Measure from the upper edge of the thyroid cartilage to tip of the jaw with the head fully extended (Fig. 2.3). A short thyromental distance equates with an anterior larynx which is at a more acute angle and also results in less space for the tongue to be compressed into by the laryngoscope blade. This is a relatively unreliable test unless combined with other tests:

• Thyromental distance >6.5 cm = easy intubation

• Thyromental distance <6.0 cm = difficult intubation.

Figure 2.3 (A) Thyromental and (B) sternomental distance.

Parameter	Risk level
Weight	0–2 (e.g. >90 kg = 1; >110 kg = 2)
Head and neck movement	0–2
Jaw movement	0–2
Receding mandible	0–2
Buck teeth	0–2
Maximum	10 points

Radiographic predictors of difficult intubation

These have the disadvantage of X-ray exposure and thus cannot be performed as routine tests.

Mandibulohyoid distance (Chou and Wu 1993)

This is the vertical distance between the anterior edge of the hyoid and the mandible vertically above measured by lateral X-ray. A distance >6 cm is suggestive of difficult intubation. A longer distance results in more of the tongue being present in the hypopharynx, which must be displaced to view the vocal cords.

Cass et al (1956) (absolute measurements not given)

• Incisor tooth to posterior border of ramus

• Alveolar margin to lower border of the mandible

• Angle of the mandible.

White and Kander (1975)

• Increased length of mandible

• Increased depth of mandible

• Reduced distance between occiput and spinous process of C₁ or reduced distance between C₁–C₂ interspinous gap.

Nichol and Zuck (1983)

These authors stressed the importance of a reduced atlanto-occipital distance as a predictor of ability to extend the head during laryngoscopy.

Combined indicators

By combining prognostic indicators, a greater specificity for predicting difficult intubation may be achieved.

• Freck (1991) found that a thyromental distance of 7 cm in patients with Mallampati class III/IV predicts a grade IV intubation. The test has high sensitivity and specificity.

• Benumof (1991) suggested that a combination of relative tongue/pharyngeal size, atlantoaxial joint extension and anterior mandibular space provides a good predictor of difficult intubation and that the tests are quick and easy to perform.

• Best multifactorial index scores the following criteria to give sensitivity and specificity >90% in prediction of difficult intubation (Arné et al 1998):

– Previous history of difficult intubation

– Pathologies associated with difficult intubation

– Clinical symptoms of a pathological airway

– Inter-incisor gap

– Thyromental distance

– Head and neck movement

– Mallampati’s modified test.

Difficult Airway Society Guidelines for Management of the Unanticipated Difficult Intubation 2004

Problems with tracheal intubation are the most frequent cause of anaesthetic death in the analyses of records of the UK medical defence societies. The Difficult Airway Society (DAS) has developed guidelines for management of the unanticipated difficult intubation in an adult non-obstetric patient, see http://www.das.uk.com/home

Figure 2.4 Simple composite chart.

(Difficult Airway Society, 2004)

Figure 2.5 Unanticipated difficult tracheal intubation.

(Difficult Airway Society, 2004)

Figure 2.6 Failed intubation.

(Difficult Airway Society, 2004)

Figure 2.7 Management of unanticipated difficult tracheal intubation.

(Difficult Airway Society, 2004)

Bibliography

Arné J., Descoins P., Ingrand P., et al. Preoperative assessment for difficult intubation in general and ENT surgery: predictive value of a clinical multivariate risk index. Br J Anaesth. 1998;80:140-146.

Benumof J.L. Management of the difficult airway. Anesthesiology. 1991;75:1087-1110.

Cass N.M., James N.R., Lines V. Difficult laryngoscopy complicating intubation for anaesthesia. BMJ. 1956;1:488-489.

Charters P. What future is there for predicting difficult intubation? Br J Anaesth. 1996;77:309-311.

Chou H.C., Wu T.L. Mandibulohyoid distance in difficult laryngoscopy. Br J Anaesth. 1993;71:335-339.

Cormack R.S., Lehane. Difficult tracheal intubation in obstetrics. Anaesthesia. 1984;39:1105-1111. Difficult Airway Society, 2004, British Airway Society Guidelines Flow-chart 2004, http://www.das.uk.com/files/rsi-Jul04-A4.pdf.

Freck C.M. Predicting difficult intubation. Anaesthesia. 1991;46:1005-1008.

Henderson J.J., Popat M.T., Latto I.P., et al. Difficult Airway Society guidelines for management of the unanticipated difficult intubation. Anaesthesia. 2004;59:675-694.

Lavery G.G., McCloskey B.V. The difficult airway in adult critical care. Crit Care Med. 2008;36:2163a-2173a.

Lee A., Fan L.T.Y., Gin T., et al. A systematic review (meta-analysis) of the accuracy of the Mallampati tests to predict the difficult airway. Anesth Analg. 2006;102:1867-1878.

Mallampati S.R., Gatt S.P., Gugino L.D., et al. A clinical sign to predict difficult intubation: a prospective study. Can J Anaesth. 1985;32:429-434.

Nichol H.L., Zuck D. Difficult laryngoscopy – the ‘anterior’ larynx and the atlanto-occipital gap. Br J Anaesth. 1983;55:141-143.

Patil V.U., Stehling L.C., Zaunder H.L. Fibreoptic endoscopy in anaesthesia. Chicago: Year Book Medical Publishers, 1983.

Popat M. The airway. Anaesthesia. 2003;58:1166-1170.

Savva D. Prediction of difficult tracheal intubation. Br J Anaesth. 1994;73:149-153.

Vaughan R.S. Predicting difficult airways. BJA CEPD Reviews. 2001;1:44-47.

White A., Kander P.L. Anatomical factors in difficult direct laryngoscopy. Br J Anaesth. 1975;47:468-474.

Wilson M.E. Predicting difficult intubation. Br J Anaesth. 1993;71:333-334.

Anaesthesia And Respiratory Disease

Smoking

Postoperative pulmonary complications occur in 22% of current smokers but only 5% of those who have never smoked.

Preoperative cessation of smoking (Box 2.1)

A study in patients undergoing CABG (Warner 2006) showed that in those stopping smoking, the incidence of postoperative pulmonary complications did not fall until at least 8 weeks had elapsed:

• current smokers – 33% incidence

• ex-smokers <8 weeks – 57% incidence

• ex-smokers >8 weeks – 15% incidence.

Box 2.1 Effects of cessation of smoking

12–24 h	Clearance of carbon monoxide
2–10 days	Decreased upper airway reactivity
1–2 months	Increase in postoperative pulmonary complications (Bluman et al 1998)
6 months	Decrease in postoperative pulmonary complications
Years	Reduced risk of COPD, ischaemic heart disease, lung cancer and cerebrovascular disease

Chronic bronchitis

Chronic bronchitis is defined as productive cough >3 months of the year for ≥2 years.

Postoperative pneumonia

Predisposed by:

• decreased ciliary activity

• sputum retention

• poor cough

• lack of humidification.

Viral upper respiratory tract infection (URTI)

Common in paediatric ENT patients. Causes worsening of asthma and ↑ bronchial reactivity for up to 6 weeks following resolution of symptoms. May be due to viral-mediated damage to vagus releasing acetylcholine and potentiating bronchoconstriction.

In children, there is a 2–7-fold increase in respiratory related adverse events, if intubated, an 11-fold increase in adverse events, and an increased risk of transient hypoxaemia in the postoperative period. In adults with URTI, upper airway reactivity is also increased by an amount related to severity of symptoms.

Therefore, postpone routine surgery for at least 2–3 weeks. If anaesthesia is given during this period, consider topical anaesthesia to larynx to reduce vagally mediated reflexes and consider the use of atropine to block hyperreactivity. Monitor O₂ saturation postoperatively.

Effects of general anaesthesia

• Central respiratory depression

• Reduced compliance

• Cranial shift of diaphragm, atelectasis, reduced tone of chest wall and reduced thoracic blood volume cause ↓ FRC (17%, 500 mL)

• FRC approaches and may exceed closing capacity (CC)

• Impaired O₂ and CO₂ exchange

• Increased spread of V/

ratios. Increased shunting (shunt fraction during GA: 11% during spontaneous breathing, 14% during IPPV)

• Hypoxic pulmonary vasoconstriction inhibited by up to 25% with volatiles but not by i.v. agents.

All these factors result in an increased A–aO₂ (difference in alveolar and arterial oxygen tensions), which persists for at least 1–2 h postoperatively. Diaphragm may recover from neuromuscular blockade prior to muscles involved in coughing and swallowing. Postoperative wound pain, abdominal distension, pulmonary venous congestion and a supine posture all increase CC–FRC and result in further alveolar collapse.

Anaesthesia for chronic respiratory disease

Anaesthetic techniques

Aims

• Avoid bronchospasm (which causes autoPEEP)

• Avoid hypoxia or hypercapnia

• Minimize postoperative complications (e.g. pain relief reduces atelectasis)

• Avoid postoperative ventilation (reduces ciliary motility, acts as route for infection, causes bronchospasm).

Use either regional/local technique or maximal support approach with GA. Plan elective surgery for summer.

Regional technique

Requires the patient to be able to lie flat for the duration of surgery and not cough. Avoid sedation which may precipitate respiratory failure. Can be combined with a light GA and spontaneous ventilation, but reactive airways are irritated by an endotracheal tube which may cause severe bronchospasm. Avoided by using local/regional technique.

General anaesthetic

The technique of choice for patients with respiratory failure or upper abdominal/thoracic surgery. Light/no premedication. Use a heat and moisture exchanger or humidifier. Use drugs allowing rapid recovery. IPPV allows control of O₂ and CO₂ and enables airway suctioning and may need to be continued postoperatively. Use slow inspiratory flow to allow equilibration of fast and slow alveoli. A long expiratory time reduces air trapping. Avoid PEEP in patients with COPD. If there are high-frequency bullae, avoid N₂O and consider double-lumen tube. Spontaneous respiration or jet ventilation (HFJV) may be appropriate with bullae.

At the end of surgery, ensure bowel is decompressed and drain any peritoneal air. Sit patient up postoperatively, which increases FRC. Epidurals also increase FRC (bupivacaine > morphine). Prior to extubation, ensure cardiovascular stability and fluid balance and ensure no residual effects of anaesthetic or neuromuscular blockade.

Anaesthesia for asthmatics

Asthma affects 4–5% of the population. There are 1400 deaths p.a. in the UK. Prevalence and mortality are increasing. Avoid factors precipitating bronchospasm (differential diagnosis = aspiration, pulmonary oedema, endobronchial intubation, patient too light, mechanical obstruction of the tube).

Preoperative

Assess severity: severe if patient unable to speak sentences, pulse >120/min, pulsus paradoxus >20 mmHg, FEV₁ <25%, ↑P_aco₂. Consider bronchodilators, hydration, antibiotics and steroids. Measure baseline arterial blood gases (ABGs). Percussive physiotherapy is contraindicated because it exhausts the patient further.

Premedication

Atropine limits vagal reflexes that cause bronchospasm. The small doses used for premedication do not cause bronchodilation but increase the viscosity of sputum. Consider nebulized salbutamol.

Anaesthetic

Use of a regional or local technique avoids most precipitating factors. Induction with ketamine (↑ secretions but is the best bronchodilator), propofol, etomidate or benzodiazepines. Thiopentone causes histamine release and may cause bronchoconstriction.

Although suxamethonium causes histamine release, there is no evidence that it precipitates bronchospasm. Intubate deep to avoid stimulating reflexes which cause bronchospasm and avoid excessively light anaesthesia which may also cause endotracheal tube irritation and bronchoconstriction. Consider topical lidocaine or lidocaine 1.5 mg.kg⁻¹ i.v. pre-intubation.

Isoflurane and sevoflurane, but not desflurane cause moderate bronchodilation. Desflurane causes bronchoconstriction in patients who currently smoke. If theophylline infusion is running (6 mg.kg⁻¹ loading dose, 0.5 mg.kg⁻¹.h⁻¹ maintenance), halve the rate because general anaesthesia decreases liver blood flow. If the patient is ventilated, aim for slow inflation for optimal alveolar gas distribution. Slow exhalation reduces air trapping. There is little work on the effects of neuromuscular blockers on asthma. Avoid those that cause histamine release. Remember to give steroid supplements if the patient is taking steroids.

Perioperative complications (bronchospasm, laryngospasm) are more common in older patients (>50 years) and those with active asthma.

Reversal

Anticholinesterases cause bronchospasm, prevented by the addition of an anticholinergic.

Figure 2.8 (A) British Guideline on the Management of Asthma. Management of Acute Asthma in Adults. (British Thoracic Society & Scottish Intercollegiate Guidelines Network 2009.) (B) British Guideline on the Management of Asthma. Management of Acute Asthma in Children aged over 2 years. (British Thoracic Society & Scottish Intercollegiate Guidelines Network 2009.) (C) British Guideline on the Management of Asthma. Management of Acute Asthma in Children aged under 2 years.

(British Thoracic Society & Scottish Intercollegiate Guidelines Network 2009.)

Anaesthesia for cystic fibrosis

Cystic fibrosis is caused by an autosomal recessive gene localized to chromosome 7, occurring in 1:2000 births. It is the commonest fatal inherited disease. The prognosis is improving, with median life expectancy of 40 years. Gene encodes for cystic fibrosis transmembrane inductance regulator, which is involved in chloride transport on epithelial cell membranes. Results in impaired chloride and sodium transport with increased electrolyte content of secretions.

Presents as meconium ileus, recurrent respiratory infections, steatorrhoea and failure to thrive. Diagnosed by sweat test with sweat sodium and chloride >60 mmol.L⁻¹.

Pathophysiology

Cardiovascular. Chronic hypoxaemia and pulmonary disease result in cor pulmonale. Left ventricular abnormalities and cardiomyopathy.

Respiratory. Chronic sinusitis, nasal polyps, turbinate hypertrophy, mucous plugging of airways, hyperinflation, bronchial hyperreactivity, bronchiectasis, chronic infection (Staphylococcus aureus, Haemophilus influenzae, Pseudomonas), obstructive and restrictive defects.

Gastrointestinal. Gastro-oesophageal reflux, impaired liver function, biliary cirrhosis causing portal hypertension, insulin-dependent diabetes and malabsorption secondary to pancreatic insufficiency causing malnutrition.

Other. Anaemia of chronic disease, renal impairment secondary to aminoglycosides, diabetes and amyloidosis.

Anaesthesia

Preoperative. Urea and electrolytes, liver function tests, glucose, full blood count, chest X-ray. Pulmonary function tests (FEV₁ <30% = poor prognosis), arterial blood gases, exclusion of active infection, vigorous physiotherapy, good diabetic control.

Premedication. Sedatives and narcotics best avoided. Anticholinergics probably of little benefit. Give H₂ antagonists if reflux.

Induction. Gas induction slow due to V/ mismatch but may be unavoidable, particularly in children with poor venous access. Coughing and laryngospasm are common. Pre-oxygenate to avoid desaturation. Ketamine increases secretions and is relatively contraindicated. Aim to intubate for most procedures to allow tracheobronchial suctioning and control of ventilation. Ensure adequate depth of anaesthesia prior to intubation in view of bronchial hyperreactivity. Low airway pressures reduce the risk of pneumothorax.

Maintenance. Humidify inspiratory gases. Sevoflurane/desflurane allows rapid recovery permitting early physiotherapy. Long-acting muscle relaxants risk incomplete postoperative reversal. Aminoglycoside antibiotics may prolong neuromuscular blockade. Aim for early extubation.

Postoperative. Effective analgesia is essential to allow good coughing and regular physiotherapy. Maintain adequate hydration.

Pulmonary hypertension

Tachycardia reduces filling time, causing ischaemia. Hypoxia causes pulmonary vasoconstriction and precipitates right heart failure. Pulmonary hypertension results in coronary filling during diastole rather than systole.

Obstructive sleep apnoea

Defined as absence of airflow for >10 s, occurring >30 times in 7 h sleep. Either obstructive or central (no respiratory movements). Associated with obesity, hypertension and diabetes. Patients are at even greater risk with i.v. sedation.

Common symptoms are snoring, daytime somnolence, restless sleep.

Reduced activity of genioglossus muscle combined with negative pressure from the diaphragm causes pharyngeal obstruction, just posterior to the soft palate. Also impaired contractility of respiratory muscles.

Nasal CPAP abolishes sleep apnoea in most patients and improves the clinical symptoms. It improves daytime oxygenation by increasing FRC and hence alveolar ventilation and improves chronic CCF and LV function. Nocturnal O₂ may also be of benefit.

Postoperative hypoxia

Severity and incidence of arterial desaturation are closely related to the surgical site and are greatest for thoracoabdominal surgery, less for upper abdominal surgery and least for peripheral surgery.

Early hypoxaemia. One-third of patients being transferred from theatre to recovery room developed O₂ saturation <90%, despite being given 100% O₂ for 5 min at the end of surgery. This early phase hypoxaemia is mostly due to upper airway obstruction, increased oxygen consumption, alveolar hypoventilation, atelectasis, V/ mismatch, diffusion hypoxia, aspiration or central or obstructive apnoea.

Late hypoxaemia is due to impaired gas exchange (atelectasis), impaired control of breathing (sleep, analgesia), impaired diaphragmatic contractility and collapse of pharynx with negative inspiratory pressures and reduced muscle tone. Persists for up to 5 days. Related temporally to hypertension, tachycardia, myocardial ischaemia and arrhythmias. Some episodes of postoperative LVF and myocardial infarction are probably related to this ischaemia. Hypoxaemia may impair wound healing and promote bacterial infection.

Nasal oxygen delivery is more comfortable than a mask and does not require additional humidification, but 35% patients fail to keep O₂ on overnight. Intratracheal and nasopharyngeal catheters may be more effective.

Recommendations (Powell et al 1996) include:

• Use of pulse oximetry to monitor all postoperative patients in the recovery room

• Patients at risk of prolonged postoperative hypoxaemia need prolonged monitoring and oxygen supplementation (obese patients with BMI >27–35 kg/m², upper abdominal surgery or thoracotomy, patients receiving opioids and those with respiratory disease)

• Patients with impaired O₂ delivery (hypovolaemia, anaemia, myocardial/cerebral ischaemia, sickle cell disease) all require postoperative oxygen therapy

• Oxygen should be continued until S_ao₂ exceeds 93% or reaches preoperative value.

Bibliography

Bluman L.G., Mosca L., Newman N., et al. Preoperative smoking habits and postoperative pulmonary complications. Chest. 1998;113:883-889.

British Thoracic Society & Scottish Intercollegiate Guidelines Network. British Guideline on the Management of Asthma, 2009 www.brit-thoracic.org.uk/ClinicalInformation/Asthma/AsthmaGuidelines/tabid/83/Default.aspx.

Edrich T., Sadovnikoff N. Anesthesia for patients with severe chronic obstructive pulmonary disease. Curr Opin Anaesthesiol. 2009. E-pub doi: 10.1097/ACO.0b013e328331ea5b

Mills G.H. Respiratory physiology and anaesthesia. BJA CEPD Rev. 2001;1:35-39.

Powell J.F., Menon D.K., Jones J.G. The effects of hypoxaemia and recommendations for postoperative oxygen therapy. Anaesthesia. 1996;51:769-772.

Stanley D., Tunnicliffe W. Management of life-threatening asthma in adults. Continuing Education in Anaesthesia, Critical Care & Pain. 2008;8:95-99.

Stather D.R., Stewart T.E. Clinical review: mechanical ventilation in severe asthma. Crit Care. 2005;9:581-587.

Sweeney B.P., Grayling M. Smoking and anaesthesia: the pharmacological implications. Anaesthesia. 2009;64:179-186.

Tonnesen H., Nielsen P.R., Lauritzen J.B., et al. Smoking and alcohol intervention before surgery: evidence for best practice. Br J Anaesth. 2009;102:297-306.

Vaschetto R., Bellotti E., Turucz E., et al. Inhalational anesthetics in acute severe asthma. Curr Drug Targets. 2009;10:826-832.

Walsh T.S., Young C.H. Anaesthesia and cystic fibrosis. Anaesthesia. 1995;50:614-622.

Warner D.O. Perioperative Abstinence from Cigarettes: Physiologic and Clinical Consequences. Anesthesiology. 2006;104:356-367.

Thoracic Anaesthesia

Anaesthesia for thoracotomy

Preoperative

Full cardiovascular and respiratory work-up, including room air ABGs and pulmonary function tests. Patient is often arteriopathic with end-organ damage.

Pulmonary artery pressure (PAP)

High risk if mean PAP >25 mmHg at rest. Hypoxic pulmonary vasoconstriction (HPV) increases shunt by diverting blood to non-ventilated lung. Worsened by most sympathomimetics, although least with dopamine.

Operative

Monitoring. ECG, good venous access, CVP line on side of thoracotomy for easier access, chest drain positioned on same side postoperatively avoids risks of pneumothorax on opposite side to surgery. Arterial line placed in contralateral radial artery. Wright’s respirometer to measure expired air volumes, pulse oximeter and capnograph.

Positioning. Take care with positioning because of risk of nerve injury (axillary rolls cause brachial plexus compression). Dependent pooling in head and legs reduces cardiac output. Worse with hypovolaemia.

Intubation and ventilation. Use bronchial blockers if patient is too small for a double-lumen tube. Intubate with double-lumen tube and use fibreoptic scope if necessary to check position. Usually intubate left main bronchus unless this would interfere with surgery. IPPV with muscle relaxation prevents coughing and high-volume IPPV ensures more even ventilation.

Maintenance. Use volatiles and high F_io₂. Intravenous anaesthetic agents may suppress hypoxic pulmonary vasoconstriction less than volatiles.

Reversal. Inflate lungs to 40 cmH₂O for 40 s to reverse atelectasis and check for leaks. Ensure complete reversal and return of protective reflexes before extubation.

Anaesthesia for one-lung ventilation

Predictors of risk for one-lung surgery

• Pulmonary hypertension

• FEV₁ <50% predicted

• FVC <50% predicted

• MBC <50% predicted.

Physiology of spontaneous ventilation in lateral decubitus position

GA reduces compliance of both upper and lower lungs, which is returned to normal values by the application of PEEP.

Weight of mediastinum and pressure of abdominal contents on diaphragm impair lower lung expansion and cause decreased FRC. However, greater curvature of the diaphragm results in more efficient contraction with greater expansion matching increased blood flow to dependent lung, i.e. remains balanced.

During spontaneous ventilation, dependent diaphragm moves cephalad on expiration, pushing the mediastinum upwards, resulting in inefficient ventilation. This mediastinal shift causes sympathetic activation, reduces venous return and reduces cardiac output.

When the upper chest is opened during spontaneous ventilation, paradoxical respiration results. During inspiration, gases are drawn from upper lung, which collapses. During expiration, gases pass from lower into upper lung causing upper lung inflation. Mediastinal shift as a result of paradoxical respiration also generates more work.

Physiology of two-lung IPPV in lateral decubitus position

IPPV results in most ventilation being directed to the upper rather than the lower lung, with perfusion remaining greatest in the lower lung, thus increasing the V/ mismatch.

• High F_io₂ (0.8–1.0) causes vasodilation and increases flow in the dependent lung

• Aim for 10 mL/kg IPPV once single-lung ventilation established

• Aim for P_aco₂ of 6 kPa. Since the overall tidal volume is decreased by about 20%, respiratory rate may need to be increased by a similar amount to maintain minute volume

• PEEP to dependent lung may improve oxygenation by recruiting closed alveoli and restoring compliance to normal, but may worsen oxygenation by compressing pulmonary vasculature and diverting more blood to the upper unventilated lung. Countered by upper lung CPAP

• Blood flow through unventilated lung is the main determinant of Po₂.

Maintain two-lung ventilation until pleura is opened.

Hypoxia during single-lung IPPV

If this occurs:

• Check position of double-lumen tube. Suction down ETT

• Non-dependent lung CPAP (5–10 cmH₂O)

• Dependent lung PEEP

• Operative lung HFJV

• Intermittent IPPV to operative lung

• Clamp pulmonary artery.

Postoperative

Any V/ mismatch is improved by nursing the patient in a lateral position with the healthy lung lowermost if breathing spontaneously, or the healthy side uppermost if IPPV.

Double-lumen tubes

Because of the wide variation in anatomical position of the right upper lobe bronchus, a left-sided tube is usually chosen unless surgery is to the left main bronchus (carina to left upper lobe = 5.0 cm; carina to right upper lobe = 2.5 cm). The presence of a carinal hook increases the stability of the tube but makes insertion more difficult.

The following are types of double-lumen tube:

• Carlens (left-sided) and White (right-sided): carinal hook; four sizes

• Robertshaw: left/right; no carinal hook; small/medium/large

• Gordon–Green: single-lumen right-sided tube; carinal hook

• Bryce–Smith: left/right; no carinal hook.

Carlens and White tubes have lumens of a smaller diameter than the Robertshaw tubes.

Indications

• Soiling below cuff (empyema, bronchiectasis, haemoptysis, tracheo-oesophageal fistula, TOF)

• Gas leak below cuff (TOF, bronchopleural fistula, ruptured cyst).

Insertion of tube with carinal hook

1. Advance tip of tube through cords and then turn 180° so that hook is anterior.

2. Once hook is through cords, rotate to correct position and advance until resistance is felt.

3. Ventilate both lungs first; then inflate tracheal cuff and listen at the mouth for any air leak. Inflate endobronchial cuff and inflate single lung through endobronchial port. Check there are no air leaks via tracheal port. Inflate opposite lung via tracheal port and check there are no air leaks via endobronchial port. Measure expired air volumes to check for leaks.

Complications

• Trauma to laryngeal cartilage and trachea during insertion

• Tube malposition resulting in hypoxia

• Surgical compression can displace tube and disrupt isolation of operative lung

• Tube displacement may result in ball valve effect with hypercapnia and prolonged expiratory flow.

Anaesthesia for bronchopleural fistula

Fistula usually occurs after lung resection; also with abscess, tumour, or bullae. Results in sudden onset of productive cough, worse at night.

Diagnosed by fall in fluid level on CXR, failure of hemithorax to opacify, return of mediastinum to midline, and consolidation of healthy lung from overspill from infected lung.

Sit patient up, with the affected side lowermost and the fistula clear of pleural fluid. Give oxygen, resuscitate preoperatively. Carry out early endobronchial intubation to isolate fistula. Induction by:

• awake intubation, but risk of coughing and contamination

• rapid sequence induction, but trachea may be distorted following pneumonectomy

• deep volatile induction, but marked CVS depression in shocked patient.

Aim for early extubation to avoid pressure from IPPV on stump sutures.

Anaesthesia for lung cysts/bullae

Lung cysts are often compliant and therefore preferentially ventilated. IPPV may deliver large volumes to the cyst, resulting in its rupture. Therefore aim for small tidal volumes, low inflation pressure, no PEEP and long expiratory phase. Spontaneous respiration until chest opening may avoid hyperinflation. A ball-valve effect may occur with mucous plugs, causing tensioning of the cyst. Avoid N₂O which may rupture the cyst. Consider spontaneous respiration or HFJV.

Good postoperative pain relief (e.g. epidural) allows quicker return of normal lung function.

Anaesthesia for tracheal resection

A partially obstructed airway is at risk of complete obstruction. Therefore avoid sedative premedication and use gas induction in case a paralysed apnoeic patient cannot be ventilated. Airway obstruction will slow induction. Since ventilation may be dependent upon a patient’s spontaneous respiratory effort, avoid neuromuscular blockers until obstruction resected.

When the trachea is divided, the surgeon places a Tovell endotracheal tube in distal trachea to continue ventilation and the original tube is then withdrawn.

When the trachea is reanastomosed, the neck is kept flexed to prevent strain on sutures. Aim to extubate as soon as possible to avoid high airway pressures on anastomosis.

Anaesthesia for bronchoscopy

Methods of anaesthesia for bronchoscopy include:

• Apnoeic oxygenation. Apnoea with insufflation of O₂ via catheter placed at carina. Arterial CO₂ rises by 0.26–0.66 kPa.min⁻¹, therefore use for short periods only

• Flexible fibreoptic bronchoscope

• Ventilating (rigid) bronchoscope with sidearm. Glass window opened for passage of instruments prevents effective ventilation

• Sanders injector. Injection of O₂ at 4 bar through 16 G cannula with entrainment of air by Venturi effect. F_io₂ uncertain.

Complications include dental and laryngeal damage, tracheal rupture, haemorrhage and pneumothorax.

Laser surgery

Carbon dioxide or Nd-Yag laser used for surgery to thoracic neoplasms. Associated with a risk of fire and explosion in the airway, risk of ignition of the endotracheal tube and risk to eyesight from laser beam.

Endotracheal tube must be shielded from the laser by coating of aluminium foil or use of a stainless steel tube. Use double cuff in case laser bursts upper cuff. Fill cuffs with water, which absorbs stray energy better than air. Both O₂ and N₂O support combustion. Reduce risk of fire by keeping F_io₂ <0.40, adding helium and using laser for as short a burst as possible. Use saline-soaked swabs to protect surrounding tissue from laser. Everyone in theatre should wear protective goggles.

Bibliography

Eastwood J., Mahajan R. One-lung anaesthesia. Br J Anaesth CEPD Rev. 2002;2:83-87.

Grichnik K.P., Shaw A. Update on one-lung ventilation: the use of continuous positive airway pressure ventilation and positive end-expiratory pressure ventilation – clinical application. Curr Opin Anaesthesiol. 2009;22:23-30.

Hillier J., Gillbe C. Anesthesia for lung volume reduction surgery. Anaesthesia. 2003;58:1210-1219.

Karzai W., Schwarzkopf K. Hypoxemia during one-lung ventilation: prediction, prevention, and treatment. Anesthesiology. 2009;110:1402-1411.

Slinger P. Update on anesthetic management for pneumonectomy. Curr Opin Anaesth. 2009;22:31-37.

Tschernko E.M., Kritzinger M., Gruber E.M., et al. Lung volume reduction surgery: preoperative functional predictors for post-operative outcome. Anesth Analges. 1999;88:28-33.

Vaughan R.S. Pain relief after thoracotomy. Br J Anaesth. 2001;87:681-683.

Mechanical Ventilation

History

Mechanical ventilation was first described in the sixteenth century by Vesalius, who used bellows to ventilate a donkey. Advances in mechanical ventilation were encouraged by the 1952 polio epidemic in Copenhagen during which Lassen organized relays of medical students to ventilate hundreds of patients by hand for many weeks.

Aims of intubation

• Establish and maintain an upper airway

• Protect the lower airway

• Facilitate IPPV ± hyperventilation

• Reduce dead space

• Facilitate airway suctioning.

Time constants

• Time constant = resistance (cmH₂O) × compliance (L/cmH₂O) =

time for 63% of change in pressure to be distributed through lungs

• Five time constants = complete equalization of pressure

• Short inspiratory time favours fast units (short time constant) with incomplete filling of slower units.

Mechanical ventilation

Ventilators

There are four main groups of ventilator:

1. Minute volume dividers, e.g. Manley Pulmovent, Blease Brompton

2. Bag squeezers, e.g. Cape Waine ventilator, Manley Servovent

3. Thumb occluders, e.g. occlusion of T-piece outlet by thumb

4. Intermittent blowers, e.g. Pneupac ventilator, Nuffield Penlon 200.

Initiation of inspiration

• Time initiated – inspiratory mode begins after a set time

• Pressure initiated – inspiratory mode begins when pressure falls below the baseline pressure.

Termination of inspiration

• Volume cycle: ends inspiration after a preset volume is delivered

• Pressure cycle: ends inspiration when circuit pressure reaches predetermined level

• Time cycle: ends inspiration after a set time. Commonest used trigger

• Flow cycle: ends inspiration when circuit flow diminishes to a predetermined level.

Infant ventilators are usually pressure-limited, time-cycled flow generators. Adult ventilators are usually volume-limited ventilators.

Ventilatory modes

IMV, SIMV and MMV

Intermittent mandatory ventilation (IMV). Patient able to breathe spontaneously on CPAP between mandatory tidal volumes.

Synchronized intermittent mandatory ventilation (SIMV). As above, but synchronized with patient’s respiratory efforts.

Mandatory minute ventilation (MMV). Spontaneous ventilation but if minute ventilation falls below set level, IPPV takes over.

Advantages of IMV, SIMV and MMV

• Lowers mean airway pressure (improves myocardial and renal blood flow)

• More physiological gas distribution

• Reduces sedation requirements

• Avoids hyperventilation causing respiratory alkalosis

• Easier and earlier weaning, exercises respiratory muscles.

Disadvantages of IMV, SIMV and MMV

• Increases work of breathing if resistance is present in spontaneous breathing circuits

• Respiratory muscle fatigue

• Prolongs weaning if decrease in IMV is too slow

• Hypoventilation may cause respiratory acidosis

• Added dead space.

High-frequency ventilation

High-frequency positive pressure ventilation (HFPPV) (1–2 Hz). Jet injector delivers gas into normal ventilator tubing. Low-velocity wavefront acts as a piston within the tracheal tube. Expiration is passive.

High-frequency jet ventilation (HFJV) (2–6 Hz). High-pressure (5 bar) pulses of gas delivered into tracheal tube, entraining air in the flow. Expiration is passive.

High-frequency oscillatory ventilation (HFOV) (3–20 Hz). Loudspeaker cone used to produce a sinusoidal pattern of gas flow superimposed on a continuous oxygen flow. Expiration is also active. Not shown to be of any benefit for preterm infants where the mortality and incidence of chronic lung disease are not improved in comparison with conventional ventilation. Associated with higher incidence of intraventricular haemorrhage (possibly from interference with cerebral vascular autoregulation) and inotropic support (possibly from interference with baroreflex).

Advantages

• ↓ mean airway pressure, thereby reducing pulmonary barotrauma

• Provides PEEP (↑ as frequency increases)

• Less depression of cardiac output

• Reduction in pulmonary shunting

• Allows patient to breathe spontaneously

• Reduced sedation requirements

• Reduced air leak with pneumothorax.

Positive end expiratory pressure (PEEP)

Effects of PEEP

• ↑ pulmonary vascular resistance. ↓ flow in West’s zone 1 causes increased dead space

• ↑ work of breathing if patient breathing spontaneously because patient must generate a negative inspiratory pressure greater than the PEEP pressure to inspire

• ↑ P_ao₂ due to ↑ FRC >CC

• Prevents surfactant aggregation, reducing alveolar collapse

• Worsens right-to-left shunt and may worsen shunt if applied just to lower lung in one-lung ventilation.

Optimum PEEP/CPAP

• Reduces physiological shunt to <15%

• Restores FRC to normal

• Corresponds to optimal compliance

• Minimizes work of breathing.

CPAP may be uncomfortable for the awake patient and cause gastric distension. Therefore, the patient must be cooperative, able to protect the airway, cough and have the energy to breathe spontaneously.