MEDICOLEGAL ASPECTS 21 Deaths which must be noti \201 ed to HM Coroner in the UK No doctor attending within prior 14 days Death without recovery from anesthesia Suicide Sudden or unexplained death Medical mishap Industrial accident or disease or related to employment Violence, accident, or misadventure Suspicious circumstances Alcoholism Poisoning Death in custody or shortly after detention 22 CHAPTER 1 Critical care organization Clinical governance Clinical governance is a framework through which health care organizati ons are accountable for continuously improving the quality of their services and safeguardi ng high standards of care by creating an environment in which excellence in clinical care w ill \202 ourish. For critical care, clinical gov- ernance requires the culture, systems, and support mechanisms to achieve good clinical performance and ensure quality improvement is embedded into the unit \200\231s routine. This includes action to ensure risks are manag ed, adverse effects are rapidly detected, openly investigated, and lessons learned, that go od practice is rapidly disseminated and that systems are in place to ensure continuous impr ovements in clinical care. There must be systems to ensure all clinicians have the right ed ucation, training, skills, and competencies to deliver the care needed by patients. There m ust also be systems in place to recognize and act on poor performance. The Critical Care Unit interfaces with most of the rest of the hospital and its clinical go vernance arrangements must contribute to patient care throughout the hospital. Some aspects of critical illness are managed outside the Critical Care Unit, yet the critical care team retains responsi- bility for ensuring quality and safety of this care. Essential components of clinical governance Clear management arrangements Everyone must kno w who they are accountable to, the limits of their decision-making, and who must be informe d in the decision-making process. Quality improvement Through the process of clinical audit, the standard of practice is moni tored and changes effected to improve quality. Clinical effectiveness Evidence-based practice is essential where sound evidence exists to support clinical decisions. Protocols and guidelines standardize practice. Risk assessment and management A register of clinical risks should be kept, to which new ri sks are appended as they are assessed. An action plan should be developed for managing each risk and its implementation monitored. Staff and organizational development Including continued professional education, clinical s upervision, and pro- fessional regulation. Patient input Complaints monitoring should be used to learn lessons and improve practice wi thin Intensive Care Unit (ICU). Patients \200\231 and relatives \200\231 sugges- tions and surveys can be used to adapt quality initiatives to the needs of patients. CLINICAL GOVERNANCE 23 See also: Audit, p24. 24 CHAPTER 1 Critical care organization Audit Audit has become an essential part of medical practice. The main purpose is to improv e quality of care. In the Critical Care Unit, this should involve all members of the multid isciplinary team. Change in practice in one dis- cipline will inevitably have a knock-on ef fect in others. Audit may involve a review of activity, performance against pre-determined indicators or cost-effectiveness. Audit may focus on speci \201 c topics or may encompass the performance of several Critical Care Units. A successful audit requires commitment from senior staff to ensure practice is de \201 ned, data are collected, and change is effecte d where necessary. Where change is sug- gested by audit, a further review is required to en sure that such change has occurred. Data collection Ideally, a basic dataset should be common to all Critical Care Units nation ally to allow meaningful comparisons to be made. This requires a dataset detailed enough to answer questions posed, but not so detailed that collection becomes unsustainable. Resourc es must be provided in terms of computer databases and staff to collect and analyze data. T his is a skilled task that should not be delegated to junior team members. The data collect or should be familiar with the fundamentals of critical care medicine, and be provided with regular summary reviews to ensure enthusiasm continues and quality control is maintained. Methods of data entry should consider the time involved and that most of those collecting d ata are not keyboard experts. Typographical mistakes destroy the value of collected data so error trapping and data validation must form part of the housekeeping in any database used . Some audit topics require data collection outside the basic dataset. Collecting appropria te data requires clarity in setting the question to be answered and care in choosing data i tems that will truly answer the question. Audit meetings Regular audit meetings should follow a pre-de \201 ned timetable. This help s to ensure maximum staff attendance and also sets target dates for data collection and ana lysis. Audit meetings should be chaired and have de \201 ned aims. Discussion of the topic being audited must lead to recommended changes in practice and these must be followed thro ugh after the meeting. It is clear that all staff cannot attend all meetings. Dissemination of infor- mation prior to implementing proposed changes is necessary to stand some chance of carrying them through. AUDIT 25 See also: Clinical governance, p22. 26 CHAPTER 1 Critical care organization Critical care scoring systems Various critical care scoring systems have evolved to provide : \200 \200 \200 An index of disease severity, e.g. APACHE, SAPS. An index of workload and consumption of re sources, e.g. TISS. A means of comparison for: \200 \200 \200 auditing performance \200\224either in the same unit or between units. research, e.g. evalu ating new products or treatment regimens. patient management objectives, e.g. sedation, pre ssure area care. The Glasgow coma scale apart, no scoring system is practiced universally. APACHE is the predominant severity score used in the USA and UK while SAPS is more popular in mainland Europe. Inter-user interpretation of the same scoring system can be highly vari able. TISS (Therapeutic intervention scoring system) \200 A score is given to procedures and techniques performed on an individual patient (e.g. use and number of vasoactive drug infusions, renal replacement therapy, administering enteral n utrition). Some units use TISS to cost individual patients by attaching a monetary value to each TISS point scored. It can be used as an index of workload activity. A discharge TISS score can be used to estimate the amount of nursing interventions required for a patient in step-down facilities or in the general ward. TISS does not accurately measure nursing work load activity as it fails to cater for tasks and duties such as coping with the irritable o r confused patient, dealing with grieving relatives, etc. \200 SoPRA (System of patient-related activities) The SoPRA score is intended to indicate the sc ope of care (medical, nursing, and other) provided to critically ill patients to assess the intensity of the impact that each patient makes on the daily workload of the Critical Care Unit. Glasgow coma scale First described in 1974, it utilizes eye opening, best motor response, a nd best verbal response to categorize neurological status (see table oppo- site). It is the only system used universally in Critical Care Units though limitations exist in mechanical ly ventilated, sedated patients. It can be used for prognostication and is often used for t herapeutic decision-making, e.g. elective ventilation in patients presenting with a GCS <8. Sedation A variety of systems gauges and records the level of sedation in a mechan- ically ventilated patient. They assist staff to titrate the dose of sedatives to avoid either over - or under-sedation. The forerunner, developed in 1974, was the Ramsay Sedation Score. This is a 6-point scoring system separated into three awake and three asleep levels where the p atient responds to a tap or loud auditory stimulus with either brisk, sluggish, or no respo nse at all. The main problem lies in achieving reproducibility of the tap or loud auditory stimulus. We currently use an 8-point system developed in-house (UCLH sedation scale) (see table opposite). CRITICAL CARE SCORING SYSTEMS 27 Glasgow coma scale Score Eyes open Best motor response Best verbal response 6 \200\223 Obeys commands \200\223 5 \200\223 Localizes pain Orientated 4 Spontaneously Flexion withdrawal Confused 3 To speech Decerebrate \202 exion Inappropriate words 2 To pain Decerebrate extension Incomprehensible sounds 1 Never No response Silent Key paper Teasdale G, Jennet B (1974). Assessment of coma and impared consciousness: a prac tical scale. Lancet 2: 81 \200\2234. UCLH sedation scale 3 2 1 0 \200\2231 \200\2232 \200\2233 A Agitated and restless Awake and uncomfortable Aware but calm Roused by voice, remains calm Roused by movement Roused by noxious or painful stimuli Unrousable Natural sleep 28 CHAPTER 1 Critical care organization APACHE scoring \200 The APACHE (Acute physiology and chronic health evaluation) score utilizes a point score de rived from the degree of abnormality of readily obtainable physiological and laboratory var iables in the \201 rst 24h of ICU admission, plus extra points for age and chronic ill he alth. The summated score provides a measure of severity while the percentage risk of subseq uent death can be computed from speci \201 c coef \201 cients applied to a wide range of admission disorders (excluding burns and cardiac surgery). APACHE I, \201 rst described i n 1981, utilized 34 physiological and biochemical variables. A simpli \201 ed version (APA CHE II) utilizing just 12 variables was published in 1985 and extensively validated in diff erent countries. A further re \201 nement published in 1990, APACHE III, claims to improve upon the statist ical predictive power by adding \201 ve new physiological vari- ables (albumin, bilirubin , glucose, urea, urine output), changing thresholds and weighting of existing variables, co mparing both admission and 24h scores, incorporating the admission source (e.g. ward, opera ting theater), and reassessing effects of age, chronic health, and speci \201 c disease ca tegory. Wide acceptance of APACHE III may be limited as its risk strati \201 cation system is proprietary and has to be purchased. Key paper Knaus WA, Draper EA, Wagner DP, et al. (1985) APACHE II: a severity of disease cl assi \201 cation system. Crit Care Med 13: 818 \200\22329. APACHE SCORING 29 Acute physiology score +4 Core temperature ( C) \211 41 39 \200\22340.9 Mean BP (mmHg) \211 160 130 \200\223159 110 \200\223129 Heart rate (bpm) \211 180 140 \200\223179 110 \200\223139 Respiratory rat e (/min) \211 50 25 \200\22334 If FIO2 \211 0.5: A \200\223aDO2 (mmHg) \211 500 350 \200 \223499 200 \200\223349 If FIO2<0.5: PaO2 (mmHg) +3 +2 +1 0 +1 +2 +3 +4 30 \200\22331.9 \211 29.9 38.2 \200\22338.9 36 \200\22338.4 34 \200\22335.9 32 \200\22333.9 \211 49 70 \200\223109 50 \200\22369 \211 39 70 \200\223109 55 \200\22369 40 \200\22354 \211 5 35 \200\22349 12 \200\22324 10 \200\22311 6 \200\2239 <200 \211 55 >70 61 \200\22370 55 \200\22360 Arterial pH \211 7.7 7.6 \200\2237.69 Serum Na+ (mmol/L) \211 180 160 \200\223179 155 \200\223159 150 \200\223154 Serum K+ (mmol/L) \211 7 Serum creatinine ( mol/L) (NB. doubl e points score if acute renal failure) \211 300 171 \200\223299 121 \200\223170 Haematocri t (%) \211 60 Leukocytes (/mm3) \211 40 Neurological points = 15 (Glasgow coma score) 7.25 \200\2237.32 7.15 \200\2237.24 \211 7.15 7.5 \200\2237.59 7.33 \200\2237.49 120 \200\223129 111 \200\223119 \211 110 130 \200\223149 <2.5 6 \200\2236.9 5.5 \200\2235.9 3.5 \200\2235.4 3 \200\2233.4 2.5 \200\2232.9 50 \200\223120 <50 50 \200\22359.9 46 \200\22349.9 30 \200\22345.9 20 \200\22329.9 <20 20 \200\22339.9 15 \200\22319.9 3 \200\22314.9 1 \200\2232.9 <1 Age points Years \211 44 45 \200\22354 55 \200\22364 65 \200\22374 \211 75 Points 0 2 3 5 6 Chronic health points Two points for elective post-operative admission or \201 ve points if emer- gency operati on or non-operative admission, if patient has either: \200 \200 \200 Biopsy-proven cirrhosis, portal hypertension, or previous hepatic failure. Chronic heart fa ilure (NYHA Grade 4). Chronic hypoxia, hypercapnia, severe exercise limitation, 2* polycyth aemia, or pulmonary hypertension. Dialysis-dependent renal disease. Immunosuppression by di sease or drugs. \200 30 CHAPTER 1 Critical care organization SAPS score \200 Has a similar role to APACHE II, but more widely utilized in mainland Europe; the Simpli \201 ed Acute Physiology Score (SAPS) was devised by LeGall et al. in 1984 (SAPS I) and mod i \201 ed by the same group in 1993 (SAPS II). As for APACHE II, burns and cardiac surgica l patients are excluded from analysis. The original version used 14 readily measured clinic al and biochemical variables while the updated version, SAPS II, comprises 12 physiology va riables, age, type of admission (medical, scheduled, or unscheduled surgical), and three un derlying disease variables (see table opposite). A point score is based on the degree and p rognostic importance of derangement of these variables in the \201 rst 24h following ICU admission. The point scoring was assigned following logistic regression modeling of data ob tained from 8,369 patients in 137 adult ICUs in both Europe and North America and validated in a further 4,628 patients. The claimed advantage of this system is that it estimates the risk of death without having to specify a primary diagnosis. SAPS SCORE 31 Key paper Le Gall JR, Lemeshow S, Saulnier F. (1993) A new Simpli \201 ed Acute Physiology Score (SAPS II) based on a European/North American multicentre study. JAMA 270: 2957 \200 \22363. SAPS II score Age <40 (0); 40 \200\22359 (7); 60 \200\22369 (12); 70 \200\22374 (15); 75 \200\22379 (16); \211 80 (18) <40 (11); 40 \200\22369 (2); 70 \200\223119 (0); 120 \200\223159 (4); \211 16 0 (7) <70 (13); 70 \200\22399 (5); 100 \200\223199 (0); \211 200 (2) <39 (0); \211 39 (3) Heart rate (bpm) Systolic BP (mmHg) Body temp (*C) PaO2/FIO2 (kPa) if ventilated/CPAP <13.3 (11); 13.3 \200 \22326.5 (9); \211 26.6 (6) Urine output (L/d) Serum urea (mmol/L) White cell count (/mm3) Serum K+ (mmol/L) Serum Na+ (mmol/L) \200\223 (mmol/L) Serum HCO3 Serum bilirubin ( mol/ L) Glasgow coma score <0.5 (11); 0.5 \200\2230.999 (4); \211 1 (0) <10 (0); 10 \200\22329.9 (6); \211 30 (10) < 1 (12); 1 \200\22319.9 (0); \211 20 (3) <3 (3); 3 \200\2234.9 (0); \211 5 (3) <125 (5); 1 25 \200\223144 (0); \211 145 (1) <15 (6); 15 \200\22319 (3); \211 20 (0) <68.4 (0); 68.4 \200\223102.5 (4); \211 102.6 (9) <6 (26); 6 \200\2238 (13); 9 \200\22310 (7); 11 \200\223 13 (5); 14 \200\22315 (0) Metastatic cancer (9); hematological malignancy (10); AIDS (17) S cheduled surgical (0); medical (6); unscheduled surgical (8) Chronic disease Type of admission Point score in brackets 32 CHAPTER 1 Critical care organization SOFA score A limitation of the APACHE and SAPS scoring systems is that they were designed a nd validated on data obtained during the \201 rst 24h of inten- sive care admission. Vari ous systems have been developed to enable daily scoring (e.g. Sequential Organ Failure Asse ssment (SOFA), Riyadh Intensive Care Program (RIP) score, Multiple Organ Dysfunction Score (MODS), etc.) to allow a better assessment of change in the patient \200\231s con- dition. As the physiological and biochemical status of the patient is determined in part by the dis ease severity, but also by the degree of medical inter- vention, these sequential scoring s ystems incorporate the use of various therapies and procedures. The SOFA system was initially designed to improve patient characteri- sation for multicentr e drug trials in sepsis (SOFA initially stood for \200\230Sepsis organ failure assessment \200\231), but has subsequently been applied to intensive care patients in general, with \200\230Sequential \200\231 being substituted for \200\230Sepsis \200\231. Although it has not been validated in the sense that a point score denoting severity of dys function in one organ system does not trans- late directly to an equivalent severity in ano ther organ, it has been used successfully to prognosticate and to follow changes in patient status throughout their intensive care stay (see table opposite). SOFA SCORE 33 Key paper Moreno R, Vincent JL, Matos R, et al. (1999) The use of maximum SOFA score to qua ntify organ dysfunction/failure in intensive care. Results of a prospective, multicentre st udy. Working Group on Sepsis related Problems of the ESICM. Intensive Care Med 25: 686 \200 \22396. SOFA score 0 >400 1 >400 2 \211 300 3 \211 200* 4 <100* Respiratory PaO2:FIO2 ratio (mmHg) <1.2 1.2 \200\2231.9 2.0 \200\2233.4 3.5 \200\2234.9 or <500mL/d \211 5.0 or <200mL/d Renal Creatinine (mg/dL) or urine output (mL/d) Hepatic Bilirubin (mg/dL) Cardiovascular Me an arterial pressure (mmHg) <1.2 1.2 \200\2231.9 2.0 \200\2235.9 6.0 \200\22311.9 12.0 No hypotension MAP >70 Dopamine \211 5 or dobutamine (any dose) \200 Dopamine >5 or epinephrine \211 0.1 epinephrine \211 0.1 \200 \211 50 Dopamine >15 or epinephrine >0.1 epinephrine >0.1 \200 \211 20 >150 \211 150 \211 100 Hematological Platelet count (x103/mm3) Neurological Glasgow coma score * With ventilatory support; \200 Adrenergic agents administered for at least 1h (doses in mcg/kg/ min). 15 13 \200\22314 10 \200\22312 6 \200\2239 <6 Conversion factors \200 \200 PaO2:FIO2 to kPa: divide by 7.5. Creatinine to mol/L: multiply by 88. Bilirubin to mol/ L: multiply by 17.1. 34 CHAPTER 1 Critical care organization Trauma score Scoring systems have been developed in trauma for: \200 \200 \200 Rapid \201 eld triage to direct the patient to appropriate levels of care. Quality assura nce. Developing and improving trauma care systems by categorizing patients and identifying problems within the systems. Making comparisons between groups from different hospitals, in the same hospital over time, and/or undergoing different treatments. The Injury severity score (ISS) is a severity scoring for patients based on the anatomical injuries sustained. The Revised trauma score (RTS) utilizes measures of physiological abnor mality to predict survival (see table oppo- site). A combination of ISS and RTS \200\224TRI SS \200\224was developed to overcome the shortcomings of anatomical or physiological scorin g alone. The TRISS methodology uses ISS, RTS, patient age, and whether the injury was blunt or penetrating to provide a measure of the probability of survival. Injury severity score Use AIS90 (Abbreviated Injury Score 1990) dictionary to score injury. Identify highest abbreviated injury scale score for each of the following: \200 \200 \200 \200 \200 \200 Head and neck. Abdomen and pelvic contents. Bony pelvis and limbs. Face. Chest. Body surfac e. Add together the squares of the three highest area scores. TRAUMA SCORE 35 Revised trauma score Measure Coded value 4 3 2 1 0 4 3 2 1 0 4 3 2 1 0 Total = revised trauma score x Weight ing = Score Respiratory rate (breaths/min) 10 \200\22329 >29 6 \200\2239 1 \200\2235 0 >89 76 \200\22389 50 \200\22375 1 \200\22349 0 13 \200\22315 9 \200\22312 6 \200\2238 4 \200\2235 3 0.2908 Systolic BP (mmHg) 0.7326 Glasgow coma scale 0.9368 See also: Multiple trauma (1), p582; Multiple trauma (2), p584. This page intentionally left blank 37 Chapter 2 Respiratory therapy techniques Oxygen therapy 38 Airway maintenance 40 Endotracheal intubation 42 Ventilatory support \200 \224indications 44 IPPV \200\224description of ventilators 46 IPPV \200\224modes of ventila tion 48 IPPV \200\224adjusting the ventilator 50 IPPV \200\224failure to tolerate ventilati on 52 IPPV \200\224failure to deliver ventilation 54 IPPV \200\224complications of ventilat ion 56 IPPV \200\224weaning techniques 58 IPPV \200\224assessment of weaning 60 High freque ncy jet ventilation 62 High frequency oscillatory ventilation 64 Positive end expiratory pr essure (1) 66 Positive end expiratory pressure (2) 68 Continuous positive airway pressure 7 0 Lung recruitment 72 Prone positioning 74 Non-invasive respiratory support 76 Extracorpore al respiratory support 78 Tracheotomy 80 Mini-tracheotomy 82 Chest drain insertion 84 Pleur al aspiration 86 Fibreoptic bronchoscopy 88 Chest physiotherapy 90 38 CHAPTER 2 Respiratory therapy techniques Oxygen therapy All critically ill patients should receive additional inspired O2 on a \200 \230more not less is best \200\231 philosophy. Principles \200 High \202 ow, high concentration O2 should be given to any acutely dyspnoeic or hypoxaemi c patient until accurate titration can be performed using arterial blood gas analysis. In g eneral, maintain SaO2 between 92 \200\22398%. Compromises may need to be made during acute on chronic hypoxaemic respiratory failure, or prolonged severe ARDS, when lower values may suf \201 ce provided tissue O2 delivery is maintained. When starting mechanical ventilatio n use a high FIO2 until accurate titration is performed using arterial blood gas analysis. Apart from patients being treated for carbon monoxide poisoning or hyperbaric therapy, e.g. diving accidents, there is no need to maintain supranormal levels of PaO2. Indeed this may cause harm. Type II respiratory failure Patients in chronic type II (hypoxaemic, hypercapnic) respirato ry failure may develop apnoea if their central hypoxic drive is removed by supple- mental O 2. This is seldom (if ever) abrupt; a period of deterioration and increasing drowsiness wil l prompt consideration of either (i) FIO2 reduc- tion if overall condition allows; (ii) non -invasive or invasive mechanical ven- tilation if fatiguing; or (iii) use of respiratory st imulants such as doxepram. Close supervision and monitoring is necessary. Oxygen toxicity This is well described in animal models. Normal volunteers become symp- tom atic (chest pain, dyspnoea) after several hours of breathing pure O2. Washout of nitrogen c an cause microatelectasis. O2 may induce direct oxidant damage to proteins, lipids, and DNA , and is a potent vasocon- strictor; high levels of PaO2 may paradoxically compromise regio nal O2 delivery. The relative importance of O2 toxicity to the lung compared to other forms of ventilator trauma in critically ill patients remains unclear. Efforts should be made to minimize FIO2 whenever possible. Debate con- tinues as to whether FIO2 or other ventilator settings (e.g. PEEP, VT, inspir- atory pressures) should be reduced \201 rst. The author s \200\231 present view is to minimize the risks of ventilator trauma and accept progressiv ely lower values of SaO2/PaO2 rather than continue with a high FIO2. Monitoring \200 A normal pulse oximetry reading may obscure deteriorating gas exchange and progressive hype rcapnia. An O2 analyzer in the inspiratory limb of the ventilator or CPAP/BiPAP circuit con \201 rms the patient is receiving a known FIO2. Some ventilators have built-in calibratio n devices. Adequacy and any changes in arterial O2 saturation can be monitored continuously by pulse oximetry and intermittently with laboratory blood gas analysis. OXYGEN THERAPY 39 Oxygen masks \200 Hudson-type masks or nasal \200\230spectacles \200\231 give an imprecise FIO2 and should o nly be used when hypoxaemia is not a major concern. Hudson- type masks do allow delivery of humidi \201 ed gas (e.g. via an \200\230Aquapak \200\231). Valves \201 tted to the Aqu apak system do not deliver an accurate FIO2 unless gas \202 ow is at the recommended leve l. Masks \201 tted with a Venturi valve deliver a reasonably accurate FIO2 (0.24 at 2L/mi n, 0.28 at 4L/min, 0.35 at 8L/min, 0.40 at 10L/min, 0.60 at 15L/min) except in patients wit h very high inspiratory \202 ow rates. Pure O2 is delivered via a \201 xed jet drawing in air from around the jet to give a known dilution of O2 to the desired concentration. The se masks do not allow delivery of humidi \201 ed gas but are preferable in the short term for dyspnoeic patients as they enable more precise monitoring of PaO2 /FIO2 ratios. A tight - \201 tting anesthetic mask and reservoir bag allows 100% O2 to be delivered. 40 CHAPTER 2 Respiratory therapy techniques Airway maintenance The airway may become occluded by secretions, vomitus, blood, or foreign body. Reduced muscle tone in the obtunded patient may result in occlusion by the tongue an d surrounding structures. Opening the airway \200 Clear secretions, vomitus, debris, or blood with a Yankauer sucker and/ or Magill \200\231s forceps. In the absence of neck injury, and with the patient supine, tilt the head back wi th one hand on the forehead, and lift the chin with the \201 ngers of the other hand. If there is a suspected neck injury or an inadequate airway with the head tilt and chin lift, perform a jaw thrust. With the patient supine, place the \201 ngers behind the angle of t he mandible on both sides and lift the mandible forward and upward until the lower teeth (o r gum) are in front of the upper teeth (or gum). Maintaining the airway If the patient can be turned and is breathing adequately, it may suf \201 ce to adopt a lateral recovery position. If manual ventilation is required or the pa tient must remain supine, an oropharyngeal or nasopharyngeal airway may be used. Oropharyngeal (Guedel) airway \200 \200 \200 This is a hard plastic tube shaped to keep the tongue forward. It should only be used in ob tunded patients. The correct size should be selected by comparing the airway to the distanc e between the teeth and the angle of the jaw. Open the patient \200\231s mouth and remove a ny obstruction by suction. Insert the airway into the mouth with the curve pointing toward the skull. Rotate the airway through 180* once the soft palate is reached. The curve of the airway will retain its position in the oropharynx once fully inserted. \200 \200 Nasopharyngeal airway \200 \200 This soft shaped plastic tube \201 ts the passage from nares to pharynx. It is better tol erated in the semi-conscious patient, but should be avoided where there is a suspected/know n basal skull fracture. Assess the correct size by approximating the diameter of the airway to the diameter of the patient \200\231s \201 fth \201 nger. Insert a safety pin throu gh the \202 ange of the airway to prevent accidental inhalation after insertion. Pass the lubricated airway into the patent nostril with a slight twisting motion. AIRWAY MAINTENANCE 41 See also: Endotracheal intubation, p42; Basic resuscitation, p338; Airway obstruction, p348 . 42 CHAPTER 2 Respiratory therapy techniques Endotracheal intubation Indications An arti \201 cial airway is necessary in the following circumstances: \200 Apnoea: provision of mechanical ventilation, e.g. unconsciousness, severe respiratory muscl e weakness, self-poisoning. Respiratory failure: provision of mechanical ventilation, e.g. ARDS, pneumonia. Airway protection: GCS <8, trauma, aspiration risk, poisoning. Airway obst ruction: maintain airway patency, e.g. trauma, laryngeal oedema, tumor, burns. Haemodynamic instability: facilitate mechanical ventilation, e.g. shock, cardiac arrest. \200 Choice of endotracheal tube Most adults require a standard high volume, low pressure, cuffe d endotra- cheal tube. Average sized adults require a size 8.0 \200\2239.0mm id tube (size 7.5 \200\2238.0mm id for females), cut to a length of 23cm (21cm for females). Particular p roblems with the upper airway, e.g. trauma, oedema, may require a smaller tube. In speci \201 c situations, non-standard tubes may be used, e.g. armored tubes to avoid external com pression or double lumen tubes to isolate the right or left lung. Route of intubation The usual routes are orotracheal and nasotracheal. Orotracheal intuba- tion is generally preferred. The nasotracheal route has the advantages of increased patient comfort, easier blind placement, and easier to secure the tube. However, there are several disadvantages. The tube is usually smaller, there is a risk of sinusitis and otitis media, and is generally contraindicated in coagulopathy, CSF leak, and nasal/base-of-skull fractu res. Dif \201 cult intubation If predicted, this should not be attempted by an inexperienced, u naccom- panied operator except in life-threatening situations. Dif \201 culty may be predi cted in patients with a small mouth, high arched palate, large upper incisors, hypognathia, large tongue, anterior larynx, short neck, immobile temporomandibular joints, immobile cer vical joints, or morbid obesity. If a dif \201 cult intubation presents unexpectedly, the use of a stylet, a straight bladed laryngoscope, a laryngeal mask airway, or a \201 breop tic laryngoscope may help. It is important not to persist for too long; revert to bag-and- mask ventilation to ensure adequate oxygenation. Complications of intubation Early complications \200 \200 Trauma, e.g. hemorrhage, mediastinal perforation. Haemodynamic collapse, e.g. positive pres sure ventilation, vasodilatation, arrhythmias, or rapid correction of hypercapnia. Tube mal position, e.g. failed intubation or endobronchial intubation. Later complications \200 \200 \200 Infection, including maxillary sinusitis if nasally intubated. Cuff pressure trauma (avoid by maintaining cuff pressure <25cmH2O). Mouth/lip or pharyngeal trauma. ENDOTRACHEAL INTUBATION 43 Equipment required \200 Suction (Yankauer tip). \200 O2 supply, rebreathing bag, and ma sk. \200 Laryngoscope (two curved blades and straight blade). \200 Stylet/bougie. \200 Endotracheal tubes (preferred size and smaller). \200 Water-based gel to lubricate tube . \200 Magill forceps. \200 Drugs (Induction agent, muscle relaxant, sedative). \200 Syringe for cuff in \202 ation. \200 Tape to secure tube. \200 Capnograph. See also: Airway maintenance, p40; Ventilatory support \200\224indications, p44; Airway obs truction, p348; Respiratory failure, p350; Coma, p438; Acute weakness, p440; Poisoning \200 \224general principles, p520. 44 CHAPTER 2 Respiratory therapy techniques Ventilatory support \200\224indications Oxygenation failure (Type I respiratory failure) Hy poxaemia is de \201 ned by PaO2 <11kPa on FIO2 \211 0.4. May be due to: \200 Ventilation/perfusion mismatch (reduced ventilation in, or preferential perfusion of, some lung areas), e.g. pneumonia, pulmonary oedema, pulmonary vascular disease, very high cardia c output. Shunt (normal perfusion but absent ventilation in some lung zones), e.g. pneumoni a, pulmonary oedema. Diffusion limitation (reduced alveolar surface area with normal ventil ation), e.g. emphysema, or reduced inspired O2 tension, e.g. altitude, suffocation. Acute v entilatory insuf \201 ciency (as above). Acute ventilatory insuf \201 ciency (Type II respiratory failure) De \201 ned by an acute rise in PaCO2 and signi \201 cant respiratory acidosis. PaCO2 is directly proportional to the body \200\231s CO2 production and inversely proportional to alveolar ventilation (minu te ventilation minus dead space ventilation). Causes include: \200 \200 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.