Oxygen delivery system Types used Properties Non-sealed masks or nasal cannulae. Oxygen at low \202 ow (2 \200\22315l.min-1). Small re servoir. Signi \201 cant entrainment of environmental air. Accurate FiO2 not possible. Com fortable and simple to use. Venturi-type masks rely on the Venturi principle to dilute oxyg en predictably to FiO2. Need to change valve to alter FiO2. Higher FiO2 valves have larger ori \201 ces, so behave more like a variable performance system. Comfortable. Simple to us e, but needs attention to detail Variable performance Nasal cannulae, semi-rigid masks (Hudson, MC), non-rebreathing masks, tracheostomy mask, T- piece systems Venturi-type masks, anesthetic breathing circuits (waters circuit, Ambu-bag) Fixed performance Anesthetic breathing systems require sealing mask to prevent entrainment. Valves prevent re breathing. Large reservoir. Accurate FiO2. Sealed mask can be uncomfortable. Knowledge of b reathing systems required. Rely on high oxygen \202 ows to match patient \200\231s inspir atory \202 ow rate. Small reservoirs and sealed mask or naso-pharynx. Requires humidi \201 cation. Accurate FiO2. Sealed mask uncomfortable with risk of mucosal dryness. More co mplicated to set up. Unusual in the self-ventilating patient. Oxygenation achieved across s ynthetic membrane. CO2 removal can be an issue. FiO2 can be dif \201 cult to measure. Comp licated and limited to specialist centers. T-piece systems, Vapotherm (humidi \201 ed high \202 ow nasal cannulae) High \202 ow systems Others Intravascular oxygenation (cardiopulmonary bypass, interventional lung assist devices (Novo lung ), ECMO) Oxygen toxicity CNS toxicity (Paul Bert effect) Seen in diving, oxygen delivered at high pr essures (>3atm) can lead to acute central nervous system (CNS) signs and seizures. Table 1.1.4 Suggested indications for hyperbaric oxygen therapy Primary therapy Adjunctive therapy Carbon monoxide poisoning Air or gas embolism Decompression sickness (the \200\230bends \200\231) Osteoreadionecrosis Clostridial myositis and myonecrosis Radiation tissue damage Crush injuries Acute blood loss Lung toxicity (Lorraine Smith effect) Prolonged exposure to a high FiO2 results in pulmonar y injury. Possibly mediated by free oxygen radicals, there is a progressive reduction in lu ng compliance, associated with interstitial oedema and \201 brosis. Avoidance of long per iods of high oxygen concentrations reduces this effect. Clinically it can be dif \201 cult to prevent long exposure times; however, in general, patients should remain below an FiO2 of 0.5 where possible and not remain above this value for much longer than 30h. Compromised skin \202 aps or grafts Refractory osteomyelitis Intracranial abscess Enhance ment of healing of problem wounds pressure therapy also has important side effects. Whilst clearly of value in these situatio ns, the availability of a hyperbaric chamber often reduces its use, particularly in carbon monoxide poisoning. Broncho-pulmonary dysplasia (BPD) A condition concerning neonates, it is a chronic \201 b rotic lung disease associated with ventilation at high FiO2. Pathologically it is similar t o the adult condition above, but with the additional effect of immaturity. Surfactant and m aternal steroid therapies have lowered the incidence and severity. Further reading Dellinger RP, Carlet JM, Masur H, et al. Surviving Sepsis Campaign guidelin es for management of severe sepsis and septic shock. Crit Care Med 2004; 32: 858 \200\22373 . Retinopathy of prematurity This is a vasoproliferative disorder of the eye affecting pre- m ature neonates. Initially thought to be solely due to the use of high FiO2, its continued i ncidence despite tighter oxygen control suggests that other factors associated with prematu rity are involved. Gattinoni L, Brazzi L, Pelosi P, et al. A trial of goal-oriented hemo- dynamic therapy in c ritically ill patients. SvO2 Collaborative Group. N Engl J Med 1995; 333: 1025 \200\22332. Grocott M, Montgomery H, Vercueil A. High-altitude physiology and pathophysiology: implicat ions and relevance for intensive care medicine. Crit Care 2007; 11: 203. Hayes MA, Timmins AC, Yau EH, et al. Elevation of systemic oxygen delivery in the treatment of critically ill patients. N Engl J Med 1994; 330: 1717 \200\22322. Hyperbaric oxygen therapy Oxygen can be delivered to patients at higher than atmos- pheric pressures (2 \200\2233atm). This serves to increase the amount of oxygen dissolved in the p lasma, rather than that bound to hemoglobin. At rest, the metabolic demands of an average p erson can be met by dissolved oxygen alone when breathing an FiO2 of 1.0 at 3atm. Hyperbari c oxygen is delivered in a sealed chamber. The gas is warmed and humidi \201 ed. The commo n indications for hyperbaric oxygen therapy are listed in Table 1.1.4. High Leigh J. Variation in performance of oxygen therapy devices. Anesthesia 1970; 25: 210 \200\22322. Stoller KP. Hyperbaric oxygen and carbon monoxide poisoning: a critical review. Neurol Res 2007; 29: 146 \200\22355. Tibbles PM, Edelsberg JS. Hyperbaric-oxygen therapy. N Engl J Med 1996; 334: 1642 \200\2238. Wagstaff TAJ, Soni N. Performance of six types of oxygen delivery devices at varying respir atory rates. Anesthesia 2007; 62, 492 \200\223503. This page intentionally left blank 6 P MACNAUGHTON Ventilatory support: indications not ventilated (e.g. atelectasis, air spaces full of \202 uid, blood or in \202 ammatory exudate). The hypoxaemia associated with shunt is not reversed by increasing the inspired oxygen tension, and treatment needs to be directed towards opening up the non-ventilated pa rts of the lung by the application of positive pressure ventilatory support. Intracardiac s hunt: results in profound hypoxaemia that is not reversed by 100% oxygen or positive pressu re ventila- tion. Although usually associated with congenital heart disease, intracardiac s hunt may develop through a patent foramen ovale (present in 25% of the population). The for amen ovale remains closed as long as left atrial pressure is higher than right atrial press ure. In right ventricular failure (e.g. pulmonary hypertension secondary to pulmo- nary emb olus, ARDS, etc.), right atrial pressure is elevated above left atrial pressure which may o pen the foramen ovale causing a right to left shunt and severe hypoxaemia. Echocardiography can be invaluable in con \201 rming right to left intracardiac shunts as a cause for prof ound hypoxae- mia that is not corrected by conventional ventilatory management. The requirement for ventilatory support is the most common reason that patients are admitte d to an Intensive Care Unit (ICU). The aims of ventilatory support are to: \200 Improve gas exchange by correcting hypoxaemia and reversing acute respiratory acidosis. Rel ieve respiratory distress by reducing the work of breathing and reducing the oxygen cost of breathing. Change the pressure \200\223volume relationships of lungs including improving c ompliance and reversing or pre- venting atelectasis. Ensure patient comfort. Avoid complica tions and permit lung healing. \200 Use of ventilatory support In addition to the treatment of acute respiratory failure, venti latory support is also used in circulatory shock (e.g. cardiogenic shock, septic shock) and in the management of cerebral injury. In a study of 1638 patients from eight coun- tries, the indications for ventilatory support were as fol- lows: \200 Ventilatory support and cardiac failure Positive pressure ventilation may have adverse and bene \201 - cial effects on cardiac function. \200 Acute respiratory failure (66%) (including acute respira- tory distress syndrome) ARDS, sep sis, cardiac failure, pneumonia, post-operative respiratory failure, trauma) Coma (15%) Acu te exacerbation of chronic obstructive pulmonary disease (COPD) (13%) Neuromuscular disease (5%) \200 Hypotension is common after commencing intermittent positive pressure ventilation (IPPV) du e to the reduction in venous return. This may precipitate myocardial ischae- mia in a patie nt with critical coronary artery disease. Left ventricular function may be improved. An inc rease in intrathoracic pressure results in a reduction in left ventricular transmural press ure and left ventricular afterload. This improves function of the failing ventricle as it m oves to a more favorable position on the left ventricular function (Starling) curve. Right ventricular function may be impaired. In addition to reduced preload, right ventricular fun ction may be impaired from an increase in pulmonary vascular resist- ance from alveolar ves sel compression associated with alveolar overdistension. Correction of hypoxaemia and respi ratory acidosis is associated with improved cardiac function. Mechanisms include a direct e ffect on cellular function and from reversal of pulmonary vasoconstriction caused by hypoxa emia and respiratory acidosis. Physiology Respiratory failure: is de \201 ned as the failure to maintain normal arterial blood gasses breathing room air: \200 Hypoxaemic (type 1) \200\224arbitrarily de \201 ned as a PaO2 of <6.7kPa (50mm Hg) breathi ng room air Hypercapnic (type 2) \200\224de \201 ned as a PaCO2 of >6.7kPa (50mm Hg). Respiratory failure may be acute, chronic or acute on chronic. Patients with chronic type 2 respiratory failure develop a compensatory metabolic alkalosis and maintain a normal pH de spite an elevated PaCO2. An acidaemia (pH <7.30) rather than the PaCO2 value indicates the need for ventilatory support. The most important mechanisms of hypoxaemia are ventilation \200\223perfusion mismatch and shunt (cardiac and intrapulmonary). Diffusion impairment and reduced inspired oxygen tension (e.g. high altitude) are less relevant. Ventilation \200 \223perfusion mismatch: describes areas of the lung which have excessive perfusion compared with ventilation (shunt-like effect) and areas which have excessive ventila- tion compared with perfusion (dead space effect). Hypoxaemia due to ventilation \200\223perfusion mismat ch is usu- ally easily corrected by increasing the inspired oxygen ten- sion. As long as th e patient is able to increase minute ventilation by increasing tidal volume and respiratory rate, an increase in carbon dioxide tension is prevented. Pulmonary shunt: describes the m ost severe form of ventilation \200\223perfusion mismatch where venous blood passes through the lungs without any involvement in gas exchange. It occurs if there are areas of the lun g which are The application of raised intrathoracic pressure with continuous positive airways pressure typically results in a rapid clinical improvement in patients with acute left ventricular f ailure. In right ventricular failure (e.g. massive pulmonary embolus), positive pressure ve ntilation with high intrathoracic pressures should be avoided in order that right ventricul ar function is not compromised further. Ventilatory support and septic shock Severe sepsis may result in hypoxaemic respiratory fai lure and is a common indication for ventilatory support. Severe sepsis is also associated w ith a severe metabolic acidosis and a markedly increased work of breathing. The high work o f breathing increases demand for oxygen consumption in a shocked patient with inadequate ut ilization of oxygen. In patients with septic shock, ventilatory support may be commenced du e to a deteriorating metabolic acidosis 7 CHAPTER 1.2 Ventilatory support: indications without respiratory failure in order to reduce the work of breathing and the oxygen cost of breathing. with acute respiratory failure, but unnecessary exposure to high inspired oxygen concentrat ions should be avoided. A PaO2 of >8kPa is an acceptable target in the majority of patients . Nosocomial pneumonia (ventilator-associated pneumonia or VAP) is the most common complica tion of mechanical ventilation and is thought to arise due to micro-aspiration of colonized upper airway secretions. Mechanical ventila- tion should be discontinued and the patient e xtubated at the earliest opportunity in order to reduce the risk of developing VAP (see \200\230Hospital-acquired pneumonia \200\231 in Chapter 125). Hypotension is common after c ommencing positive pres- sure ventilation due to the reduction in venous return. It may be severe if the patient is hypovolaemic. Barotrauma describes pressure-related damage to the lungs resulting in extrapulmonary air which may cause pneumothorax, subcutaneous emphysema, mediastinal emphysema and systemic air embolism. Incidence is 10% of patients with acute lung injury receiving mechanical ventilation. Although recent studies have suggested that b arotrauma is more related to the degree of damage to the underlying lung than the use of hi gh airway pressures, it is prudent to avoid high airway pressures (e.g. peak pressure <45cm H2O and plateau pressure <35cm H2O). Ventilator-associated lung injury Laboratory studies and recent clinical trials have demon- strated that exposing already injured lungs to high tidal volumes and pressures results in an insidious and progres- sive worsening of the unde rlying lung injury. Overdistension ( \200\230volutrauma \200\231) and tidal lung recruitmen t \200\223derecruitment ( \200\230atelectrauma \200\231) appear to be the important mechani sms. Selecting an inappropriately high tidal volume increases mortality in patients with ac ute lung injury Assessment of a patient with respiratory failure Severe hypoxaemia (PaO2 <8kPa) despite high \202 ow oxygen or a deteriorating respiratory acidosis (pH <7.30) are common indications for commencing ventilatory support. Blood gas v alues re \202 ect on both the severity of the acute episode and the degree of chronic impa irment of respira- tory function. Clinical assessment is more important than arbitrary arte rial blood gas values when considering venti- latory support. Clinical signs of severe resp iratory failure indicating the need for ventilatory support may include: \200 Altered con scious level (from agitation to coma) \200 Increased work of breathing including tachypno ea (respiratory rate >30), use of accessory muscles and nasal \202 aring Paradoxical brea thing pattern re \202 ecting diaphragmatic fatigue when the \202 accid diaphragm paradox ically moves cephalad during inspiration causing inward movement of the abdominal wall Cent ral cyanosis Signs of excessive catecholamine release including diaphoresis, tachycardia, c ardiac arrhythmias and hypertension. \200 Lung function tests may be of value in indicating the need for ventilatory support in selec ted patients at risk of respi- ratory failure due to neuromuscular disease. A vital capacit y of <10ml/kg is associated with a markedly impaired ability to cough and, if untreated, a progressive decline in res- piratory capacity occurs due to atelectasis, ending with respir atory arrest. Serial measurements of vital capacity are helpful in predicting the need for ventilatory support in the Guillian \200\223Barre syndrome. Ventilatory support should be i nstituted when vital capacity falls to between 10 and 15ml/kg and before there is deteriora tion in arterial blood gasses. Measurements of vital capacity appear to be less predictive of the need for ventilatory support in myasthe- nia gravis, probably due to the unpredictab le and variable course of muscle function in this condition. Outcome from mechanical ventilation The outcome of mechanical ventilation was reported in a n international study of 361 ICUs. Over 5000 patients received ventilation for a mean of du ration if 5.9 days. The mortality of patients receiving ventilation for acute respiratory d istress syndrome was 52%, and 22% in patients being treated for an acute exacerbation of CO PD. The survival of unselected patients receiving ventilation for >12h was 69%. Complications of ventilatory support These relate either to the requirement for tracheal in tuba- tion or to the effects of positive pressure ventilation. Upper airway trauma is not i nfrequent and increases with the duration of intubation. Complications of endotracheal intu bation include laryngeal swelling, prolonged larygneal dysfunction (dysphonia and impaired swallowing) and, rarely, tracheal stenosis. Pulmonary oxygen toxicity describes airway and lung parenchyma damage secondary to prolonged exposure to high inspired oxygen tensions. Pr olonged (>24h) exposure of the normal lung to a partial pressure of oxygen of >0.5bar has b een associated with damage in previously normal lungs (atelectasis, reduced CO transfer fac tor). The priority is to correct hypoxaemia in the patient Further reading Esteban A, Anzueto A, Alia I, et al. How is mechanical ventilation employed in the intensive care unit. Am J Resp Crit Care Med 2000; 161: 1450 \200\2238. Marples IL, Heap MJ, Suvarna SK, Mills GH. Acute right to left inter- atrial shunt: an impo rtant cause of profound hypoxaemia. Br J Anaesthes 2000: 85: 921 \200\2235. Esteban A, Anzueto A, Frutos F, et al. Characteristics and outcomes in adult patients recei ving mechanical ventilation. A 28-day inter- national study. JAMA 2002; 287: 345 \200\22355 . 8 P MACNAUGHTON IPPV \200\224description of ventilators Classi \201 cation of positive pressure ventilation The wide and often confusing modes of ventilation offered by an ICU ventilator can be simpli \201 ed by considering the followin g: \200 \200 Ventilators generate a pressure gradient between the upper airway and the alveoli that resu lts in a controlled \202 ow of gas (air and or oxygen) into the lungs. This can be achiev ed either by creating a negative pressure around the chest wall whilst the upper airway rem ains at atmospheric pressure (e.g. tank ventilator or a curaiss) or more com- monly by crea ting a positive pressure in the airway. Negative pressure ventilators are rarely used in mo dern intensive care practice. Positive pressure ventilation may be applied via an arti \201 cial airway (invasive ventilation) or by a mask (non=invasive ventilation) Are the breaths volume or pressure targeted (or both)? Are the breaths initiated by the ven tilator or by the patient \200\231s efforts (or both)? How is the duration of inspiration c ontrolled? Volume- or pressure-targeted breaths In volume-controlled ventilation the tidal volume is s et, and the airway pressure generated depends upon the com- pliance and resistance of the r espiratory system (lungs and respiratory circuit). The inspiratory \202 ow waveform is co n- stant during volume ventilation whilst the airway pressure gradually increases to a peak (see below). In pressure-controlled ventilation the ventilator delivers a set inspiratory airway pressure and the tidal volume that is delivered will depend upon the compliance and resistance of the respiratory system. The inspiratory \202 ow waveform has a decelerating envelope whilst airway pressure remains constant throughout inspiration (see below). Many modern ICU ventilators now offer dual control of the inspiratory phase where the breath is both volume targeted and pressure limited. This results in a breath with the characteristic s of a pressure breath (constant pressure, decelerating flow) together with a predictable t idal volume. ICU ventilators Positive pressure ventilators used in the ICU are complex microprocessor-co ntrolled pieces of equipment. They require a high pressure (4bar) source of oxygen and air, and a power source from mains electricity. There may be a battery as a short-term (e.g. 10 \200\22330min) back-up power source in case of failure of the mains supply. Inspiration is the active phase of mechanical ventilation that is controlled by the ventilator. Expiratio n is passive and occurs when the expiratory valve is opened, with gas \202 ow depending o n the elastic recoil forces of the lungs and chest wall combined with the expiratory airway resistance. Ventilator circuit The ventilator circuit (Fig. 1.3.1) comprises inspiratory and expiratory limbs which connect to the relevant ventilator port. The two limbs are joined close to the patient by the \200\230Y \200\231 piece. The Y piece may be attached directly to the air- way (endotracheal tube (ETT) or tracheostomy) or with the aid of a catheter mount. A humid i \201 er must be included in the circuit. An active humidi \201 er (heated water bath) o r a passive heat and moisture exchanger (HME) may be used. Any additional tubing (e.g. cath eter mount, heat and mois- ture exchanger/bacterial \201 lter) between the airway and the Y piece is termed equipment dead space as it results in rebreathing of exhaled CO2, reduci ng the effective tidal volume. Triggering: time, pressure or \202 ow triggered Breaths may be delivered according to a s et frequency (ventilator or mandatory breaths) or in response to the patient making an atte mpt to inhale (spontaneous or sup- ported breaths). Some modes allow a mixture of manda- to ry and spontaneous breaths. Triggering describes what parameter the ventilator uses to init iate a breath and cycle to inspiration. In time triggering, breaths are delivered according to a pre-set frequency. This is also termed controlled ventila- tion (e.g. controlled mech anical ventilation) as there is no interaction between ventilator and spontaneous respira- tory efforts. Pressure or \202 ow triggering are used to detect spontane- ous respiratory efforts to allow supported breaths. In pressure triggering, the ventilator detects the dro p in air- way pressure that occurs when the patient makes a spon- taneous inspiratory effor t with the inspiratory valve closed. As soon as the pressure drop exceeds the trigger limit , the ventilator will cycle to inspiration. The sensitivity of the trigger may be adjustabl e by setting the pressure drop that will initiate inspiration (e.g. 0.5 \200\2232cm H2O). I n \202 ow triggering, the patient \200\231s inspiratory effort is detected from a change in \202 ow in the ventilator circuit. This is usually achieved by maintaining a \202 ow rate in the ventilator circuit during the expiratory phase and monitoring the flow returni ng to the expiratory valve. If the patient makes an inspiratory effort, the \202 ow retur ning to the expiratory valve falls below the background \202 ow rate and the ventila- tor cycles to inspiration. Ventilator Expiratory limb Inspiratory limb Bacterial filter/ humidifier Fig. 1.3.1 Diagram of a ventilator circuit. 9 CHAPTER 1.3 IPPV \200\224description of ventilators O 2 H m C Peak airway pressure Inspiratory pause or plateau pressure 40 30 20 10 0 \210\22210 e r u s s e r P Missed breath with patient effort but no ventilator breath Patient effort initiates ventilator breath L/min 50 n m / L w o F 25 i Fig. 1.3.2 An airway pressure trace from a ventilator showing poor triggering with \200 \230missed breaths \200\231. 0 \210\22225 \210\22250 l Flow triggering is considered the most sensitive method of triggering that improves synchro ny between patient and ventilator. Optimal setting of the trigger ensures that all patient efforts are detected by the ventilator and that auto-triggering does not occur. Autotrigger ing describes the ventilator incorrectly cycling to inspiration when the patient has not ma de an inspiratory effort. It occurs due to the trigger being set at a too sensi- tive level with the result that small changes in pressure or \202 ow within the ventilator circuit that are not due to patient effort (e.g. movement) erroneously initiate inspiration. time Fig. 1.3.3 Diagram of volume-controlled ventilation. peak during inspiration. If an end-inspiratory pause has been set, the plateau pressure can be observed. The difference in the peak and plateau pressure re \202 ects the pressure re quired to overcome resistive forces and increases as inspiratory \202 ow rate or airway r esistance increase. If inspiratory \202 ow rate remains constant, the peak to plateau gra dient changes proportionately with changes in airway resistance. The plateau pressure re \202 ects the pres- sure required to overcome elastic forces during inspiration and depends upon tidal volume and respiratory system compliance (lung and chest wall). Inspection of t he airway pressure trace during volume-controlled ventilation can therefore provide useful information about the elastic and resistive properties of the respiratory system. Cycling: time, \202 ow or time The ventilator can use volume, time or \202 ow to dictat e when the inspiratory phase is complete and when cycling to expiration should occur. Volum e cycling: expiration occurs as soon as the set tidal volume is delivered. There is no end- inspiratory pause. If a pause is added, the tidal volume is held within the lungs for a sho rt period at the end of inspiration before expiration, then cycling can be considered to be by both volume and time. Time cycling is most common and describes the inspira- tory metho d used in most ICU ventilators. The inspiratory time is either set directly or derived from the set frequency and inspiratory to expiratory time ratio. Pressure-control- led breaths are always time cycled. Flow cycling is used in pressure support ventilation to ter- minate the inspiratory phase. The inspiratory \202 ow has a decelerating \202 ow pro \201 le and when inspiratory \202 ow falls to a predetermined percentage of the peak \202 ow r ate the ven- tilator cycles to expiration. In most ventilators this \202 ow rate is set a t 25% of the peak \202 ow rate although some ventilators now have the facility for the us er to choose the \202 ow rate at which cycling occurs (e.g. between 10 and 90% of peak \202 ow rate). O 40 2 H 30 m 20 C 10 e r u 0 s s \210\22210 e r P L/min 50 25 n m / L w o F i 0 \210\22225 l Graphic waveforms \210\22250 Most ICU ventilators display continuous graphical displays of airway pressure, gas \202 o w and volume plotted against time. Observation of these displays can provide useful informa - tion regarding the mode of ventilation and ventilator set- tings, adequacy of patient ven tilator synchrony, evidence of gas trapping and an indication of the mechanical properties of the respiratory system. In volume-controlled ventilation with a constant inspira- tory \202 ow rate, the airway pressure gradually increases to a Fig. 1.3.4 Diagram of pressure-controlled ventilation. In pressure-controlled ventilation (and in dual modes) the inspiratory pressure is constant throughout the inspiratory phase and it is not possible to differentiate the elastic and r esistive properties of the lung from observation of the airway pressure trace. However, man y modern ICU venti- lators will calculate and display continuously values of res- piratory system resistance and compliance. 10 P MACNAUGHTON IPPV \200\224modes of ventilation patient \200\231s respiratory rate is above the pre-set frequency, the mandatory breaths ar e inhibited and the mode functions as a spontaneous mode with all breaths being patient tri g- gered. Cycling may be by volume or time. Assist pressure control is analogous to assist volume con- trol but with a pressure-targeted breath. An inspiratory pressure is set and th e delivered tidal volume will depend upon the respiratory system compliance and resistance. Cycling is always by time, which differentiates this mode from pressure support (see below ) where cycling is by \202 ow. The modern ICU ventilator offers a complex and wide range of ventilation modes. Unfortunate ly, there is little standardization of terminology between the different ven- tilator manuf acturers, and modes that are essentially the same may have different names depending upon t he par- ticular ventilator. To understand how a particular mode functions and interacts wit h the patient the following should be considered: \200 Are the breaths volume or pressure targeted (or a com- bination)? Is inspiration initiated by ventilator (controlled mode) or following patient effort (spontaneous or assist mode) or are there a combination of ventilator and spontaneous breaths (synchronized intermittent m andatory ventilation)? How is the duration of inspiration controlled (cycling)? Although th ere are a large number of modes available, there is little evidence that one mode improves clinical outcomes compared with another mode. The majority of patients can be managed with two modes: one controlled mode and one spontaneous mode. Synchronized intermittent mandatory ventilation (SIMV) In this mode a mandatory frequency o f breaths is delivered which will be synchronized to any spontaneous patient effort occurri ng within a time window that follows the pre- ceding breath (trigger window). If the patien t breaths at a rate greater than the set rate, the additional breaths will be allowed but u nsupported unless pressure support is also set. Thus a mixture of two breaths is delivered, mandatory ventilator breaths and pressure-supported breaths for any efforts above the mand atory frequency. Cycling of the mandatory breaths is by time, while the pressure-sup- porte d breaths are \202 ow cycled. When \201 rst developed, the mandatory breaths in SIMV we re volume targeted. This mode is now available with pressure-targeted breaths (SIMV pressur e control). Controlled modes Controlled mandatory ventilation (other terms CMV, IPPV, volume control) T his describes a fully controlled mode where the respira- tory rate is set by the ventilator and the breaths are usually volume targeted. Cycling from the inspiratory to expira- tory phase is usually by time or by volume. There is no interaction or synchronization with the patient \200\231s efforts, and additional breaths cannot be triggered. CMV is typi- cally u sed when patients are anesthetized and paralyzed (e.g. in the operating theater). CMV may a lso be applied with a pressure-targeted breath (pressure control). + 0 \210\222 SIMV with pressure support Fig. 1.4.3 Pressure \200\223time plot of SIMV with pressure support. + Dual control modes This term is used to describe modes that deliver breaths that are both v olume and pressure targeted. A range of names are used by the manufacturers, including Auto \202 ow , Pressure Regulated Volume Control , volume assured pressure control and volum e control plus . The ventilator delivers a breath with the characteristics of a pressure-t argeted breath (constant inspiratory pressure and decelerating \202 ow pro \201 le) comb ined with a guaranteed tidal volume (within certain pressure limits). On commenc- ing a dua l mode, a volume-targeted test breath is delivered \201 rst to assess the compliance and resistance. Subsequent breaths are pressure controlled using an inspiratory pres- sure that ensures delivery of the set tidal volume. The ven- tilator monitors the tidal volume on a breath-by-breath basis and can automatically change the inspiratory pres- sure (usually in 2 \200\2233cm H2O increments) to ensure that the desired tidal volume is delivered. In dual modes, the maxi- mum inspiratory pressure that may be delivered is a func- tion of the hig h airway pressure alarm setting. This varies between manufacturers but is usually 5 or 10cm H2O less than the high pressure alarm limit setting. Dual control can be applied to a wide range of modes including volume control, assist volume control, SIMV and pressure support. 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.