F
F wave, see Atrial flutter.
Facemasks. The traditional black antistatic rubber anaesthetic masks, with soft edges or inflatable rims, have largely been replaced by clear, disposable, plastic masks. Ideally, they should have minimal dead space and make an airtight seal with the patient’s face. Some are malleable to improve fit. Damage may be caused to eyes, nose and face if excessive pressure is used. Dead space may be measured using water, and may be up to 200 ml if the elbow attachment is included. Paediatric facemasks may be small versions of adult ones or specially designed to minimise dead space, e.g. Rendell-Baker’s (anatomically moulded to fit the face). Others are specifically designed for delivery of CPAP or non-invasive ventilation.
[Leslie Rendell-Baker (1917–2008), British-born US anaesthetist]
Facet joint injection. Injection of the posterior facets of the intervertebral joints, performed in patients with mechanical low back pain not associated with leg symptoms or signs of root irritation/compression. The posterior primary ramus of each spinal nerve divides into lateral and medial branches; the latter supplies the lower portion of the facet joint capsule at that spinal level and the upper portion of the capsule below. Thus two posterior primary rami must be blocked to anaesthetise one facet joint.
With the patient prone, the joint is located using image intensification radiography, and a needle inserted under local anaesthesia. It is walked medially and superiorly off the transverse process of the vertebra to reach the angle where the lateral edge of the facet joint meets the superomedial aspect of the transverse process. Local anaesthetic agent may be injected, or longer-lasting relief obtained by destroying the facet joint nerve using radiofrequency rhizolysis.
Facial deformities, congenital. Patients may present for radiological assessment and corrective cosmetic surgery.
• Anaesthetic considerations are usually related to:
airway difficulties, including difficult intubation.
other congenital abnormalities, e.g. CVS, renal, CNS.
general problems of paediatric anaesthesia and plastic surgery, e.g. fluid balance, heat and blood loss during prolonged procedures. Topical vasoconstrictors may be used to reduce bleeding.
cleft lip and palate: incidence is about 1 in 600; it may involve the lip (right, left or bilateral), palate, or combinations thereof. Other abnormalities are present in up to 15% of cases. Swallowing abnormalities may be present, with risk of aspiration pneumonitis. Surgery for cleft lip is usually performed at 3–6 months, for cleft palate at 6–12 months.
Induction of anaesthesia is as for standard paediatric anaesthesia, but tracheal intubation may be difficult if the laryngoscope blade slips into the cleft. To prevent this the cleft may be packed with gauze or the Oxford blade used. Preformed or rigid tracheal tubes are usually employed, with a throat pack. Further surgery may be required in later years.
mandibular hypoplasia: e.g. in Pierre Robin syndrome (macroglossia, cleft palate and cardiac defects) and Treacher Collins syndrome (choanal atresia, downwards sloping eyes, deafness, low-set ears and cardiac defects). The small mandible leaves little room for the tongue, the larynx appearing anterior. Intubation may be extremely difficult; deep inhalational anaesthesia, awake or blind nasal intubation, cricothyrotomy and tracheostomy have been employed.
other deformities that may produce airway problems include macroglossia, cystic hygroma and branchial cyst. Raised ICP may occur with hydrocephalus and craniosynostosis (premature closure of the cranial sutures).
Facial nerve block. Performed to prevent blepharospasm during ophthalmic surgery, e.g. with retrobulbar block.
Facial trauma. Anaesthetic and resuscitative considerations include: possible airway obstruction and difficult tracheal intubation; risk of aspiration of gastric contents; postoperative management of the airway; and the presence of other trauma (especially to head, eyes, chest and neck).
• Classification of facial injuries:
– I: transverse fractures of mid-lower maxilla.
– II: triangular fracture from top of the nose to base of the maxilla.
zygomatic fractures: may hinder mouth opening.
– gastric contents, including swallowed blood. Fractures rarely require immediate surgery; preoperative fasting is usually possible.
– the patient should be warned about postoperative inability to open the mouth if the jaw is wired.
– rapid sequence induction may be necessary. Other techniques may be required if airway obstruction or cervical instability is present (e.g. awake fibreoptic tracheal intubation, tracheostomy).
– tracheal extubation should be performed when the patient is awake and in the lateral position. If severe oedema is anticipated, the tracheal tube is left in place postoperatively until it has subsided. Oral suction may be impossible. Dexamethasone is often given intraoperatively to reduce oedema.
– the tracheal tube may be withdrawn into the pharynx to act as a nasal airway or an airway exchange catheter placed.
[René Le Fort (1829–1893), French surgeon]
See also, Dental surgery; Maxillofacial surgery; Induction, rapid sequence; Intubation, difficult
Facilitation, post-tetanic, see Post-tetanic potentiation
Faculty of Anaesthetists, Royal College of Surgeons of England. Founded in 1948 at the request of the Association of Anaesthetists, in order to manage the academic side of anaesthesia whilst the latter body concentrated on general and political aspects. Administered and regulated the FFARCS examination and training of junior anaesthetists, until it became the College of Anaesthetists in 1988 and thence the Royal College of Anaesthetists in 1992. The corresponding Faculty in Ireland was founded in 1959, becoming a College in 1998.
Faculty of Intensive Care Medicine, Royal College of Anaesthetists. Established in 2010 by seven parent Colleges, its remit is to define and promote standards of education and training in critical care. Replaces the Intercollegiate Board for Training in Intensive Care Medicine. Responsible for developing a primary specialty training programme for intensive care medicine.
Faculty of Pain Medicine, Royal College of Anaesthetists. Established in 2007, to promote education, training and excellence in the delivery and management of pain medicine.
Factor VIIa, recombinant, see Eptacog alfa
Fade. Progressive reduction in strength of muscle contraction during tetanic or intermittent stimulation (e.g. train-of-four), exaggerated in non-depolarising neuromuscular blockade. Thought to be caused partly by inadequate mobilisation of acetylcholine in presynaptic nerve endings at the neuromuscular junction compared with the rate of release. Block of prejunctional acetylcholine receptors, which normally increase mobilisation by a positive feedback mechanism, is thought to be involved during neuromuscular blockade. Thus patterns of fade vary between blocking drugs, reflecting their differing affinities for prejunctional receptors (e.g. greater with tubocurarine than with pancuronium).
Failed intubation, see Intubation, failed
Fallot’s tetralogy. Commonest cause of cyanotic heart disease (65%), accounting for 5–10% of congenital heart disease.
hypoxaemia and cyanosis, usually from birth, with secondary polycythaemia. Dyspnoea occurs on effort.
acute exacerbations of shunt are attributed to infundibular spasm and increased pulmonary vascular resistance secondary to hypoxia. Features include worsening cyanosis, syncope and metabolic acidosis. Symptoms are relieved by squatting; thought to increase SVR and encourage pulmonary blood flow.
supraventricular arrhythmias; right heart failure in adults.
a loud pulmonary murmur suggests mild stenosis. A large VSD may be unaccompanied by a murmur.
as for congenital heart disease, VSD, cardiac surgery, paediatric anaesthesia.
infundibular spasm is provoked by fear and anxiety, and may be treated with β-adrenergic receptor antagonists. Sedative premedication is often given.
avoidance of air bubbles in iv injectate, because of the risk of systemic embolisation.
peripheral vasodilatation worsens shunt and cyanosis. Vasopressor drugs (e.g. phenylephrine) may be used to increase SVR and pulmonary blood flow.
False negative/false positive, see Errors
Familial periodic paralysis. Rare group of autosomal dominant myopathies due to defects in ion channels in skeletal muscle; characterised by episodes of severe weakness, often precipitated by extremes of temperature, physical activity, stress and large carbohydrate loads. Although traditionally classified into hypo- or hyperkalaemic variants, the condition may be associated with normal plasma potassium levels. Diagnosis may be difficult, but exercise EMG has a high level of sensitivity; detection of known gene mutations can be helpful. Treatment depends on type of disease but includes the use of carbonic anhydrase inhibitors (e.g. acetazolamide), oral potassium supplements (for hypokalaemic variant) and thiazide diuretics (for hyperkalaemic variant).
Careful use of neuromuscular blocking drugs is required, with close monitoring of perioperative potassium levels. Arrhythmias may accompany potassium changes. Glucose-containing intravenous fluids should be avoided in the hyperkalaemic form of the disease. Increased susceptibility to MH is thought to be unlikely.
A needle is inserted 0.5 cm caudal to the junction of the lateral third of the inguinal ligament with the medial two-thirds. A click or ‘give’ (the latter if continuous pressure is applied to the plunger of the syringe) is felt as the needle passes through the fascia lata, followed by a second click as the fascia iliaca is pierced. An ultrasound-guided in-plane approach may also be used. 30–40 ml local anaesthetic agent (e.g. 0.25% bupivacaine) is then injected. Distal pressure is advocated to encourage cranial extension of the solution. A catheter may be inserted to allow continuous infusion of local anaesthetic.
Dalens B, Vanneuville G, Tanguy A (1989). Anesth Analg; 69: 705–13
Fascicular block, see Bundle branch block
Fasciculation. Visible contraction of skeletal muscle fibre fasciculi, seen following use of suxamethonium and other depolarising neuromuscular blocking drugs. Possible damage to fibres is suggested by increased serum myoglobin and creatine kinase following suxamethonium; it may also be partly responsible for the raised potassium that occurs. May be related to post-suxamethonium myalgia, since measures to reduce the latter often reduce visible fasciculation.
Also occurs in motor neurone disease, spinal motor neurone lesions, and rarely in myopathies. Muscle fibre fibrillation (e.g. occurring after denervation injury) is invisible.
Fasciitis, necrotising, see Necrotising fasciitis
Fat embolism. Dispersion of fat droplets into the circulation, usually following major trauma. Also occurs in acute pancreatitis, burns, diabetes mellitus, joint reconstruction (possibly related to use of methylmethacrylate cement), cardiopulmonary bypass, liposuction, bone marrow harvest/bone marrow transplantation and parenteral infusion of lipids. Post-mortem evidence of fat embolism is found in 90% of fatal trauma cases. The mechanical (infloating) theory proposes that fat liberated from fractured bone enters the venous system and impacts in pulmonary capillaries, resulting in pulmonary dysfunction. Systemic embolism may occur via pulmonary arteriovenous shunts or a patent foramen ovale. The biochemical theory suggests that free fatty acids released following trauma induce an inflammatory response that causes pulmonary dysfunction, possibly mediated via an increase in plasma lipase. Both processes may occur.
confusion, restlessness, coma, convulsions, cerebral infarction.
dyspnoea, cough, haemoptysis. Hypoxaemia is almost inevitable. Pulmonary hypertension and pulmonary oedema may occur. Typically, gives a ‘snowstorm’ appearance on the CXR, but radiography may be normal. May contribute to development of ARDS.
petechial rash, typically affecting the trunk, pharynx, axillae and conjunctivae.
tachycardia, hypotension, pyrexia.
platelets are reduced in 50%; hypocalcaemia is also common. Coagulation disorders may occur.
fat droplets are detected in cells obtained by bronchopulmonary lavage in 70% of cases. The presence of fat droplets in the urine is a non-specific finding following trauma. Retinal examination may reveal intravascular fat globules.
O2 therapy; IPPV may be required.
supportive therapy. Fluid restriction has been advocated for reducing lung water.
corticosteroids have been shown to reduce mortality in several small studies, but optimum dosage, timing and patient selection remain unclear.
heparin, aprotinin, aspirin, clofibrate, prostacyclin, dextran and alcohol infusion have all been tried, without conclusive benefit.
Prognosis is variable and unrelated to initial severity. Mortality is 10–20%.
Fats (Lipids). Four main classes are present in plasma and cells:
– composed of glycerol and fatty acids. Formed in the GIT, liver and adipose tissue.
– endogenous triglycerides are synthesised in the liver and secreted as very low-density lipoproteins (VLDLs). These are hydrolysed in the blood by lipoprotein lipase; the FFAs released are taken up by tissues for resynthesis of triglycerides or remain free in the plasma. During starvation, intracellular hormone-sensitive lipase breaks down adipose triglycerides to FFAs and glycerol (increased by β-adrenergic stimulation; decreased by insulin).
– include corticosteroids, bile salts and cholesterol (from which the former two are derived).
– plasma cholesterol is esterified with fatty acids, or circulates within low-density, high-density and intermediate-density lipoproteins (LDLs, HDLs and IDLs respectively) and VLDLs, especially the first. Unesterified cholesterol forms a major component of cell membranes.
– mainly synthesised in the liver and small intestine mucosa.
– circulate in the plasma in lipoproteins and constitute important cellular components, but not part of the depot fats. Present in myelin and cell membranes.
Lipoproteins are classified according to their size: chylomicrons 80–500 nm; VLDLs 30–80 nm; IDLs 25–40 nm; LDLs 20 nm; HDLs 7.5–10 nm. LDLs and IDLs are formed from VLDLs; HDLs are formed in the liver. High levels of cholesterol, LDLs and VLDLs are associated with ischaemic heart disease, although the role of each is controversial. HDLs may be protective.
Fazadinium bromide. Obsolete non-depolarising neuromuscular blocking drug, introduced in 1972. Acts within 60 s and marketed as an alternative to suxamethonium. Withdrawn because of marked cardiovascular effects due to ganglion and vagal blockade.
Felypressin. Synthetic analogue of vasopressin, used as a locally acting vasoconstrictor. Has minimal effects on the myocardium, therefore safer than adrenaline during anaesthesia with halothane. Available in combination with prilocaine for local infiltration.
Femoral artery. Continuation of the external iliac artery; enters the thigh below the inguinal ligament midway between the anterior superior iliac spine and symphysis pubis, where it lies between the femoral vein medially and femoral nerve laterally. Descends through the femoral triangle and enters (and runs in) the subsartorial canal. Ends by piercing adductor magnus 10 cm above the knee joint where it becomes the popliteal artery.
May be cannulated for arterial BP measurement, dialysis and use of the intra-aortic counter-pulsation balloon pump as well as providing access for angiography.
Femoral nerve block. Useful as an adjunct to general anaesthesia for operations involving the anterior thigh, hip, knee and medial lower leg. May be combined with sciatic nerve block and/or obturator nerve block for more extensive surgery to the lower limb. Also used for analgesia in leg and thigh fractures.
• Anatomy:
the femoral nerve (L2–4) arises from the lumbar plexus, passing under the inguinal ligament to enter the femoral triangle lateral to the femoral artery. Divides into terminal branches within 3–6 cm.
supplies hip and knee joints and muscles of the anterior thigh. Also supplies skin of the anterior thigh and knee, and medial lower leg and foot via the saphenous branch (Fig. 66).
Fig. 66 Nerve supply of leg (for nerve supply of ankle and foot, see Fig. 11 Ankle, nerve blocks)
• Block:
after aspiration to exclude vascular puncture, 10–15 ml local anaesthetic agent is injected. A further 5–10 ml is injected in a fan laterally as the needle is withdrawn, in case cutaneous branches arise higher than normal.
injection of 30–40 ml solution at the initial site, with distal compression, has been claimed to force solution cranially to the lumbar plexus, lying between psoas and quadratus lumborum muscles (three-in-one block). In fact, a continuous femoral ‘sheath’ probably does not exist as a separate entity; the ‘three-in-one block’ is thought to represent combined femoral and lateral cutaneous nerve blocks below the inguinal ligament as a result of non-specific spread. Fascia iliaca compartment block is a more reliable and anatomically sound method of producing block of the three nerves.
Femoral triangle. Compartment of the anterior upper thigh; its borders are the inguinal ligament superomedially, the medial border of adductor longus medially and the medial border of sartorius laterally (Fig. 67). Its floor is formed by adductor longus, pectineus, psoas and iliacus muscles, and its roof by the fascia lata of the thigh. Contains the femoral artery, vein and canal within the femoral sheath; the femoral nerve and lateral cutaneous nerve of the thigh lie laterally.
Femoral venous cannulation. The femoral vein is the continuation of the popliteal vein and accompanies the femoral artery in the femoral triangle, ending medial to the latter at the inguinal ligament, where it becomes the external iliac vein. Following skin cleansing, the patient’s leg is extended and slightly abducted at the hip. The femoral vein lies 1–1.5 cm medial to the femoral artery, 2–3 cm below the inguinal ligament. The needle is inserted here and advanced at an angle of 45–60° to the frontal plane. When venous blood is aspirated, the syringe is lowered to lie flat on the skin. A Seldinger technique is usually employed thereafter. Ultrasound guidance may be useful.
May be performed for central venous cannulation; traditionally avoided if other routes are available because of (probably unfounded) fears of infection or thrombosis. May be useful in superior vena caval obstruction.
Fenoldopam mesylate. Selective D1–dopamine receptor partial agonist, introduced in the USA in 1998 as an iv vasodilator drug. Also has mild α2-adrenergic agonist properties. Causes increased renal blood flow, diuresis and sodium excretion. Given as an infusion for hypertensive crisis, its short half-life of 5 min results in rapid offset of action. Metabolised in the liver to inactive compounds.
Fenoterol hydrobromide. β-Adrenergic receptor agonist, used as a bronchodilator drug. Similar in action to salbutamol and terbutaline but less β2-selective. Now only available in the UK as part of a compound aerosol formulation.
Fentanyl citrate. Synthetic opioid analgesic drug, derived from pethidine. Developed in 1960. 100 times as potent as morphine. Widely used perioperatively as an analgesic, for sedation (e.g. on ICU) and in chronic pain. Onset of action is within 1–2 min after iv injection; peak effect is within 4–5 min. Duration of action is about 20 min, terminated by redistribution initially as plasma clearance is less than for morphine. Postoperative respiratory depression is possible if large doses are used, especially in combination with opioid premedication and other depressant drugs. Causes minimal histamine release or cardiovascular changes, although may cause bradycardia.
• Dosage:
to obtund the pressor response to laryngoscopy: 7–10 µg/kg iv.
as a co-induction agent/during anaesthesia: 1–3 µg/kg iv with spontaneous ventilation; 5–10 µg/kg with IPPV. Up to 100 µg/kg is used for cardiac surgery. Muscular rigidity and hypotension are more common after high dosage. Has been used in neuroleptanaesthesia.
by infusion: 1–5 µg/kg/h, e.g. for sedation. For patient-controlled analgesia: 20–100 µg bolus with 3–5 min lockout.
25, 50, 75 or 100 µg/h transdermal patch placed on the chest or upper arm and replaced (using a different site) every 72 h. A patch employing iontophoresis has been developed for postoperative patient-controlled analgesia but is not currently marketed.
Commonly used for epidural and spinal anaesthesia (see Spinal opioids).
Fetal circulation. Oxygenated blood from the placenta passes through the single umbilical vein and enters the inferior vena cava, about 50% bypassing the liver via the ductus venosus. Most of it is diverted through the foramen ovale into the left atrium, passing to the brain via the carotid arteries (Fig. 68). Deoxygenated blood from the brain enters the right atrium via the superior vena cava, and passes through the tricuspid valve to the right ventricle. Because the resistance of the pulmonary vessels within the collapsed lungs is high, the blood passes from the pulmonary artery trunk through the ductus arteriosus to enter the aortic arch downstream from the origin of the carotid arteries. Thus relatively O2-rich blood is conserved for the brain, and the rest of the body is perfused with the less oxygenated blood. Deoxygenated blood reaches the placenta via the two umbilical arteries, arising from the internal iliac arteries; they receive about 60% of cardiac output.
– pH 7.2
At birth, placental blood flow ceases, and peripheral resistance increases. Lung expansion lowers pulmonary vascular resistance, both directly and via reduction of hypoxic pulmonary vasoconstriction. Thus pulmonary and right heart pressures fall, and aortic and left heart pressures rise. Pulmonary blood flow increases and flow through the ductus arteriosus and foramen ovale ceases. The ductus arteriosus usually closes within 48 h due to the high PO2. Pulmonary artery pressure, pulmonary vascular resistance and pulmonary blood flow approach adult values by 4–6 weeks.
Neonates may revert to persistent fetal circulation, with decreased pulmonary blood flow and right-to-left shunt through the ductus arteriosus, foramen ovale, or both. This may occur if pulmonary vascular resistance is increased, e.g. by hypoxia, hypothermia, hypercapnia, acidosis or polycythaemia. It may occur during surgery if anaesthesia is too light or if the patient strains on the tracheal tube. Right-to-left shunt increases with worsening hypoxia and further reflex vasoconstriction. Ductal shunting may be demonstrated clinically by measuring O2 saturation (e.g. by pulse oximetry) in the arm and leg simultaneously; a large difference (higher saturation in the arm) represents significant ductal blood flow (i.e. pulmonary artery pressure exceeds aortic pressure). If the right ventricle fails, right atrial pressure exceeds left atrial pressure, increasing shunt through the foramen ovale.
Treatment of persistent fetal circulation includes: O2 therapy; correction of acidosis, hypercapnia and hypothermia; and inotropes and fluid administration. Drugs that lower pulmonary vascular resistance (e.g. tolazoline, isoprenaline) may be given. Extracorporeal membrane oxygenation has been used.
Fetal haemoglobin. Consists of two α chains and two γ chains, the latter differing from β chains by 37 amino acids. Binds 2,3-DPG less avidly than haemoglobin A (adult), thus shifting the oxyhaemoglobin dissociation curve to the left (P50 is 2.4 kPa [18 mmHg]) and favouring O2 transfer from mother to fetus. At the low fetal PO2, it gives up more O2 to the tissues than adult haemoglobin would, because its dissociation curve is steeper in this part. Forms 80% of circulating haemoglobin at birth; replaced by haemoglobin A normally within 3–5 months. May persist in the haemoglobinopathies. Reactivation of production of fetal haemoglobin using hydroxyurea has been used in the treatment of sickle cell anaemia.
A variety of embryonic haemoglobins are present up to 2–3 months of gestation.
Fetal monitoring. Methods include:
heart rate, especially related to uterine contractions. May be performed intermittently using a trumpet-shaped stethoscope (Pinard) or portable ultrasound machine, or continuously using a cardiotocograph (CTG), a device that measures heart rate by external ultrasonography or fetal scalp electrode, and contractions by external transducer or intrauterine probe:
– accelerations usually indicate reactivity and well-being.
– decelerations; usual significance:
– early (type I), i.e. with contractions: vagally mediated, due to head compression.
– late (type II), i.e. after contractions: represent hypoxia, although not always with acidosis.
– variable: usually due to cord compression; they may indicate compromise if severe.
Prolonged decelerations are more sinister, and may represent severe fetal compromise.
Recent NICE guidelines classify the CTG according to the baseline rate, variability, accelerations and decelerations as being ‘normal’ (all four criteria are normal), ‘suspicious’ (one of the four is ‘non-reassuring’) or ‘pathological’ (two or more of the four are non-reassuring or one is ‘abnormal’). Predictive value of cardiotocography is poor in low-risk patients, hence its routine use is controversial. Combination with fetal electrocardiography (ST waveform analysis) is thought to increase its sensitivity.
Signs of fetal compromise may be related to treatable conditions, e.g. uterine hypertonicity associated with excessive oxytocin administration, maternal hypotension. Aortocaval compression should always be considered, especially if regional analgesia has been provided.
Post-delivery, cord blood gas interpretation (pH represents degree of acidosis at time of delivery), Apgar scoring, time to sustained respiration and neurobehavioural testing of neonates may be assessed; these may be useful prognostically.
Fetus, effects of anaesthetic drugs on. The fetus is usually defined as such from the ninth week of gestation. Most major organ structures develop earlier than this.
• Main anaesthetic considerations:
effect of anaesthetic drugs on fetal development and spontaneous abortion:
– animal studies suggest increased fetal loss and abnormalities following prolonged exposure to high concentrations of volatile agents and N2O.
