Investigation These will depend on the mode and severity of presentation. The respiratory t eam will be involved both with patients at risk of developing ARDS (e.g. those with pneumon ia) also with management and investigation of patients on ITU with the condition. \200 Ra diology: CXR and CT to exclude other diagnoses. \200 Physiology: blood gasses will establ ish severity of respira- tory failure. Bronchoscopy and BAL, will be useful both diagnostically (especially in the immunocom promi sed) and therapeuti- cally to remove mucus plugs. Risk factors \200 Direct injury: pneumonia, aspiration, pulmonary contu- sion, fat emboli, near-drowning, inhalational injury. Indirect injury: sepsis, trauma, cardiopulmonary by pass, drug overdose, acute pancreatitis , massive blood transfusion. AUTHOR \200\231S TIP Sepsis is the factor most associated with development of ARDS (40% of cases) and the presence of multiple pre- disposing factors substantially increases the risk . CHAPTER 17.4 Acute respiratory distress syndrome 431 Mechanical ventilation is discussed in detail in Chapter 17.6. Low tidal volumes have been shown to be protec- tive but can result in reduced carbon dioxide clearance. Permissive hyp ercapnia is acceptable as long as oxy- genation is not compromised and the pH is maintained above 7.2. The use of positive end expiratory pressure (PEEP) and prone ventilation are ot her techniques which may be helpful. Corticosteroids: these drugs remain controversial and no clear cut advantage has been shown by Cochrane review. \200 Inhaled nitric oxide: an improvement in oxygenation occurs in 6 0% of patients but the effect is transient (48 hours) and does not improve mortality. Nebulised prostacyclin: this is another vasodilator with similar physiological effects to n itric oxide. When nebu- lised, it has an equivalent effect on pulmonary vasodi- lation and oxygenation but is easier to administer, and requires no special monitoring. Outcome \200 Most studies until recently have reported a mortality rate of 40 \200\22360%. Death occurs mainly due to sepsis or multiorgan dys- function and not respiratory failure. The therapeutic success of low tidal volume ventilation in the ARDS Network Trial indicates some deaths are directly related to lung injury. Some data suggest mortality is falling. Possible reasons for this include improved treatmen t of sepsis, better ventilation strategies and improved supportive care. \200 Pulmonary f unction in most survivors returns to normal Fig. 17.4.1 A typical CXR of ARDS showing widespread diffuse alveolar shadowing. or near-normal levels by 6 months. Mild restriction, reduced, bronchial hyper-reactivity and air trapping can persist. AUTHOR \200\231S TIP ARDS survivors may have a persistent extrapulmonary functional disabil ity 12 months after discharge mainly due to muscle wasting and weakness with minimal lung f unction changes. Further reading Bernard GR, Artigas A, Brigham KL, et al. The American-European consensus c onference on ARDS. De \201 nitions, mechanisms, rele- vant outcomes, and clinical trial co ordination. Am J Respir Crit Care Med 1994; 149: 818 \200\223824. Fig. 17.4.2 A CT scan showing widespread ground glass showing with areas of consolidation a nd some areas of more normal appearance. Gattinoni L, Caironi P, Cressoni M, et al. Lung recruitment in patients with the acute resp iratory distress syndrome. N Engl J Med 2006; 354: 1775 \200\2231786. Treatment Treatment is essentially supportive ventilation with aggres- sive management of t he precipitating condition. Nutritional support and tight glycaemic control are essential C omplica- tions include the exacerbation of lung injury, multiple organ system failure, noso comial pneumonia, deep vein thrombosis, and gastrointestinal bleeding must be minimized. Peter JV, John P, Graham PL, et al. Corticosteroids in the prevention and treatment of acut e respiratory distress syndrome (ARDS) in adults: meta-analysis. BMJ 2008; 336: 1006 \200 \2231009. Useful Website: NHLBI Acute Respiratory Distress Syndrome network for trial details and results. www.ardsnet.org S POUTANEN 432 17.5 Severe acute respiratory syndrome Epidemiology \200 SARS was \201 rst recognized i n Guangdong Province, Chi- na in November 2002 and spread to 26 countries over the subseque nt 9 months. Clinical course Clinical presentation \200 Clinical presentation ranges from asymptomatic disease to mild respiratory symptoms to the severe acute respira- tory syndrome after whic h the virus was named. 8098 infected people and 774 deaths were reported to the World Health Organization before t he outbreak was declared over in July 2003. Typical SARS presents with fever, chills, malaise, head- ache, and myalgia; non-productive cough, dyspnoea, and sometimes watery diarrhea seen 3 to 5 days later. \200 If infants an d children acquire the infection (rare), they Four isolated cases of SARS with no associated trans- mission were identi \201 ed in China in December 2003 and January 2004. Two isolated cases and a cluster of 11 cases (one death ) were identi \201 ed in South-East Asia related to breaches in biosafety practices in lab oratories culturing SARS-CoV. follow a milder course frequently with rhinorrhea. Routine laboratory investigations \200 Normal total white blood cell count, lymphopenia, increased lactate dehydrogenase and creatinine kinase levels are typical. Whether or not a large-scale re-emergence of SARS will occur is debatable. Laboratory abnormalities progress and peak at/just after Etiology \200 SARS Coronavirus (SARS-CoV) was identi \201 ed in 2003. \200 SARS-CoV li kely evolved from animal SARS-like CoV (found most frequently in Himalayan civet cats and b ats in China). the second week of disease. Chest radiography \200 75% of patients have uni- or bilateral in \201 ltrates on CXR at the time of presentation. If CXR clear, ground glass opacities often detectable on SARS-CoV, like other coronaviruses, is an enveloped non-segmented, single-stranded, positiv e sense, RNA virus. HRCT or will progress to develop CXR in \201 ltrates. Typically see air-space opacities with ill-de \201 ned margins in a predominant peripheral location progressing from unilateral focal involvement to unilateral or bilateral multifoc al involvement. Incubation period \200 Based on the 2003 outbreak, the typical incubation period for SARS is 2 to 10 days (mean of 4 to 6 days). A small proportion of cases may have incubation per iods as short as 1 day and as long as 14 days. CXR opacities peak between 8 and 10 days after illness onset and then improve. Progressive radiographic deterioration may occur asso- ciated with a more protracted clinical course. SARS is not communicable prior to symptom onset but transmission may occur soon after. Risk of transmission increases as symptoms progress, peaking during the second week of illness corresponding to peak viral load. Most countries considered patients to be potentially infe ctious and kept them in isolation precautions un- til 10 days after resolution of fever and signs of clinical improvement. There was no evidence of transmission from anyone treated i n this manner, and it is possible that isolation for a shorter period of time may be suf \201 cient. Cavitation, lymphadenopathy, and pleural effusions are not typically seen. Pneumothoraces h ave been found in critically ill patients receiving mechanical ventilation. Prognosis \200 20% of patients develop worsening respiratory distress requiring intensive care. Approximately 10% of patients die from progressive respiratory distress or complications of their hospital admission, typically during the third or fourth week of symptomatic illness . Increased risk of death with age (50% mortality if >60 years), co-morbidity, elevated lacta te dehydrogenase, elevated CRP, and elevated neutrophil counts. Modes of transmission \200 SARS-CoV has been found in respiratory specimens, stool, and t o a lesser extent, blood, urine, and conjunc- tival secretions antemortem. At autopsy, SARS -CoV has been found in lung, gastrointestinal and lymphopoetic tissue and to a lesser exten t heart and kidney tissues. \200 Transmission primarily occurs by nasal mucosa or con- ju nctiva exposure to respiratory droplets either directly from an infected person or indirect ly through inocula- tion with contaminated hands. It is possible that airborne transmission or transmission via contaminated fomites may also with SARS, but infrequently, if at all. Complications \200 In women infected during pregnancy who survive, high incidences of spo ntaneous miscarriage, preterm deliv- ery, and intrauterine growth restriction have been see n. \200 At 3 months post symptom onset, most survivors have normal lung function but musc le weakness fatigue may account for residual disability. Pathogenesis \200 SARS-CoV most likely enters the human body via the respiratory tract mu cosa, leading to viraemia and then replication in the lung and gastrointestinal tract. Fecal-oral or fecal-droplet transmission has also been postulated but plays only a minor role if any. Given that SARS-CoV has been found in multiple organs and body substances, transmission thr ough blood and organ transplantation is possible but there is no evi- dence of such transmi ssion to date. \200 No evidence of vertical transmission. \200 In the 2003 outbreak, tr ansmission was mostly limited to Viral replication is maximal during the second week of symptoms, correlating with worsening of symptoms and increased ef \201 ciency of transmission to others. Paradoxically, despite a fall in SARS-CoV viral load and a rise in SARS-speci \201 c antib odies during the third week of illness, clinical deterioration may occur in some. Immune dy sregulation may play a role in these situations. households, hospitals/immediate pre-hospital care. CHAPTER 17.5 Severe acute respiratory syndrome 433 Diagnosis The diagnosis of SARS relies on the combination of: \200 identifying epidemiolo gic and clinical features consistent Treatment \200 During the 2003 outbreak, ribavirin, steroids, type 1 interferons, convale scent plasma, and lopinavir/ritonavir were used in varying doses and combinations to treat patients with SARS. with SARS; ruling out infections other than SARS; \200 laboratory con \201 rmation of SARS-CoV infe ction. SARS-CoV laboratory tests \200 Available tests include reverse-transcription PCR ( RT- PCR), enzyme immunoassays (EIAs), and viral culture for the detection of SARS-CoV. Sero logical tests includ- ing immuno \202 uorescent assays, EIAs, immunoblots, and neutralizat ion assays for the detection of IgM and IgG directed against SARS-CoV. All of these agents have varying reports of associated anecdotal clinical improvement and s ome have been supported by studies using in-vitro assays and animal models. Some, such as r ibavirin, were associated with signi \201 cant toxicity. No de \201 nitive conclusions re garding the ef \201 cacy of any of these treatments can be made. \200 Currently, of all of the agents studied that are already approved for clinical use, type 1 interferons, stero ids, and lopinavir/ritonavir appear to be the most promising. RT-PCR is the mainstay of laboratory diagnosis at the time of patient presentation. Highest percent RT-PCR positivity seen in upper and lower respiratory samples (such as nasopharyng eal swabs/aspirates and sputum), stool samples, and serum or plasma. Prevention \200 One of the keys to prevention is the early identi \201 ca- tion of cases of SARS through surveillance i.e. screening of patients who have compatible clinical featu res in the context of potential SARS \200\223CoV exposure followed by appropriate laborator y testing. Epidemiologic risks to consider include: 1) exposure to settings where SARS acti vity is suspected or documented; and/or 2) being a laboratory worker in a laboratory that c ontains live SARS-CoV. During the \201 rst 5 days of symptoms RT-PCR yield from serum or plasma 80%, whereas th e yield from respi- ratory and stool specimens is considerably lower. Days 10 \200\22314, y ield from respiratory and stool specimens increases to 80 to 90%. Serologic tests are useful for the retrospective diagnosis of SARS in the weeks following i llness. Seroconversion (IgM and IgG) usually 1 to 4 weeks after symptom onset, occasionally later at weeks 7 and 8. Droplet, contact, and respiratory precautions should be used when caring for patients with SARS in order to prevent transmission to health care providers (gown, gloves, eye protectio n, in addition to an N95 respirator and private negative pressure room) Laboratory con \201 rmation of SARS-CoV infection Laboratory con \201 rmation of SARS-CoV infection is based on one or more of the following diagnostic criteria: (a) Detection of S ARS-CoV by a validated RT-PCR method Attempts should be made to: minimize the time spent by healthcare workers and visitors in t he room and spe- ci \201 cally minimize the time spent in close contact with the patient; keep to the side of the patient out of direct droplet range; assign the most experienced pe rsonnel to perform procedures on the patient; and avoid transportation- ing SARS patients w here possible. from: Two or more clinical specimens from different sources or Two or more clinical specimens collected from the same source at different time periods or Public health authorities should immediately be noti \201 ed of any suspected or con \201 rmed case of SARS in order to search for and isolate symptomatic contacts and quar- antine asymptomatic contacts for the 10 day incubation period following exposure. Two different RT-PCR assays or repeat RT-PCR using a new RNA extract from the original clin ical sample on each occasion of testing (b) Detection of SARS-CoV antibodies in any of the following ways using a validated test: Many candidate SARS vaccines have been proposed but Negative SARS-CoV antibody test result on acute phase serum and positive SARS-CoV antibody test results on convalescent phase serum tested in parallel or none are currently available for clinical use. Further reading Kamps BS, Hoffman C (eds.). SARS Reference. www.sarsrefer- A fourfold or greater rise in antibody titre between acute and convalescent phase sera test ed in parallel (c) Isolation in cell culture of SARS-COV from a clinical specimen in a refe rence laboratory, with con \201 rmation using a validated method such as RT-PCR. ence.com/index.htm. Accessed April 2008. Poutanen SM, Low DE. SARS. In Torres A, Ewig S, Mandell L, et al. (eds.) Respiratory Infect ions, pp. 515 \200\22334. Hodder Arnold: London. World Health Organization. Severe acute re spiratory syndrome. www.who.int/csr/sars/en/. Accessed April 2008. AUTHOR \200\231S TIPS \200 A single test result is insuf \201 cient for the de \201 nit ive diagnosis of SARS-CoV infection because both false- negative and false-positive results are known to occur. \200 Testing for SARS-CoV in the 2003 outbreak period needs to be do ne with caution given the potential for false-positives and the associated major public hea lth and economic implications. T PALFREYMAN & T EVANS 434 17.6 The ventilated patient Intensive care units (ICUs) were \201 rst developed in the 1950s to provide acute respira tory support for the victims of polio epidemics in Europe and North America. Ventila- tory management remains a core competency for the intensivist today and continues to present sig ni \201 cant chal- lenges. This chapter outlines the principles underpinning the care of t he intubated, ventilated patient. exhausted and cerebrally obtunded they will need intuba- tion and conventional ventilatory support. If in doubt, it is usually safer to intubate a patient with severe hypoxaemia, (e. g. with a PaO2 <8kPa, receiving an FiO2 of 0.6 or above). This permits greater control of t he patient \200\231s physiology and avoids the risk of respiratory arrest. Hypercapnic (type II) respiratory failure The most common cause of type II respiratory fail ure in the ICU is exhaustion due to increased work of breathing. This usually occurs in pat ients who have already developed type I respiratory failure, or in those with severe metabo lic acidosis (e.g. septic shock) who attempt to compensate through hyperventilation. In suc h cases, a rising arterial car- bon dioxide tension (PaCO2) may be a sign of impending resp iratory arrest, even if the level remains within normal limits, and invasive ventilation sh ould be considered immediately. Other causes of type II failure include acute on chronic re spiratory failure, acute neuromuscular diseases (Guillain \200\223Barr syndrome, myasthen ia gravis, botulism), chest wall or diaphragmatic trauma, drug overdose, post-operative pai n, opiate analgesia, intracranial pathology, and partial airway obstruction. Once again, th e decision to intubate depends on assessment of the patient as a whole, including the sever ity of respiratory acidosis, the ability of the patient to protect their airway, and the re versibility of the pathology, as well as physiological parameters such as PaCO2 and FVC. Re duction of oxygen demand Invasive ventilation is indicated in the initial resuscitation of some patients (e.g. those with severe sepsis) in order to reduce tissue oxygen requirements , even in the absence of respiratory failure or other absolute indications for ventilation. Epidemiology A recent, large international study found that 33% of patients admitted to an ICU required mechanical ventila- tion for at least 12 hours: \200 Indications for ventila tion included acute respiratory failure (ARF) (69%), coma (16%), and respiratory failure on a background of chronic lung (13%) or neuro-muscular (2%) diseases. Duration of ventilation was for a median of 5 days, but 1% of patients required support for more than 28 days. \200 Overall mortality was 31% (ICU) and 39% (hospital). ICU mortalit y was associated with age, severity of illness, prior functional impairment, severe hypoxae mia, dif \201 cult ventilation, and speci \201 c clinical conditions (coma, sepsis, ARDS) . Those who developed ARDS, coagulopathy or metabolic acidosis while ventilated, or who dev eloped a second organ failure, were at greatest risk (mortality 60 \200\22370%). Ventilated patients usually die from multiple or- gan failure rather than from hypoxaemia. A study of over 20,000 medical ICU patients in the USA found that units treating over 400 v entilated patients per year had a lower hospital mortality (25.5%) compared with those trea ting less than 150 ventilated patients per year (34.2%). Patients with an acute exacerbation of COPD who received mechanical ventilation suffered mo rtality of 22% (ICU) and 28% (hospital), which is lower than for ventilated patients in gen eral. The duration of ventila- tory support (median 6 days), and ICU (8 days) and hospital (17 days) length of stay were similar to those for ventilated patients as a whole. These re sults prob- ably indicate that more patients with COPD should be offered mechanical ventila tion, but a dif \201 cult decision remains to be made for each individual patient. Post-operative management Ventilation for 4 \200\22312 hours is routine after certain types of surgery, including cardiothoracic surgery requiring cardio- pulmonary bypass, and major head and neck surgery. Decreased conscious level Intubation and ventilation may be indicated in order to: \200 M aintain a patent airway. In patients with a traumatic brain injury, hypoxaemia related to a irway obstruction is a major cause of secondary brain injury. In patients with ARDS, ICU mortality was 52 \200\22363%, in accordance with other cohort st udies. Mortality in clinical trials is lower (e.g. 31 \200\22340%), possibly due to trial s elec- tion criteria. Protect the lungs from aspiration of gastric contents. \200 Control PaCO2 between 4.5 \200\2235.0kPa as part of an algo- rithm to control raised intra-cranial pressure (ICP). \200 Enable deep sedation in patients with status epilepti- cus or severe traumatic brain injury, in order to reduce cerebral oxygen demand. Indications for invasive ventilation Acute hypoxic (type I) respiratory failure Common caus es include community-acquired or nosoco- mial pneumonia, cardiogenic pulmonary oedema, ARDS , atelectasis after major abdominal or thoracic surgery, severe asthma and COPD. There is n o absolute value for arterial oxygen tension (PaO2), or for the ratio of PaO2 to fractional inspired oxygenation concentration (FiO2) which triggers the need for invasive ventilation . That decision also depends upon the underlying pathology, the likelihood of success using non-invasive ventilation (NIV), and the mental and physical condition of the patient. For example, a patient with cardiogenic pulmonary oedema will often recover rapidly from severe hypoxaemic respiratory failure using only continuous positive airways pressure (CPAP) or N IV and standard drug therapies, but if the patient is A Glasgow Coma Score (GCS) of 7 is sometimes used as a threshold for intubation. However, o ther factors may favor intubation when the GCS is higher. The role of NIV and facemask CPAP NIV and facemask CPAP have an established role in pa- tie nts with an exacerbation of COPD, acute on chronic respiratory failure from chest wall defo rmities and neuro- muscular disease, cardiogenic pulmonary oedema, thoracic trauma, respira tory failure after thoracic surgery, and respiratory failure in the setting of immunosuppre ssion. There are many reports of the successful use of NIV and CPAP in other conditions. Fo r some patients these tech- niques may represent an appropriate ceiling to support CHAPTER 17.6 The ventilated patient 435 especially if the patient has only recently been extubated or is hypoproteinemic. It is ess ential that RSI is performed by those who are familiar with a dif \201 cult airway algorit hm, and who know how to use the dif \201 cult airway equipment. A maximum of four attempts should be made at intu- bation before handing over to a more experienced col- league. The emphasis should be on maintaining oxygen- ation rather than on achieving intubation. Other means of oxygenation including bag-and-mask ventilation, inser- tion of a laryngeal mask ai rway, or cricothyroid puncture should be considered without delay. when invasive ventilation is not considered to be in a patient \200\231s best interests. Ho wever, when NIV or CPAP fail and intubation beomes necessary, prognosis may be worse than i f intubation had been performed at the outset. In ARDS, an attempt at NIV before intubation was associated with an increase in ICU mortality from 31% to 48%. In patients who were wea ned from invasive ventilation but in whom respiratory failure recurred, NIV did not reduce the rate of re-intubation, and was associated with a mortality increase from 14% to 25%. NI V should therefore be used with caution in the majority of patients admitted to the ICU. Be yond its recognized indications it should be used only when the underlying condition is lik ely to improve rapidly. Patients should be monitored closely. Those who fail to improve rap idly should be considered for early intubation before they become exhausted. Patients are at increased risk of regurgitation and aspi- ration until the endotracheal tub e is in place with the cuff in \202 ated. They should therefore be anesthetized and intuba ted in the head-up position. Cricoid pressure helps to prevent regurgitation, but may make intubation more dif \201 cult, and may have to be relaxed to allow the endotracheal tube t o pass through the larynx. Ethical considerations The decision to commence or withhold invasive mechani- cal ventilati on is frequently dif \201 cult. In the UK, the decision should be made in accordance with the guidance of the General Medical Council on withholding and withdrawing treatment. In su mmary, competent adults have the right to refuse treatment, even if this results in harm to themselves or death, but do not have a right to demand treatment which the doctor thinks i s not clinically indicated. The aim should be to achieve consensus between the patient, the ir close family and friends and the healthcare team. A second opinion should be sought wher e there is disagreement. There is no ethical or legal distinction between withhold- ing and withdrawing treatment. When there is uncertainty about the patient \200\231s best interest s, as in many emergency situations, treatment should be started until a clearer assessment of best interests can be made. A critically ill patient is at risk of cardiovascular col- lapse due to the negative inotro pic and vasodilatory effects of anesthetic drugs, and due to positive pressure ventilation which increases the intra-thoracic pressure and reduces cardiac preload. To minimize these risks, ensure reliable IV access for \202 uid loading. Invasive arte- rial blood pressure monitoring is desirable before induc- tion if time allows. Reduced and incremental doses o f the IV anesthetic agent should be used, with a short- acting vasopressor agent such as me taraminol imme- diately available. The choice of induction agent is less important than the dose that is given. However, many ICU doctors avoid etomidate despite its cardiovascu- lar stability, as even a single dose may cause adrenal suppression. The paralyzing agent suxamethonium should be used with caution. It provides optimum conditi ons for intuba- tion, but may cause an exaggerated release of potassium from muscle cells i n patients with burns or neuromuscu- lar diseases, including those with prolonged immobilit y or ICU neuro-myopathy. Cardiac arrests from hyperka- laemia have occurred in ICU patients as a result. Airway management Rapid sequence intubation (RSI) The intubation of a critically ill patien t is a time of particular risk, with high rates of complications including severe hypoxaemi a (26%), dif \201 cult intubation (12%), oesophageal intubation (5%), aspiration of gastri c contents (2%), haemo- dynamic collapse (25%), arrhythmias (10%), and cardiac arrest (2%). Although intubation is traditionally an area of expertise of the anesthetist, it is increa singly seen as a core skill for all physicians working in the critical care setting. Speci \201 c considerations are: \200 The patient may need to be intubated on a ward distant f rom the ICU or theater complex with limited equip- ment or assistance. Essential equipment, drugs, and a trained assistant should be immediately available to go to a ward to manage t his situation. If possible, the patient should be attached to a monitor and transferred to a more suitable location before intubation. Given the signi \201 cant risk of oesophageal intubation, cap- nography should always be u sed to con \201 rm the position of the ETT in the trachea. Listening for breath sounds wit h a stethoscope may be misleading. Management of the endotracheal tube (ETT) The most common arti \201 cial airway when invas ive ventila- tion begins is a cuffed oral ETT. Nasotracheal tubes are preferred in pediatri c ICUs, but in adults are only generally employed after major head and neck surgery when su rgical access to the oral cavity has been required. A small number of patients already have a tracheostomy in situ (2%). \200 The ETT should be secured \201 rmly, but without obs truct- ing venous drainage from the head (especially if there is raised ICP). Accidental ex tubation occurs in 3 \200\2235% of ventilated patients. If this occurs, the priority is to main- tain oxygenation and ventilation via a bag-and-mask until equipment and drugs are pre pared for re-intubation, but this may only be necessary in 41%. Critically ill patients desaturate quickly during apnoea at the time of intubation. It is t herefore vital to pre- oxygenate fully before induction. This requires at least 3 minutes o f normal tidal breathing while inhaling 100% oxygen (but as few as 5 vital capacity breaths ). To maxi- mise the functional residual capacity (FRC), i.e. the oxy- gen reservoir in the lungs, the patient should be kept head-up and positive pressure applied via the anesthetic breathing system to recruit collapsed airways. An air leak around the cuff of the ETT may indicate cuff rupture, but more commonly the tub e has migrated above the vocal cords. Further cuff in \202 ation stops the leak temporaril y but also pushes the ETT further up into the pharynx, so the leak soon recurs. The correct response is to check the position of the ETT immedi- ately, and if necessary push it back down the trachea to prevent accidental extubation. ICU patients have an increased risk of dif \201 cult intubation. Even if a pre-intubation assessment of the airway is nor- mal, dif \201 culties may arise (e.g. due to laryngeal oe dema), T PALFREYMAN & T EVANS 436 notch should have an open surgical tracheostomy rather than a percutaneous procedure. Percu taneous trache- ostomy may be performed in morbidly obese patients, but the risk of complic ations is much higher, and many ICU doctors routinely refer these patients for surgical tra cheostomy. Modern ETTs typically have a high-volume/low-pressure cuff to spread the pressure over the tracheal mucosa and minimize the risk of pressure necrosis and subse- quent tracheal stenos is. Cuff pressures should be mea- sured regularly and should not exceed 30cmH2O. Pharyngeal secretions pool above the ETT cuff and can pass into the lower airway. Such micr o-aspiration occurs in 89% of intubated critically ill patients, and is thought to be the m ain route of access for organisms causing ventilator-associated pneumonia (VAP). To minimiz e the problem a subglottic drainage tube (an integral part of the ETT) just above the cuff should be aspirated either periodically or continuously. Subglottic drainage reduces the in cidence of VAP by 50%, the duration of ventilation by 2 days, and the length of stay in ITU by 3 days. How- ever, these tubes are not widely used, partly because of concern about an increased risk of mucosal injury. The optimal timing for tracheostomy is unknown. As an aid to weaning, a tracheostomy is of no bene \201 t until a patient has recovered from the acute phase of their illness and is ready to wean from ventilatory support. However, one study found a reduction in mortality f rom 61.7% to 31.7% when tracheostomy was performed within 48 hours of intubation rather tha n 14 \200\22316 days after intubation. The Tracman study is currently recruit- ing patients to compare tracheostomy performed at day 1 \200\2234 versus day 10 after ICU admission. Ventilator terminology \200 Intermittent positive pressure ventilation (IPPV) is a genera l term for all forms of positive pressure ventila- tion. However, it is also sometimes used to indicate con- trolled mechanical ventilation (CMV). Suction via the ETT lumen is performed routinely, both to reduce micro-aspiration and to ma intain tube patency. Closed suction systems have not been found to reduce the incidence of VAP, mortality or ICU length of stay compared with open suction. Ventilator cycling refers to the signal which tells the ventilator to switch from inspirati on to expiration. Time cycling occurs after a set inspiratory time. Pressure, vol- ume or \202 ow cycling occurs after the target pressure, volume or \202 ow has been reached. Th e method of cycling depends on the mode of ventilation used. Arti \201 cial humidi \201 cation is necessary to prevent drying of the airways and thick ening of secretions. This is normally achieved with a heat and moisture exchanger (HME), wh ich also functions as the breathing system \201 lter. How- ever, HMEs can increase work o f breathing, particularly when saturated with water vapor. The alternative, water- bath hum idi \201 ers, may increase the risk of VAP. CMV delivers a set tidal volume and respiratory rate, and is time-cycled. The tidal volume is usually delivered in the \201 rst part of the inspiratory phase, and is followed by th e inspiratory plateau before expiration begins. Peak inspiratory pressure depends on the in teraction of tidal volume, inspiratory \202 ow rate, airway resistance, and lung complian ce. Plateau pressure is an indicator of the pressure transmitted to the alveoli, and is an important determinant of ventilator-induced lung injury (VILI). CMV does not allow spontane ous breaths, and is approp- riate for patients who have no respiratory effort. If the patie nt coughs or tries to take a breath, high airway pressures and work of breathing may be gen erated. \200 Pressure controlled ventilation (PCV) delivers a set air- way pressure and r espiratory rate, and is time-cycled. Tidal volume depends upon the inspiratory pressure, in spiratory time, airway resistance and lung compliance. PCV does not permit spontaneous resp iration. The risk of high airway pressure is avoided, but tidal volumes and minute ventilat ion are variable. Tracheostomy Until the mid-1980s, tracheostomy was almost exclusively performed as an open, surgical procedure. Since that time several percutaneous techniques have been described wh ich can be performed at the bedside in the ICU. The most pop- ular is that described by Cia glia, using a seldinger guidewire and either serial dilators or a single tapered dilator. \200 The most common indication for tracheostomy in the ICU is to aid weaning from respira tory support in patients who need ventilation for more than a few days. Other indications i nclude upper airway obstruction and impaired bulbar function. A mini-tracheostomy may help in the management of secretions in self-ventilating patients with an inadequate cough. The major bene \201 t is improved comfort (compared to an oral ETT), allowing sedation to be stopped. Airway resistance and anatomical dead space are reduced, and easier mouth care may reduce the risk of VAP. Assist-control ventilation (ACV) delivers a set tidal vol- ume. Each breath is triggered by the patient \200\231s inspiratory effort (assist). If the patient does not trigger the ven tila- tor, the set tidal volume is delivered at a set back-up respiratory rate (control). A CV is the mode of ventila- tion employed in the ARDS Network studies. Risks of tracheostomy include hypoxaemia, bleeding, infection, and damage to the trachea or esophagus. Severe hypoxia may be due to loss of airway control at the time of tracheostomy formation, or dislodgement or obstruction of the tube at a later time. To reduce the risk of blockage, a tracheostomy tube may have an inner lining tube which can be removed and cle aned. Bleed- ing may occur at the time of the procedure or due to erosion through an adjace nt vessel days or weeks later. Infection is usually not severe but mediastinitis, especiall y in the presence of a median sternotomy wound, may be catastrophic. The risk of infection is less with percutane- ous tracheostomy than with open tracheostomy, proba- bly due to the difference in the amount of tissue trauma. \200 Contra-indications to tracheostomy inclu de soft tissue infection of the neck, and signi \201 cant thrombocytopenia or coagulopathy . Patients with abnormal neck anatomy such as a goiter or a pulsatile vessel above the ster nal Synchronized intermittent mandatory ventilation (SIMV) enables a set number of ventilator b reaths (either volume controlled or pressure controlled) to be syn- chronised with the pati ent \200\231s spontaneous respiratory efforts. Patients can also breathe between these mand a- tory breaths, with pressure support added to the extra breaths. Patient-ventilator dyssy nchrony may still occur, with increased work of breathing. Biphasic positive airway pressure (BIPAP) alternates between two levels of airway pressure, providing tidal ventilation but permitting spontaneous breaths through- out the ventilator cycle. Spontaneous breaths can be CHAPTER 17.6 The ventilated patient 437 augmented by pressure support. Like SIMV, BIPAP can provide complete or partial ventilatory support, but the ability to take a spontaneous breath at any time renders it better tolera ted than SIMV. Extra-corporeal membrane oxygenation (ECMO) achieves gas exchange via an extra-corporeal circuit similar to that used for cardio -pulmonary bypass during surgery. It is used as a rescue therapy in patients with severe, r efractory hypoxia. There is currently no good evi- dence of bene \201 t in adults, but the results of the CESAR trial in patients with severe ARDS are awaited. Pressure support ventilation (PSV). The patient trig- gers each breath. The ventilator deli vers a set level of inspiratory pressure, and cycles to expiration when the inspiratory \202 ow rate drops below a certain level. Tidal volume depends upon the interaction between inspiratory pressure, inspiratory time, airway resistance and lung compliance. PSV is used for weaning patients from respiratory support, once they have recovered from the acute pha se of critical illness. A mandatory mode of ventilation acts as a back up, activated by apn oea. Ventilator settings It is important to understand the various modes of ventila- tion, but c urrent evidence suggests that other ventilator settings such as tidal volume and airway pre ssure have more in \202 uence on outcome: \200 FiO2 should start at 0.6 \200\2231.0, and be titrated according to PaO2 (aiming for 8 \200\22310kPa) and SpO2 (aiming for at least 9 0 \200\22395%). Until the patient has been stabilized, the over-riding concern is to avoid hypoxaemia. In patients with severe chronic respiratory failure or severe ARDS, a lower PaO 2 or SpO2 may be accepted, as long as tissue oxygenation appears to be adequate, as assesse d by end-organ function, central venous oxygen satura- tion, lactate and base de \201 cit. The duration and severity of an SpO2 less than 90% is correlated with cognitive impairment in survivors of severe ARDS. The effect of oxygen therapy on the hypoxic respiratory drive is ir- relevant in the mechanically ventilated patient in the acute setting. However, it m ay become important dur- ing weaning. Hyperoxia is bene \201 cial in the treatment of carb on monoxide poisoning but should be avoided in other circumstances. Oxygen toxicity occurs after 12 \200\22336 hours at an FiO2 above 0.5, and is characterized by lung in \202 ammat ion and atelectasis, the clinical importance of which is not clear. Triggering is the mechanism by which the ventilator recognizes a patient \200\231s attempt to take a spontaneous breath. The ventilator measures either a small negative de \202 ecti on in airway pressure, or a change in the rate of air \202 ow within the breathing system . Modern ICU venti- lators measure changes in both pressure and \202 ow. Flow can be meas ured earlier, and provides a more sensitive trigger which reduces work of breathing. Positive end-expiratory pressure (PEEP) occurs when airway pressure remains above atmospher ic pressure at the end of expiration. It may be set externally by the ventilator, or may be intrinsic (PEEPi) when there is increased resistance to expiratory \202 ow in the airway s, as in asthma or COPD. PEEP is used therapeutically to recruit collapsed areas of lung, i ncrease FRC, and improve ventilation-perfusion matching, leading to better arterial oxygena tion. There is less cyclical opening and closing of small airways with each breath, reduc-