(BQ) Part 2 book Basic physiology for anaesthetists has contents: Cerebrospinal fluid, cerebral blood flow, skeletal muscle, cardiac muscle, the electrocardiogram, autonomic nervous system, immune system, resting membrane potential,.... and other contents.
Section Chapter Neurophysiology Intracranial pressure and head injury 46 What is intracranial pressure? How is it measured? The ICP is simply the hydrostatic pressure within the skull, but reflects the pressure of the CSF and brain parenchyma At rest in a normal supine adult, ICP is 5–15 mmHg; ICP varies throughout the cardiac and respiratory cycles Even in a normal brain, coughing, straining and sneezing can transiently increase ICP to as high as 50 mmHg Unfortunately, ICP cannot be estimated, only invasively measured ICP may be measured by a variety of devices, each with their advantages and disadvantages: By an EVD: a catheter inserted into the lateral ventricle, which is considered the ‘gold standard’ for measuring ICP In addition to ICP measurement, an EVD can be used to remove CSF for diagnostic and therapeutic purposes (to reduce ICP – see later) and for the administration of intrathecal medication However, to measure ICP, the EVD must be ‘clamped’; that is, CSF cannot be simultaneously drained An EVD may be surgically challenging to insert, especially if the ventricles are small or displaced Also, EVDs are frequently complicated by blockage and are associated with an infection risk of up to 5% Intraparenchymal probe: a fibre-optic-tipped catheter placed within the brain parenchyma through a small burr hole An intraparenchymal probe is much easier to insert than an EVD, and can be used in situations where the ventricles are compressed or displaced Measurement of ICP using an intraparenchymal probe is almost as accurate as an EVD, and infection rates are substantially lower However, there are concerns about the accuracy of intraparenchymal catheters used for prolonged periods: the catheter is zeroed at the time of insertion, and cannot be recalibrated in vivo However, drift has been shown to be as little as mmHg after days’ use An intraparenchymal probe only measures the pressure of the brain parenchyma in which it is located, which may not represent global ICP Subarachnoid probe: now considered relatively obsolete The subarachnoid probe is easier to insert and is associated with a low infection rate, but is much less accurate than the first two methods Subdural probe: also considered obsolete Like the subarachnoid probe, the subdural probe is easier to insert and has a lower infection risk than the first two methods, but is less accurate and prone to blockage, requiring regular flushing What is the Monro–Kellie hypothesis? The Monro–Kellie hypothesis states that the cranium is a rigid box of fixed volume, which contains: Brain tissue, 1400 g or approximately 80% of the intracranial volume CSF, 150 mL or approximately 10% of intracranial volume Arterial and venous blood, 150 mL or approximately 10% of intracranial volume An increase in the volume of any of these intracranial contents will increase ICP, unless there is also a corresponding reduction in the volume of one or both of the other contents For example: An increase in the volume of brain tissue may be localized (for example, a brain tumour or abscess) or generalized (such as occurs with cerebral oedema) The volume of CSF may be increased in hydrocephalus (see Chapter 43) 201 Downloaded from Cambridge Books Online by IP 216.195.11.197 on Thu Nov 05 03:42:07 GMT 2015 http://dx.doi.org/10.1017/CBO9781139226394.048 Cambridge Books Online © Cambridge University Press, 2015 Section 4: Neurophysiology Figure 46.1 Change in ICP with increasing intracranial volume Intracranial pressure (mmHg) 60 Global ischaemia 50 40 Focal ischaemia 30 20 Compensatory mechanism s 10 Point of decompensation Volume of expanding intracranial mass (mL) The volume of intracranial blood may be increased following haemorrhage (extradural, subdural or intraparenchymal) or venous sinus thrombosis When one of the intracranial contents increases in volume, there is a limited capacity for displacement of the other contents: Some CSF is displaced from the cranium into the spinal subarachnoid space Whilst the rate of CSF production remains approximately the same, CSF absorption by the arachnoid villi is increased Dural venous sinuses are compressed, displacing venous blood into the internal jugular vein, thus reducing the volume of intracranial blood After these small compensatory changes have occurred, ICP will rise The only options left are then potentially disastrous: a reduction in arterial blood volume or displacement of brain parenchyma through the foramen magnum (Figure 46.1) Symptoms suggesting raised ICP include: – A headache that is worse in the morning and is exacerbated by straining and lying flat – Nausea and vomiting Signs of raised ICP include: – A bulging fontanelle in infants and neonates – Papilloedema – Altered level of consciousness Severe intracranial hypertension may result in additional signs, as a result of brain displacement: – Cranial nerve palsies – most commonly the abducens (cranial nerve VI) – Pupillary dilatation – caused by compression of the oculomotor nerve (cranial nerve III) – Cushing’s triad: ▪ systemic hypertension ▪ bradycardia ▪ abnormal respiratory pattern Can you explain Cushing’s triad? As discussed in Chapter 45, CPP is related to ICP: CPP ¼ MAP À ICP According to this equation, an increase in ICP results in a decrease in CPP, unless MAP also increases Between a CPP of 50 and 150 mmHg, cerebral autoregulation maintains CBF at its normal value of 50 mL/100 g of brain tissue/min (see Chapter 45 and Figure 45.1) The Cushing response is a late physiological response to increasing ICP When CPP falls below 50 mmHg, the cerebral arterioles are maximally vasodilated and cerebral autoregulation fails CBF falls below the ‘normal’ value of 50 mL/100 g/min, resulting in cellular ischaemia 202 Downloaded from Cambridge Books Online by IP 216.195.11.197 on Thu Nov 05 03:42:07 GMT 2015 http://dx.doi.org/10.1017/CBO9781139226394.048 Cambridge Books Online © Cambridge University Press, 2015 Chapter 46: Intracranial pressure and head injury In the event of brainstem ischaemia, the brain has an ‘emergency’ hypertensive mechanism: the vasomotor area dramatically increases sympathetic nervous system outflow, triggering an intense systemic arteriolar vasoconstriction that results in systemic hypertension The rise in MAP restores perfusion, and hence CBF, to the brainstem In response to systemic hypertension, the arterial baroreceptors induce a reflex bradycardia If ICP continues to rise, the brain parenchyma starts to be displaced downwards The cerebellar tonsils are pushed through the foramen magnum, a process referred to as ‘tonsillar herniation’ or ‘coning’ The cerebellar tonsils compress the brainstem, causing the failure of brainstem functions: Irregular breathing and apnoea through compression of the respiratory centre Decreased consciousness: Glasgow coma scale (GCS) of 3–5 is usual Hypotension, as the vasomotor centre is compressed The Cushing reflex is a desperate attempt to maintain CPP (and therefore CBF) in the face of substantially increased ICP Unless (and often despite) swift action is taken, brainstem death is inevitable How may intracranial pressure be reduced? The Monro–Kellie hypothesis states that an increase in the volume of one of the three intracranial contents will cause an increase in ICP, unless there is also a reduction in the volume of one or both of the other components It therefore follows that ICP may be reduced if the volume of one or more of the intracranial contents is reduced: Reduction in the volume of CSF by means of an EVD This method can be used to reduce ICP even when hydrocephalus is not the cause Even the removal of a few millilitres of CSF can result in a significant decrease in ICP Reduction in the volume of blood: if the cause of raised ICP is a haematoma, this should be urgently evacuated Otherwise, in the context of raised ICP, intracranial venous and arterial blood can be considered as two entirely different entities: – Venous blood Intracranial venous blood serves no useful purpose and should be permitted to drain from the cranium As ICP increases, the dural venous sinuses are compressed, displacing blood into the internal jugular vein, thereby reducing the volume of intracranial venous blood As discussed in Chapter 42, the dural venous sinuses not have valves Therefore, venous drainage from the cranium is entirely dependent on the venous pressure gradient between the venous sinuses and the right atrium Venous drainage is therefore promoted by: ▪ Keeping the head in a neutral position and removing neck collars and tight-fitting ETT ties, which prevents kinking or occlusion of the internal jugular veins ▪ Nursing the patient in a 30° head-up tilt ▪ Using minimal PEEP Positive intrathoracic pressure reduces the venous pressure gradient Therefore, in ventilated patients, PEEP should be reduced to the lowest value required to achieve adequate oxygenation ▪ Using muscle relaxants to prevent coughing and straining, both of which transiently increase intrathoracic pressure – Arterial blood An adequate volume of well-oxygenated arterial blood is essential to meet the metabolic demands of the brain, but CBF in excess of that required merely serves to increase ICP Therefore, the aim is to provide just sufficient CBF to meet the brain’s metabolic needs Two main strategies are employed: ▪ Reducing CMR Owing to flow– metabolism coupling, CBF is related to CMR Seizure activity substantially increases CMR, which in turn increases CBF and consequently increases ICP – seizures should be rapidly treated with benzodiazepines and anti-epileptic drugs CMR may be reduced to sub-normal levels through the use of drugs (propofol, thiopentone or benzodiazepines such as midazolam) or through therapeutic cooling (CMR is reduced by 7% per °C reduction in brain temperature) Therapeutic cooling has not yet been proven to reduce mortality, and is not recommended unless the patient is pyrexial 203 Downloaded from Cambridge Books Online by IP 216.195.11.197 on Thu Nov 05 03:42:07 GMT 2015 http://dx.doi.org/10.1017/CBO9781139226394.048 Cambridge Books Online © Cambridge University Press, 2015 Section 4: Neurophysiology ▪ Preventing hypoxaemia or hypercapnoea As discussed in Chapter 45, hypoxaemia and hypercapnoea both trigger cerebral arteriolar vasodilatation, which increases CBF and consequently increases ICP In situations of raised ICP, PaO2 should be maintained above 10 kPa, and PaCO2 between 4.5 and 5.0 kPa Reduction in the volume of brain parenchyma: – Severely raised ICP may be temporarily reduced by decreasing brain ECF volume through osmotherapy, following intravenous administration of an osmotic diuretic; for example, mannitol or hypertonic saline – When raised ICP is caused by a brain tumour, the volume of surrounding oedema may be reduced by using dexamethasone, or surgical excision may be considered – The volume of a cerebral abscess may be reduced by surgical drainage and by antibiotic therapy How is head injury classified? Head injury is defined as any trauma to the head, whether or not brain injury has occurred Head injury may be classified by: Mechanism of injury, which may be blunt (road traffic collision or fall) or penetrating (gunshot or stab wounds) In the military setting, blast injury can also occur Blunt head injury may be: – Closed, where the dura mater remains intact – Open, where the dura mater is breached, exposing the brain and CSF to environmental microorganisms Penetrating head injury is, by definition, open Presence of other injuries Following trauma, patients may have an isolated head injury or there may be accompanying traumatic injuries Where a head injury results in a TBI, further classifications can be made: Severity of injury On arrival to hospital, the severity of TBI is commonly assessed using the GCS: – Mild TBI corresponds to a GCS score of 13–15 – Moderate TBI corresponds to a GCS score of 9–12 – Severe TBI corresponds to a GCS score of 3–8 Patients presenting with mild TBI have a good prognosis with a mortality of 0.1% However, patients with moderate and severe TBI have a much higher mortality, around 10% and 50% respectively Many survivors are left with severe disability Area of brain injury Brain injury can be focal (for example, extradural haematoma, contusions) or diffuse (for example, diffuse axonal injury, hypoxic brain injury), but both types of injury commonly coexist What is the difference between primary and secondary brain injury? Brain injury may be classified as primary or secondary: Primary brain injury is damage to the brain during the initial injury caused by mechanical forces: stretching and shearing of neuronal and vascular tissue Neuronal tissue is more susceptible to damage than blood vessels; this is why diffuse axonal injury frequently accompanies injuries where there has been vessel disruption; for example, extradural haematoma or traumatic subarachnoid haemorrhage Secondary brain injury refers to the further cellular damage caused by the pathophysiological consequences of the primary injury Cells injured in the initial trauma trigger inflammatory reactions, resulting in cerebral oedema and an increase in ICP Secondary brain injury occurs hours to days after the primary injury through a number of different mechanisms: – – – – – – damage to the BBB cerebral oedema raised ICP seizures ischaemia infection Once primary brain injury has occurred, it cannot be reversed Prevention of trauma is the best method of reducing primary brain injury: reducing speed limits, safer driving strategies, and so on The impact of trauma on the brain can be reduced by the use of airbags and seatbelts in cars, and of helmets for cyclists and motorcyclists Medical and surgical efforts are concentrated on preventing secondary brain injury: preserving as many neurons as possible 204 Downloaded from Cambridge Books Online by IP 216.195.11.197 on Thu Nov 05 03:42:07 GMT 2015 http://dx.doi.org/10.1017/CBO9781139226394.048 Cambridge Books Online © Cambridge University Press, 2015 Chapter 46: Intracranial pressure and head injury How would you approach the management of a patient with traumatic brain injury? Patients with TBI frequently present with other, more immediately life-threatening injuries The broad principles of initial trauma management are the same whether in the emergency department or the pre-hospital setting: with a multidisciplinary team following an airway–breathing–circulation–disability– exposure (ABCDE) approach, ensuring spinal immobilization and treating life-threatening injuries first Following the initial resuscitation phase, patients with suspected TBI will require rapid transfer for brain imaging, the results of which will help guide further medical and surgical management What are the main principles of medical management in a patient with traumatic brain injury? The medical management of TBI is concerned with preventing secondary brain injury and reducing ICP It is divided into maintenance of: Normoxia Hypoxaemia (defined as PaO2 < kPa) is associated with a worse outcome following TBI, due to its detrimental effects on CBF and hence ICP Hypoxaemia may occur for a number of reasons, such as airway obstruction, associated chest injuries and aspiration pneumonitis In the initial resuscitation phase, all trauma patients should have high-flow O2 administered, and patients with the potential to develop hypoxaemia (for example, those with a low GCS) should be intubated at an early stage Normotension A fall in CPP below 50 mmHg leads to failure of cerebral autoregulation, reduced CBF and cellular ischaemia Therefore, in the neurointensive care unit, when ICP is being measured, CPP should be kept above 60 mmHg Unfortunately, trauma patients not arrive in hospital with ICP monitoring in situ – the Association of Anaesthetists of Great Britain and Ireland (AAGBI) recommends maintaining MAP >80 mmHg This should be achieved initially using fluid resuscitation, and then by using vasopressors Even a single episode in which SBP is 37.6 °C) increases CMR, which leads to an increase in CBF and consequently an increase in ICP Hyperthermia should therefore be treated promptly using an antipyretic (such as paracetamol) and external cooling devices Venous drainage This is promoted by nursing the patient in a 30° head-up tilt, with a neutral head position and ensuring that ETT ties are loose Minimal PEEP should be used 205 Downloaded from Cambridge Books Online by IP 216.195.11.197 on Thu Nov 05 03:42:07 GMT 2015 http://dx.doi.org/10.1017/CBO9781139226394.048 Cambridge Books Online © Cambridge University Press, 2015 Section 4: Neurophysiology Further reading R T Protheroe, C L Gwinnutt Early hospital care of severe traumatic brain injury Anaesthesia 2011; 66(11): 1035–47 I K Moppett Traumatic brain injury: assessment, resuscitation and early management Br J Anaesth 2007; 99(1): 18–31 H B Lim, M Smith Systemic complications after head injury: a clinical review Anaesthesia 2007; 62(5): 474–82 L A Steiner, P J D Andrews Monitoring the injured brain: ICP and CBF Br J Anaesth 2006; 97(1): 26–38 K Pattinson, G Wynne-Jones, C H E Imray Monitoring intracranial pressure, perfusion and metabolism Contin Educ Anaesth Crit Care Pain 2005; 5(4): 130–3 K Girling Management of head injury in the intensive-care unit Contin Educ Anaesth Crit Care Pain 2004; 4(2): 52–6 206 Downloaded from Cambridge Books Online by IP 216.195.11.197 on Thu Nov 05 03:42:07 GMT 2015 http://dx.doi.org/10.1017/CBO9781139226394.048 Cambridge Books Online © Cambridge University Press, 2015 Section Chapter Neurophysiology The spinal cord 47 Describe the anatomy of the spinal cord The spinal cord is part of the CNS, located within the spinal canal of the vertebral column The spinal cord begins at the foramen magnum, where it is continuous with the medulla oblongata The spinal cord is much shorter than the vertebral column, ending at a vertebral level of L1/2 in adults, but at a lower level of around L3 in neonates Like the brain, the spinal cord is enveloped in three layers of the meninges: pia, arachnoid and dura mater CSF surrounds the spinal cord in the subarachnoid space, and extends inferiorly within the dural sac to approximately S2 level After the spinal cord terminates, the pia and dura merge to form the filum terminale, which tethers the cord to the coccyx The spinal cord is divided into 31 segments, each emitting a pair of spinal nerves There are: Eight cervical segments Note: there is one more pair of cervical nerves emitted than there are cervical vertebrae Twelve thoracic segments Five lumbar segments Five sacral segments One coccygeal segment With the exception of C1 and C2, the spinal nerves exit the spinal canal through the intervertebral foramina The spinal cord enlarges in two regions: The cervical enlargement at C4–T1, corresponding to the brachial plexus, which innervates the upper limbs The lumbar enlargement at L2–S3, corresponding to the lumbar plexus, which innervates the lower limbs At the terminal end of the spinal cord: The conus medullaris is the tapered terminal portion of the cord The cauda equina is the collection of spinal nerves that continue inferiorly in the spinal canal after the cord has ended, until they reach their respective intervertebral foramina Describe the cross-sectional anatomy of the spinal cord In cross-section the spinal cord is approximately oval, with a deep anterior median sulcus and a shallow posterior median sulcus The centre of the cord contains an approximately ‘H’-shaped area of grey matter, surrounded by white matter: The grey matter contains unmyelinated axons and the cell bodies of interneurons and motor neurons Located in the centre of the grey matter is the CSF-containing central canal The points of the ‘H’ correspond to the dorsal and ventral (posterior and anterior) horns There are also lateral horns in the thoracic region of the cord, which correspond to pre-ganglionic sympathetic neurons The white matter contains columns of myelinated axons, called tracts These tracts are organized into: – ascending tracts, containing sensory axons; – descending tracts, containing motor axons The most important ascending tracts are shown in Figure 47.1: The dorsal (posterior) columns contain axons of nerves concerned with proprioception (position sense), vibration and two-point discrimination (fine touch) The anterior and lateral spinothalamic tracts carry sensory information about pain, temperature, crude touch and pressure The anterior and posterior spinocerebellar tracts carry proprioceptive information from the muscles and joints to the cerebellum 207 Downloaded from Cambridge Books Online by IP 216.195.11.197 on Thu Nov 05 03:42:20 GMT 2015 http://dx.doi.org/10.1017/CBO9781139226394.049 Cambridge Books Online © Cambridge University Press, 2015 Section 4: Neurophysiology ASCENDING Cuneate tract Dorsal columns DESCENDING Gracile tract Central canal Posterior spinocerebellar tract Dorsal (posterior) horn Lateral corticospinal tract Anterior spinocerebellar tract Lateral horn (present in thoracic segments only) Ventral (anterior) horn Lateral spinothalamic tract Anterior spinothalamic tract Anterior corticospinal tract Anterior median sulcus Figure 47.1 Cross-section of the spinal cord (extrapyramidal tracts not shown) The most important descending tracts are (Figure 47.1): The anterior and lateral corticospinal tracts, also known as the pyramidal tracts, carry the axons of upper motor neurons In the ventral horn of the spinal cord, these axons relay to α-motor neurons (or lower motor neurons) that innervate muscle The extrapyramidal tracts: rubrospinal, tectospinal, vestibulospinal, olivospinal and reticulospinal tracts The extrapyramidal neurons originate at brainstem nuclei and not pass through the medullary pyramids Their primary role is in the control of posture and muscle tone Describe the blood supply to the spinal cord The spinal cord is supplied by three arteries, derived from the posterior circulation of circle of Willis (see Chapter 42) However, the blood flow through these vessels is insufficient to perfuse the cord below the cervical region – an additional contribution from radicular arteries is essential The three spinal arteries are: One anterior spinal artery, which arises from branches of the right and left vertebral artery (see Figure 42.1) The anterior spinal artery descends in the anterior median sulcus and supplies the anterior two-thirds of the spinal cord, essentially all the structures with the exception of the dorsal columns The anterior spinal artery is replenished along its length by several radicular arteries, the largest of which is called the artery of Adamkiewicz The location of this vessel is variable, but is most commonly found on the left between T8 and L1 Two posterior spinal arteries, which arise from the posterior inferior cerebellar arteries (see Figure 42.1) The posterior spinal arteries are located just medial to the dorsal roots, and supply the posterior one-third of the cord Again, the posterior spinal arteries are replenished by radicular arteries 208 Downloaded from Cambridge Books Online by IP 216.195.11.197 on Thu Nov 05 03:42:20 GMT 2015 http://dx.doi.org/10.1017/CBO9781139226394.049 Cambridge Books Online © Cambridge University Press, 2015 Chapter 47: The spinal cord Blood from the spinal cord is drained via three anterior and three posterior spinal veins, located in the pia mater, which anastomose to form a tortuous venous plexus Blood from this plexus drains into the epidural venous plexus Clinical relevance: anterior spinal artery syndrome The artery of Adamkiewicz most commonly arises from the left posterior intercostal artery, a branch of the aorta Damage or obstruction of the artery can occur through atherosclerotic disease, aortic dissection or surgical clamping during aortic aneurysm repair As the anterior spinal artery supplies the anterior two-thirds of the spinal cord, cessation of blood flow can have profound consequences (see Figure 47.4) Signs and symptoms of anterior spinal artery syndrome are: Paraplegia, as a result of involvement of α-motor neurons within the anterior horn of the cord (i.e a lower motor neuron deficit at the level of the lesion), and the corticospinal tracts carrying the axons of upper motor neurons (i.e an upper motor neuron deficit below the level of the lesion) Loss of pain and temperature sensation, due to involvement of the spinothalamic tracts Autonomic dysfunction involving the bladder or bowel, due to disruption of the sacral parasympathetic neurons Crucially, proprioception and vibration sensation remain intact These sensory modalities are carried in the dorsal columns, which are supplied by the posterior spinal arteries and thus remain unaffected Describe the main sensory afferent pathways The somatosensory nervous system consists of: Sensory receptors, which encode stimuli by repetitive firing of action potentials The different sensory receptor types are specific to their sensory modalities: proprioceptors, nociceptors, thermoreceptors and mechanoreceptors relay sensory information concerning limb position, tissue damage (potentially causing pain), temperature and touch respectively The perception of the stimulus is dependent upon the neuronal pathway rather than the sensory receptor itself For example, pressing on the eye activates the optic nerve and gives the impression of light, despite the stimulus being pressure rather than photons First-order neurons transmit action potentials from sensory receptors to the spinal cord, where they synapse with second-order neurons These neurons are pseudounipolar with their cell bodies located in the dorsal root ganglion, a swelling of the dorsal root just outside the spinal cord Second-order neurons conduct action potentials to the thalamus, where they synapse with thirdorder neurons Third-order neurons relay action potentials to the cerebral cortex via the internal capsule The primary somatosensory cortex is the area of the cerebral cortex that receives and performs an initial processing of the sensory information The primary somatosensory cortex is located in the post-central gyrus of the parietal lobe It is organized in a somatotropic way with specific areas of cortex dedicated to specific areas of the body, known as the sensory homunculus Of note: the hands and lips make up a major component, reflecting their tactile importance Inputs from specific sensory modalities end in specific columns of cerebral cortical tissue There are two major pathways by which sensory information ascends in the spinal cord: The dorsal column–medial lemniscal (DCML) pathway carries sensory information about twopoint discrimination, vibration and proprioception (Figure 47.2a) The name of the pathway comes from the two structures through which the sensory signals pass: the dorsal columns of the spinal cord and the medial lemniscus in the brainstem: – The first-order neuron is extremely long It enters the dorsal root of the spinal cord and ascends in the dorsal columns on the same side (ipsilateral) Sensory neurons from the lower body travel in the medial gracile tract and synapse in the gracile nucleus in the medulla oblongata, whilst sensory neurons from the upper body travel in the lateral cuneate tract and synapse in the cuneate nucleus – In the medulla, first-order neurons synapse with second-order neurons, which then cross over to the contralateral side and ascend to the 209 Downloaded from Cambridge Books Online by IP 216.195.11.197 on Thu Nov 05 03:42:20 GMT 2015 http://dx.doi.org/10.1017/CBO9781139226394.049 Cambridge Books Online © Cambridge University Press, 2015 Section 4: Neurophysiology (a) Dorsal column–medial lemniscuspathway (b) Spinothalamic pathway Somatosensory cortex Third-order neurons Thalamus Second-order neurons Medial lemniscal tract Gracile nucleus Cuneate nucleus Third-order neurons Medulla oblongata Fibres cross the midline Second-order neurons within spinothalamic tract Cuneate tract First-order neuron from upper limbs Second-order fibres cross in anterior commissure First-order neuron from upper limbs Gracile tract Dorsal root ganglion First-order neuron from lower limbs First-order neuron from lower limbs Figure 47.2 The two major sensory pathways: (a) DCML; (b) spinothalamic thalamus After this sensory decussation, the fibres ascend through the brainstem in a tract called the medial lemniscus The spinothalamic tract carries sensory information about crude touch, pressure, temperature and pain (Figure 47.2b) In contrast to the DCML pathway, the spinothalamic tract crosses the midline at the level of the spinal cord rather than the medulla: – The first-order neurons enter the dorsal root of the spinal cord, and may ascend or descend one or two vertebral levels (along Lissauer’s tract) before synapsing with second-order neurons in the dorsal horn – The axons of the second-order neurons decussate anterior to the central canal of the spinal cord, in an area called the anterior commissure, before ascending to the thalamus in the contralateral spinothalamic tract Clinical relevance: dissociated sensory loss Dissociated sensory loss is a relatively rare pattern of neurological injury characterized by the selective loss of two-point discrimination, vibration-sense and proprioception without the loss of pain and temperature, or vice versa This is due to the different points of decussation of the DCML and spinothalamic tracts Causes of dissociated sensory loss include: Brown-Séquard syndrome, in which a hemi-section of the spinal cord causes ipsilateral motor weakness, ipsilateral loss of two-point discrimination, proprioception and vibration sensation with contralateral loss of pain and temperature sensation below the level of the lesion (see Figure 47.4) Hemi-section of the cord may be the result of trauma (such as a gunshot wound), inflammatory disease (for example, multiple sclerosis), or by local compression: spinal cord tumour or infection (for example, tuberculosis) 210 Downloaded from Cambridge Books Online by IP 216.195.11.197 on Thu Nov 05 03:42:20 GMT 2015 http://dx.doi.org/10.1017/CBO9781139226394.049 Cambridge Books Online © Cambridge University Press, 2015 Chapter 83: Temperature regulation Renal Suppression of ADH secretion results in a ‘cold diuresis’ Haematological Hypothermia has been implicated in platelet and clotting dysfunction, but it is likely that these effects are only minor Clinical relevance: adverse effects of intraoperative hypothermia There are a number of adverse effects associated with mild perioperative hypothermia: Myocardial ischaemia, infarction and arrhythmias Increased intraoperative blood loss, and increased requirement for transfusion Increased incidence of postoperative wound infection Prolonged postoperative recovery and prolonged hospital stay Common measures to prevent intraoperative hypothermia include: Active warming with forced-air warmers and heated mattresses Warming of intravenous fluids and blood Humidification of inspired gases Further reading C M Harper, J C Andrzejowski, R Alexander NICE and warm Br J Anaesth 2008; 101(3): 293–5 S C Kettner, C Sitzwhol, M Zimpfer, et al The effect of graded hypothermia (36 °C–32 °C) on haemostasis in anaesthetized patients without surgical trauma Anesth Analges 2003; 96(6): 1772–6 D A Kirkbride, D J Buggy Thermoregulation and mild perioperative hypothermia Contin Educ Anaesth Crit Care Pain 2003; 3(1): 24–8 433 Downloaded from Cambridge Books Online by IP 216.195.11.197 on Thu Nov 05 18:38:22 GMT 2015 http://dx.doi.org/10.1017/CBO9781139226394.085 Cambridge Books Online © Cambridge University Press, 2015 Index abciximab, 339 ABO blood group system, 29, 345 acetylcholine (ACh), 234 acetylcholine receptors (AChRs), 234–5, 267–8 acetylcholinesterase (AChE), 20, 232 acid Brønsted–Lowry definition, 328 definitions, 328 strong and weak acids (pKa), 328–9 acid–base disorders, 121, 329–30, 336 acid–base physiology, 330–1, 333–6 acidaemia, 328 acidosis, 329–30 acromegaly, 391 action potential, 221 acute high-altitude illness, 427 acute kidney injury (AKI), 309–10 acute pancreatitis, 289 acute respiratory distress syndrome (ARDS), 51, 157, 329, 357 Addison’s disease, 326 adenine (A), ADP (adenosine diphosphate) receptor antagonists, 339 adrenal glands, 397–400 adrenaline, 20, 400 adrenergic receptors (adrenoceptors), 268 adrenocorticotropic hormone (ACTH), 384, 389–90 aerobic metabolism, 64 ageing, 119, 420–4 Acquired immunodeficiency syndrome (AIDS) patients, 364 airway devices effects on the respiratory system, 108 airway resistance, 88–9 and anaesthesia, 90–1 albumin, 366–7 alcohol acute binge, 301 chronic abuse, 301 metabolism, 301 aldosterone, 387, 398 alkalaemia, 328 alkalosis, 330 allergens, 355 allergic reactions, 356 allergic rhinitis, 363–4 allodynia, 272 allopurinol, 301, 310 altitude physiology, 42, 78–9, 81, 99, 425–8 alveolar–arterial (A–a) gradient, 78 alveolar–capillary barrier, 24, 40, 42–3 alveolar dead space (V Alv D ), 45–6 alveolar diffusion, 40–4, 64–5 rate of diffusion equation, 40 alveolar gas equation (AGE), 64, 77–9 alveolar surface tension, 83–4, 88 alveolar ventilation, 46–8, 69 alveolar volume (VA), 45 alveoli, 24 cell types, 24 determining the PAO2, 77 aminophylline, 301 amoxicillin, 410 anabolism, 369 anaemia, 351–3 global oxygen delivery in an anaemic patient, 74–5 anaemic hypoxia, 64 anaerobic metabolism, 81 anaesthesia and airway resistance, 90–1 and global oxygen consumption, 76 and global oxygen delivery, 76 at altitude, 427–8 effects of hypoxic pulmonary vasoconstriction (HPV), 99–100 effects on normal thermoregulatory mechanisms, 431–2 effects on the immune system, 364–5 emergency anaesthesia, 55 for thyroid surgery, 394–5 halothane hepatitis, 295–6 heat loss during, 431–2 hypercapnoeic acidosis, 329–30 hypotensive anaesthesia, 149 low flow anaesthesia, 29 management in sickle cell disease, 33 minimal flow anaesthesia, 29 See also general anaesthesia anaesthetic agents negative inotropic effects, 121 anaesthetic breathing systems mechanical dead space, 47–8 re-breathing effect, 47–8 anaesthetic drugs effects on the respiratory system, 107–8 effects on ventilation control, 95 anaphylaxis, 363–5 anatomical dead space Fowler’s method of measurement, 48 anatomical shunt, 96 anaxonic neurons, 184 angina anti-anginal drugs, 157 anion gap, 330–1 equation, 330 anorexia nervosa, 382–3 Anrep effect, 121 anterior spinal artery syndrome, 209, 214 antiarrhythmic drugs, 253–4 antibiotics, 195, 364 antibodies (immunoglobulins), 358–60, 362–3, 409 antidiuretic hormone (ADH), 149, 318, 321, 324, 387, 390–1 antiemetic drugs, 284 antifibrinolytic drugs, 344 antigens, 355 anti-platelet drugs, 116, 338–40 aortic stenosis, 122–3 apneustic centre, 92 apnoea, 38–9 test for brainstem death, 52 arachnoid mater, 188 area postrema, 195 arginine vasopressin See antidiuretic hormone (ADH) arterial baroreceptor reflex, 166–7 arterial CO2 tension, 46–8, 66 arterial pressure wave Windkessel effect, 150 arterial pressure waveform, 150–2 arterial pulse contour analysis, 152 arterial system, 144–9 arterioles, 146–8 arteriovenous anastomoses, 158 aspiration pneumonia, 277, 281 434 Downloaded from Cambridge Books Online by IP 216.195.11.197 on Thu Nov 05 18:38:34 GMT 2015 http://ebooks.cambridge.org/ebook.jsf?bid=CBO9781139226394 Cambridge Books Online © Cambridge University Press, 2015 Index aspirin, 116, 312, 339 asthma, 89, 329, 356, 363–4 astrocytes, 188 atelectasis, 21 caused by general anaesthesia, 108 ATP (adenosine triphosphate), 5–6, 369, 373 ATPases, 14 atracurium, 424 atropine, 410 autonomic nervous system (ANS), 172, 184–5, 265–8 autonomic neurons, 184–5 autosomal dominant inheritance, 11 autosomal recessive inheritance, 11 autotransfusion, 156 axons, 183 Bain circuit (Mapleson D), 47 Bainbridge reflex, 166–7 balloon-tipped pulmonary artery catheter, 100 See also pulmonary artery catheter Bamford classification of ischaemic stroke, 189 barbiturates, 301 barotrauma, 51 Barrett’s oesophagus, 277 basal ganglia of the brain, 186 basal metabolic rate (BMR), 379 base Brønsted–Lowry definition, 328 definitions, 328 base excess, 330 basophils, 356 Bazett’s formula, 262 Becker's muscular dystrophy, 242 benzodiazepines, 195, 231, 423 β-blockers, 116, 121 bipolar neurons, 184 bisoprolol, 116 bleomycin-induced oxygen toxicity, 103 bleomycin treatment pulmonary fibrosis related to, 103 blood constituents, 366 blood–brain barrier (BBB), 153, 196 blood haematocrit influence on cerebral blood flow (CBF), 198 blood oxygen content equation, 28 blood pressure diastolic blood pressure (DBP), 148 in tachycardia, 148 invasive measurement method, 148 manipulation in clinical practice, 149 non-invasive measurement, 148 systolic blood pressure (SBP), 148 See also mean arterial pressure (MAP) blood substitutes (O2-carrying solutions), 350 blood transfusion allogenic transfusion, 346 autologous transfusion, 346, 349 blood groups, 29 blood substitutes (O2-carrying solutions), 350 cell salvage, 349 complications of massive transfusion, 349–50 cross-match tests, 347 haemolytic transfusion reaction, 346–7 infectious disease transmission, 348 iron overload (haemosiderosis), 348 massive transfusion, 349–50 O2 binding in transfused blood, 32 potential complications, 348 storage of blood products, 347–8 universal donor, 347 universal recipient, 347 blood velocity and flow equation, 142 body compartments, 316 general organization, 1–4 organs, systems, 1–2 body plethysmography calculation of FRC, 53–4 Bohr effect, 37 Bohr equation, 45, 49 Bohr method measurement of physiological dead space, 49 bone disease and kidney dysfunction, 397 and liver dysfunction, 397 bone mineral density effects of weight-bearing exercise, 182 botulinum toxin, 234 Bowditch effect, 122 Boyle’s law, 53–4 brain, 184 cerebral arterial blood supply, 188–9 electroencephalogram (EEG), 189–90 extrapyramidal system, 186 stroke, 189 venous drainage, 189 ventriculomegaly, 192 brain anatomy, 186–7 basal ganglia, 186 cerebellum, 187 cerebral cortex, 186 cerebral hemispheres, 186 corpus callosum, 186 diencephalon, 186–7 embryological classification, 187 frontal lobe, 186 hypothalamus, 186–7 lateral geniculate nucleus, 187 limbic system, 186 medial geniculate nucleus, 187 medulla oblongata, 187 meninges, 187–8 mesencephalon (midbrain), 187 metathalamus, 187 occipital lobe, 186 parietal lobe, 186 pons, 187 prosencephalon (forebrain), 187 rhombencephalon (hindbrain), 187 subthalamus, 187 telencephalon (cerebrum), 186 temporal lobe, 186 thalamus, 186 Wernicke’s area, 186 brain injury primary, 204 secondary, 204 See also traumatic brain injury brainstem death testing apnoea test, 52 bronchial circulation, 96 and lung transplant surgery, 96 Brønsted–Lowry definitions of acid and base, 328 Brown-Séquard syndrome, 210, 214 butyrylcholinesterase, 20 calcitonin, 397 calcium (Ca2+) in the body, 219–20, 395–7 calcium channel blockers, 116, 121 calcium resonium, 327 capillaries, 153–6 capillary–tissue exchange, 153–4 carbamazepine, 301 carbaminohaemoglobin, 37 carbohydrates digestion and absorption, 287 carbon dioxide (CO2) Bohr effect, 37 diffusion rate, 40 Haldane effect, 37 methods of transport in the circulation, 36–7 physiological effects of apnoea, 38–9 production and storage, 36 435 Downloaded from Cambridge Books Online by IP 216.195.11.197 on Thu Nov 05 18:38:34 GMT 2015 http://ebooks.cambridge.org/ebook.jsf?bid=CBO9781139226394 Cambridge Books Online © Cambridge University Press, 2015 Index carbon dioxide (CO2) (cont.) proportion in each transport form, 37–8 carbon dioxide (CO2) arterial partial pressure effects on cerebral blood flow, 198 carbon dioxide (CO2) dissociation curve, 38–9 carbon monoxide carboxyhaemoglobin, 32 diffusion rate, 41–2 effects on O2-carrying capacity, 34 lung diffusion capacity (DLCO), 43 carboxyhaemoglobin, 32 cardiac action potential action of the pacemaker currents, 255 conduction through the heart, 255–6 differences from nerve action potential, 250–1 pacemaker cells, 254–5 pacemaker potential, 255 phases, 251–3 refractory periods, 253 cardiac arrhythmias, 161, 253–4 cardiac cycle definition, 117 events, 117–19 phases, 117 cardiac failure, 130–4, 139–40 cardiac index (CI), 122 cardiac muscle contraction mechanism, 256–7 excitation–contraction coupling, 256 function, 130 functional syncytium, 112 influence of the autonomic nervous system, 257–8 resting membrane potential (RMP) in cells, 250 structural features, 250 termination of contraction, 257 cardiac output (CO) Bowditch effect, 122 calculation from the arterial pressure waveform, 152 cardiac index (CI), 122 definition, 120 effects of ageing, 119 effects of aortic stenosis, 122–3 ejection fraction (EF), 119 factors affecting stroke volume (SV), 120 influence of afterload, 120–1 influence of heart rate (HR), 121 influence of myocardial contractility, 120–1 influence of preload, 120–1 myocardial ischaemia, 121 regulatory factors, 120–1 relationship to mean arterial pressure (MAP), 122 cardiac output (CO) equation, 120 cardiac output (CO) measurement invasive methods, 123–7 methods based on the Fick principle, 123–6 methods of measurement, 123 minimally invasive methods, 127–9 pulse contour analysis, 126–7 cardiac resynchronization therapy (CRT), 114 cardiac toxicity effects of local anaesthetics, 258 cardiac work relationship to left ventricular pressure–volume loop, 137–8 cardiogenic pulmonary oedema, 99 cardiogenic shock, 149 cardiopulmonary bypass, 335 cardiovascular reflexes arterial baroreceptor reflex, 166–7 Bainbridge reflex, 167 classes of haemorrhagic shock, 169 classification, 166 consequences of peripheral chemoreceptor activation, 167–8 Cushing’s reflex, 167 decompensated shock, 169 physiological response to haemorrhage, 168–9 cardiovascular system components, 1, 141 effects of exercise, 176–8 effects of physical training, 182 effects of the Valsalva manoeuvre, 171 See also pulmonary circulation; systemic circulation catabolism, 369 production of ATP, 369 catalysts, 18 catecholamines, 194–5, 312, 387, 399–400 cauda equina syndrome, 214 cell basic structure, organelles, 5–7 cell membrane, active transport across, 16 carriers, 14 cholesterol, 13 endocytosis, 17 enzymes, 14 exocytosis, 17 functions of transmembrane proteins, 13–14 glycolipids, 13 glycoproteins, 13 ion channels, 14 mechanisms of transport across, 14–17 passive transport across, 15–16 peripheral proteins, 13 pumps (ATPases), 14 receptors, 14 structure, 13 transcytosis, 17 transmembrane proteins, 13 transport of hydrophilic substances across, 14–17 transport of lipophilic substances across, 14 vesicular transport across, 17 cell nucleus, cell salvage for autologous transfusion, 349 cellular respiration, 369 central cord syndrome, 214 central nervous system (CNS), 184 brain, 184 neuroglia, 188 oxygen toxicity effects, 102 spinal cord, 184 central venous cannulation, 164–5 central venous oxygen saturation (ScvO2), 163 central venous pressure (CVP), 161–3 central venous pressure (CVP) waveform, 161 centrilobular necrosis of the liver, 295–6 cerebellum, 187 cerebral arterial blood supply, 188–9 cerebral autoregulation, 197 cerebral blood flow (CBF) cerebral autoregulation, 197 cerebral perfusion pressure (CPP), 197 effects of anaesthetic drugs, 198–200 effects of CO2 arterial partial pressure, 198 effects of low CBF on neurons, 197–8 effects of O2 arterial partial pressure, 198 436 Downloaded from Cambridge Books Online by IP 216.195.11.197 on Thu Nov 05 18:38:34 GMT 2015 http://ebooks.cambridge.org/ebook.jsf?bid=CBO9781139226394 Cambridge Books Online © Cambridge University Press, 2015 Index factors affecting global CBF, 198 flow–metabolism coupling, 198 influence of blood haematocrit, 198 measurement, 197 methods of measurement, 200 normal level, 197 proportion of cardiac output (CO), 197 cerebral blood supply stroke, 189 cerebral cortex, 186 voluntary control of breathing, 94 cerebral hemispheres, 186 cerebral perfusion pressure (CPP), 197 cerebrospinal fluid (CSF), 191–2 cerebrum (telencephalon), 186 Charcot–Marie–Tooth disease, 235 chemoreceptors central, 93 peripheral, 92–3 choroid plexus, 195 chromosomes, chronic obstructive pulmonary disease (COPD), 53, 89–90, 93, 99–100, 105–6, 329 chyle, 164 chylomicrons, 164 chylothorax, 165 ciclosporin, 301 cimetidine, 301 circle of Willis, 188–9 circle system (anaesthetic breathing system), 47 circulatory system, circumventricular organs, 195–6 citric acid cycle, 369, 371–2 clopidogrel, 116, 339 closing capacity (CC), 55 clotting laboratory tests, 341–3 coagulation cell-based model, 341 coagulation cascade, 338–41 cocaine, 232 codeine, 301 codons, 10 coenzymes, 19–20 cofactors, 19–20 compensated heart failure, 132–3 complement system, 357–8 complex regional pain syndrome (CRPS), 273 compliance of the venous system, 158–9 congestive heart failure, 156 Conn’s syndrome, 327 contact dermatitis, 364 continuous positive airway pressure (CPAP), 100 cor pulmonale, 99 coronary blood flow, 114–16 coronary circulation, 112–13 corpus callosum, 186 corticospinal tract, 211–12 corticotropin-releasing hormone (CRH), 389 cortisol, 386–7, 398–9 creatinine, 312 critical illness causes of peripheral oedema, 156 complex acid–base disturbance, 336 global oxygen delivery, 76 hyperglycaemia, 385 hypoalbuminaemia, 156 myopathy, 242 risk associated with etomidate, 399 Cushing’s disease, 391, 398 Cushing’s reflex, 167, 202–3 cyanide poisoning, 32, 34–5 cyanohaemoglobin, 32 cyclizine, 284 cyclo-oxygenase (COX) inhibitors, 339 cystic fibrosis, 10 cytochrome P450 enzymes, 20 cytoplasm, cytosine (C), cytotoxic hypoxia, 64 cytotoxic T-cells (CD8+ T-cells), 361–2 Dalton’s law, 425 dantrolene, 240 Darcy’s law, 97, 122, 145, 147 decompensated heart failure, 133–4 decompensated shock, 169 demyelinating disease, 224 dendrites, 183 denervation hypersensitivity, 235 deoxyhaemoglobin, 30, 37 desmopressin (DDAVP), 341 diabetes insipidus, 321 diabetes mellitus, 312 diabetic autonomic neuropathy, 172 diabetic ketoacidosis, 374, 378 diamorphine, 195 diarrhoea oral rehydration therapy (ORT), 287 diastolic blood pressure (DBP), 148 diencephalon, 186–7 dietary nutrients carbohydrate digestion and absorption, 287 lipid digestion and absorption, 288 main classes, 287 protein digestion and absorption, 287–8 DiGeorge syndrome, 358 digestion role of the lymphatic system, 164 digestive system, digoxin, 121–2, 366 dipyridamole, 339–40 dissociated sensory loss, 210–11 disulfiram, 301 diuretics, 324 diving airway resistance, 89 ambient pressure change during descent, 429 breath-hold and SCUBA compared, 430 decompression sickness, 430 effects on air within lungs on a breath-hold dive, 429–30 physiology of a body during head-out immersion, 429 risk of oxygen toxicity, 102–3 diving reflex, 429 DLCO (lung diffusion capacity for carbon monoxide), 43–4 DNA (deoxyribonucleic acid), 5, 8–9 dobutamine, 121, 149 domperidone, 284 l-DOPA, 194–5, 399 dopamine, 20, 389 dorsal respiratory group (DRG) of neurons, 92 double-lumen endotracheal tubes (DLETTs), 23 doxapram, 95 drug metabolism inter-patient variability, 301 processes in the liver, 301 drugs effects on ventilation control, 95 transport across the blood–brain barrier (BBB), 195 Duchenne’s muscular dystrophy, 242 duodenal ulcers, 281 dura mater, 187–8 ectoderm, eicosanoids, 309, 357, 387 Einthoven’s triangle, 113 ejection fraction (EF) equation, 119 electrocardiogram (ECG), 113–14, 117, 261–4 electroencephalogram (EEG), 189–90 electrolytes, 2, 121, 219–20 electron transport chain, 369, 372–3 Embden–Meyerhof pathway, 369–70 endocrine signalling, 183 437 Downloaded from Cambridge Books Online by IP 216.195.11.197 on Thu Nov 05 18:38:34 GMT 2015 http://ebooks.cambridge.org/ebook.jsf?bid=CBO9781139226394 Cambridge Books Online © Cambridge University Press, 2015 Index endocrine system components, effects of the stress response, 384–5 endoderm, endoplasmic reticulum (ER), 6–7 endothelin (ET), 157 endothelium functions, 156–7 anticoagulant properties, 157 haemostasis, 157 inflammatory system, 157 procoagulant properties, 157 synthesis of vasoactive substances, 157 endotracheal tubes (ETTs), 91 choice for children, 416–17 enoximone, 121 enteric nervous system, 184 enteric neurons, 184 enzymes catalysis, 18 coenzymes, 19–20 cofactors, 19–20 definition, 18 hydrolases, 19 importance in anaesthetic practice, 20 isomerases, 19 ligases, 19 lyases, 19 main features, 18 mode of action, 18 oxidoreductases, 19 regulation of biochemical pathways, 18 specificity, 18 transferases, 19 types of, 19 eosinophils, 356 ependymal cells, 188 ephedrine, 423 epidural anaesthesia, 386 erythromycin, 301 erythropoiesis, 29, 351 erythropoietin (EPO), 351 esmolol, 149 etomidate, 231, 386, 399 excess post-exercise oxygen consumption (EPOC), 181–2 excitation–contraction coupling cardiac muscle, 256 skeletal muscle, 239 smooth muscle, 247–8 exercise effects on RBC transit time, 42 effects on venous return, 160 hypoxaemia induced by, 42 exercise physiology changes with physical training, 182 dynamic exercise, 174 effects on bone mineral density, 182 effects on skeletal muscle, 176 effects on the cardiovascular system, 176–8 effects on the respiratory system, 178–9 effects on thermoregulation, 179 elite athletes, 182 excess post-exercise oxygen consumption (EPOC), 181–2 meaning of V_ O2 max , 179–80 muscle fatigue, 175 O2 consumption after exercise, 181–2 oxygen debt, 181–2 physiological challenges of exercise, 174 physiological changes in anticipation of exercise, 175–6 skeletal muscle energy sources, 175 skeletal muscle fibre types, 174–5 static exercise, 174 expiratory flow–volume curve, 58–60 expiratory reserve volume (ERV), 50 extracellular fluid (ECF) volume regulation by the kidneys, 316–17 extrapyramidal system, 186 factor VIII, 341 Fahraeus–Lindqvist effect, 145 farmer’s lung, 364 fats metabolism, 374 fentanyl, 386 fetal haemoglobin (HbF), 32 fetal physiology causes of fetal distress, 411–12 circulation, 99 double Haldane effect, 411 features of the fetal circulation, 412 features of the fetal respiratory system, 414 fetal cardiovascular reflexes during labour, 412–14 functions of the placenta, 408 mechanisms for transfer across the placenta, 409–10 oxygen delivery, 410–11 oxygenation during labour, 411–12 physiological changes at birth, 414–15 placental anatomy related to function, 408–9 placental antibody transfer, 409 placental development, 408–9 placental drug transport, 410 pre-eclampsia, 408–9 reversion to a transitional circulation, 415 fibrinogen, 366 fibrinolysis pathway, 343–4 Fick’s law, 28, 40 flail chest, 329 flavin adenine dinucleotide (FAD), 369 flow–metabolism coupling, 198 flow–volume curve, 60–1 flow–volume loop, 60–1 fluid balance role of the lymphatic system, 164 fluid management, 162–3 follicle-stimulating hormone (FSH), 387, 389–90 forced spirometry, 56–7 expiratory flow–volume curve, 58–9 forebrain (prosencephalon), 187 Fowler’s method, 45 measurement of anatomical dead space, 48 measurement of closing capacity (CC), 55 Frank–Starling mechanism, 121, 130 frontal lobe of the brain, 186 functional magnetic resonance imaging (fMRI) measurement of CBF, 200 functional residual capacity (FRC), 50 calculation using body plethysmography, 53–4 calculation using gas dilution, 52–3 calculation using multiple breath nitrogen washout method, 54–5 factors affecting FRC volume, 51–2 importance in emergency anaesthesia, 55 importance of, 51 pre-oxygenation for general anaesthesia, 52 ganglia (PNS), 183 gas dilution technique, 52–3 gastric dumping syndrome, 282 gastric ulcers, 281 gastrointestinal (GI) tract organs involved in digestion, 286 gastro-oesophageal reflux disease (GORD), 277–8, 281 general anaesthesia atelectasis caused by, 108 effects of airway devices, 108 effects on lung volumes, 108 effects on the lungs, 108–9 postoperative effects on lung function, 109–10 438 Downloaded from Cambridge Books Online by IP 216.195.11.197 on Thu Nov 05 18:38:34 GMT 2015 http://ebooks.cambridge.org/ebook.jsf?bid=CBO9781139226394 Cambridge Books Online © Cambridge University Press, 2015 Index ventilation–perfusion mismatch, 109 See also anaesthesia general anaesthetics mechanisms of action, 230–2 genetic mutations, 10 genetics chromosomes, codons, 10 Mendelian inheritance patterns, 10–12 germ cell layers, Glasgow coma score (GCS), 204 global oxygen consumption, 74 and anaesthesia, 76 global oxygen delivery anaemic patient, 74–5 anaerobic threshold, 75–6 and anaesthesia, 76 critically ill patient, 76 definition, 74 typical resting global oxygen delivery, 74–5 globulins, 366 glomerular filtration rate (GFR), 313–15 glucagon, 121, 377–9 gluconeogenesis, 377 glyceryl trinitrate, 116, 149, 157 glycolysis, 369–70 glycoprotein IIb/IIIa inhibitors, 339 glycopyrrolate, 410 glymphatic system, 191 Goldman–Hodgkin–Katz equation, 218 Golgi apparatus, Golgi tendon organs, 243 gonadotropin-releasing hormone (GnRH), 389 Goodpasture’s disease, 309, 364 graft-versus-host disease in blood transfusion, 348 Graham’s law, 40 Graves’ disease, 394 growth hormone (GH), 376, 389–90 growth-hormone-releasing hormone (GHRH), 389 guanine (G), Guillain–Barré syndrome, 57–8, 224, 329 haemochromatosis, 353 haemoglobin carboxyhaemoglobin, 32 cooperative binding of oxygen, 30 cyanohaemoglobin, 32 effects of carbon monoxide poisoning, 34 fetal haemoglobin (HbF), 32 HbA form, 32 HbA2 variant, 32 HbS in sickle cell disease, 32 methaemoglobin, 32 methaemoglobin clinical significance, 33–4 oxyhaemoglobin dissociation curve, 30–2 single point mutation in sickle cell disease, 32–3 structure, 29 types of, 32 haemophilia, 341 haemorrhage physiological responses, 156, 168–9 haemorrhagic shock, 169 haemostasis anti-platelet drugs, 338–40 cell-based coagulation model, 341 coagulation cascade, 338–41 coagulation disorders, 341 components involved, 337 definition, 337 fibrinolysis pathway, 343–4 functions of the endothelium, 157 haemostatic response, 337 inhibition of fibrinolysis, 344 initiation, 337–8 laboratory tests of clotting, 341–3 platelet activation and aggregation, 338 role of the vascular endothelium, 337 steps in clot formation, 337 thromboelastography, 343 thrombolysis, 343–4 Hagen–Poiseuille equation, 89, 144–6 Haldane effect, 37–8, 411 halothane hepatitis, 295–6 haptens, 355 head injury classification systems, 204 heart blood flow to the myocardium, 114 functions, 111 influence of the autonomic nervous system, 257–8 structure, 111 venous drainage, 113 heart failure, 130–4, 139–40 heart rate (HR), 261 heart transplant:, 258–60 Henderson–Hasselbalch equation, 329–30 Henry’s law, 28 hepatopulmonary syndrome, 65 hepcidin, 353 hexose monophosphate shunt, 377 hindbrain (rhombencephalon), 187 His–Purkinje system, 117 homeostasis, 2–4 homeostatic control mechanisms, 3–4 hormones, 387 classification, 387 released by the pituitary gland posterior lobe, 390–1 secreted by the hypothalamus, 389 secreted by the pituitary gland anterior lobe, 389–90 synthesized by the thyroid gland, 392 Hudson mask, 47 Hüfner’s constant, 28 human genome project, humidification of inspired gases, 22 Huntingdon's disease, 10 hyaline membrane disease, 414 hydrocephalus, 192 hydrogen peroxide (H2O2), 102 hydrolases, 19 hydroxyl free radicals (OH•), 102 hyoscine, 284 hyperalgesia, 271–2 hypercapnoea, 94 hyperglycaemia, 312 hyperkalaemia, 219, 326–7 hypersensitivity, 363–4 hyperthyroidism, 394 hyperventilation, 46–7, 94 hypervolaemia, 324–5 hypoalbuminaemia, 156 hypokalaemia, 219, 327 hypomagnesaemia, 327 hyponatraemia, 219, 318 hypotension, 149 hypotensive anaesthesia, 149 hypothalamic–pituitary axis, 389 hypothalamus, 186–7, 195, 387–9 hypothermic cardiopulmonary bypass, 335 hypothyroidism, 394 hypotonicity, 318 hypoventilation, 64, 78, 81 hypovolaemia, 152, 323–4 hypoxaemia, 42, 64–5, 71, 94 hypoxaemic hypoxia, 64 hypoxia, 64–5 hypoxic pulmonary vasoconstriction (HPV), 98–100 hysteresis, 85 439 Downloaded from Cambridge Books Online by IP 216.195.11.197 on Thu Nov 05 18:38:34 GMT 2015 http://ebooks.cambridge.org/ebook.jsf?bid=CBO9781139226394 Cambridge Books Online © Cambridge University Press, 2015 Index idiopathic thrombocytopaenic purpura, 364 IgA nephropathy, 310 immune complex disease, 364 immune system active immunity, 360 adaptive immune system, 355, 358–60 antibodies (immunoglobulins), 358–60, 362–3 cell-mediated immunity, 361–2 complement system, 357–8 components, cytotoxic T-cells (CD8+ T-cells), 361–2 definition of allergen, 355 definition of antigen, 355 definition of hapten, 355 development of antibodies to RBC antigens, 345–6 effects of anaesthesia and surgery, 364–5 hypersensitivity, 363–4 inflammation, 356–7 innate immune system, 355 lymphocytes, 358 lymphoid tissue, 358 passive immunization, 361 primary immune response, 358–60 role of eicosanoids, 357 role of kinins, 357 role of the lymphatic system, 164 secondary immune response, 360 white blood cells (leucocytes) involved in the immune response, 355–6 immunodeficiency classification, 363 immunoglobulins (Igs), 362–3, 366 See also antibodies infant respiratory distress syndrome (IRDS), 84, 88, 414 inflammation, 356–7 inspiratory capacity (IC), 50 inspiratory reserve volume (IRV), 50 insulin, 377–9, 387 integumentary system, intensive care risks related to oxygenation, 103 internal carotid arteries, 188–9 intra-aortic balloon pump, 149 intracranial pressure (ICP) Cushing’s triad, 202–3 definition, 201 factors influencing, 201–2 methods of measurement, 201 Monro–Kellie hypothesis, 201–2 normal range, 201 raised, 21–2 signs and symptoms of raised pressure, 202 ways to reduce, 203–4 ion channels, 14 ionotropic receptors, 229–30 iron control of iron homeostasis, 353 handling in the body, 352–3 iron overload (haemosiderosis) related to blood transfusion, 348 irritant receptors, 94 ischaemic heart disease, 121 isomerases, 19 isoniazid, 301 isoprenaline, 121 jaundice, 299–300 Jehovah’s Witnesses, 349–50 Jendrassik manoeuvre, 245 jugular bulb catheterization, 200 juxtacapillary receptors (J-receptors), 94 ketamine, 231, 410 ketone bodies, 374 Kety–Schmidt technique, 200 kidney actions of diuretics, 324 active secretion of waste products, 312 acute interstitial nephritis, 310 acute tubular necrosis (ATN), 309 anatomy, 305 clearance of drugs from the blood, 312 effects of ADH, 318 effects of Starling filtration forces, 156 filtration fraction, 315 filtration process, 311 functions, 305 generation of high osmolarity in the renal medulla, 319–20 GFR as indicator of kidney function, 314 glomerular filtration rate (GFR), 313–14 glomerulonephritis, 309–10 handling of urea, 322 histology, 305–7 influence of eicosanoids on blood flow, 309 influence of renin–angiotensin–aldosterone axis on blood flow, 308–9 juxtaglomerular apparatus, 307 measurement of renal blood flow, 310 mechanism of ADH action on, 318 nephron structure and function, 305–7 pathophysiology of acute kidney injury (AKI), 309–10 reabsorption from tubular fluid, 311 reabsorption limit in hyperglycaemia, 312 reglation of renal blood flow, 307 regulation of extracellular fluid volume, 316–17 regulation of Na+ excretion, 322 regulation of plasma volume, 316–17 renal autoregulation, 307 renal autoregulation mechanism, 307–8 renal clearance definition, 313 renal clearance equation, 313 renal replacement therapy (RRT), 314–15 renal transplant, 315 role in regulation of plasma K+ concentration, 325–6 Starling forces and the GFR, 313 use of clearance in GFR measurement, 314 kidney dysfunction and bone disease, 397 kinins, 357 knee-jerk reflex, 244–5 Krebs cycle See citric acid cycle labetalol, 149 lactic acidosis, 370–1 Laplace’s law, 83 laryngeal mask airway (LMA), 91 larynx, 21 lateral geniculate nucleus, 187 lateral medullary syndrome, 211 left ventricular pressure–volume loop, 135–40 ligases, 19 limbic system, 94, 186 lipase inhibitors, 288 Listeria monocytogenes, 409 liver blood supply, 292 centrilobular necrosis, 295–6 halothane hepatitis, 295–6 intraoperative liver blood flow, 293 living donor transplantation, 297 macroscopic anatomy, 293 main cell types, 294–5 microscopic anatomy, 293–4 440 Downloaded from Cambridge Books Online by IP 216.195.11.197 on Thu Nov 05 18:38:34 GMT 2015 http://ebooks.cambridge.org/ebook.jsf?bid=CBO9781139226394 Cambridge Books Online © Cambridge University Press, 2015 Index physiological reserve, 297 regeneration capability, 297 regulation of hepatic blood flow, 292 respiratory cycle influence on venous blood flow, 292–3 liver dysfunction and bone disease, 397 liver function classification of functions, 297 drug metabolism, 301 endocrine functions, 300 exocrine functions, 298–9 factors affecting drug metabolism, 301 immunological functions, 300 jaundice, 299–300 liver function tests, 302–3 metabolic functions, 297–8 physiological changes in cirrhosis, 302 physiological functions, 301–2 substances synthesized by the liver, 300–1 testing in paracetamol overdose, 303 liver transplantation criteria, 303 local anaesthetics action on nerve axons, 185 forms of toxicity, 258 placental transfer, 410 response of different types of nerve fibre, 225–6 Lorraine Smith effect, 102 low flow anaesthesia, 29 lung capacities closing capacity (CC), 55 distinction from lung volumes, 50 functional residual capacity (FRC), 50–2 inspiratory capacity (IC), 50 methods of measurement, 52 total lung capacity (TLC), 50 vital capacity (VC), 50 lung compliance component of respiratory compliance, 82 definition, 82 dynamic compliance, 84–5 effects of surface tension in alveoli, 83–4 effects of surfactant, 83–4 factors affecting, 82 measurement, 85 mechanism of pulmonary surfactant action, 84 static compliance, 84–5 lung diffusion capacity for carbon monoxide (DLCO), 43–4 lung resection, 43–4 preoperative work using spirometry, 61–3 lung transplantation and the bronchial circulation, 96 lung ventilation regional differences in, 85–7 static compliance curve, 85–7 lung volumes distinction from lung capacities, 50 effects of general anaesthesia, 108 expiratory reserve volume (ERV), 50 inspiratory reserve volume (IRV), 50 methods of measurement, 52 residual volume (RV), 50 tidal volume (VT), 50 tidal volume in mechanically ventilated patients, 51 lungs alveolar dead space (V Alv D ), 45–6 alveolar volume (VA), 45 anatomical dead space (V Anat D ), 45 anatomy, 23 atelectasis caused by general anaesthesia, 108 causes of pulmonary oedema, 156 components of tidal volume (VT), 45 defence mechanisms, 25–7 definition of dead space (VD), 45 definition of dead-space ventilation, 46 effects of general anaesthsia, 108–9 effects of gravity on perfusion, 69 effects of physical training, 182 endocrine functions, 27 immunological functions, 25–7 inflation and deflation during tidal breathing, 24–5 metabolic functions, 27 non-respiratory functions, 21, 25–7 oxygen toxicity effects, 102 Phys physiological dead space (V D ), 45 pneumothorax, 25 postoperative effects of general anaesthesia, 109–10 pulmonary circulation, 27 respiratory functions, 21 types of dead space, 45 vascular functions, 27 West zones, 72–3 luteinizing hormone (LH), 387, 389–90 lyases, 19 lymph fluid, 164 lymphatic system, 164 lymphocytes, 164, 358 lymphoid tissue, 358 lysosomes, macrophages, 356 malignant hyperthermia, 239–40 mannitol, 195 mast cells, 356, 358, 363–4 mean arterial pressure (MAP), 120, 148 arterial baroreceptor reflex, 166–7 Bainbridge reflex, 167 classes of haemorrhagic shock, 169 classification of cardiovascular reflexes, 166 consequences of peripheral chemoreceptor activation, 167–8 Cushing’s reflex, 167 decompensated shock, 169 effects of the Valsalva manoeuvre, 171 importance of minimizing fluctuations, 166 manipulation in clinical practice, 149 physiological response to haemorrhage, 168–9 relationship to cardiac output (CO), 122 mean arterial pressure (MAP) equation, 122 mechanical ventilation, 51 mechanoreceptors, 93–4 medial geniculate nucleus, 187 medulla oblongata, 187 area postrema, 195 melatonin, 195 Mendelian inheritance patterns, 10–12 Mendelson’s syndrome, 278 meninges, 187–8 meningitis, 195 mesencephalon (midbrain), 187 mesoderm, metabolic acidosis, 326, 330 metabolic alkalosis, 330 metabolic equivalent (MET), 379 metabolism aerobic and anaerobic generation of ATP, 373–4 ATP generated from a molecule of glucose, 373–4 basal metabolic rate (BMR), 379 catabolism of carbohydrates, fats and proteins to ATP, 369 cellular respiration, 369 citric acid cycle, 369, 371–2 definition, 369 effects of glucagon, 377–9 effects of insulin, 377–9 electron transport chain, 369, 372–3 441 Downloaded from Cambridge Books Online by IP 216.195.11.197 on Thu Nov 05 18:38:34 GMT 2015 http://ebooks.cambridge.org/ebook.jsf?bid=CBO9781139226394 Cambridge Books Online © Cambridge University Press, 2015 Index metabolism (cont.) fats, 374 gluconeogenesis, 377 glycolysis, 369–70 lactic acidosis, 370–1 pentose phosphate pathway (PPP), 377 production of ketone bodies, 374 protein catabolism, 374 storage and release of nutrients, 374–7 metabotropic receptors, 232 metaraminol, 149 metarterioles, 156 metastases and the lymphatic system, 164 metathalamus, 187 metformin, 370–1 methaemoglobin, 32–4 methotrexate, 195 microglia, 188 midbrain (mesencephalon), 187 minimal flow anaesthesia, 29 minute ventilation, 46 mitochondria, 5–6 mivacurium, 20, 424 molarity, 317 monoamine oxidase (MAO), 20 monoamine oxidase (MAO) inhibitors, 20 monocytes, 356 Monro–Kellie hypothesis, 201–2 morphine, 195, 312 motor (efferent) neurons, 184 motor units, 241 multiple breath nitrogen washout method, 54–5 multiple sclerosis, 224 multipolar neurons, 184 muscarinic ACh receptors, 268 muscle relaxants, 234, 364, 410, 419, 424 muscle spindles, 243 muscle tone, 245–6 muscular system, myasthenia gravis (MG), 105, 234–5, 329 Mycobacterium tuberculosis infection, 364 myelin, 183, 188 myelinated nerve axons, 185 effects of demyelinating disease, 224 effects on propagation of nerve action potential, 224 myocardial blood flow, 114 myocardial contractility information from the arterial pressure waveform, 152 myocardial ischaemia, 121 changes in ECG, 113–14 myocarditis, 121 myoglobin, 35 myotonia congenita, 242 myotonic dystrophy, 242 Na+ (sodium) in the body, 219, 322–3 Na+/K+-ATPase contribution to resting membrane potential, 218–19 naloxone, 169 natural killer (NK) cells, 356 near-drowning cases loss of pulmonary surfactant, 84 negative-feedback loops, 3–4 neostigmine, 20 Nernst equation, 218 nerve action potential definition, 221 effects of demyelinating disease, 224 effects of myelination on propagation, 224 events leading to, 221 propagation along nerve axons, 222–4 refractory period, 226–7 nerve fibres, 185 functional classification, 224–5 response of different types to local anaesthetics, 225–6 nervous system central nervous system (CNS), 184 component systems, 184–5 components, functions, 183 motor output, 183 peripheral nerve structure, 185 peripheral nervous system (PNS), 184–5 sensory input, 183 sensory integration by the CNS, 183 signalling systems, 183 neural signalling, 183 neuraxial blockade, 149 neuroglia, 188 neuromuscular junction (NMJ), 183, 232–4 neurons autonomic, 184–5 enteric, 184 morphologic classes, 184 motor (efferent), 184 of the CNS, 188 sensory (afferent), 183 signalling systems, 183 structure, 183–4 neuropathic pain, 272–3 neurotransmitters, 228–9 ionotropic receptors, 229–30 metabotropic receptors, 232 release at the synaptic cleft, 229 reuptake inhibitors, 232 termination of neurotransmission, 232 neutrophils, 355–6 nicorandil, 116 nicotinamide adenine dinucleotide (NAD+), 369 nicotinic ACh receptors, 267–8 nifedipine, 116 nitrate drugs, 116 nitric oxide (NO), 157 nitric oxide synthase (NOS), 157 nitrous oxide (N2O), 41–2, 231–2 nociception distinction from pain, 269 nociceptive pain, 269 nociceptor nerve fibres, 269 nociceptors, 269 non-steroidal anti-inflammatory drugs (NSAIDs), 309–10, 366–7 noradrenaline, 20, 149, 400 nuclei (CNS), 183 nucleobases, nutrients control in the body, obesity, 88 obesity hypoventilation syndrome, 329–30 obstructive lung disease, 90 occipital lobe of the brain, 186 oesophageal phase of swallowing, 276–7 oesophagus functional anatomy, 277 gastro-oesophageal reflux disease (GORD), 277–8 oestrogen, 387 olanzapine, 301 oligodendrocytes, 188 omeprazole, 281, 301 ondansetron, 284 one-lung ventilation and PEEP, 100 opioid drugs, 386, 410 perioperative effects, 365 respiratory depression, 95, 329 oral contraceptive pill, 301 oral phase of swallowing, 276 oral rehydration therapy (ORT), 287 organs components of body systems, 1–2 development, Orlistat, 288 osmolality, 317 442 Downloaded from Cambridge Books Online by IP 216.195.11.197 on Thu Nov 05 18:38:34 GMT 2015 http://ebooks.cambridge.org/ebook.jsf?bid=CBO9781139226394 Cambridge Books Online © Cambridge University Press, 2015 Index osmolar gap equation, 317 osmolarity, 317 osteoporosis, 397 oxidoreductases, 19 oxygen (O2) cooperative binding to haemoglobin, 30 ROS role in normal body functions, 102 oxygen arterial partial pressure effects on cerebral blood flow, 198 oxygen binding myoglobin structure and properties, 35 oxygen-carrying capacity effects of carbon monoxide poisoning, 34 oxygen-carrying solutions (blood substitutes), 350 oxygen cascade anaerobic metabolism, 81 definition, 80 effects of high altitude, 81 effects of hypoventilation, 81 effects of pneumomia, 81 Pasteur point, 81 steps along, 80–1 oxygen consumption after exercise, 181–2 compared with oxygen stores, 28–9 meaning of V_ O2 max , 179–80 V_ O2 max and surgical risk, 180–1 oxygen debt, 181–2 oxygen diffusion compared with gases related to anaesthesia, 41–2 compared with other gases, 41 rate compared with CO2, 40 oxygen extraction ratio (OER), 75 oxygen flux equation, 74 oxygen levels physiological effects of apnoea, 38–9 oxygen partial pressure regulation in the body, oxygen stores compared with oxygen consumption, 28–9 oxygen toxicity antioxidants, 102 CNS toxicity, 102 effect on the retina, 102 harmful effects on the body, 102 harmful levels of oxygen, 102–3 induced by bleomycin, 103 Lorraine Smith effect, 102 lung toxicity, 102 mechanism, 102 oxygenation in intensive care, 103 Paul Bert effect, 102 protection against oxidative stress, 102 reactive oxygen species (ROS), 102 risk for divers, 102–3 oxygen transfer diffusion limitation, 42 effects of altitude, 42 perfusion limitation, 42 oxygen transport blood oxygen content equation, 28 bound to haemoglobin, 28 dissolved in plasma, 28 methods of transport in the blood, 28 oxygenation distinction from ventilation, 104 oxygenation function gas-exchange system, 104 oxyhaemoglobin, 30 oxyhaemoglobin dissociation curve, 30–2 Bohr effect, 37 O2 binding in transfused blood, 32 oxymyoglobin dissociation curve, 35 oxytocin, 391 pacemaker cells, 254–5 pacemaker potential, 255 PaCO2 equation, 46 paediatric anatomy and physiology choice of ETT for children, 416–17 classification of age groups, 416 differences between children and adults, 416–19 pharmacokinetics in children, 419 pain allodynia, 272 classification, 269 complex regional pain syndrome (CRPS), 273 definition, 269 distinction from nociception, 269 hyperalgesia, 271–2 modulation mechanisms, 270–1 neuropathic pain, 272–3 nociceptive type, 269 pain signal pathways to the brain, 270 referred pain, 271 role of the sympathetic nervous system, 273 types of nociceptor nerve fibre, 269 pain management sympathetic blockade, 267 pain receptors, 94 pancreas, 288–90 paracetamol overdose, 295 liver function testing, 303 parasympathetic nervous system, 184–5, 265–7 parathyroid gland, 397 parathyroid hormone (PTH), 396 parietal lobe of the brain, 186 Parkinson’s disease, 195 Pasteur point, 81 patellar reflex, 244–5 patent ductus arteriosus, 65 Paul Bert effect, 102 penicillins, 310, 312, 364 pentose phosphate pathway (PPP), 377 perioperative care effects of proceures on the immune system, 364–5 enhanced recovery programme, 382 methods of reducing the stress response, 386 risks associated with polycythaemia, 353–4 perioperative hypothermia, 431–3 peripheral chemoreceptors, 167–8 peripheral nerve structure, 185 peripheral nervous system (PNS), 184–5 peripheral oedema, 156 pethidine, 410 pH definition, 328 equation, 328 homeostatic mechanisms, 331–3 regulation in the body, relationship to pKa, 329 pH of blood change with temperature, 334–5 in hypothermic cardiopulmonary bypass, 335 pharmacokinetics differences between children and adults, 419 pharmacology effects of ageing, 423–4 pharyngeal phase of swallowing, 276 phenobarbitone, 301 phenotype (trait), 10–11 phenylephrine, 149, 423 phenytoin, 195, 301 phosphodiesterase inhibitors, 339–40 physiological dead space Bohr method of measurement, 49 physiological fitness assessment metabolic equivalents (MET), 379 pia mater, 188 pineal gland, 195 pituitary adenoma, 391 pituitary gland, 186, 195 anatomy, 388 blood supply, 388–9 443 Downloaded from Cambridge Books Online by IP 216.195.11.197 on Thu Nov 05 18:38:34 GMT 2015 http://ebooks.cambridge.org/ebook.jsf?bid=CBO9781139226394 Cambridge Books Online © Cambridge University Press, 2015 Index pituitary gland (cont.) hormones released by the posterior lobe, 390–1 hormones secreted by the anterior lobe, 389–90 hypothalamic–pituitary axis, 389 pKa, 329 equation, 328–9 placenta anatomy related to function, 408–9 development, 408–9 functions, 408 mechanisms for transfer across, 409–10 transfer of drugs across, 410 placental antibody transfer, 409 plasma constituent of blood, 366 hyperkalaemia, 326–7 hypokalaemia, 327 mechanisms to regulate potassium (K+) concentration, 325–6 plasma cholinesterase, 20 plasma glucose concentration effects of insulin and glucagon, 377–9 plasma osmolarity clinical disorders of osmolarity, 320–1 definition of osmolarity, 317 estimated plasma osmolarity equation, 317 feedback loop control, 318 hypotonicity, 318 importance of regulation, 317–18 interaction with plasma volume regulation, 324 plasma pH Henderson–Hasselbalch equation, 329 plasma proteins classification, 366 functions of albumin, 366–7 plasma volume interaction with plasma osmolarity regulation, 324 physiological response to high volume, 324–5 physiological response to low volume, 323–4 regulation, 316–17 platelets, 338 anti-platelet drugs, 116, 338–40 pneumonectomy, 43–4 pneumonia, 99 effects on the oxygen cascade, 81 pneumotachograph, 56 pneumotaxic centre, 92 pneumothorax, 25 polycythaemia, 353–4 pons, 187 portal veins, 158 positive end-expiratory pressure (PEEP), 21–2, 44, 87 extrinsic, 91 influence on venous return, 159 one-lung ventilation, 100 physiological, 90 positive feedback, positive pressure ventilation influence on venous return, 159 one-lung ventilation, 100 positron emission tomography (PET) measurement of CBF, 200 postoperative nausea and vomiting (PONV), 284 potassium (K+) in the body, 219, 325–7 potassium channel openers, 116 pregnancy, 379 alterations in endocrine function, 401–2 challenges of general anaesthesia, 403 incidence of glycosuria, 312 physiological changes and anaesthesia, 402–6 pre-eclampsia, 408–9 vena cava compression, 159–60 preoperative fasting, 282–3 pre-oxygenation for general anaesthesia, 52 probenecid, 312 prolactin (PRL), 387, 389–90 propofol, 195, 231, 365, 410 proprioception, 243 prosencephalon (forebrain), 187 prostacyclin (PGI2), 157 protein, 374 digestion and absorption, 287–8 proteinuria, 156 proton-pump inhibitors (PPIs), 281, 285 pseudocholinesterase, 20 pseudounipolar neurons, 184 pulmonary arteriovenous malformation (AVM), 65 pulmonary artery catheter (PAC), 73, 100 pulmonary circulation calculation of pulmonary vascular resistance (PVR), 96–7 comparison with the systemic circulation, 141 factors affecting PVR, 97–9 PVR compared with SVR, 96–7 reason for normal low pressure, 96 unique features, 96 pulmonary embolism (PE), 71 pulmonary fibrosis, 88, 99 related to bleomycin treatment, 103 pulmonary function tests (PFTs), 56 pulmonary hypertension, 157 pulmonary oedema, 96, 156 pulmonary surfactant, 83–4 pulmonary vascular resistance (PVR), 96–100 pyramidal cells, 184 pyramidal tract, 211–12 ranitidine, 281 rapid sequence induction (RSI), 55 reactive oxygen species (ROS), 102 red blood cell (RBC) antigens ABO blood group system, 345 antibody development by the immune system, 345–6 range of antigen systems, 345 Rhesus blood group system, 345 Rhesus disease, 346 red blood cells (RBCs) cell membrane antigens, 29 erythropoiesis, 351 stages of erythropoiesis, 29 steps in production, 351 structure and function, 29 refeeding syndrome, 382 referred pain, 271 reflex arcs, 243–4 knee-jerk reflex, 244–5 remifentanil, 20 renal clearance equation, 313 renin–angiotensin–aldosterone axis, 308–9 Renshaw cells, 184 reproductive system, residual volume (RV) of the lungs, 50 respiration regulatory role of cerebrospinal fluid, 191 respiratory acidosis, 329–30 respiratory alkalosis, 330 respiratory centre effects of opioid drugs, 95 inputs, 92–4 reflex desensitization, 105 role in ventilation control, 92 respiratory compliance, 82–3 respiratory compliance equation, 82 respiratory failure chronic hypercapnoea in stable COPD patients, 105 definition, 104 exacerbation of COPD, 106 in patient with myasthenia gravis (MG), 105 processes which cause type failure, 104–5 444 Downloaded from Cambridge Books Online by IP 216.195.11.197 on Thu Nov 05 18:38:34 GMT 2015 http://ebooks.cambridge.org/ebook.jsf?bid=CBO9781139226394 Cambridge Books Online © Cambridge University Press, 2015 Index type 1, 104 type 2, 104 respiratory quotient (R), 77–8 respiratory system, effects of airway devices, 108 effects of anaesthetic drugs, 107–8 effects of exercise, 178–9 oxygenation function (gas exchange), 104 ventilation function (bellows), 104 respiratory system functional anatomy, 21–4 alveoli, 24 bronchi, 23 bronchioles, 23–4 conducting zone, 22–4 larynx, 21 lungs, 23 mucociliary escalator, 22 respiratory bronchioles, 24 respiratory zone, 24 trachea, 22–3 tracheobronchial tree, 22–4 upper airway, 21 resting membrane potential (RMP) cardiac muscle cells, 250 contribution of Na+/K+-ATPase, 218–19 definition, 217 effects of electrolyte disturbances, 219–20 Goldman–Hodgkin–Katz equation, 218 Nernst equation, 218 Nernst equation applied to explain RMP, 218 production of, 217–18 restrictive lung disease, 90 reticulocytes, 29 retina oxygen toxicity effects, 102 retinopathy of prematurity, 102 retrolental fibroplasia, 102 reverse Fick principle, 74 Reynolds number, 88–9 Rhesus blood group system, 29, 345 Rhesus disease, 346 rhombencephalon (hindbrain), 187 rifampicin, 301 right ventricular pressure-volume loop, 138 RNA (ribonucleic acid), 8–10 salbutamol, 327 saliva, 275–6 salivary glands, 275–6 sarcomeres, 236–9 Schwann cells, 185 selective serotonin reuptake inhibitors (SSRIs), 232 semi-permeable membranes, 40 sensory (afferent) neurons, 183 sepsis, 121 septic shock, 149 serotonin, 387 shunt equation, 66–8 shunts, 65–8 sickle cell disease, 10, 348 anaesthesia management, 33 effects of a single point Hb mutation, 32–3 HbS abnormal haemoglobin, 32 operative management issues, 33 testing patients for, 33 sickle cell trait, 32 testing patients for, 33 skeletal muscle anatomy, 236 differences from smooth muscle, 247 disorders, 242 effects of exercise on, 176 effects of physical training, 182 energy sources, 175 excitation–contraction coupling, 239 factors which determine muscle tension, 241–2 fibre types, 174–5 functions, 236 malignant hyperthermia, 239–40 mechanism of contraction, 240–1 motor units, 241 muscle fatigue, 175 sarcomeres, 236–9 Type I (slow-twitch, fatigueresistant) fibres, 174–5 Type II (fast-twitch) fibres, 174–5 skeletal system, skin integumentary system, small intestine, 286–7 intestinal motility, 290–1 smoking effect on hepatic enzymes, 301 smooth muscle adaptation to its function, 249 contraction mechanism, 248–9 description, 247 differences from skeletal muscle, 247 excitation–contraction coupling, 247–8 excitatory inputs, 247–8 locations in the body, 247 types of, 247 sodium (Na+) in the body, 219, 322–3 sodium nitroprusside, 149 somatostatin, 389 spinal anaesthesia, 386 spinal cord, 184 anatomy, 207 anterior spinal artery syndrome, 209 blood supply, 208–9 corticospinal tract, 211–12 cross-sectional anatomy, 207–8 dissociated sensory loss, 210–11 main sensory afferent pathways, 209–10 meninges, 187–8 spinal cord injury, 172 classification, 212 effects related to level of complete injury, 212–13 initial management of acute spinal cord injury, 214–16 patterns of incomplete spinal cord injury, 214 spinal shock, 245–6 spirometers, 56 spirometry dynamic spirometry, 56 expiratory flow–volume curve, 58–9 forced spirometry, 56–7 lung variables measured, 56 measurement of lung volumes and capacities, 52 preoperative work before lung resection, 61–3 static lung volume measurements, 56 spironolactone, 326 stagnant hypoxia, 64 staircase effect, 122 Starling filtration equation, 154 Starling forces and the glomerular filtration rate (GFR), 313 and transmembrane fluid flow, 154–6 Starling’s law of the heart, 120–1, 130 starvation, 374, 381–3 static compliance curve, 85–7 static lung volumes use of spirometer to measure, 56 steatorrhoea, 288 Stewart–Fencl–Story approach to acid–base physiology, 335–6 stomach control of gastric emptying, 281–2 functions, 279 gastric acid secretion by parietal cells, 280–1 gastric dumping syndrome, 282 neutralization of gastric acid, 281 445 Downloaded from Cambridge Books Online by IP 216.195.11.197 on Thu Nov 05 18:38:34 GMT 2015 http://ebooks.cambridge.org/ebook.jsf?bid=CBO9781139226394 Cambridge Books Online © Cambridge University Press, 2015 Index stomach (cont.) phases of gastric secretion, 281 preoperative fasting, 282–3 substances secreted by, 279–80 time taken for gastric emptying, 282 See also vomiting stress response, 384–6 stroke Bamford classification, 189 stroke volume (SV), 120, 152 stroke volume (SV) equation, 119 stroke volume index (SVI), 122 subarachnoid space, 188 subdural space, 188 subthalamus, 187 sulphonamide drugs, 301 superoxide anion (O2•À), 102 surfactant See pulmonary surfactant surgical risk and V_ O2 max , 180–1 Surviving Sepsis Campaign guidelines, 163 suxamethonium, 20, 234–5, 239, 326, 419, 424 suxamethonium apnoea, 20 swallowing, 276–7 Swan–Ganz catheter, 100 sympathetic blockade, 267 sympathetic nervous system, 184–5, 265–7, 273 synapses definition, 228 ionotropic receptors, 229–30 metabotropic receptors, 232 neurotransmitter reuptake inhibitors, 232 neurotransmitters, 228–9 termination of neurotransmission, 232 types of, 228 See also neuromuscular junction (NMJ) synaptic cleft release of neurotransmitters, 229 syndrome of inappropriate ADH secretion, 321 syringomyelia, 211 systemic circulation, 141 changes in blood flow, 142–3 comparison with the pulmonary circulation, 141 constituent parts, 141 functions, 141 See also arterial system; venous system systemic inflammatory response syndrome (SIRS), 357 systemic lupus erythematosus, 310, 364 systemic vascular resistance (SVR), 96–7, 120, 147–8, 152 systolic blood pressure (SBP), 148 tachycardia blood pressure calculation, 148 Bowditch effect, 122 effects on cardiac output (CO), 119 telencephalon (cerebrum), 186 temperature regulation, adverse efects of hypothermia, 432–3 adverse effects of intraoperative hypothermia, 433 effects of anaesthesia on normal mechanisms, 431–2 effects of exercise, 179 mechanisms, 431 role of the venous system, 158 temporal lobe of the brain, 186 testosterone, 387 tetanus, 361 thalamus, 94, 186 thalassaemia, 348 thalidomide, 410 thiopentone, 195, 231, 365–6, 410, 419 thoracic cage compliance, 82 thromboelastography, 343 thrombolysis, 343–4 thrombosis risk in polycythaemia, 353 thymine (T), thymus, 358 thyroid gland anaesthesia for thyroid surgery, 394–5 Graves’ disease, 394 hormones synthesized by, 392 physiological effects of T3 (triiodothyronine), 392 regulation of plasma thyroid hormones, 393–4 synthesis of T3 and T4, 392–3 thyroid-stimulating hormone (TSH), 387, 389–90 thyrotropin-releasing hormone (TRH), 387 thyroxine, 387 tidal volume (VT), 50 in mechanically ventilated patients, 51 TLCO (lung transfer factor for CO), 43 tonsillectomy, 22 total lung capacity (TLC), 50 trait (phenotype), 10–11 tranexamic acid, 344 transcranial Doppler ultrasonography, 200 transferases, 19 transfusion-related acute lung injury (TRALI), 348 transfusion-related immunomodulation (TRIM), 365 traumatic brain injury (TBI), 204–5 Treppe effect, 122 tricarboxylic acid cycle See citric acid cycle tuberculosis, 364 unipolar neurons, 184 urea handling by the kidney, 322 urinary system, valproate, 301 Valsalva manoeuvre, 171–3 varicella zoster, 361 vascular endothelium role in haemostasis, 337 vasoactive substances synthesis in the endothelium, 157 vasopressin See antidiuretic hormone (ADH) veins, 158 vena cava compression in pregnancy, 159–60 venous cannulation, 164–5 venous pressure effects on resistance to blood flow, 160 venous pressure waveforms features of the CVP waveform, 161 venous return to the heart, 158–60 venous system, 158–60 ventilation alveolar ventilation, 46 definition of dead-space ventilation, 46 distinction from oxygenation, 104 minute ventilation, 46 ventilation control anatomical sites involved, 92 effects of drugs on, 95 neuronal feedback loops, 92 respiratory centre inputs, 92–4 role of the respiratory centre, 92 ventilation–perfusion matching, 71 ventilation–perfusion mismatch, 21, 65–6, 70–1, 109 ventilation–perfusion ratio, 69–70 ventilator-associated lung injury, 51 446 Downloaded from Cambridge Books Online by IP 216.195.11.197 on Thu Nov 05 18:38:34 GMT 2015 http://ebooks.cambridge.org/ebook.jsf?bid=CBO9781139226394 Cambridge Books Online © Cambridge University Press, 2015 Index ventilatory response to hypercapnoea, 94 to hypoxaemia, 94 ventral respiratory group (VRG) of neurons, 92 ventricular septal defect, 65 vertebral arteries, 188–9 vital capacity (VC), 50 vitalograph, 56 vitamin D, 396–7 V_ O2 max and surgical risk, 180–1 meaning of, 179–80 vocal cords, 21 volatile anaesthetics, 41–2, 149, 195, 239 voluntary control of breathing, 94 volutrauma, 51 vomiting, 283–4 von Willebrand disease, 341 von Willebrand factor (vWF), 157 warfarin, 366–7 waste products removal from the body, water distribution in the body, 316 measurement within body compartments, 316 regulation in the body, Wernicke’s area, 186 West zones of the lung, 72–3 Willis, circle of, 188–9 Windkessel effect, 150 work of breathing, 88–91 X-linked recessive inheritance, 11–12 xenon-133 isotope, 200 xenon anaesthesia, 231–2 447 Downloaded from Cambridge Books Online by IP 216.195.11.197 on Thu Nov 05 18:38:34 GMT 2015 http://ebooks.cambridge.org/ebook.jsf?bid=CBO9781139226394 Cambridge Books Online © Cambridge University Press, 2015 ... Anaesth Crit Care Pain 20 04; 4 (2) : 52 6 20 6 Downloaded from Cambridge Books Online by IP 21 6.195.11.197 on Thu Nov 05 03: 42: 07 GMT 20 15 http://dx.doi.org/10.1017/CBO978113 922 6394.048 Cambridge Books... indirectly affected as a result of 21 2 Downloaded from Cambridge Books Online by IP 21 6.195.11.197 on Thu Nov 05 03: 42: 20 GMT 20 15 http://dx.doi.org/10.1017/CBO978113 922 6394.049 Cambridge Books Online... by high-flow O2 administration in a conscious 21 5 Downloaded from Cambridge Books Online by IP 21 6.195.11.197 on Thu Nov 05 03: 42: 20 GMT 20 15 http://dx.doi.org/10.1017/CBO978113 922 6394.049 Cambridge