0 \210\222 Controlled Mechanical Ventilation (CMV) Fig. 1.4.1 Pressure \200\223time plot of controlled mechanical ventilation (CMV). Assist volume control (other terms CMV assist, IPPV assist) This is similar to CMV but the patient is able to trigger ventilator breaths. All breaths are volume targeted. If the pati ent does not make any respiratory efforts the respira- tory rate remains at the set frequen cy and the mode is effectively identical to CMV. Any spontaneous effort will trigger a vent ilator breath of the pre-set tidal volume. If the + 0 \210\222 Assist Control Ventilation Fig. 1.4.2 Pressure \200\223time plot of assist volume control. 11 CHAPTER 1.4 IPPV \200\224modes of ventilation Spontaneous modes Continuous positive airways pressure (CPAP) This is the simplest mode of respiratory support for spon- taneously breathing patients where a constant pressure above atmospheric is maintained throughout inspiration and expiration. Airway pressure release ventilation is a variant of bilevel ventilation where the higher ai rway pressure is maintained for a relatively prolonged period (e.g. 10s) with brief epi- so des when the pressure falls to the lower value (0.5s). Spontaneous breathing is maintained throughout. It may be used in acute lung injury and ARDS where the high mean airway pressur e improves oxygenation, the transient fall in airway pressure assists CO2 clearance and the small tidal volumes ensure a lung protective mode of support. Pressure support (other terms assisted spontaneous breathing) This is a spontaneous mode wh ere the ventilator provides an inspiratory assist by increasing airway pressure to a set le vel following each patient effort. The pressure support equals the difference in pressure d uring inspiration and expiration (PEEP). In this mode there is no set rate and the ventilat or will only deliver inspiratory assistance in response to patient efforts. It may be combi ned with a back-up mandatory mode (apnoea ventilation) that will take over if the patient h as a prolonged period without any inspiratory effort (e.g. >15s). P Bi-level 20 Pressure support 40 cmH2O e r u s s e r P 15 10 Spontaneous breathing APRV 100 L/min 5 w o F Release pressure l 0 \210\222100 800 ml Fig. 1.4.5 Bilevel and assisted pressure release ventilation (APRV). Fig. 1.4.4 Pressure and \202 ow waveforms with pressure support. Automatic tube compensation (ATC) The resistance of the endotracheal or tracheostomy tube i ncreases the work of breathing that is re \202 ected by a pres- sure gradient across the t racheal tube. This pressure drop, which changes during the respiratory cycle in proportion to the gas \202 ow, can be estimated continuously by the ven- tilator. With automatic tub e compensation, the ventilator increases airway pressure during inspiration and reduces air way pressure during expiration to offset the estimated pressure gradient across the breathi ng tube. ATC effec- tively removes the imposed work of breathing from the ETT and can be us ed during spontaneous breathing trials to assess readiness for extubation. In pressure support, cycling is by \202 ow. The inspiratory \202 ow follows a decelerat ing pro \201 le that is monitored by the ven- tilator. In most ventilators, cycling to exp iration occurs when inspiratory \202 ow has fallen to 25% of the peak inspira- tory \202 ow. Some ventilators offer the facility to adjust the \202 ow at which cycling occur s (e.g. 10 \200\22390% of peak \202 ow). This may be useful for improving patient ventila tor syn- chrony when the duration of the inspiratory phase is either longer or shorter than desired by the patient. Bilevel ventilation (BIPAP, DuoPAP) This can be considered as a mode of ventilatory support where there is cycling between two different levels of CPAP at the set ventilator frequenc y. There is no synchro- nization with spontaneous respiratory efforts although the patient is able to breath without support at any time. An adaptation of this mode may offer pressur e support for spontaneous breaths during the lower pressure phase. If the patient makes no spontaneous efforts, bilevel ventila- tion functions in an identical manner to pressure con trol. Proposed advantages of bilevel ventilation are improved patient comfort, as spontaneo us breathing is allowed at any point of the respiratory cycle, and better gas exchange, as maintaining spontaneous breathing enhances ventilation \200\223 perfusion matching. Automated modes Some manufacturers offer modes that may automatically adjust certain ventil ator parameters that would normally be set by the operator. Modes that switch between con- trolled and spontaneous modes according to patient effort are available (e.g. adaptive supp ort ventilation, automode). A mode that automatically adjusts the level of pressure support (Smart care ) has been developed with the aim of weaning the patient as long as the patie nt does not have signs of respiratory distress. 12 P MACNAUGHTON IPPV \200\224adjusting the ventilator Initial settings Chose a mode of ventilation that is familiar and appropri- ate for the cli nical situation. This will usually be a control- led mode (e.g. volume or pressure control) as the patient will often have received sedative agents and muscle relax- ants to assist i ntubation. The following parameters are set: \202 ow patterns. Constant \202 ow ventilation is the most com- monly used, although de celerating \202 ows are increasingly available and have the advantage of reduced peak air way pressure and improved patient ventilator synchrony. Sinusoidal \202 ow mimics the nor mal \202 ow pattern during spontaneous breathing although it is unknown if it is associ- ated with any clinical bene \201 ts Inspired oxygen tension In an unstable patient, ventilatory support should be com- menced w ith an FiO2 of 1.0. This can then be adjusted according to arterial saturations recorded by pulse oxime- try and from blood gas analysis. A saturation >92% and a PaO2 >8kPa are appro priate targets in the majority of patients. To avoid oxygen toxicity, inspired oxygen tensi on should be adjusted to the lowest level that maintains these values. Tidal volume Regardless of mode used, the desirable tidal volume should be based on the pat ient \200\231s ideal body weight (IBW). This can be calculated from the patient \200\231s h eight using the following formulas: Males IBW = 50 + 0.91 (height in cm \200\223 152.4) Fe males IBW = 45.5 + 0.81 (height in cm \200\223 152.4) In normal lungs, a tidal volume of 8 \200\22310ml/kg is acceptable, while in patients with acute lung injury a lung protective strategy with a reduced tidal volume of 6 \200\2238ml/kg is appropriate. When using pressur e control modes, the inspiratory pressure is adjusted once ventilation is commenced to achi eve the desired tidal volume. Positive end-expiratory pressure The initial PEEP setting is 5cm H2O in the majority of pat ients. This maintains the \200\230physiological PEEP \200\231 that occurs in spontaneous b reathing due to exhalation through a partially closed glottis. Trigger There is no advantage to preventing the patient initiating spontaneous breaths, and the trigger should always be switched on unless the patient is sedated and receiving muscl e relaxants. The mode of triggering (pressure or \202 ow) and sensitivity may be adjustab le according to the ventilator used. The trigger sensitivity should be set to ensure that a ll spontaneous patient efforts are detected by the ventilator. Auto-triggering occurs if th e trigger is too sensitive when the ventilator delivers a breath in response to minor \202 uctuations in airway pressure caused by patient movement, airway manipulation, etc., a nd not from patient inspiratory effort. Careful patient observation allows appropriate trig ger setting. Respiratory rate An initial rate between 10 and 20 breaths/min is set to achieve the requir ed minute ventilation in order to main- tain pH within normal limits (7.35 \200\2237.45). A patient with underlying metabolic acidosis (e.g. septic shock or cardio- genic shock) will require a high respiratory rate to ensure respiratory compensation with a low PaCO2. The p atient with a metabolic alkalosis secondary to chronic CO2 reten- tion will maintain a norm al pH with a low rate and high PaCO2. As the underlying metabolic abnormality improves, the respiratory rate will need to be adjusted to ensure that pH remains within the normal rang e. Inspiratory phase In controlled modes of ventilation the duration of the inspiratory phase is pre-set. How this is achieved varies according to the individual ventilator and may be b y setting total inspiratory time, by selecting the inspiratory:expira- tory time ratio (I:E ) or from the inspiratory \202 ow rate (volume control modes). Appropriate initial settin gs are: \200 \200 \200 Alarms The alarm parameters vary according to the individual ventilator. Usually there will be alarms to monitor the following: \200 \200 \200 \200 Exhaled tidal volume Minute ventilation (high and low) Airway pressure (high and low) Respi ratory rate (high and low) Inspiratory time 1.0 \200\2231.5s I:E ratio 1:2 \200\2231:3 Inspiratory \202 ow rate 30 \200\22360l/min An appropriate alarm setting for each parameter is when the measured value deviates by 25% from the desired setting. Patient disconnection will activate a number of alarms including low pressure, low tidal volume, low minute ventilation or low rate (or apnoea). The high pr essure alarm limit is usually set to activate at between 30 and 40cm H2O. If set too close to the peak airway pressure, it will activate frequently, which could result in an inadequa te minute ventilation as the ventilator will cycle to expiration as soon as the alarm is tr iggered. If using a ventilator where the I:E ratio is directly set, this may need to be adjusted fol lowing changes to the respira- tory rate in order to ensure an inspiratory time >1s. Inspir atory times if <1s may not allow adequate time for ventilation of lung units with long time constants, resulting in impaired gas exchange. In volume modes, inspiration is divided int o an active inspiratory phase and the end-inspiratory pause. Setting an inspiratory pause d uring volume-controlled modes allows the plateau (end-inspiratory pause) pressure to be mea sured. An inspiratory pause may improve gas exchange. Commencing ventilation The ventilator should be checked before connecting to the patient. M any ventilators include an automatic pre-use test that occurs whenever first switched on. T ypically this includes a circuit check (leak and compliance) and sensor (pressure, \202 o w and oxygen) calibration. Once the initial Inspiratory waveform Some ventilators allow the pro \201 le of the inspiratory \202 ow w aveform to be changed in volume-controlled modes. Options may include constant, deceleratin g and sinusoidal 13 CHAPTER 1.5 IPPV \200\224adjusting the ventilator High airway pressures When the high airway pressure alarm is activated, the ventilator imme diately cycles to expiration that will reduce the inspired tidal volume and rapidly results in the patient receiving inadequate ventilation. Causes of high airway pressures include: \200 Low lung compliance (e.g. ARDS) \200 Hyperin \202 ation gas trapping \200 exces sive tidal volumes \200 Low chest wall compliance \200 \200 \200 Increased airway r esistance \200 \200 \200 Patient \200\230 \201 ghting the ventilator \200\231 agita tion, coughing, straining \200 settings have been set, the ventilator can be connected to the patient. Clinical assessment after commencing venti- latory support should include: \200 \200 \200 \200 Adequacy and symmetry of chest wall movement, Synchronization of the ventilator with the pa tient \200\231s efforts Vital signs including heart rate and blood pressure Gas exchange (p ulse oximetry, capnography and arterial blood gasses) The expired tidal volume displayed by the ventilator should be checked and should be simila r to the set tidal volume. Airway pressures should be monitored with the aim of keeping ins piratory plateau pressure as low as possible and certainly <30cm H2O in the majority of pat ients. morbid obesity intra-abdominal distension chest wall rigidity (e.g. secondary to high dose opiates) Hypoxaemia Only two parameters directly in \202 uence arterial oxygen tension, the inspire d oxygen concentration and the mean airway pressure. Mean airway pressure can be adjusted b y prolonging the inspiratory time (adding an inspiratory pause) or by apply- ing PEEP. Incr easing mean airway pressure may increase haemodynamic instability as it may reduce venous r eturn. Increasing PEEP will increase peak airway pressures and increase the risk of barotra uma. Increasing inspiratory time may result in gas trapping due to the reduction in expira- tory time. Prolonged exposure of normal lungs to high inspired oxygen concentrations is da maging and, although it is unknown whether oxygen has the same effect on abnormal lungs, it would seem prudent to minimize the inspired oxygen concentration. A PaO2 of >8 kPa (SaO2 > 92%) is a satisfactory target in the majority of patients and is achieved by a combination of selecting an appropri- ate FiO2 and level of PEEP. When assessing a patient with hypoxae mia during mech- anical ventilation, reversible causes should always be considered such as endobronchial intubation, atelectasis secondary to sputum plugs, and pulmonary oedema. bronchospasm airway obstruction (secretions) airway occlusion due to compression/kinking Reversible causes of high airway pressures should be treated if possible (e.g. removal of s ecretions, administration of bronchodilator). Patient ventilator asynchrony This describes poor synchronization between the patient \200\231s inspiratory efforts and inspiration appl ied by the ventilator. It is common and has a number of adverse effects including increased work of breathing, impaired gas exchange, increased requirement for sedation and prolonged wean- ing from mechanical ventilation. When severe, it presents as the patient \200\230 \201 ghting the venti- lator \200\231 with failure to settle, frequent coughing, straining and agitation. It is more common when \201 rst commencing a patient on ventilatory suppor t and results in poor gas exchange as minute ventilation is not maintained due to frequent activation of the high pressure alarm. A number of factors may contribute to asynchroncy: V entilator factors \200 \200 \200 \200 \200 Hypercapnia The CO2 tension is in \202 uenced by minute ventilation, dead space and CO2 pr oduction. Minute ventilation is adjusted by changing the tidal volume and/or respiratory ra te in order to maintain pH within the normal range (7.35 \200\2237.45). If this cannot be a chieved without exposing the patient to excessive tidal volumes (>6 \200\22310ml/kg dependi ng on under- lying lung diagnosis) or high airway pressures (plateau pres- sure >30cm H2O), it is invariably safer to limit tidal volumes and accept the associated respiratory acidos is. This permissive hypercapnia is well tolerated unless the patient has raised intracrania l pressure (e.g. head injury) and is associated with an improved outcome in acute lung inju ry and acute severe asthma. An increase in dead space will raise PaCO2. Reversible causes o f increased pulmonary dead space include low cardiac output, hypovolaemia and high intratho racic pres- sures (secondary to externally applied PEEP or intrinsic PEEP from gas trapping ). Equipment dead space may be minimized by removing the catheter mount and using a water b ath humidi \201 er rather than an HME. Reducing CO2 production with therapeutic hypothermi a combined with deep sedation and muscle relaxation may be of value in managing severe resp iratory acidosis in the dif \201 cult to ventilate patient (e.g. severe asthma). Inadequate trigger sensitivty (missed breaths) Autotriggering Inspiratory \202 ow wavefor m (e.g. constant \202 ow) Inspiratory \202 ow rate does not match patient effort Rise t ime setting (time to reach maximum inspiratory pressure) Patient factors \200 \200 \200 \200 Lung pathology (e.g. high resistance and compliance AutoPEEP (impairs ability to trigger) H igh inspiratory effort/drive (e.g. metabolic acidosis) Sedation level, inadequate pain cont rol Asynchrony may occur at different times in the respiratory cycle: \200 \200 \200 Triggering of inspiration During active inspiratory \202 ow Termination of inspiratory \202 ow Treatment of patient \200\223ventilator asynchrony requires rec- ognition and correction of the underlying cause(s) with optimal setting of the ventilator. However, increasing the le vels of sedation and the administration of a non-depolarizing muscle relaxant is often requ ired. 14 J COCKINGS & G YAP IPPV \200\224barotrauma Introduction Mechanical ventilation, particularly in the setting of acute lung injury, alth ough life-saving, has been shown also to cause signi \201 cant lung injury. Only in recent times has the signi \201 cance of ventilator-induced lung injury (VILI) been more widely acknowledged. The incidence of barotrauma complicating the management of ARDS; recent \201 gures include 6.5% by Anzueto et al., 11% in the ARDS network, and 13% by Brochard et al. These contrast with \201 gures of between 40 and 60% 10 \200\22315yrs ago. Gross baro trauma manifesting as pneumothorax is the most frequently and easily recognized complicatio n of mechanical ventilation. Barotrauma is, however, only one manifestation of VILI. Other types of injury are described: Volutrauma \200\224direct injury to the alveoli from overdis ten- sion of the lung. Atelectrauma \200\224shearing injury to the alveoli resulting from r epetitive collapse and opening of distal airways or alveoli. Biotrauma \200\224injury to th e lung (and distant organs) result- ing from the release of in \202 ammatory mediators int o the airspaces and systemic circulation. The increased intrathoracic pressures from mechanical ventilation affect venous drainage fr om other sites, with reduction in venous return and increased venous pressures from the bra in and abdomen. Biotrauma in the lung increases leukocytes, tumor necrosis factor, interleu kin-6 (IL-6) and IL-8. These are the same cytokines implicated in the systemic in \202 amm atory response syndrome and in sepsis. Imaging studies A high clinical index of suspicion with radiological con \201 r- mation is often required for diagnosis in an asymptomatic patient. Chest radiographs Radiological \201 ndings in PIE include: \200 \200 \200 \200 \200 \200 \200 Parenchymal cysts Lucent lines directed towards the hilum Subpleural air cysts Presence of gas around large vessels Pneumatoceoles Pneumomediastinum outling the great vessels Pneumop ericardium outlining the pericardium and con- tiguous diaphragm Pathophysiology A mechanism for the development of extra-alveolar air has been described wh ereby an initial site of disruption occurs in the base of the perivascular alveoli. The ris k of such a disruption is consequent to the pressure gradient between the alveolus and the vascular sheath. Air in the vascular sheath, which was termed pulmonary interstitial emphy- sema (PIE), is the \201 rst manifestation of barotrauma. In the mediastinum, air can tra ck along the tissue planes creating a pneumomediastinum, or the increased pressure can rupt ure through the mediastinal pleura to produce a pneumothorax. Pneumothoraces especially small ones may be dif \201 cult to diagnose on portable chest ra diographs. CT scanning Computed tomography (CT) scanning is rarely indicated to establish the diagnosi s of barotraumas but it may be helpful in determining the size of a pneumothorax and is oft en an incidental \201 nding when imaging for other indica- tions. It is also easier to ap preciate pneumothoraces that are primarily anterior or basilar than on a two-dimensional ch est radiograph. CT scans may be useful in guiding the placement of thoracostomy tube(s) in loculated pneumot- horaces or where draining more than one tube is required. Clinical History Often mechanically ventilated patients are unable to communicate, but the history can often be gleaned from their medical records or from other staff. Those at highe st risk of barotraumas from mechanical ventilation are those with acute lung injury (ALI) o r ARDS. Co-existing lung pathology such as interstitial lung disease, COPD, Pneumocystis ca rinii pneumonia (PCP) or blunt thoracic injuries increases the risk. Protective mechanical ventilation Protective mechanical ventilation is the practice of adju st- ing ventilator parameters to minimize lung injury. There is no agreed single approach t o protective ventilation, yet most authorities now share the basic principles of low tidal volumes and permissive hypercapnea as long as arterial pH remains in an acceptable range. PEEP The pressure \200\223volume curve of the lung has both upper and lower in \202 ection points. The upper in \202 ection point is the pressure at which the lung volume ceases to increase sharply with rising airway pressure. The lower in \202 ection point is the press ure at which the lung volume begins to decline sharply with falling airway pressure. Lung i njury might be avoided by ventilating the lung at a PEEP above the lower in \202 ection po int to prevent atelectrauma while restricting tidal volumes so that the end-inspiratory pre s- sure does not exceed the upper in \202 ection point. Eisner et al. in the ARDSNetwork t rial showed that by decreasing tidal volume from 12 to 6ml/kg the mortality rate fell from 40 to 30% in ARDS patients. An important component of this trial was the selection of PEEP and FiO2 parameters. Thoracic The manifestations of barotrauma span from the asympto- matic to cardiac arrest fr om an unrecognized tension pneumothorax. The severity depends on the degree of extra-alveol ar air present. Signs of respiratory distress, e.g. ventilator \200\223patient dys-synchron y, use of accessory muscles, etc., may be the earliest clinical manifestation in the patien t unable to communicate. The earliest clinical signs of a pneumothorax may be decreased bre ath sounds and hyper-resonance on percussion. These signs are often less apparent in the me chanically ventilated compared with the conscious self-ventilating patient. Extrathoracic A systemic gas embolus is the most dramatic extrathoracic manifestation of ba rotrauma. These may cause cerebral air emboli, myocardial infarction and livido reticularis . 15 CHAPTER 1.6 IPPV \200\224barotrauma Further reading Amato MBP, Barbas CS, Medeiros DM, et al. Bene \201 cial effects of the op en lung approach with low distending pressure in acute respiratory distress syndrome; a pro spective randomized study on mechanical ventilation. Am J Respir Crit Care Med 1995; 23: 1 \200\22315. Plateau pressure This provides the best approximation of transalveolar pressure. Amato et a l. have shown that failure to limit pla- teau pressures is associated with a high incidence of baro- traumas and an increased mortality. It is widely agreed that plateau pressures >3 5mm H2O leads to increase incidence of barotraumas. Amato MBP, Barbas CSV, Medeiros D, et al. Improved survival in ARDS: bene \201 cial effect s of a lung protective strategy. Am J Respir Crit Care Med 1996; 153 suppl: A531. Surgical treatment Only rarely is surgical repair of the lung required for the treatment of barotrauma. However, the effective manage- ment of pneumothorax requires evacuation of ple ural air and placement of a pleural drain to permit the gas to escape. The urgency and type of tube placement depends on the patient \200\231s clinical status. In most instances, lea ks asso- ciated with ventilator-induced barotrauma are small, and tension pnuemothoraces de velop slowly. Anzueto A, Frutos-Vivar F, Esteban A. et al. Incidence, risk factors and outcome of barotra umas in mechanically ventilated patients. Intensive Care Med 2004; 30: 612 \200\2239. Brochard L, Roudot-Thoraval F, Roupie E, et al. Tidal volume reduc- tion for the prevention of ventilator-induced lung injury in acute respiratory distress syndrome. Am J Respir Crit Care Med 1998; 158: 1831 \200\2238. Eisner MD, Thompson BT, Schoenfeld D, et al.; Acute Respiratory Distress Syndrome Network. Airway pressures and early baro- trauma in patients with acute lung injury and acute respir atory distress syndrome. Am J Respir Crit Care Med 2002; 165: 978 \200\22382. Tube thoracostomy Many commercial kits are available using a Seldinger tech- nique as an al ternative to the traditional intercostal drain insertion using blunt dissection. Fuhrman BP. Avoidance of ventilator induced lung injury. Acta Pharmacol Sin 2002; Suppl 23: 44 \200\2237. Gammon RB, Shin MS, Buchalter SE. Pulmonary barotraumas in mechanical ventilation. Patterns and risk factors. Chest 1992; 102: 568 \200\22372. Emergency needle thoracostomy This is indicated for patients with a tension pneumothorax an d cardiovascular compromise requiring immediate decompression. In mechanically ventilated p atients, the ventilator should be removed and replaced with a bag valve device connected to oxygen. In this way the clinician can assess the lung compliance and eliminate the deleter i- ous effect of PEEP on the cardiovascular system. Following emergency needle decompressio n, a thoracostomy tube placement is required. Gropper MA. New approaches to mechanical ventilatory support. 56th Annual Refresher Course Lectures and Basic Science Reviews. Presented in October 2005 during the Meeting of the Ame rican Society of Anaesthesiologist. Hoo GWS. Emedicine.com/topic209.htm Ricard J-D. Editori al. Intensive Care Med 2004; 30: 533 \200\2235. 16 C DAVIDSON IPPV \200\224weaning techniques The weaning process The progressive reduction in the degree of ventilatory sup- port that l eads to the re-establishment of spontaneous breathing (SB) is conventionally termed weaning . Liberation might be a better descriptive as we now better appreciate the potential risks of invasive mechanical ventilation (IPPV) such as ventilator-induced lung injury (VILI) and ventilator- associated pneumonia (VAP). The start of weaning coin- cides with clinical sta bility and the beginnings of recovery from the critical illness that precipitated ICU admis sion. When weaning is prolonged, it extends into the period of general rehabilitation, e.g. sitting out of bed or even ambu- latory mechanical ventilation. Weaning is unnecessary whe n mechanical ventilation is employed, for instance, to manage major elective surgery. In su ch circumstances, con- trolled ventilation may be employed to allow for the initial recover y from surgery and is followed by cessation of sedation, establishment on low level pressur e support and rapid extubation. Weaning occupies >40% of ICU stay and therefore is of major economic importance. Weaning delay is associated with a high mortality, 51% in one large U S report, and is not uncommon. Patient case mix determines how common but, in one large UK report, weaning delay (>3 days but <2 weeks) occurred in 8% of all ICU patients, and in a f urther 7% weaning failed as de \201 ned by the requirement of >6h per day ventilatory assi stance >3 weeks after treat- ment of the initiating illness. Skeletal myopathy is almost un iversal in critical illness, and involvement of the respiratory muscles is a major factor i n weaning delay. The role of disuse atrophy vs diaphragmatic dysfunction is uncertain. The link between paralytic agents, steroids and critical illness neuropathy/myopathy (CINM) may be more an indicator of severity of illness rather than purely a causative factor. The bal ance between reduced respiratory pump function and an increased ventilatory load, arising a s a result of air \202 ow obstruction and reduced lung, chest and abdominal wall complianc e, will determine whether weaning can successfully proceed or whether improvement is requir ed before progress can be made. Trails of SIMV with pressure support of SB (and a gradual reduction in the number of mandat ory breaths and in degree of pressure support) vs either progressive reduc- tion in pressur e support or intermittent CPAP/T-tube SB trials (SBTs) have demonstrated that SIMV is a poo r wean- ing strategy. The relative merits between progressive pres- sure support reduction and intermittent SBTs have not yet been established. The value of periods of unsupported ve ntilation is to detect when patients can wean faster than their carers believe possible! Non-ventilatory aspects of weaning Optimal \202 uid balance, treatment of heart failure, ensuring adequate nutrition and avoiding, or treating, nosocomial infection are all importa nt. Psychological and rehabilitation aspects are equally so. For instance, improving commun ica- tion, with a speaking valve in the ventilator tubing, manag- ing anxiety and delirium, and re-establishing the sleep/wake cycle are crucial steps in rehabilitation. Feelings of depend- ency and fear may need to be addressed. Weaning centers Economic pressure has led to the development of special- ist weaning center s in the USA. The bene \201 ts may be more than simply economic. IPPV/assessment of weaning Weaning stages The initial step in weaning is the decision to al low/encour- age supported SB. This coincides with evidence of a response to treatment such as a reduction in inotrope requirement or FiO2. Suggested pre-requisites for stage 1 \200 Respiratory variables: \200 \200 \200 Cardiovascular variables: \200 Heart rate \211 120bpm \200 Mean arterial blood pressure stable (with or without inotropes) FiO2 <0.5 PEEP \211 10cm H2O pH >7.3 or PaCO2 <6.5kPa Causes of weaning delay/failure \200 Unresolved primary illness \200 Pre-morbid (neurom uscular disease or severe COPD) \200 Sepsis \200 Weak muscles ineffective cough (bul bar disease or depressed respiratory drive, CINM, malnutrition) CNS (brain injury, sedation , anxiety depression) Physician related (failure to recognize imbalance between pump and lo ad, ventilator \200\223patient dys-synchrony). Neurological variables: \200 Adequate analgesia \200 Awake and cooperative Nutrition: \200 \200 Potassium and phosphate levels normalized No severe abdominal distension \200 VILI remains a consideration. Pressure support should be titrated to limit the tidal volume to between 6 and 8ml/kg whilst monitoring for signs of fatigue as indicated by a rising re spiratory rate, blood pressure or heart rate, or the development of agitation or a change i n conscious level. Stage 2 is characterized by a period during which pressure support and P EEP are reduced. This may be a continual and progressive process or be associated with setb acks when more support will be required, e.g. a septic episode. Initially controlled ventil atory modes may be better at night to ensure that the gains by day are not compromised by i nad- equate support during sleep. Weaning techniques Two contrasting philosophies lie behind the strategies that can be adopt ed. When the load/capacity ratio is unfavour- able, a slowly progressive reduction in press ure support is appropriate. If disuse atrophy and diaphragm retraining is required, intermi ttent T-tube SB or CPAP trials might be a better strategy. Direct measurements of diaphragm strength and ventilatory load are, however, technically demanding and have not yet been sh own to in \202 uence outcome. What evidence is there for choosing the right strategy? 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.