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• W2095278742 abstract "Amongst adults, prolonged breath-holding is the domain of free-divers and illusionists. Although their prolonged periods of apnoea are not typically preceded by breathing high concentrations of oxygen, these characters do not appear to suffer any long-term sequelae. However, such long durations of apnoea during anaesthesia can result in lethal consequences, despite the availability of oxygen-enriched gas mixtures and skilled personnel. Apnoea, which may be defined as the cessation of ventilation, is a common occurrence in anaesthetic practice [1, 2]. In the peri-operative context, apnoea is initiated by suppression of the drive or ability to breathe. Causes include failed airway management [3], respiratory depressant drugs and equipment malfunction [4]. Apnoea is most prevalent soon after induction and during emergence from anaesthesia [5]. The Confidential Enquiry into Maternal and Child Health report for 2000–2002 highlighted seven direct anaesthesia-related deaths, three of which resulted from oesophageal intubation and subsequent apnoea [6]. Furthermore, a cohort study of almost 870 000 patients over 2 years demonstrated that 10% of direct anaesthesia-related deaths were due to inadequate ventilatory management [7]. Despite its obvious importance, our understanding of the processes and events occurring during apnoea has been limited because of ethical and practical obstacles to clinical research. What has been widely (although only qualitatively) understood is that apnoea results in hypoxaemia, hypercapnia, acidaemia, atelectasis, loss of a monitoring modality (i.e. expired gas analysis) and loss of the inhaled and exhaled routes of drug administration and elimination [8]. However, we have not had a quantitative understanding of apnoea – When does haemoglobin desaturation commence? How quickly does hypoxaemia progress once established? Does an open airway make a difference during apnoea? How can we slow or delay de-oxygenation during apnoea? Which patients will become hypoxic most quickly? How do children differ in their de-oxygenation during apnoea? It is clear that apnoea is common, dangerous and poorly understood. Apnoea, the anaesthetist's ubiquitous adversary, lurks whenever unconsciousness is induced. How then may we understand this important topic better? The advent of sophisticated and credible physiological models has allowed research approaches to apnoea that provide us with some of the answers we require [9-14]. Hypercapnia occurs inevitably and predictably during apnoea. Once ventilation ceases, carbon dioxide is no longer removed from the alveoli. Within the first few seconds of apnoea, alveolar partial pressure of carbon dioxide (PAco2) increases to match the mixed venous partial pressure. The diffusion gradient for carbon dioxide from mixed venous blood to alveolar gas is thus removed and the arterial carbon dioxide tension (Paco2) rises by approximately 0.8 kPa over the first few seconds of apnoea. Subsequently, Paco2 increases steadily at a rate of approximately 0.5 kPa.min−1 (30 kPa.h−1) [15, 16]. The retention of carbon dioxide results in an inevitable reduction in arterial pH through the formation of carbonic acid; arterial pH typically decreases at a rate of approximately 1.5 units.h−1. Thus, 10 min of apnoea typically produces a Paco2 of 10.5 kPa and a pH of 7.15 (assuming normal baseline measurements). While these figures are hardly desirable, they are usually far from lethal. However, life-threatening hypoxaemia may well have developed during this 10-min period [12]. Haemoglobin desaturation does not usually occur until the alveolar partial pressure of oxygen reaches approximately 12 kPa. However, there is marked interpatient variability in the rate of haemoglobin desaturation during apnoea [17-19]. Once the haemoglobin begins to desaturate, its rate of fall is roughly constant in all patients, and desaturation from normal to brain-injurious levels occurs in just 3 min in a healthy subject with an airway open to room air. Recent investigations have highlighted risk factors for the rapid development of hypoxaemia during apnoea [12, 17, 18]. These risk factors are additive and include a reduced functional residual capacity (FRC), absent or inadequate pulmonary de-nitrogenation, hypoventilation prior to apnoea, increased oxygen consumption and airway obstruction during apnoea. Patients with a combination of these risk factors (e.g. young age, pregnancy, obesity, sepsis) should be recognised in advance of induction of anaesthesia and their management adjusted appropriately. It is widely recognised that de-oxygenation occurs more rapidly in apnoeic children than in apnoeic adults. Recent research findings [20] indicate that children differ from adults in the time from the start of apnoea to the onset of haemoglobin desaturation, but that the rate of desaturation after it has begun is relatively constant between ages, and is approximately 30%.min−1. The timing of the onset of desaturation is highly variable, however, with neonates beginning to desaturate almost immediately following apnoea. Prior to apnoea, de-nitrogenation of the lungs (which is often referred to as ‘pre-oxygenation’ in the UK) generates a reservoir of oxygen within the FRC; this reservoir delays the development of dangerous hypoxaemia during apnoea. The efficacy of such de-nitrogenation is determined by the inspired oxygen fraction, the minute ventilation, the size of the FRC, a good facemask seal and, to a lesser extent, the oxygen consumption [12, 21, 22]. The adequacy of pre-oxygenation may only be assessed (at the bedside) through examination of the expired gas; arterial oxygen saturation may be misleading as a guide to de-nitrogenation, giving falsely reassuring or falsely alarming results. The achievement of Spo2 100% is most definitely not a reason to cease de-nitrogenation, and may occur well before the lungs are adequately de-nitrogenated. Conversely, failure of Spo2 to increase substantially during de-nitrogenation does not necessarily indicate failure of de-nitrogenation or lack of its usefulness; patients with substantial pulmonary shunting may achieve excellent pulmonary oxygen reservoirs while remaining hypoxaemic. The adequacy of pulmonary de-nitrogenation is indicated by an end-tidal oxygen fraction greater than 80%. This is achieved by a good facemask seal [22] and the prevention of air breathing during pre-oxygenation. However, minor errors in allowing room air to be inhaled, particularly during the initial stages of the process, cause little change in the safe duration of apnoea. Very young children can be de-nitrogenated very quickly because of their large minute-ventilation to FRC ratio, and 3 min of de-nitrogenation produces little advantage compared to 1 min [20]. Theoretically, a similar situation applies in third-trimester gravid patients, where increased pulmonary ventilation and reduced FRC facilitate rapid de-nitrogenation. However, in the majority of situations, assurance of adequate de-nitrogenation will take precedence over expediting the induction of anaesthesia. Clinical research indicates that non-gravid adults require 3 min to achieve adequate de-nitrogenation during tidal breathing [23, 24]. Until recently, the evidence suggested that de-nitrogenation could be achieved in an urgent situation with three to four vital capacity breaths [25, 26]. However, Baraka et al. [27] recommend a technique using eight deep breaths prior to induction as this provides a longer period of ‘safe’ apnoea compared to usual techniques. In addition to a high FIo2, some authors [28] have advocated the use of continuous positive airway pressure (CPAP) or a head-up position [29] to increase FRC and thus delay hypoxaemia during apnoea. The problem with using CPAP in de-nitrogenation is that the effect disappears once the face-mask is removed to allow airway instrumentation. Despite its demonstrated efficacy in non-pregnant patients, de-nitrogenation in the head-up position in third-trimester pregnant patients does not appear to confer any advantage with respect to the progression of hypoxaemia [30]. The dynamic equilibrium that exists during steady-state ventilation, where similar volumes of carbon dioxide and oxygen move between the pulmonary blood and the alveoli, changes radically at the onset of apnoea. The large volume of body tissues and the relatively large solubility of carbon dioxide in them cause the liquid sump for carbon dioxide to be 20–25 times larger than the gaseous sump (the FRC). In combination with the loss of a carbon dioxide tension gradient into the alveoli, this causes only a small fraction of the produced carbon dioxide to enter the lungs during apnoea; the large majority dissolves in tissue water, with only approximately 4% (8 ml.min−1) entering the alveoli. This is in contrast to the behaviour of oxygen, which is extracted from the alveoli at its usual rate of approximately 250 ml.min−1. Consequently, the net gas flow from alveoli to blood is much closer to basal oxygen consumption than is commonly appreciated [13]. This has the fortunate consequence that gas applied to an open airway will be drawn into the alveoli at a rate of approximately 242 ml.min−1[13]. This passively inspired gas will be drawn most quickly into those alveoli with the most blood flow, producing an automatic (and fortuitous) ventilation-perfusion matching. Except for a small proportion (6%) that is added water vapour, this 242 ml.min−1 contains whichever gas is applied to the apnoeic patient's airway. Therefore, there is the potential for the passive inhalation of approximately 228 ml.min−1 of oxygen even in the absence of tidal ventilation; this value represents 91% of the body's oxygen requirement. Recent computational modelling studies have demonstrated the ability of very high oxygen fractions to extend the safe duration of apnoea [13]. Indeed, it is apparent that the survivable duration of open-airway apnoea is more than doubled by increasing the oxygen fraction applied to the airway from 90 to 100%[12, 13]. Remarkably, this effect is greater than that achieved by increasing the oxygen fraction applied to the airway from 21 to 90%. During periods of high oxygen consumption (e.g. during the fasciculations caused by suxamethonium, or in pyrexial or pregnant patients) the mass inflow of gas through an open airway will be increased. Therefore, provision of 100% oxygen at such times substantially extends the safe duration of apnoea. In the past, this technique was used to keep patients oxygenated during lung surgery, because it had the advantage of providing a motionless lung. Deprived of an open airway during apnoea, patients do not have the luxury of passive inhalation. The ongoing extraction of oxygen from the alveoli causes a reduction in intrathoracic pressure. This ‘thoracic depressurisation’ compounds the developing arterial hypoxaemia because alveolar oxygen tensions are the product of intra-alveolar pressure and intra-alveolar oxygen fraction. The rate of change in the intrathoracic mass of gas is relatively constant, but the change in intrathoracic volume and pressure are determined by the compliance of the thorax and the rate of oxygen consumption. Thus, a non-patent airway during apnoea accelerates de-oxygenation through two mechanisms: the denial of passive inhalation and the compounded reduction of PAo2 through thoracic depressurisation. Atelectasis increases the risk of chest infection, hypoxaemia and postoperative pyrexia. On occasion, atelectasis may cause severe hypoxaemia that risks organ ischaemia. Through their effect on FRC, the supine position and general anaesthesia exacerbate pulmonary atelectasis to a degree dependent on the patient's age, weight and existing lung pathology. Periods of superimposed apnoea, when the lung volume is less than the patient's usual (awake) FRC, extend these areas of collapse. In addition to position and anaesthesia, a high concentration of inspired oxygen (i.e. larger than 60%) is thought to cause atelectasis through absorption collapse. Advances in patient monitoring have made possible the excellent safety record of anaesthesia. One such advance is exhaled gas monitoring, which provides information on the arterial partial pressure of volatile anaesthetic agents, respiratory rate, cardiac output, alveolar carbon dioxide tension, ventilation-perfusion matching and airway patency. During apnoea, this wealth of information is unavailable and, as a result, patient safety is compromised. Apnoea deprives us of an important route for drug administration and elimination during anaesthesia. The tidal administration of volatile anaesthetic agents and nitrous oxide ceases during apnoea, although a patent airway will allow a degree of drug delivery through passive mass-flow. The amount of volatile agent delivered in this fashion is substantially less than is required during the immediate postinduction phase of anaesthesia. Indeed, it should be noted that apnoea during the early part of a volatile agent anaesthetic will usually result in lightening of the anaesthetic through drug redistribution from vessel-rich areas (e.g. brain) to vessel-poor (e.g. adipose tissue). Conversely, apnoea during the emergence phase of general anaesthesia delays the elimination of volatile agents. Rapid de-oxygenation may be anticipated in patients with risk factors; these include reduced FRC (e.g. obesity, pregnancy) and increased oxygen consumption (e.g. children, pregnancy, pyrexia, suxamethonium). Steps should be taken prior to apnoea to prolong the expected safe duration of apnoea and to provide appropriate tools for creating and maintaining an open airway. Actions before and during the patient's apnoea may radically alter the progression of the ensuing hypoxaemia, hypercapnia and acidosis. In situations of enforced apnoea (e.g. rapid sequence induction), it is our duty to ensure that steps are taken to minimise its impact. Such steps include adequate de-nitrogenation and the maintenance of a patent airway. Even in the absence of ventilation, the open airway will prolong the safe duration of apnoea through passive mass-flow and through the prevention of ‘thoracic depressurisation’. This beneficial effect is greatly magnified by the provision of 100% oxygen to the open airway. In the presence of a difficult airway, transtracheal oxygen insufflation will ensure an ambient oxygen fraction of 100%, very effectively delaying haemoglobin desaturation [12, 31, 32]; such transtracheal insufflation may be commenced prior to the induction of anaesthesia. Although oxygen insufflation is effective in delaying desaturation (even in the already hypoxaemic patient), it will not reverse hypoxaemia caused by apnoea unless a significantly negative intrathoracic pressure exists to cause a large, passive inhalation of oxygen (as occurs following opening of an obstructed airway). Therefore, where apnoea is associated with an obstructed airway, it is useful to apply oxygen to the airway while it is opened to take advantage of this one-time opportunity for re-oxygenation. In the more common scenario of airway intervention in an apnoeic, hypoxaemic patient with a normobaric thorax, tidal ventilation is required to restore normoxaemia. Restoration of normocapnia will require the washout of accumulated carbon dioxide over several minutes, but restoration of normoxaemia may be accomplished with very small minute ventilation if 100% oxygen is supplied. It is widespread practice to wait for the apnoeic patient's PaCO2 to increase enough to drive spontaneous ventilation; this practice is not without dangers. In addition to risking awareness through drug redistribution and impaired administration, we risk the patient's PaCO2 increasing to dangerous levels without our knowledge; we are blinded by the loss of exhaled gas monitoring and falsely reassured of adequate gas exchange by the SpO2, which remains high because of passive inhalation of oxygen-enriched mixtures. A more practical and safer alternative to this ‘permissive apnoea’ is reduction of the ventilatory rate, thus maintaining alveolar patency, exhaled gas monitoring and volatile agent administration or elimination. Apnoea is extremely common in anaesthetic practice. It is potentially lethal or organ-injuring if inadequately managed. An understanding of the pathophysiology of apnoea allows anaesthetists to enhance patient safety by anticipating and thwarting our patient nemesis." @default.
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• W2095278742 title "Fighting for breath: apnoea vs the anaesthetist" @default.
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