are designed such that the jet of oxygen administered entrains a fixed proportion of air by the Venturi effect; this phenomenon is known as high air flow oxygen enrichment (HAFOE). The design also ensures that the total flow (oxygen dialed plus air entrained) is greater than the expected PIFR of patients likely to need oxygen therapy, normally 30l/min; this avoids rebreathing gas poor in oxygen.
These masks are usually indicated for patients who require a constant and accurate oxygen concentration, usually those with ventilation-perfusion mismatch (shunt or dead space) or chronic obstructive airways disease. High concentrations of oxygen (up to 60%) can be used in the former; low concentrations (24-28%) are normally used in the latter.
In addition to hypoxaemia, hypoventilation also causes hyper-carbia. Many of the factors involved are interdependent and have been already discussed. In the postoperative period reduced minute ventilation has two main aetiologies: reduced central respiratory drive and peripheral muscle weakness.
There are several important causes of hypotension. Vasodilatation
Anaesthetic agents, opioids, phenothiazines, and other drugs often used have central and peripheral vasodilatory properties. The lack of efferent sensory stimuli under anaesthesia also contributes to a decreased sympathetic tone and vasodilatation. The treatment is adequate cardiovascular monitoring and intravascular volume expansion with i.v. fluids.
Low cardiac output
There are a multitude of causes of low cardiac output postoperatively and only the most important are discussed.
All anaesthetics and opioids are, to a variable extent, direct myocardial depressants and their effect can extend hours into the postoperative period.
Certain anaesthetic drugs, particularly halothane, can cause supraventricular, and very occasionally, ventricular arrhythmias, as can electrolyte imbalances, particularly potassium, calcium and magnesium deficits. Intraoperative events leading to hypoxaemia and/or hypercarbia, can cause serious arrhythmias which may extend into the recovery period. Some patients have pre-existing arrhythmias; others may have an irritable myocardium.
The detailed treatment of arrhythmias is beyond the scope of this chapter. The important issues are to assess the haemodynamic impact, to distinguish between supraven-tricular and ventricular arrhythmias, to determine and treat the cause, and to decide which drug, if any, to use. The most common and best tolerated antiarrhythmic agents are amiodarone, digoxin and lignocaine.
Normally effective compensatory mechanisms to hypo-volaemia (peripheral vasoconstriction, tachycardia) develop early and only quite marked hypovolaemia causes hypotension. Hypovolaemia should be diagnosed by looking for these earlier clinical signs before hypotension develops. Drugs given during anaesthesia can impair the sympathetic response and mask hypovolaemia.
A relatively low intravascular volume amidst anaesthetic induced vasodilatation is a common cause of cardiovascular instability and hypotension. Treatment is based on fluid administration in anticipation of these events.
Haemorrhage, most commonly from the operative site, may be difficult to detect in the recovery room and must always be considered.
The diagnosis is made by suspicion in those at risk, exclusion of other causes of low cardiac output, clinical examination, ECG and serial enzyme changes. The importance of tachycardia, hypotension, hypoxaemia, shivering, and pain, as causes of myocardial ischaemia cannot be over-emphasised.
Even the most fulminant presentation of sepsis usually develops several hours after colonisation by the infective agent. Correspondingly, sepsis should be considered in those with potential entry sites of infection (peritonitis, trauma, compound fractures, skull fractures, abscesses, etc.).
Pain and anxiety on awakening are commonly associated with hypertension. Some patients may have preoperative hypertension, requiring target values to be adjusted accordingly. In addition, the late stages of hypoxaemia can cause a reflex mediated hypertensive response.
The cause of the hypertension must be addressed. For example, in a semiconscious patient hypertension and agitation may be due to pain; sedatives may worsen the situation. Conversely, hypertension and anxiety arising from partial paralysis will not respond to vasodilators or analgesics.
Pain after surgery is distressing; although common, it has until recently received little attention. Pain has been the subject of a report by the Royal Colleges of Surgeons and Anaesthetists . It recommended regular assessment, prevention and treatment of postoperative pain, the establishment of dedicated multidisciplinary acute pain teams, staff training, and appropriate facilities.
Opioids constitute the drugs of choice for severe visceral pain. Unfortunately side-effects can limit their use. Some of the more important side-effects are nausea and vomiting, drowsiness and/or dysphoria, reduced intestinal motility, cardiovascular depression, especially in the frail, and respiratory depression. Opioids are customarily given i.v. or i.m. They can also be given by i.v. or regional (epidural) infusions, by patient controlled analgesia (PCA), or orally.
The NSAIDs can reduce opioid requirements. They are given rectally, orally, or i.v. Their side-effects are mediated by inhibition of cyclo-oxygenase and its deleterious effect on the prostacycline-prostaglandin-thromboxane ratio, which alters platelet aggregation, gastric mucosal protection and renal blood flow.
Paracetamol is an analgesic antipyretic with no clinically significant action on cyclo-oxygenase. It is therefore devoid of the side-effects but also of the anti-inflammatory properties associated with NSAIDs. At high doses it can cause hepatic necrosis. Many anaesthetists commence regular oral paracetamol or preparations of paracetamol with a weak opioid as soon as possible in an attempt to reduce the doses of stronger analgesics.
Epidural analgesia has established its place in surgery to the lower limbs, pelvis, upper abdomen and chest, as it can reduce i.v. opioid requirements and speed mobilisation. Most hospitals place patients receiving postoperative epidural analgesia in high dependency or intensive care wards.
Currently there is considerable interest on combining drugs and techniques. This should make it easier to adapt regimes to individual patient requirements and to minimise side-effects .
Postoperative nausea and vomiting (PONV) are amongst the commonest and disturbing complications of surgery and anaesthesia. Despite even the most effective regimes about 10-20% of patients suffer troublesome PONV There are many causes; some easier to treat than others.
Anaesthetic drugs (opioids, nitrous oxide, and inhalational agents) and general anaesthesia per se cause emesis. Surgical factors, such as traction to the eyes, trauma and shock, peritonitis, and ENT, dental, upper gastrointestinal, and gynaecological surgery are associated with a higher incidence of emesis. Gastrointestinal conditions, such as delayed gastric emptying, oesophageal reflux, duodenal ulcers, and paralytic ileus are also associated with PONV Finally, certain individuals are more susceptible to experiencing emesis, which also occurs more often in females.
Treatment may be difficult; it should involve the avoidance of predisposing factors, including excessive starvation and dehydration, together with the judicious use of the available antiemetics before, during and after surgery.
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