Recovery from anaesthesia is considered to start when the patient is no longer under the direct care of an anaesthetist. It should take place in a specifically designated area.
The recovery unit should be staffed by appropriately trained personnel in a ratio of staff to patients of not less than one to one. It should have enough equipment and monitors to care for a wide range of patients, which will vary among different hospitals. Specifically, each patient should have dedicated oxygen and suction ports, a trolley or bed with head-down tilt, and similar monitoring to that used in theatre. In addition, every recovery unit must have a full range of anaesthetic and resuscitation equipment.
Communication between medical staff and recovery room personnel is extremely important. Anaesthetists must relay patient characteristics to the recovery nurses, and these in turn should keep anaesthetists informed of the patient's progress.
There are a multitude of potentially serious problems which can arise in the recovery room, many with little warning; some of the more common ones are discussed below.
Hypoxaemia can be defined as low arterial oxygen content. It is a relative concept; nevertheless in healthy subjects breathing air an arterial saturation below 90% and/or a PaO2 of less than 9 kPa normally represent hypoxaemia. In addition even moderate anaemia, say Hb below 10mg/dl, causes significantly impaired oxygen carriage.
For purposes of discussion, hypoxaemia is divided into early, occurring up to 4 h postoperatively, and late, extending several days after surgery and anaesthesia.
This constitutes a spectrum which presents as respiratory distress characterised by inspiratory stridor, use of the accessory muscles of respiration, straining, and asynchrony between chest and abdominal excursion. In its most extreme form there is insufficient airflow to cause even these signs, with no air entering the lungs.
There are three main causes of airway obstruction. The first is loss of airway muscle tone, due to decreased consciousness or to residual neuromuscular paralysis. The second is laryngeal spasm caused by inappropriate stimulation of the pharyngo-larynx, or by blood, secretions, or stomach contents in the airway. Thirdly, surgical and anaesthetic factors, such as local haemorrhage, recurrent laryngeal nerve trauma, and foreign objects (throat packs, swabs, etc.) can cause airway obstruction.
Airway obstruction requires immediate treatment. Positioning the patient in the left lateral position may prevent posterior displacement of the tongue and collapse of the pharyngeal muscles. The chin lift and jaw thrust manoeuvres contribute to airway stability and may definitively solve the problem. An oropharyngeal airway may help to maintain the airway patent. However, in some patients, especially if they are too 'awake', an oropharyngeal airway may provoke coughing or laryngeal spasm. If all else has failed it becomes necessary to paralyse, intubate and ventilate the patient.
The causes of alveolar hypoventilation are respiratory depression, unresolved neuromuscular paralysis, and closure of lung units.
The latter has a complex mechanism but is very important. Anaesthesia causes a decrease in functional residual capacity (FRC), which often leads to closure of small airways while breathing within the tidal volume range. This reduction in alveolar volume causes relative underventilation of perfused areas, leading to venous admixture (low ventilationperfusion ratio or shunt).
Common causes include hypovolaemia, poor ventricular function (see below), and cardiodepressant effects of anaesthetics, opioids, and other medications. In states of low cardiac output there is relative underperfusion of ventilated areas (high ventilation-perfusion) which creates alveolar dead space.
This occurs minutes after discontinuation of nitrous oxide. It should be prevented by prompt administration of oxygen.
When not compensated by increased extraction or increased cardiac output an increase in oxygen consumption, say in shivering or agitation, causes hypoxaemia. This may worsen the equilibrium between myocardial oxygen consumption and demand.
Pain impairs the ability to cough efficiently, which can lead to sputum retention and consolidation. The postoperative reduction in lung volume already discussed, if allowed to persist unimpaired, leads to reduction in respiratory excursion and small lung volumes, which ultimately can cause lobar collapse.
In practice consolidation and collapse often coexist. They constitute a spectrum which presents clinically as pyrexia, purulent sputum, tachycardia and tachypnoea. Patients most at risk are smokers, the obese, those with chronic obstructive airways disease, and those undergoing high abdominal or thoracic surgery.
Treatment consists of close observation in an adequately staffed and equipped unit, oxygen therapy (see below) physiotherapy, analgesia, and appropriate antibiotics. Many anaesthetists consider epidural analgesia has certain advantages for this patient population; it provides effective analgesia and can reduce opioid requirements and side-effects.
This is usually due to a decrease in airway muscle tone, which may persist up to 5 days postoperatively. In the first 48 h these muscle tone changes are thought to be related to opioids. From about 48 h onwards changes in sleep pattern, not unlike obstructive sleep apnoea, are implicated.
Due to changes in lung mechanisms intrinsic to general anaesthesia, particularly a reduction in FRC, and to the diffusion hypoxia of nitrous oxide, most patients require at least a brief period of supplemental oxygen therapy. Many anaesthetists administer oxygen enriched air for a period equal to the duration of the operation, unless circumstances dictate otherwise.
Oxygen resolves the hypoxaemia of reduced minute ventilation, a common condition after surgery (Fig. 2.2). Administration of oxygen can maintain an adequate saturation even in serious hypoventilation , creating a false sense of well-being when, for example, a worsening hypercarbia is developing. Administration of oxygen to patients with chronic obstructive airways disease who rely on a certain hypox-aemic drive to stimulate their respiratory centre may abolish this stimulus and lead to apnoea.
In hypoxaemia of venous admixture (low ventilationperfusion ratio or shunt typically caused by pneumonia, lung collapse, or pulmonary oedema) a high proportion
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