Neurology

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Chapter 3 Neurology

Neurology and neuromuscular disorders

Epilepsy

Affects 1/200 of the general population. Continue anticonvulsants perioperatively.

Anaesthetic problems

• Enzyme induction. Chronic medication induces hepatic enzymes with resistance to i.v. induction agents and volatiles.

• Risk of seizures. Particularly with enflurane in a hypocapnic patient, methohexitone, ketamine and etomidate. Although propofol has not been demonstrated to cause significant EEG changes, excitatory phenomena are more common. Because patients risk losing their driving licence after an epileptiform event, it is recommended to avoid propofol in patients who are driving. Several case reports document successful use of propofol for the treatment of status epilepticus.

• Underlying pathology causing epilepsy.

Cerebrovascular disease

A cerebrovascular accident (CVA) is defined as a rapidly evolving episode of loss of cerebral function with symptoms lasting more than 24 h (<24 h = transient ischaemic attack) or leading to death. Annual incidence is 1–2/1000 in the UK, with a mortality of 15–30%.

Risk of perioperative stroke following general surgery is 0.2–0.7% in patients without a history of cerebrovascular disease. Most CVAs occur 2–10 days postoperatively, with an average of 7 days, and have an associated mortality of 26%. In those with a history of cerebrovascular disease, the risk is 2.9% with a mortality of 60%.

Risk factors include age, systolic hypertension, atrial fibrillation (AF), peripheral vascular disease and diabetes. Hyperextension or rotation of the patients neck during head surgery may reduce flow in vertebral and internal carotid arteries.

Preventative measures

Preoperative measures include treating risk factors and anticoagulation for patients in AF. The European Carotid Surgery Trial (ECST) and the North American Symptomatic Carotid Endarterectomy Trial (NACEST) suggest that carotid endarterectomy would benefit symptomatic patients with >70% carotid stenosis. Surgery should be deferred for 4–6 weeks after an acute event.

Intraoperative measures. Avoid hypocapnia (steal syndrome) or hypercapnia (inverse steal syndrome), avoid hypo- or hyperglycaemia, and avoid extreme cervical spine rotation or extension. Maintain BP within normal range.

Postoperative measures. Avoid hypotension, dehydration and hypoxia.

Parkinsons disease

Disorder of the extrapyramidal system with degeneration of dopaminergic neurones in the substantia nigra of the basal ganglia, giving rise to intention tremor, ‘cogwheel’ rigidity, akinesia and postural changes. Dysautonomia also common (orthostatic hypotension, urinary dysfunction, sleep disorders). Prevalence 1% in those >65 years age. First described as ‘the shaking palsy’ by James Parkinson in 1817.

Patients are already confused in a strange environment, which is worsened by GA. Patients are often difficult to assess preoperatively, with reduced pulmonary function, upper airway obstruction, weakness and incoordination of inspiratory and expiratory muscles. The usual drug regimen should be continued preoperatively. If patient is well controlled on l-DOPA, both general and regional anaesthesia is usually well tolerated. Avoid drugs that exacerbate Parkinson’s (phenothiazines, droperidol, metoclopramide).

Continue anti-Parkinsonian medication immediately postoperatively, via nasogastric (NG) tube if necessary. Delayed mobilization postoperatively increases risk of respiratory complications and deep vein thrombosis (DVT). Avoid antiemetics that are dopamine antagonists (e.g. prochlorperazine), although all may cause extrapyramidal and movement disorders.

Multiple sclerosis (MS)

Chronic progressive demyelinating disease characterized by repeated exacerbations and partial remissions. Affects 1:2000; equal incidence in both sexes. Upper motor neurone lesions, cerebellar lesions and sensory deficits are common.

General anaesthesia does not exacerbate MS. Use normal doses of muscle relaxants.

Regional blockade. New lesions may develop coincidentally at the time of regional blockade and subsequent symptoms may be difficult to differentiate from nerve injury or may be blamed on the block. Therefore regional blockade is relatively contraindicated.

Motor neurone disease

Progressive degeneration of motor function with sparing of higher mental function and sensory function. Involves both upper and lower motor neurones. Progressive muscle atrophy, spasticity, pseudobulbar palsy. Affects smooth, striated and cardiac muscle.

General anaesthesia. Risk of aspiration from delayed gastric emptying and bulbar weakness. Weak respiratory muscles. Suxamethonium may cause hyperkalaemia. Increased sensitivity to non-depolarizing relaxants and induction agents.

Regional anaesthesia. Avoid impairment of respiratory muscles but otherwise safe.

Autoimmune disease

Myasthenia gravis

Affects 1:20 000. A result of autoantibodies directed against the neuromuscular junction. Ocular, facial, bulbar and limb weakness in 85% of patients.

Preoperative. Continue anticholinesterases and steroids. Intubate if vital capacity falls below 1000 mL. Consider β-blockers and atropine to stabilize the autonomic nervous system.

GA. Greatly increased sensitivity to non-depolarizers; decreased sensitivity to depolarizing blockers. Give conventional anticholinesterase dose at end of surgery and then restart anticholinesterases at a decreased dose. Extubate when inspiratory pressure >−30 cmH₂O or FVC >15 mL.kg⁻¹.

Postoperative. Risk factors for postoperative ventilation are:

• disease for >6 years

• chronic respiratory disease

• pyridostigmine >750 mg.day⁻¹

• FVC <2.9 L.

Eaton–Lambert syndrome

Severe muscle weakness found in association with 1% of patients with bronchial carcinoma, thyroid disease and connective tissue disorders (systemic lupus erythematosus, polyarteritis nodosa). Unlike myasthenia gravis, causes proximal rather than bulbar weakness, muscle power increases with exercise and no fade occurs on tetanic stimulation.

Increased sensitivity to both non-depolarizing and depolarizing blockers.

Associated with ↑ ACTH (hypertension, diabetes) and ↑ PTH (↑ Ca²⁺, dehydration).

Myotonia

Myotonic dystrophy

Affects 1:25 000. Autosomal dominant. Myotonia with difficulty releasing hand grip, muscle weakness, cataracts, ‘inverted smile’, bilateral ptosis, frontal balding, masseter and sternomastoid wasting, and bulbar weakness (aspiration and chest infections); also cardiac conduction defects, cardiomyopathy, valve defects, obstructive sleep apnoea, dysphagia and reduced gastric emptying.

Sensitivity to sedatives, induction agents (barbiturates, propofol), opioids and non-depolarizing neuromuscular blockers. Anticholinesterases, cold and shivering may worsen myotonia. Suxamethonium may produce a generalized myotonic response. Non-depolarizing relaxants are safe. Myotonic contraction with surgical diathermy may be a major problem. Postoperative complications are usually related to cardiac pathology or muscle weakness leading to aspiration. Postoperative shivering may induce a myotonic crisis.

Pregnancy may exacerbate myotonia and muscle weakness.

Myotonia congenita (Thomsen’s disease)

Affects 1:25 000. Autosomal dominant. Generalized muscular hypertrophy, stiffness on initiating movement, relieved by exercise. Myotonia may be severe but no muscle weakness. Anaesthetic problems are as for myotonic dystrophy. Association with malignant hyperthermia.

Familial periodic paralysis

Hyperkalaemic periodic paralysis

Episodes of flaccid paralysis associated with hyperkalaemia. Paralysis may occur with potassium levels no greater than 4.0 mmol, possibly due to a defect in the sarcolemma causing spontaneous depolarization. Triggered by stress, cold, hunger and exercise. Vital to avoid hyperkalaemia perioperatively, using insulin/dextrose and loop diuretics. Suxamethonium may cause sufficient hyperkalaemia to precipitate an attack.

Hypokalaemic periodic paralysis

Unrelated to hyperkalaemic periodic paralysis. Asymmetric paralysis involving arms, legs, trunk and neck. Usually spares diaphragm and facial muscles. Associated with reduced cell membrane potential, making muscle more excitable. Precipitated by heavy carbohydrate meals, diuretics, alkalosis and hypothermia. The effect of muscle relaxants may be clinically similar to the paralysis itself.

Neuroanaesthesia

Physiology

Cerebrospinal fluid (CSF)

Secreted by the choroid plexus in the lateral, III and IV ventricles. Flows through foramen of Magendie and Lushka and is absorbed by arachnoid villi: 720 mL.day⁻¹. Contents are:

• CSF >plasma: Na⁺, Cl⁻, Mg²⁺

• CSF <plasma: K⁺, HCO₃⁻, glucose, protein.

Intracranial pressure (ICP)

Munro–Kelly hypothesis (1852) stated that the contents of cranium are not compressible (60% water, 40% solid). Therefore, increasing the volume within the cranium causes a rapid increase in pressure (Fig. 3.1).

Figure 3.1 Theoretical intracranial pressure–volume relationship.

However, compression of veins and communication of CSF with spinal column result in a small range of compensation before pressure increases (Fig. 3.2).

Figure 3.2 Actual intracranial pressure–volume relationship.

Normal CSF pressure = 0–10 mmHg. Neurosurgical patients often have raised ICP and so are already on the steep part of curve. Active treatment is needed if ICP >25–30 mmHg. CSF pressure oscillates with arterial pulse and swings with respiration.

Cushing reflex. Increased ICP causes hypertension and bradycardia.

Coning

All coning causes an autonomic storm. High pulmonary artery pressures may then result in neurogenic pulmonary oedema. ECG changes are now thought to be indicative of myocardial ischaemia. Reduced ADH secretion causes diabetes insipidus. Metabolic response is similar to that of the stress response following surgery.

• Temporal (tentorial) coning. Ipsilateral III nerve palsy, ↓ consciousness, Cushing reflex, decerebrate rigidity

• Cerebellar (medullary) coning. Cheyne–Stokes breathing, sudden apnoea, neck stiffness.

Pressure waves in CSF (described by Lundberg in 1960)

• A-waves – large amplitude waves lasting 5–20 min. Indicate failure of vasomotor compensation for raised ICP

• B-waves – 1/min. Associated with brainstem disorders

• C-waves – 6/min. Indicative of cerebral disorders.

Cerebral circulation

where CPP = cerebral perfusion pressure, MAP = mean arterial pressure, ICP = intracranial pressure, CVP = central venous pressure at jugular bulb (usually zero).

Raised intrathoracic pressure increases CVP and reduces CPP further.

• Normal flow = 50 mL.100 g⁻¹.min⁻¹ ≡ 15–20% of cardiac output.

• Critical flow occurs if MAP <50 mmHg, i.e. <20 mL.100 g⁻¹.min⁻¹.

Local metabolites are the main regulator of cerebral blood flow (CBF) by effects on extracellular H⁺ concentration. Lactic acid metabolites maximally vasodilate diseased tissues, e.g. infarct, tumour, head injury, subarachnoid haemorrhage. Subsequently, any cerebral vasodilator will increase flow to normal tissue and may reduce flow in diseased tissue. Known as ‘reverse steal’.

Normal brain autoregulates over a range of 50–130 mmHg (Fig. 3.3). Hypertension shifts the curve to the right. Autoregulation is lost with volatile anaesthetic agents, tumour, trauma, infarction, intracranial bleed, hypoxia, hypercarbia, seizure disorders, hypotension and hypertension. In these conditions, CBF ∝ MAP.

Figure 3.3 Autoregulatory limits of cerebral blood flow.

CO₂

Affects CBF through vasodilation by changing the pH of extracellular fluid (ECF) (Fig. 3.4). Aim for a P_aco₂ of 3.5 kPa to lower ICP without excessive vasoconstriction and prevent ‘reverse steal’. Volatile agents increase effects of CO₂ on vasodilation. A 3% change in CBF occurs for each 0.1 kPa change in P_aco₂.

Figure 3.4 Effect of P_aco₂ on cerebral blood flow.

Acute changes of hyperventilation return to normal values after 48 h due to normalization of CSF pH and a compensatory increase in CSF volume.

O₂

Has less influence on CBF until P_ao₂ <8 kPa (Fig. 3.5). Hyperoxia causes mild cerebral vasoconstriction of 5–10% at 60 kPa.

Figure 3.5 Effect of P_ao₂ on cerebral blood flow.

Monitoring

Table 3.1 Glasgow Coma Scale

Evoked potentials

Measure latency and amplitude.

• Somatosensory: e.g. median or posterior tibial nerve. Record over sensory cortex. Used for spinal cord and posterior fossa surgery

• Auditory: auditory clicks. Record over mastoid to assess brainstem function, e.g. acoustic neuroma surgery

• Visual: flashes of light over eyes. Record over visual cortex, e.g. for pituitary surgery.

Measurement of intracranial pressure

• Intraventricular catheter: attached to transducer. Most accurate but risk of infection

• Subdural bolt: tends to under-read at high pressures

• Subdural catheter

• Extradural catheter: either pressure transducer at tip of catheter or fibreoptic light shining onto mirror at tip which is displaced as ICP increases and alters amount of light reflected back onto the catheter.

Anaesthetic drugs

Alter CBF by effects on vascular smooth muscle, cerebral metabolism and alveolar ventilation (P_aco₂).

Figure 3.6 Percentage change in middle cerebral artery blood flow with increasing minimum alveolar concentration (MAC).

Volatile agents

All volatiles with the exception of desflurane reduce cerebral metabolism and oxygen demand. Effect is most marked with isoflurane. All increase ICP and abolish autoregulation in sufficient doses. Halothane causes most cerebral vasodilation (Table 3.2). At 1 MAC (minimum alveolar concentration), isoflurane has minimal effect on ICP, autoregulation or EEG depression. At 2.5 MAC, the EEG becomes isoelectric. Isoflurane reduces cerebral O₂ demand more than any other volatile and reduces cerebral blood flow without evidence of ischaemia. Sevoflurane and desflurane appear similar to isoflurane in their CNS and CVS effects.

Table 3.2 Cerebral effects of anaesthetic drugs

N₂O is a weak vasodilator causing moderate increases in CBF and cerebral metabolic rate (CMR). Changes in CBF are variable and may be more related to changes in F_io₂.

Intravenous agents

All i.v. induction agents, except ketamine, decrease ICP, and all have little effect on autoregulation. Both thiopentone and propofol cause dose-related decreases in CBF and O₂ demand and both are good attenuators of increased ICP during intubation. Propofol has nine Committee on Safety of Medicines reports (August 1987) warning of grand mal seizures.

Ketamine increases CBF, ICP and O₂ demand. Avoid in neuroanaesthesia.

Suxamethonium causes a transient rise in ICP through muscle fasciculations, increasing venous pressure and muscle spindle efferents activated by fasciculations.

Anaesthesia for neurosurgery

Aims

• Maintain safe airway

• Maximize O₂ delivery

• Minimize O₂ demand

• Avoid sudden hypertensive insults

• Maintain CPP (→ MAP, ↓ ICP, ↓ CVP)

• Use agents allowing rapid postoperative recovery.

Preoperative

Assess gag reflex (?aspiration), ↓ cough reflex (?sputum retention), drowsiness (?drug-induced or CNS pathology), nausea and vomiting causing electrolyte disturbance and dehydration. Assess signs of raised ICP (headache, nausea and vomiting, Cushing reflex, downward gaze of eyes). Assess drug treatment: steroids decrease ICP, anticonvulsants induce liver enzymes. Assess pituitary dysfunction.

Premedication

Avoid drugs causing neurological or respiratory depression. Prescribe midazolam and glycopyrrolate if necessary.

Monitoring

Arterial line, CVP via long line (neck lines impair venous drainage of head and may require head-down position for insertion), ECG, temperature, end-tidal CO₂, S_ao₂, neuromuscular stimulator, regular blood gases and electrolytes.

Positioning

Avoid obstructing venous drainage of head. 15° head up. Protect eyes.

Induction

Thiopentone is often the drug of choice because of its anticonvulsant properties. Give slowly to avoid a decrease in BP reducing CPP. Propofol is also popular and appears not to cause postoperative seizures. Consider additional agent to attenuate pressor response to intubation, e.g. lidocaine, high-dose opioids, β-blockers, hydralazine. Topical anaesthesia to larynx. Etomidate causes coughing, hiccoughs and vomiting which raises ICP. Propofol may cause epileptiform EEG but lowers ICP and is suitable for induction and maintenance.

Suxamethonium causes hyperkalaemia in the presence of spastic paraplegia. Wait for full paralysis before intubation to avoid coughing and straining on endotracheal tube (ETT). Use armoured ETT to prevent kinking. Tape ETT, because a tie may cause venous obstruction of head and neck, increasing ICP. Consider NG tube.

Maintenance

Use a balanced technique with opioid in combination with O₂ and N₂O/air and muscle relaxants, which produces good cardiovascular stability. N₂O may increase ICP but detrimental affects of using this as part of balanced anaesthesia have not been demonstrated. Sevoflurane is the volatile of choice as it causes less vasodilation (↑ ICP) and preserves autoregulation compared with isoflurane and desflurane. If greatly increased ICP, avoid volatiles until dura has been opened. Vecuronium/rocuronium are the relaxants of choice – use high dose to avoid coughing or straining. Ventilate to maintain P_aco₂ at 3.5 kPa. Fentanyl is a suitable opioid, but remifentanil may allow faster waking and neuroassessment. TIVA is gaining popularity using propofol/remifentanil infusion, but some concern that it increases cerebral oxygen demand.

Reversal

Avoid coughing. Early extubation allows CNS monitoring for signs of deterioration. Avoid sudden hypertension which causes cerebral oedema through loss of autoregulation.

Fluids

Maintain plasma osmolality at the upper end of normal. Avoid fluids with low osmolality which increase free brain water (Table 3.3). Avoid glucose-containing solutions which accelerate anaerobic metabolism and may worsen neurological morbidity.

Table 3.3 Osmolality of intravenous fluids

Solution	Osmolality (mOsm.L⁻¹)
Normal saline	310
Mannitol	300
Hartmann’s solution	272
Dextrose saline	262
5% dextrose	250

Postoperative

Any change in Glasgow Coma Scale can be assumed to be due to surgical complications. Aim for a similar BP as the preoperative value. Codeine phosphate is usually sufficient for analgesia. Start anticonvulsants. Watch for diabetes insipidus, tension pneumocephalus and cranial nerve injury.

Anaesthesia for intracranial aneurysm

Nimodipine reduces the risk of re-bleeding in patients following a subarachnoid haemorrhage and may reduce the severity of vasospasm. Vasospasm is maximal between days 3 and 10. Generally, aim for early surgery (within 48 h) if no severe neurological deficit, or late surgery if patient is comatose (to assess potential degree of recovery over about 10 days). Hyperventilation may worsen vasospasm.

Opening the dura reduces ICP, resulting in increased transmural pressure across the aneurysm wall. Therefore, may need perioperative hypotensive anaesthesia. Vasodilation with sodium nitroprusside causes increased ICP unless dura is opened. Trimetaphan can be used with the dura closed but is of slower onset, causes dilated pupils (ganglion blockade), making CNS assessment difficult, and triggers histamine release. Both drugs may cause rebound hypertension on cessation.

If aneurysm ruptures, press on ipsilateral carotid artery, give 100% O₂ and consider transient hypotension with sodium nitroprusside.

Anaesthesia for posterior fossa surgery

The posterior fossa comprises midbrain, pons, medulla, cerebellum and cranial nerves V–XII. Patient position to be either:

• sitting – reduces blood loss but high risk of air embolus and hypotension

• park bench position – greatly reduces the risk of air embolus.

Complications of surgery

Air embolus. Usually gradual leak rather than sudden bolus. Occurs due to veins being prevented from collapsing by tethering to dura (dural sinuses) or periosteum (emissary sinuses). Reduce incidence with 10 cm PEEP, neck tourniquet and G-suit.

Spontaneous respiration provides further indicators of brainstem function but increased risk of air embolus (negative intrathoracic pressure) and hypercapnia.

Sensitivity of detection. Precordial Doppler >P_ao₂ >P_ETco₂ >PAP >P_aco₂ >CVP >CO >BP >ECG>‘mill-wheel’ murmur using stethoscope.

Treatment. Occlude wound with wet swab, 100% O₂, raise CVP by levelling table and neck compression, aspirate CVP line (tip should be placed in RA preoperatively), position patient in left lateral position with head down if possible.

Other complications

• Stimulation of posterior fossa causing the Cushing reflex

• Vagal stimulation causes bradycardia

• Stimulation of V (trigeminal) cranial nerve causes hypertension

• Damage to dorsal group neurones causes postoperative apnoea

• Bulbar palsy

• Increased sensitivity to respiratory depressants.

Postoperative

Loss of gag (glossopharyngeal (IX) damage) increases risk of aspiration following extubation. Therefore assess prior to extubation. Watch for respiratory failure and hydrocephalus.

Treatment of raised ICP

• 15° head-up tilt. Ensure good venous drainage of head and neck

• Avoid hypoxia. Keep P_aco₂ lower limit of normal. No PEEP

• Keep CVP low

• Avoid cerebral vasodilating drugs

• Adequate muscle relaxation

• Osmotic/loop diuretics (mannitol 1 g.kg⁻¹; effect prolonged by furosemide). Consider hypertonic saline as an alternative to mannitol.

• Consider CSF drainage.

Recommendations for the Safe Transfer of Patients with Brain Injury

Association of Anaesthetists of Great Britain and Ireland 2006

Summary

1. High quality transfer of patients with brain injury improves outcome.

2. There should be designated consultants in the referring hospitals and the neuroscience units with overall responsibility for the transfer of patients with brain injuries.

3. Local guidelines on the transfer of patients with brain injuries should be drawn up between the referring hospital trusts, the neurosciences unit and the local ambulance service. These should be consistent with established national guidelines. Details of the transfer of responsibility for patient care should also be agreed.

4. While it is understood that transfer is often urgent, thorough resuscitation and stabilization of the patient must be completed before transfer to avoid complications during the journey.

5. All patients with a Glasgow Coma Scale (GCS) ≤8 requiring transfer to a neurosciences unit should be intubated and ventilated.

6. Patients with brain injuries should be accompanied by a doctor with appropriate training and experience in the transfer of patients with acute brain injury. They must have a dedicated and adequately trained assistant. Arrangements for medical indemnity and personal accident insurance should be in place.

7. The standard of monitoring during transport should adhere to previously published standards.

8. The transfer team must be provided with a means of communication – a mobile telephone is suitable.

9. Education, training and audit are crucial to improving standards of transfer.

Association of Anaesthetists of Great Britain and Ireland. Recommedations for The Safe Transfer of Patients With brain injury. Reproduced with the kind permission of the Association of anaesthetists of Great Britain and Ireland, 2006.

Dinsmore J. Anaesthesia for elective neurosurgery. Br J Anaesth. 2007;99:68-74.

Hancock S.M., Nathanson M.H. Nitrous oxide or remifentanil for the ‘at risk’ brain. Anaesthesia. 2004;59:313-315.

Hirsch N. Advances in neuroanaesthesia. Anaesthesia. 2003;58:1162-1165.

Moss E. The cerebral circulation. BJA CEPD Rev. 2001;1:67-71.

Pasternak J.J., William L.W. Neuroanesthesiology update. J Neurosurg Anesth. 2009;21:73-97.

Autonomic Nervous System

Sympathetic nervous system (Fig. 3.7)

Centres in the brainstem give rise to descending tracts which innervate SNS preganglionic neurones in intermediolateral columns in the spinal cord. They emerge at T₁–L₂, then either synapse in SNS chain or synapse at a distance, e.g. coeliac plexus (splanchnic) or hypogastric plexus (bladder). SNS fibres for skin and vessels re-enter the cord to re-emerge with skeletal nerves.

Figure 3.7 SNS synapse. N, nicotinic receptor; M, muscarinic receptor; NA, noradrenaline; Ad, adrenaline; , ganglia; , adrenal medulla.

Parasympathetic nervous system (Fig. 3.8)

Parasympathetic nerve fibres run in cranial nerves II, V, VII, IX, X, S₂–S₄. 75% of PNS fibres run in the vagus to supply heart, lungs, upper GI tract and liver. Preganglionic fibres terminate in the end organ and postganglionic fibres are very short.

Figure 3.8 PNS synapse. N, nicotine receptor; M, muscarinic receptor; ACh, acetylcholine; O, ganglia.

Autonomic neuropathy

Causes

• Diabetes (IDDM >NIDDM)

• Guillain–Barré syndrome

• Parkinson’s disease

• Shy–Drager syndrome

Symptoms and signs

• Loss of diurnal BP variation

• Fixed heart rate (tachycardia) and loss of R–R′ variation

• Orthostatic hypotension

• Painless MI

• Failure of kidneys to concentrate urine at night, causing nocturia

• Increased gastric emptying time.

Anaesthetic problems

• Blood pressure dependent upon ECF volume with subsequent hypotension on induction

• Arrhythmias common

• Reduced sensitivity to hypoxia and hypercapnia

• Ventilation not associated with the usual Valsalva-type response

• Reduced response to indirect-acting catecholamines (e.g. ephedrine) but exaggerated response to direct catecholamines (e.g. adrenaline) due to a denervation hypersensitivity.

Foëx P. The heart and autonomic nervous system. In: Nimmo W.S., Rowbotham D.J., Smith G., editors. Anaesthesia. ed 2. Oxford: Blackwell Scientific Publications; 1994:195-242.

Keyl C., Lemberger P., Palitzsch K.D., et al. Cardiovascular autonomic dysfunction and haemodynamic response to anesthetic induction in patients with coronary artery disease and diabetes mellitus. Anesth Analg. 1999;88:985-991.

Tusiewicz K. The autonomic nervous system. In: Kaufman L., editor. Anaesthesia Review 5. Edinburgh: Churchill Livingstone; 1988:54-66.

Related

Clinical Notes for the FRCA