute Respiratory Distress Syndrome Network. (2000) Ventilation with lower tidal volumes compared with traditional tidal volumes for acute lung injury and the acute respira tory distress syndrome. N Engl J Med 342: 1301 \200\2238. See also: IPPV \200\224modes of ventilation, p48; High frequency jet ventilation, p62; Hig h frequency oscillatory ventilation, p64; Continuous positive airway pressure, p70; Non-inv asive respiratory support, p76. 48 CHAPTER 2 Respiratory therapy techniques IPPV \200\224modes of ventilation Controlled mechanical ventilation (CMV) A preset number o f breaths are delivered to supply all the patient \200\231s venti- latory requirements. Bre aths may be at a preset VT (volume-controlled) or at a preset inspiratory pressure (pressur e-controlled). Assist-control mechanical ventilation (ACMV) Patients can breathe, triggering the ventilato r to determine the respira- tory rate. However, a preset number of breaths are delivered if the spon- taneous respiratory rate falls below the preset level. Intermittent mandatory ventilation (IMV) A number of breaths are preset, but patients are f ree to breathe sponta- neously in between. Mandatory breaths may be synchronized with spon- taneous efforts (synchronized IMV) to avoid mandatory breaths occurring on top of spontane ous breaths ( \200\230stacking \200\231). This may lead to excessive VT, high airway pressu re, incomplete exhalation, and air trapping. Positive pressure support may be added to spon taneous breaths to reduce the work of breathing. Pressure support ventilation (PSV) A preset positive inspiratory pressure is added to the v entilator circuit during inspiration in spontaneously breathing patients. Preset pressures should be adjusted to an adequate (but not excessive) VT. Volume support ventilation (VSV) A target VT is set and pressure support is adjusted to ach ieve the target volume. Choosing the appropriate mode Pressure-controlled ventilation avoids the dangers associated with high airway pressure, although it may result in marked changes in VT if respira- tory compliance alters. Allowing the patient to make some spontaneous respiratory effort may re duce sedation requirements, retrain respiratory muscles, and reduce mean airway pressure. Apnoeic patient Use of IMV or ACMV in totally apnoeic patients provides total minute volume requirement if the preset rate is high enough (effectively CMV), but allows spontaneous re spiratory effort on recovery. Patient taking limited spontaneous breaths A guaranteed minimum minute volume is assured wi th both ACMV and IMV, depending on the preset rate. The work of spontaneous breathing is re duced by supplying the preset VT for spontaneously triggered breaths with ACMV or by adding pressure support to spontaneous breaths with IMV. With ACMV, the spontaneous tidal volume is guaranteed, whereas with IMV and pressure support, spontaneous tidal volume depends on l ung compliance and may be less than preset tidal volume. The advantage of IMV and pressure support is that gradual reduction of preset rate, as spon- taneous effort increases, allows a smooth transition to pressure support ventilation. Subsequent weaning is by reduction of pressure support level. IPPV \200\224MODE OF VENTILATION 49 See also: IPPV \200\224description of ventilators, p46; High frequency jet ventilation, p62 ; High frequency oscillatory ventilation, p64; Continuous positvie airway pressure, p70; No n-invasive respiratory support, p76. 50 CHAPTER 2 Respiratory therapy techniques IPPV \200\224adjusting the ventilator Adjustments are usually made in response to blood gas ses, pulse oximetry or capnography, patient agitation or discomfort, or during weaning. \200\230Migration \200\231 of the endotracheal tube, either distally to the carina or beyon d, or proximally such that the cuff is at vocal cord level, may result in agitation, excess coughing, and a deterioration in blood gasses. Tube migra- tion or obstruction should be c onsidered and recti \201 ed before changing ventilator settings or sedative dosing. The choice of ventilator mode depends upon conscious level, the number of spontaneous breat hs being taken, and blood gas values. Many spontaneously breathing patients can cope adequa tely with pressure support ventilation alone. However, a few intermittent mandatory breaths (SIMV) may be needed to assist gas exchange or slow an excessive spon- taneous rate. The p aralyzed/heavily sedated patient will require either volume- or pressure-controlled mandato ry breaths. The order of change will be dictated by the severity of respiratory failure and individual operator preference. Earlier use of increased PEEP is advocated to recruit collapsed alveol i and thus improve oxygenation in severe respiratory failure. Low PaO2 considerations \200 \200 Increase FIO2. Increase PEEP (may raise peak airway pressure or reduce cardiac output). Inc rease I:E ratio. Consider tolerating low PaO2 ( \200\230permissive hypoxaemia \200\231). Co nsider increasing pressure support/pressure control or VT. In CMV, consider increasing seda tion 9 muscle relaxants. Prone ventilation, inhaled nitric oxide. \200 \200 \200 \200 High PaO2 considerations \200 \200 \200 \200 Decrease FIO2. Decrease I:E ratio. Decrease PEEP. Decrease level of pressure control/pressu re support if VT adequate. High PaCO2 considerations \200 \200 \200 \200 \200 \200 Consider tolerating high level ( \200\230permissive hypercapnia \200\231). Increase VT (if low and peak airway pressure allows). Increase respiratory rate. Reduce rate if too high (t o reduce intrinsic PEEP). Reduce dead space. In CMV, increase sedation 9 muscle relaxants. Low PaCO2 considerations \200 Decrease respiratory rate. \200 Decrease VT. IPPV \200\224ADJUSTING THE VENTILATOR 51 See also: IPPV \200\224modes of ventilation, p48; IPPV \200\224failure to tolerate ventilat ion, p52; IPPV \200\224failure to deliver ventilation, p54; IPPV \200\224complications of v entilation, p56; IPPV \200\224weaning techniques, p58; IPPV \200\224assessment of weaning, p60. 52 CHAPTER 2 Respiratory therapy techniques IPPV \200\224failure to tolerate ventilation Agitation or \200\230 \201 ghting the ventil ator \200\231 may occur at any time. If paralyzed or heavily sedated, poor ventilator toler ance may be indicated by hypox- aemia, hypercapnia, ventilator alarms, or cardiovascular in stability. The \201 rst priority is to assess the patient. \200 \200 \200 \200 \200 Is the patient cyanosed? Is the chest moving? Are breath sounds present and equal? Are ther e abnormal breath sounds? Has the SpO2 changed? Basic clinical assessment is necessary to judge how serious the problem is and whether imme diate resuscitative steps are required. If the problem is serious, the \201 rst response must be to disconnect the ventilator and manu- ally ventilate. Manual ventilation with 100% O2 and a non-rebreathing bag allows assessment of how dif \201 cult it is to in \202 ate the lungs, how long exhala- tion takes, and whether the pro blem with ventilation relates to patient (problem persists) or ventilator (problem resolved ) factors. Poor initial tolerance \200 \200 Increase FIO2 to 1.0 and start manual ventilation. Check endotracheal tube is correctly pos itioned and both lungs are being in \202 ated. Consider tube replacement, intra-tracheal o bstruction, pneumothorax, or bronchospasm. Check ventilator circuit is both intact and pate nt, and ventilator is functioning correctly. Check ventilator settings, including FIO2, PEE P, I:E ratio, set tidal volume, respiratory rate, and/or pressure control. Check \200\230p ressure limit \200\231 settings as these may be set too low causing ventilator to cycle to expiration prematurely. Poor tolerance after previous good tolerance If agitation occurs in a patient who has previ ously tolerated mechanical ven- tilation, either the patient \200\231s condition has deteri orated, or there is a problem in the ventilator circuit (including arti \201 cial airway) or the ventilator itself. \200 The patient should be removed from the ventilator and plac ed on manual ventilation with 100% O2 while the problem is resolved. Resorting to increased sedation 9 muscle relaxation in this circumstance is dangerous until the cause is understo od. Check patency of the endotracheal tube (e.g. with a suction catheter) and re-intubate i f in doubt. Consider chest X-ray to identify endotracheal tube malposition (e.g. cuff above vocal cords, tip at carina, tube in main bronchus). Seek and treat changes in the patient \200\231s condition, e.g. bronchospasm, tension pneumothorax, sputum plug, pain, raised int ra-abdominal pressure, pulmonary oedema. Where patients are making spontaneous respiratory effort, consider increasing pressure support or adding mandatory breaths. If patients fail to synchronize with IMV by stacking spontaneous and mandatory breaths, increasing pressure support and reducing mandatory rate may help. Use of pressure support ventilation may also be appropriate. IPPV \200\224FAILURE TO TOLERATE VENTILATION 53 See also: IPPV \200\224modes of ventilation, p48; IPPV \200\224adjusting the ventilator, p5 0; IPPV \200\224failure to deliver ventilation, p54; IPPV \200\224complications of ventilat ion, p56; IPPV \200\224weaning techniques, p58; IPPV \200\224assessment of weaning, p60. 54 CHAPTER 2 Respiratory therapy techniques IPPV \200\224failure to deliver ventilation Failure to ventilate despite apparently appropr iate ventilator settings and exclusion of patient factors requires assessment of which vent ilator settings are not being delivered. Poor gas exchange \200 \200 \200 Increase FIO2 to 1.0 and start manual ventilation. Exclude patient factors. Check endotrach eal tube is correctly positioned, patent, and both lungs are being in \202 ated. Consider tube replacement. Check ventilator circuit is both intact and patent, and ventilator is fun ctioning correctly. Check ventilator settings, including FIO2, PEEP, I:E ratio, set VT, res piratory rate and/or pressure control. Low VT or low pressure alarm Expired VT will be lower than inspired VT with bronchopleural \201 stula. In other situations where expired VT is suddenly signi \201 cantly lower tha n inspired VT, or maintenance of circuit pressure is not possible, there is a leak in the v entilator circuit. The patient should be manually ventilated while the leak is identi \201 ed and corrected. If the leak persists with manual ventilation, repositioning or replaceme nt of the endotracheal tube is required. High pressure alarm A sudden increase in airway pressure indicates a change in resistance t o gas \202 ow. After patient factors have been excluded: \200 Check patency of the endotracheal tube (e.g. with a suction catheter); re-intubate if in do ubt. Check patency of ventilator circuit and catheter mount. Look for excessive trapped wat er partially occluding the catheter mount. Check for sputum obstructing the HME. Consider a chest X-ray to identify endotracheal tube malposition (e.g. cuff above vocal cords, tip at carina, tube in main bronchus). \200 IPPV \200\224FAILURE TO DELIVER VENTILATION 55 See also: IPPV \200\224modes of ventilation, p48; IPPV \200\224adjusting the ventilator, p5 0; IPPV \200\224failure to tolerate ventilation, p52; IPPV \200\224complications of ventila tion, p56; IPPV \200\224weaning techniques, p58; IPPV \200\224assessment of weaning, p60; F ibreoptic bronchoscopy, p88; Chest physiotherapy, p90; Bronchodilators, p254; Positive end expiratory pressure (1), p66; Positive end expiratory pressure (2), p68. 56 CHAPTER 2 Respiratory therapy techniques IPPV \200\224complications of ventilation Haemodynamic complications Venous return depends on passive \202 ow from central veins to right atrium. An increase in intrathoracic press ure is transmitted across compliant lungs to increase right atrial pressure and reduce veno us return. This is less of a problem with stiff lungs (e.g. ARDS), but will be exacerbated by inverse I:E ratio and high PEEP. As lung volume is increased by IPPV, the pulmonary vasc ulature is constricted. Pulmonary vascular resistance and diastolic volume of the right ven tricle rise and, by septal shift, left ventricular \201 lling is impeded. These effects a ll contribute to a reduced stroke volume. This can be minimized by reducing airway pressure , avoiding prolonged inspira- tory time, and maintaining blood volume. Ventilator trauma Barotrauma relates to gas escape into cavities and interstitial tissues d uring IPPV. Distending volume and high shear stress are probably responsible rather than hi gh pressures. It is most likely to occur with high VT. It occurs in IPPV and conditions ass ociated with lung overin \202 ation (e.g. asthma). Tension pneumothorax is life-threatenin g and should be suspected in any patient on IPPV who becomes suddenly agitated, tachycardic , hypotensive, or exhibits sudden deterioration in their blood gasses. An immediate chest d rainage tube should be inserted if tension pneumothorax develops. Prevention of venti- lato r trauma relies on avoidance of high VT and high airway pressures. Nosocomial infection Endotracheal intubation bypasses normal defense mechanisms. Ciliary ac tivity and cellular morphology in the tracheobronchial tree are altered. The requirement fo r endotracheal suction further increases susceptibility to infection. In addition, the norm al heat and moisture exchanging mecha- nisms are bypassed, requiring arti \201 cial humidi \201 cation of inspired gasses. Failure to provide adequate humidi \201 cation increases the risk of sputum retention and infection. Maintaining ventilated patients at 30* upright , head tilt reduces the incidence of nosocomial pneumonia. Acid \200\223base disturbance Over-ventilating patients with chronic respiratory failure ma y, by rapid correction of hypercapnia, cause respiratory alkalosis. This reduces pulmonary blood \202 ow and may contribute to hypoxaemia. Respiratory acidosis due to hypercapnia m ay be due to inappropriate ventilator settings or may be desired to avoid high VT and venti lator trauma. Water retention Vasopressin released from the anterior pituitary is increased due to a redu ction in intrathoracic blood volume and psychological stress. Reduced urine \202 ow thus contributes to water retention. In addition, the use of PEEP reduces lymphatic \202 ow wi th consequent peripheral oedema, especially affecting the upper body. High airway pressure reduces venous return, again contributing to oedema. Respiratory muscle wasting Prolonged ventilation may lead to disuse atrophy of the respirat ory muscles with subsequent weaning dif \201 culty. IPPV \200\224COMPLICATIONS OF VENTILATION 57 See also: IPPV \200\224modes of ventilation, p48; IPPV \200\224adjusting the ventilator, p5 0; IPPV \200\224failure to tolerate ventilation, p52; IPPV \200\224failure to deliver venti laion, p54; High frequency jet ventilation, p62; Positive end expiratory pressure (1), p66; Positive end expiratory pressure (2), p68. 58 CHAPTER 2 Respiratory therapy techniques IPPV \200\224weaning techniques Patients may require all or part of their respiratory suppo rt to be pro- vided by a mechanical ventilator. Weaning from mechanical ventilation may fol low several patterns. In patients ventilated for short periods (no more than a few days), i t is common to allow 20 \200\22330min breathing on a \200\230T \200\231 piece before remov ing the endotracheal tube. For patients who have received longer term ventilation, it is un likely that mechanical support can be withdrawn suddenly; several methods are commonly used to wean these patients from mechanical ventilation. There is no strong evidence that any t echnique is superior in terms of weaning success. Intermittent \200\230T \200\231 piece or continuous positive airway pressure (CPAP) Sponta neous breathing is allowed for increasingly prolonged periods with a rest on mechanical ven tilation in between. The use of a \200\230T \200\231 piece for longer than 30min may lead to basal atelectasis since the endotracheal tube bypasses the physiological PEEP effect of the larynx. Therefore, it is common to use 5cmH2O CPAP as spontaneous breathing periods get longer. In the early stages of weaning, mechanical ventilation is often continued at night to encourage sleep, avoid fatigue, and rest respiratory muscles. Intermittent mandatory ventilation (IMV) The set mandatory rate is gradually reduced as the spontaneous rate increases. Spontaneous breaths are usually pressure-supported to over- co me circuit and ventilator valve resistance. With this technique, it is important that the p atient \200\231s required minute ventilation is provided by the combination of mandatory br eaths and spontaneous breaths without an excessive spontaneous rate. The reduction in manda tory rate should be slow enough to maintain adequate minute ventilation. It is also importa nt that the patient can synchronize his own respiratory efforts with man- datory ventilator breaths; many cannot, particularly where there are frequent spontaneous breaths, some of w hich may \200\230stack \200\231 with mandatory breaths causing hyperin \202 ation. Pressure support ventilation All respiratory efforts are spontaneous but positive pressure is added to each breath, the level being chosen to maintain an appropriate tidal volume. We aning is performed by a gradual reduction of the pressure support level while the respirato ry rate is <30/min. The patient is extu- bated or allowed to breathe with 5cmH2O CPAP when pressure support is minimal (<10 \200\22315cmH2O with modern ventilators). Choice of ventilator Modern ventilators have enhancements to aid weaning; however, weaning most patients from ventilation is possible with a basic ventilator and the intermittent \200\230T \200\231 piece technique, provided an adequate fresh gas \202 ow is provided. I f IMV and/or pressure support are used, the ventilator should provide the features listed i n the table opposite. IPPV \200\224WEANING TECHNIQUES 59 Key features in the choice of ventilator Ventilator must allow patient triggering (i.e. not a minute volume divider). Fresh gas \202 ow must be greater than spontaneous peak inspiratory \202 ow. Minimum circuit resist ance (short, wide bore, and smooth internal lumen). Low resistance ventilator valves. Sensi tive pressure or \202 ow trigger (ideally monitored close to the ET tube). Synchronized I MV (avoids \200\230stacking \200\231 mandatory on spontaneous breaths). \200 See also: IPPV \200\224modes of ventilation, p48; IPPV \200\224assessment of weaning, p60; Continuous positive airway pressure, p70; Non-invasive respiratory support, p76. 60 CHAPTER 2 Respiratory therapy techniques IPPV \200\224assessment of weaning Prior to weaning, it is important that the cause of resp iratory failure and any complications arising have been corrected. \200 \200 \200 Sepsis should be eradicated as should factors that increase O2 demand. Attention is require d to nutrition, \202 uid and electrolyte balance. The diaphragm should be allowed to cont ract unhindered by choosing the optimum position for breathing (sitting up unless the diaph ragm is paralyzed) and ensuring that intra-abdominal pressure is not high. Adequate analges ia must be provided. Sedatives are often withdrawn by this point, but may still be needed i n speci \201 c situations, e.g. residual agitation, raised intracranial pressure. Weaning should start after adequate explanation has been given to the patient. Factors predicting w eaning success are detailed in the table oppo- site. Spontaneous (pressure-supported) breat hing should generally start as soon as possible to allow a reduction in sedation levels and to main- tain respiratory muscle function. Weaning with the intention of removing mechanic al support is unlikely to be successful while FIO2 >0.4. Continuous pulse oximetry and regu lar clinical review are essential during weaning. Arterial blood gasses should be taken aft er 20 \200\22330min of spon- taneous breathing. After short-term ventilation, extubate if a rterial gasses and respiratory pattern remain satisfactory, the cough re \202 ex is adequa te, and the patient can clear sputum. Patients being weaned from longer-term ventilation (> 1wk) should generally be allowed to breathe spontaneously for at least 24h before extubatio n. Indications for re-ventilation If spontaneous respiration is discoordinate or the patient i s exhausted, agitated, or clammy, the ventilator should be reconnected. Successful weaning is more easily accomplished if excessive fatigue is not allowed to set in. Tachypnoea (>30/ min), tachycardia (>110/min), respiratory acidosis (pH <7.2), rising PaCO2, and hypoxaemia (SaO2 <90%) should all prompt reconnection of the ventilator. Factors associated with weaning failure Failure to wean is associated with: \200 Increase d O2 cost of breathing. \200 Muscle fatigue (malnutrition, peripheral neuropathy or myopa thy, drugs, (e.g. muscle relaxants, aminoglycosides), and electrolyte abnormalities (e.g. l ow Mg2+, K+, and perhaps phosphate). Inadequate respiratory drive (alkalosis, opiates, seda tives, malnutrition, cerebrovascular accident, coma). Inadequate cardiac reserve and heart failure. In the latter case, monitor cardiac function during spontaneous breathing periods. Any dete rioration in cardiac function should be treated aggres- sively (e.g. optimal \202 uid the rapy, vasodilators, inotropes). Early muscle fatigue due to prolonged disuse requires regul ar and controlled exercise after correction of nutritional de \201 cit. Weaning should be stopped during periods when exercise is provided. Patients who are building up muscle on an exercise program may also bene \201 t from rest periods at night so that the time free of mechanical ventilator support is gradually increased. IPPV \200\224ASSESSMENT OF WEANING 61 Factors predicting weaning success \200 \200 \200 \200 \200 \200 \200 \200 PaO2 >11kPa on FIO2 = 0.4 (PaO2/FIO2 ratio >27.5kPa). Minute volume <12L/min. Vital capacit y >10mL/kg. Maximum inspiratory force (PImax) >20cmH2O. Respiratory rate/tidal volume <100. Qs/Qt <15%. Dead space/tidal volume <60%. Haemodynamic stability. A ratio of respiratory r ate to tidal volume (f/VT, shallow breathing index) \211 105 has a 78% positive predictive value for successful weaning. Key paper Yang KL, Tobin MJ. (1991) A prospective study of indexes predicting the outcome o f trials of weaning from mechanical ventilation. N Engl J Med 324: 1445 \200\22350. See also: IPPV \200\224weaning techniques, p58; Pluse oximetry, p144; CO2 monitoring, p146; Pulmonary function tests, p148; Blood gas analysis, p154. 62 CHAPTER 2 Respiratory therapy techniques High frequency jet ventilation \200 High frequency jet ventilation (HFJV) involves a high pressure jet of gas entraining furthe r fresh gas which is directed by the jet towards the lungs. Respiratory rates of 100 \200 \223300/min ensure minute ventilation of about 20L/min although tidal volume may be lower t han dead space. CO2 elimination is usually more ef \201 cient than conventional IPPV. The method of gas exchange is not fully elucidated, but includes turbulent gas mixing and conve ction. Oxygenation is dependent on mean airway pressure. Peak airway pressures are lower th an with conventional mechanical ventilation, but auto-PEEP and mean airway pressures are ma intained. SaO2 often falls when starting HFJV, but usually improves with time. The high gas \202 ow rates employed require additional humidi \201 cation (30 \200\223100mL/h); this is usually nebulised with the jet. \200 Indications Bronchopleural \201 stula is the only proven ICU indication for HFJV. It may assist weaning from mechanical ventilation as the open circuit allows spontaneous breaths w ithout the drawbacks of demand valves. HFJV also ensures adequate ventilation if the patien t fails to breathe adequately. Reducing the driving pressure and increasing the respiratory rate may facilitate weaning further. In ARDS, conventional ventilation can lead to ventila tor trauma if a high VT is used. HFJV avoids problems associated with high VT, but is often unable to provide adequate ventilation in isola- tion for patients with severe ARDS. Setting up HFJV \200 A jet must be provided via a modi \201 ed endotracheal tube or catheter mount. Entrainment gas is provided via a T-piece. VT cannot be set directly, but is altered by adjusting jet size, I:E ratio, driving pressure, and respiratory rate from inbuilt algorithms. Respirator y rate is usually set between 100 \200\223200/min. As the rate increases at a constant driv ing pressure, PaCO2 may increase (increasing PEEPi increases effective physiological dead s pace). The I:E ratio is usually set between 1:3 and 1:2. VT is determined by airway pressur e and I:E ratio. Driving pressure is usually set between 1 \200\2232bar. These pressures ar e much higher than the 60 \200\223100cmH2O used in conventional ventilation. PEEPi is relat ed to the driving pressure, I:E ratio, and respiratory rate. External PEEP may be added to increase mean airway pressure should this be necessary to improve oxygenation. Combined HFJV and conventional CMV May be useful in conditions of poor lung compliance wher e HFJV alone cannot provide adequate gas exchange. Low frequency pressure limited ventilati on with PEEP provides an adequate mean airway pressure to ensure oxygenation while CO2 clea rance is effected by HFJV. Care must be taken to avoid excessive peak airway pressure when HFJV and CMV breaths stack. HIGH FREQUENCY JET VENTILATION 63 Adjusting HFJV according to blood gasses Increasing PaO2 \200 Increase FIO2. \200 Incre ase I:E ratio. \200 Increase driving pressure. \200 Add external PEEP. \200 Consider reducing respiratory rate. Decreasing PaCO2 \200 \200 Increase driving pressure. Decrease respiratory rate. See also: IPPV \200\224description of ventilators, p46; IPPV \200\224modes of ventilation, p48; High frequency oscillatory ventilation, p64; Positive end expiratory pressure (1), p66 ; Positive end expiratory pressure (2) p68; Acute respiratory distress syndrome (1), p360; Acute respiratory disress syndrome (2), p362; Pneumothorax, p368. 64 CHAPTER 2 Respiratory therapy techniques High frequency oscillatory ventilation High frequency oscillation (HFO) is an extreme form of standard ventila- tion with high rates, sub-deadspace tidal volumes (1 \200\2233mL/kg), and signi \201 - cantly higher levels of PEEP (equal to the continuous distending pressure or mean airway pressure during HFO). It may thus be viewed as a CPAP device that allows ge neration of pressure oscillations around a continuous distending pressure eliminating CO2 b y accelerating molecular diffusion processes. Precise mechanisms of action on gas exchange are uncertain. Whereas bulk convection and diffusion predominate, during standard ventilati on, HFO may provide: \200 Inter-regional gas mixing between respiratory units with different time constants (Pendellu ft ventilation). Convective transportation from asymmetric inspiratory and expiratory veloc ity pro \201 les. Longitudinal dispersion via interaction between the axial velocity pro \201 le and the radial concentration gradient. During HFO, high frequencies (180 \200\223360bpm = 3 \200\2236Hz) generally maintain normal PaCO2 levels. At lower frequencies (3Hz), CO2 clearance usually improves because of the la rger VT generated. CO2 clearance can also be enhanced by higher proximal driving pressures (range 60 \200\22390cmH2O) and longer inspiratory times (range 30 \200\22350%) \200\224both have a similar effect on VT. Indications This technique is used as a rescue therapy for refractory hypoxaemia or ventila tory failure in ARDS. It is now being considered as an early strategy in patients with mild er forms of acute lung injury to prevent further deterioration. However, there are no contr olled data showing superiority over conventional techniques. Theoretically, low VT and high PEEP in HFO reduce the risk of cyclical alveolar collapse and over-distension, both import ant factors in ventilator-induced lung injury (VILI). The higher mean airway pressure, but lower cycling and plateau pressures, will also improve oxygenation and allow reduction in t he FIO2. Lung recruitment can often be achieved by temporarily increasing lung volumes by a stepwise increase in continuous distending pressure to an oxygenation or chest X-ray target. The incidence of pneumothorax is thought to be similar to conventional ventilation in adult s. HFO may reduce the size of an air leak and promote healing by reducing high peak airway pressures and the alveolar \200\223pleural pressure gradient. Reducing the diameter of the leak increases resistance to gas \202 ow and this facilitates lung healing. Changes in me an airway pres- sure will result in the greatest percentage change in the size of the air l eak. Potential problems with HFO \200 Inability to maintain spontaneous breathing such that the patient often requires heavy seda tion 9 paralysis. Novel technical developments incorporating a \202 ow-demand system to e nable \202 ow compensation may reduce the imposed work of breathing, increase patient com fort, and allow continued spontaneous breathing. Haemodynamic compromise that usually respo nds to volume loading. This is more common during recruitment maneuvers. HIGH FREQUENCY OSCILLATORY VENTILATION 65 See also: IPPV \200\224description of ventilators, p46; IPPV \200\224modes of ventilation, p48; High frequency jet ventila- tion, p62; Positive end expiratory pressure (1), p66; Posi tive end expiratory pressure (2), p68; Acute respiratory distress syndrome (1), p360; Acute respiratory distress syndrome (2), p362; Pneumothorax, p368. 66 CHAPTER 2 Respiratory therapy techniques Positive end expiratory pressure (1) Positive end expiratory pressure (PEEP) is a modality used in positive pressure ventilation to prevent the alveoli returning to atmospheric pres- sure during expiration. It is routinely set between 3 \200\2235cmH2O; however, in severe r espiratory failure, it will often need to exceed 10cmH2O to be above the lower in \202 exi on point of the pressure \200\223volume curve. This has been suggested as bene \201 cial i n patients with severe ARDS. It rarely needs to exceed 20cmH2O to avoid cardiorespiratory c omplications and alveolar over-distension (see below). It neither prevents nor attenuates A RDS, reduce capillary leak, or lung water. Respiratory effects PEEP improves oxygenation by recruiting collapsed alveoli, re-distribut ing lung water, decreasing A \200\223V mismatch, and increasing functional residual capacit y (FRC). Haemodynamics PEEP usually lowers both left and right ventricular preload, and increases RV afterload. Though PEEP may increase cardiac output in left heart failure and \202 uid ov erload states by preload reduction, in most other cases, cardiac output falls, even at rela tively low PEEP levels. PEEP may also compro- mise a poorly functioning right ventricle. Im proved PaO2 resulting from decreased venous admixture may sometimes arise solely from reduc tions in cardiac output. Physiological PEEP A small degree of PEEP (2 \200\2233cmH2O) is usually provided physiologi cally by a closed larynx. It is lost when the patient is intubated or tracheostomised and b reathing spontaneously on a T-piece with no CPAP valve (see CPAP). Intrinsic PEEP (auto-PEEP, air trapping, PEEPi) Increased level of PEEP due to insuf \201 cient time for expiration, leading to \200\230air trapping \200\231, CO2 retention, increa sed airway pressures, and increased FRC. Seen in pathological conditions of increased air \202 ow resistance (e.g. asthma, emphysema) and when insuf \201 cient expiratory time is s et on the ventilator. Used clinically in inverse ratio ventilation to increase oxygenation and decrease peak airway pressures. However, high levels of PEEPi can slow weaning by an in creased work of breathing; use of extrinsic PEEP may overcome this. PEEPi can be measured b y temporarily occluding the expiratory outlet of ventilator at end-expiration for a few sec onds to allow equilibration of pressure between upper and lower airway, and then reading th e ventilator pressure gauge (or print-out). \200\230Best \200\231 PEEP Initially described as the level of PEEP producing the lowest s hunt value. Now generally considered to be the lowest level of PEEP that achieves SaO2 \211 90% allowing, wherever possible, lowering of FIO2 (ideally \211 0.6), though not at t he expense of peak airway pressures >35 \200\22340cmH2O or signi \201 cant reductions in D O2. POSITIVE END EXPIRATORY PRESSURE (1) 67 See also: IPPV \200\224description of ventilators, p46; IPPV \200\224modes of ventilation, p48; IPPV \200\224adjusting the ventilator, p50; IPPV \200\224complications of ventilation, p56; Positive end expiratory pressure (2), p68; Continuous positive airway pressure, p70; Lung recruitment, p72; Atelectasis and pulmonary collapse, p352. 68 CHAPTER 2 Respiratory therapy techniques Positive end expiratory pressure (2) Adjusting PEEP 1. 2. 3. 4. Measure blood gasses and monitor haemodynamic variables. If indicated, alter level of PEEP by 3 \200\2235cmH2O increments. Re-measure gasses and haemodynamic variables after 15 \200 \22320min. Consider further changes as necessary (including additional changes in PEEP, \202 uid challenge, or vasoactive drugs) A number of clinical trials have adjusted PEEP levels according to FIO2 requirements (see t able below). Although unlikely to constitute \200\230optimal PEEP \200\231 for an individu al patient, this provides a useful approximation and starting point for further titration o f therapy. FIO2 PEEP (cmH2O) 0.3 0.4 0.4 0.5 0.5 0.6 0.7 0.7 0.7 0.8 0.9 0.9 0.9 1.0 18 \211 18 5 5 8 8 10 10 10 12 14 14 14 16 Indications \200 \200 \200 \200 \200 \200 Hypoxaemia requiring high FIO2. Optimizing the pressure \200\223volume curve in severe resp iratory failure. Hypoxaemia secondary to left heart failure. Improvement of cardiac output in left heart failure. Reduced work of breathing while weaning patients with high PEEPi. Ne urogenic pulmonary oedema (i.e. non-cardiogenic pulmonary oedema following relief of upper airway obstruction).