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CHAPTER 12 Endocrine System
Osteoporosis
Centripetal
251
Plethora
'moon face'
High blood
pressure
Poor wound
healing
Striae
Acne
'Buffalo
hump'
obesity
Bruising
Thin skin
Proximal
myopathy
Oedema
Fig. 12.6 Features of Cushing’s syndrome.
Adrenogenital syndrome
• Also known as congenital adrenal hyperplasia (CAH),
it results from genetic deciencies in the enzymes in the
synthesis of cortisol. e commonest defect aects the
enzyme 21-hydroxylase.
• e lack of this enzyme leads to a decrease in cortisol secretion and as a result increases in ACTH secretion; this has the eect of driving the unused cortisol
precursors into the androgenic hormone synthetic
pathways.
• e clinical eects depend on the sex of the aected
individual:
• male: there is rapid growth in childhood and early
sexual development (precocious puberty); due to
early fusion of the epiphysis, these patients are oen
shorter than average
• female: there is masculinization of the external geni-
talia with hypertrophy of the clitoris, a male body
shape and hair distribution.
Phaeochromocytoma
• A rare condition characterized by oversecretion of catecholamines (epinephrine and norepinephrine) from
the adrenal medulla.
• A tumour of the chroman cells causes the condition:
10% are malignant, 10% are multiple and 10% arise outside of the adrenal medulla (‘rule of 10 s’).
• e eects of the increased circulating catecholamines
include:
• palpitations and arrhythmias
• tremors
• sweating and ushing
• ↑ blood pressure (episodic)
• hyperglycaemia (episodic).
Growth Hormone
• Human growth hormone (hGH) is the main form of
growth hormone; it is a large protein composed of 191
amino acids.
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SECTION II Physiology
• Secretion is stimulated by growth hormone releasing
hormone (GHRH) released by the hypothalamus and
inhibited by somatostatin.
• GH is released in a pulsatile manner and demonstrates
a circadian rhythm, with elevation in secretion during
periods of deep sleep.
• Hypoglycaemia is a potent stimulator of GH secretion;
it stimulates GHRH release and inhibits somatostatin
secretion.
• A number of other stimuli promote GH secretion:
• anxiety
• pain
• hypothermia
• haemorrhage
• trauma
• fever
• exercise.
• e eects of GH can be divided into those predominating in childhood and adolescence, and those that predominate in adulthood:
• childhood and adolescence: GH stimulates skeletal
growth by stimulating mitosis in the cartilage cells in
the epiphyseal plates at the ends of the long bones; this
process is aided by insulin-like growth factors (IGFs)
that encourage matrix secretion from cartilage cells
• adulthood: aer fusion of the epiphyseal plates, GH
no longer has any inuence on skeletal growth; however, it still has an important role in a number of
metabolic functions:
• ↑glycogenolysis
• ↓glucose uptake by cells
• promotes amino acid uptake into cells
• promotes protein synthesis
• ↑lipolysis and release of free fatty acids (FFAs)
• ↓LDL cholesterol.
Clinical Physiology
Disorders of Growth Hormone Secretion
Gigantism
• Caused by growth hormone hypersecretion prior to
epiphyseal fusion; there is increased growth, particularly
of the limbs – this results in the condition of gigantism.
Acromegaly
• In this condition there is also hypersecretion of growth
hormone, but it occurs in adult life aer epiphyseal
fusion.
• Hypersecretion of growth hormone in adult life is called
acromegaly, and results from a pituitary tumour.
• e symptoms and signs of acromegaly can be divided
into those produced by the tumour and those produced
by the growth hormone excess (see Fig. 12.7).
ENDOCRINE FUNCTION OF THE PANCREAS
• e exocrine role of the pancreas has been discussed in
Chapter 10.
• Exocrine secretions are produced in the pancreatic acini
and then discharged into the ductal system; the endocrine secretions are produced in the islets of Langerhans.
• e islets of Langerhans are highly vascular and are
innervated by the sympathetic and parasympathetic
nervous system.
• ree main hormones produced in the islet of
Langerhans play a role in the regulation of plasma glucose levels:
• insulin (secreted by β-cells)
• glucagon (secreted by α-cells)
• somatostatin (secreted by δ-cells).
Insulin
• Insulin is a small peptide consisting of 91 amino acids; it
is derived from the precursor proinsulin.
• Proinsulin undergoes cleavage to form insulin.
• Insulin is stored within granules in β-cells and is
secreted into the circulation by exocytosis.
• Insulin has a short half-life in the circulation (5–10 min);
it is rapidly broken down by the liver and kidney.
• A number of factors are able to inuence the secretion of
insulin; the level of glucose is the most potent stimulus.
• Increased glucose stimulates insulin release from the
β-cells; this decreases glucose concentration in the
plasma and acts as a negative feedback.
• Other regulators of insulin secretion include:
• fatty acids (+)
• ketone bodies (+)
• parasympathetic stimulation (+)
• amino acids, i.e. arginine, leucine (+)
• gastrin, cholecystokinin (CCK), secretin, gastric
inhibitory polypeptide (GIP) (+)
• prostaglandins (+)
• drugs, e.g. sulfonylureas (+)
• sympathetic stimulation (−)
• dopamine (−)
• serotonin (−)
• somatostatin (−).
• Insulin is an anabolic hormone; it has a variety of
actions, which can be divided into:
• carbohydrate metabolism
• protein metabolism
• lipid metabolism.
Carbohydrate Metabolism
• Promotes glucose uptake, except in brain cells; these are
freely permeable to glucose.
CHAPTER 12 Endocrine System
Galactorrhoea
Carpal tunnel
253
Prominent
supra-orbital
ridge
Heart failure
High blood
pressure
Thick 'greasy'
skin
Visual field
defects
Broad nose
Large tongue
syndrome
'Spade-like'
hands
Fig. 12.7 Features of acromegaly.
• Promotes glycogen storage via ↑ glycogenesis and ↓ glycogenolysis; this allows glucose storage in the post-prandial
period. Liver glycogen is converted to glucose and is able
to maintain plasma glucose levels. Muscle glycogen acts
as an energy store. Muscle lacks the phosphatase enzyme
necessary to release free glucose and thus muscle glycogen can only be used in the muscle cells for glycolysis.
• Stimulates the use of glucose (glycolysis).
Protein Metabolism
• Stimulates amino acid uptake.
• Stimulates protein synthesis.
Oedema
• Inhibits protein degradation.
• Inhibits amino acid conversion to glucose.
Lipid Metabolism
• Inhibits lipolysis by lipase.
• Stimulates lipogenesis.
Glucagon
• Glucagon is a catabolic hormone. It is a 29-amino-acid
polypeptide and is released from the α-cells of the pancreas; like insulin it has a short half-life in the circulation (approximately 5 min).
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SECTION II Physiology
• e actions of glucagons can be divided into those
aecting carbohydrate metabolism and those aecting
lipid metabolism.
Carbohydrate Metabolism
• ↑ Glycogenolysis.
• ↑ Gluconeogenesis.
• Glucose sparing by preferential oxidation of fatty
acids; this produces ketones, i.e. acetone, acetoacetate,
β-hydroxybutyrate.
Lipid Metabolism
• Stimulates lipase activity to increase plasma FFAs and
glycerol.
Somatostatin
• Somatostatin is released by δ-cells in the pancreas.
• Secretion is stimulated by:
• ↑ plasma glucose
• ↑ plasma amino acids
• ↑ plasma glycerol.
• e eects of somatostatin include:
• inhibits the release of insulin and glucagons
• ↓ gastrointestinal motility, secretion and absorption.
Effects of Other Hormones on Glucose Regulation
Glucocorticoids
• Released in response to hypoglycaemia, the eects
include:
• anti-insulin: inhibit glucose uptake
• promote lipolysis: FFAs and glycerol are used in pref-
erence to glucose
• promote gluconeogenesis
• promote glycogen production.
Growth Hormone
• Released in times of fasting, the eects include:
• anti-insulin: inhibits glucose uptake
• promotes lipolysis
• stimulates glycogenolysis.
Thyroid Hormone
• e role of thyroid hormone is complex: at low concentrations it is anabolic and reduces plasma glucose; at high
concentrations it is catabolic and induces hyperglycaemia.
• e eects of thyroid hormone include:
• ↑glycogenolysis
• ↑gluconeogenesis
• ↑absorption of glucose from the gastrointestinal tract
• ↑uptake of glucose into cells
• enhances the rate of insulin-dependent glycogenesis.
Catecholamines
• Release of catecholamines is stimulated when the plasma
glucose falls below 4 mmol/L; their eects include:
• ↑glycogenolysis
• enhanced glycogen secretion
• inhibited insulin secretion
• lipolysis (FFAs and glycerol metabolized in prefer-
ence to glucose).
Clinical Physiology
Disorders of the endocrine pancreas
Diabetes Mellitus
• Diabetes mellitus encompasses a number of conditions
in which there is either a lack of insulin or a relative
resistance to its eects.
e causes of diabetes mellitus include:
• Primary:
• type I insulin-dependent diabetes mellitus (IDDM)
• type II non-insulin-dependent diabetes mellitus
(NIDDM).
• Secondary:
• pancreatic disease:
• pancreatitis
• pancreatic cancer
• pancreatectomy
• cystic brosis
• antagonists to insulin:
• acromegaly (GH)
• Cushing’s syndrome (glucocorticoids)
• hyperthyroidism (thyroid hormone)
• phaeochromocytoma (catecholamines)
• glucagonoma (glucagon)
• drugs, e.g. corticosteroids, thiazide diuretics
• liver disease
• genetic syndromes, e.g. Down’s syndrome, Friedreich’s
ataxia
• insulin receptor abnormalities, e.g. congenital
lipodystrophy
• Diabetes mellitus has a number of complications, these
can be divided into:
Acute
• Hypoglycaemia: very common complication of insulin therapy in patients with diabetes; symptoms usually develop when blood glucose falls <3 mmol/L.
Symptoms include sweating, tremor and palpitations
(adrenergic symptoms); in patients with long-standing
disease these warning signs may not be present.
• Diabetic ketoacidosis (DKA): occurs when the body
produces ketones in an uncontrolled manner. Glucose
is not taken up into cells and is lost in the urine, producing an osmotic diuresis. e abnormal glucose handling
CHAPTER 12 Endocrine System
255
is associated with increased lipolysis, which leads to
increased circulating levels of fatty acids; these are converted to acetyl-CoA and then to ketones. e ketones
lead to a severe metabolic acidosis and dehydration due
to nausea and vomiting.
• Hyperglycaemic hyperosmolar non-ketotic coma
(HONK): occurs in the absence of ketosis; it is typically
seen in patients with NIDDM. e patients present with
severe dehydration and a decreased level of consciousness with a very high plasma glucose level.
• Lactic acidosis: occurs in patients on biguanide therapy;
it rarely occurs nowadays as long as the dosage is not
exceeded and is not used in patients where it can accumulate, i.e. renal or hepatic failure.
Chronic
• Macrovascular
• Diabetes mellitus is a risk factor in the development
of atherosclerosis. is tends to be widespread and
more severe as it tends to aect vessels distally (thus
making bypass surgery technically harder).
• Disorders caused by atherosclerosis are all increased
in diabetics, i.e. ischaemic heart disease (IHD), stroke,
myocardial infarction (MI) and peripheral vascular
disease.
• Microvascular
• Small blood vessels are predominantly aected; this
has its greatest eect at three sites:
• eye: diabetic retinopathy
• kidney: diabetic nephropathy
• nerves: diabetic neuropathy.
Pancreatic Endocrine Tumours
Tumours can arise in the endocrine cells of the pancreas.
When these are ‘functioning’ and secrete excess hormone
they can lead to clinical syndromes; examples include:
• Insulinoma: 75% of endocrine tumours; they are derived
from β-cells; the classic presentation is with ‘Whipple’s
triad’ – hypoglycaemic symptoms during fasting, a
reduced blood sugar during these periods, and relief
with intravenous glucose; 10% are malignant.
• Gastrinoma (Zollinger–Ellison syndrome): arise from
pancreatic G-cells; malignant in >50% of cases; the
excess gastrin leads to gastric hypersecretion, diarrhoea
and widespread peptic ulceration.
• VIPomas: associated with excess secretion of VIP (vasoactive intestinal peptide); they lead to severe watery
diarrhoea, ↓ K+, and achlorhydria (absence of HCl in
the stomach).
• Glucagonoma: a rare cause of secondary diabetes mellitus; other symptoms include anaemia, weight loss and a
characteristic rash called necrolytic migratory erythema;
the tumour arises from the α-cells; 75% are malignant.
• Somatostatinoma: a very rare tumour derived from the
δ-cells of the pancreas; they cause diabetes mellitus,
cholelithiasis and steatorrhoea.
Hormonal Response to Trauma/Surgery
• e body responds to a variety of noxious stimuli such
as pain, infection, trauma and surgery.
• is response aims to limit the injuring process and
allow the body to heal; this involves a variety of hormonal changes that alter the metabolism of carbohydrates, proteins and fats, and also involves stimulating
the immune and clotting systems.
• ere are four systems involved in the body’s response
to injury:
1. Sympathetic nervous system: this response is the ini-
tial phase of a response to injury and occurs at the
time of injury. It prepares the body for action, i.e.
‘ght or ight’; the release of epinephrine and norepinephrine has a number of eects:
• blood is redistributed to non-essential organs,
thus supplying more to the heart, skeletal muscle
and brain
• ↑ glucose: provides energy
• ↑ lipolysis: provides energy
• ↑ ketone production: provides energy
• inhibition of non-essential visceral functions, e.g.
bowel peristalsis.
2. Acute phase system: the acute phase response refers
to the cytokine and inammatory mediator production that occurs following tissue injury; this has local
and systemic eects:
• local eects: this involves the rapid inux of inam-
matory cells such as neutrophils and macrophages
(see below) into the wound; these release a variety
of cytokines such as IL-1, 2, 6, TNF-α, and interferons and inammatory mediators such as the
prostaglandins, histamine, serotonin, etc. ese
mediators aim to limit tissue injury by producing
vasodilatation, increased vascular permeability,
attraction and migration of neutrophils, broblasts
and endothelial cells, and stimulation of the clotting system and complement cascade
• systemic eects: the cytokine cascade associated
with local injury is usually limited to the area of
injury; however, if the insult is severe, it may lead
to cytokines spilling into the circulation; this produces systemic eects such as:
• tachypnoea
• fever
• tachycardia
• increased vascular permeability (↓ blood
pressure)
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SECTION II Physiology
• vasodilatation (↓ blood pressure)
• immune cell activation
• increased leukocyte adhesion
• eects on glucose metabolism (see below).
3. Endocrine response: a variety of hormones are
involved in the response to tissue injury; these are
shown in Box 12.2.
4. Vascular endothelium: the endothelium should
be considered as an organ in its own right. e
response to trauma has both local and systemic
eects:
• increased adhesion molecule expression: this
action attracts cells such as neutrophils to destroy
bacteria and digest foreign bodies; however,
enzymes released and production of free radicals
can lead to additional tissue damage
• nitric oxide (NO): produces vasodilatation; this
may lead to hypotension. NO also increases the
number of antigen-presenting cells
• endothelins: these oppose the action of NO and
produce vasoconstriction
• platelet-activating factor (PAF): released in
response to cytokines such as IL-1 and TNF-α.
e main eect is to stimulate platelet aggregation and produce vasoconstriction
• prostaglandins: reduce platelet aggregation and
cause vasodilatation.
• e changes associated with trauma and surgery lead to
wide-ranging local and systemic changes and production of numerous cytokines and humoral mediators;
together they produce a number of clinical changes:
• hypovolaemia: this type of uid loss is referred to as
‘third space’ loss; the vasodilatation and increased vascular permeability lead to uid being sequestered in the
interstitial space
• renal changes: following injury there is reduced excretion of free water and sodium; this continues for about
24 h and is due to the release of aldosterone and ADH
• fever: injury (even in the absence of infection) is associated with a rise in temperature; this is due to changes in the
thermoregulatory set point in the hypothalamus by IL-1
• haematological changes: there is a leukocytosis; albumin levels fall due to decreased production and loss into
injured tissue. e coagulation system is activated. is
is primarily to reduce bleeding aer the injury; however,
it leads to a state of hypercoagulability and an increased
risk of deep vein thrombosis (DVT)
• electrolyte and acid–base changes: the electrolyte changes
include ↓Na+ (due to dilution from retained water), ↑K+
(as a result of cell death and tissue injury), metabolic alkalosis (the absorption of Na+ stimulated by aldosterone
leads to K+ and H+ excretion) and metabolic acidosis
(this occurs with more severe injuries with hypotension,
poor perfusion and consequent anaerobic metabolism).
BOX 12.2 Summary of the Action of Various Hormones in the Body’s Response to Trauma
Hormone Action
ACTH Stimulates glucocorticoid release and potentiates the actions of catecholamines on the heart
Glucocorticoids
Aldosterone
ADH Increased water absorption from the collecting ducts, vasoconstriction (particularly
Insulin
Glucagon Stimulates glycogenolysis, gluconeogenesis, ketogenesis, and lipolysis
Thyroxine See Sick euthyroid syndrome section
Serotonin
Histamine
Growth hormone Stimulates protein synthesis, lipolysis and glycogenolysis
Protein → glucose, glucose → glycogen. Inhibits insulin and stimulates gluconeogenesis,
decreases vascular permeability, potentiates catecholamine-induced vasoconstriction, antiinflammatory (suppresses prostaglandin synthesis), immunosuppressant (inhibits secretion
of IL-2)
Stimulates reabsorption of Na+ (water follows by osmosis; this leads to a reduced urine
volume) and secretion of K
splanchnic), and stimulates glycogenolysis and gluconeogenesis
Low in the ebb phase (due to ↓ β-cell sensitivity to glucose levels; glucagon inhibits its
secretion and cortisol reduces its peripheral action), levels increase in the flow phase but
hyperglycaemia remains due to continued resistance
Causes vasoconstriction, bronchoconstriction, ↑ heart rate and contractility, and stimulates
platelet aggregation
Causes vasodilatation and ↑ vascular permeability
+
CHAPTER 12 Endocrine System
257
• Metabolic changes: the altered metabolism seen aer
trauma or surgery can be divided into two phases: the
ebb phase and the ow phase:
• the ebb phase is the initial response to injury and is a
phase of reduced energy expenditure and metabolic rate
that lasts for approximately 24 h
• the ow phase follows: this is a catabolic phase with
increased metabolic rate, hyperglycaemia, negative
nitrogen balance and increased O2 consumption. e
ow phase has signicant eects on the metabolism of
carbohydrates, lipids and proteins:
• carbohydrates: hyperglycaemia is seen post-injury
due to mobilization of liver glycogen; this is stimulated by catecholamines and glucocorticoids (insulin
resistance prevents cell uptake). Aer 24 h the glycogen is exhausted and the hyperglycaemia is maintained by gluconeogenesis
• lipids: lipolysis is stimulated by catecholamines, the
sympathetic nervous system, cortisol and growth
hormone. ey provide the primary source of energy
for all tissues (leaving the brain and blood cells to
utilize glucose)
• proteins: the demand for amino acids is met by skeletal muscle breakdown; the greater the insult, the
greater the breakdown and nitrogen loss. e amino
acids are used in gluconeogenesis and synthesis of
acute phase proteins.
• Respiratory changes: there is increased respiratory drive
that leads to a respiratory alkalosis (due to ↓ PaCO2); in
addition, the systemic eects of the cytokine release and
immune cell activation can lead to ARDS and severe
hypoxia. e metabolic alkalosis created by H+ excretion aects the oxygen dissociation curve, making it
harder for O2 to dissociate into tissues – thus exacerbating hypoxia.
• Cardiac changes: the cardiac output increases dramatically following injury.
• Immune system changes: there are a variety of defects in
the immune system that occur following trauma:
• cell-mediated immunity
• antigen presentation
• neutrophil function
• opsonization of bacteria.
OSCE SCENARIOS
OSCE Scenario 12.1
A 32-year-old female is admitted with suspected acute appendicitis. She is sweating, agitated, confused and complaining
of palpitations. Her symptoms do not t with a straightforward diagnosis of acute appendicitis. Examination reveals a
temperature of 40°C and a tachycardia of 140 with an irregular pulse. You check her thyroid function, which reveals an
elevated T3 and T4 with suppressed TSH.
1. What is the most likely diagnosis?
2. What may precipitate the condition?
3. How is the condition managed?
OSCE Scenario 12.2
A 40-year-old male presents to his GP with intermittent
headaches, palpitations, sweating, anxiety and intermittent chest pains. Examination reveals a blood pressure of
180/110 mmHg.
1. What endocrine condition do you need to consider?
Explain the condition.
2. How could you conrm the diagnosis?
3. What measures would you take to prepare the patient
for surgery?
OSCE Scenario 12.3
A 64-year-old female is admitted for major gastrointestinal surgery. She is taking 5 mg Prednisolone and has been
doing so for six months.
1. What are the risks of failing to replace steroids
pre-operatively?
2. How would you manage her steroid administration
prior to major surgery?
3. How long aer stopping steroids would a patient not
require pre-operative replacement?
OSCE Scenario 12.4
A 46-year-old female has undergone a total thyroidectomy –
you are called to the ward as the patient is suering from
severe cramps and numb peripheries.
1. What are Chovstek’s and Trousseau’s signs?
2. What is causing the above symptoms and why? What
would you expect to see on an ECG and how would you
treat it?
3. Why has the hypocalcaemia happened and what will be
the long-term treatment?
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SECTION II Physiology
OSCE Scenario 12.5
A 45-year-old male attends a GP surgery with some strange
symptoms – he describes episodes of sweating, palpitations,
being confused and forgetting things, and also abdominal
pain and diarrhoea. A friend thought it might be diabetes
1. What is the diagnosis and what is the classic triad asso-
ciated with this condition?
2. What cells does the disorder arise from?
3. What percentages are benign or malignant?
4. What syndrome are they associated with?
and measures his blood sugar during an episode and found
it to be 3 mmol/L.
Answers in Appendix pages 457–458
Please check your eBook at https://studentconsult.inkling.com/ for more self-assessment questions. See inside cover for
registration details.
13
Cerebral Perfusion Pressure (CPP)
Cerebral Blood Flow (CBF)
Cerebral Blood Volume (CBV)
Nervous and Locomotor Systems
INTRODUCTION
Components
• e nervous system is composed of two components:
• central
• peripheral: sensory and motor.
• e nervous system can also be divided into somatic
and autonomic:
• somatic: supplies the skin and muscles
• autonomic: supplies glands, sphincters and smooth
muscles within blood vessels, etc.
• e central nervous system (CNS) is composed of the
brain and spinal cord; it is composed of numerous specialized cells called neurons.
• e neurons are supported by neuroglia (or glial cells);
these are cells that have a variety of ancillary functions
including:
• astrocytes: form the ‘blood–brain barrier’
• microglia: perform a phagocytic role in the CNS
• oligodendroglia: produce myelin.
• e CNS is organized into two distinct areas:
• grey matter: contains the neuronal cell bodies
• white matter: contains the axon of the neurons.
• e peripheral nervous system consists of the cranial
and spinal nerves and the autonomic nervous system
and their associated ganglia. ey link the CNS with
sensory receptors (e.g. pain receptors) and eectors (i.e.
muscles).
Functions
• e functions of the nervous system include:
• the interpretation of sensory input such as touch,
temperature, proprioception and pain
• interpretation of electrical impulses from the special
senses leading to our ability to taste, smell, hear and
see
• the initiation and co-ordination of movement and
muscle contraction
• higher functions such as thought, memory and the
ability to learn.
CENTRAL NERVOUS SYSTEM
Cerebral Blood Flow (Fig. 13.1)
• Blood ow to the brain is via the internal carotid and
the vertebral arteries; they anastomose to form a circle
of arteries that supply the brain: the circle of Willis.
• e control of cerebral blood ow is maintained within
very close limits. e brain is particularly sensitive to
ischaemia, with loss of consciousness occurring within
5 s of the interruption of cerebral circulation, and irreversible damage within 2–3 min.
• e brain receives approximately 10–15% of the cardiac
output.
• Cerebral blood ow is controlled by three mechanisms:
• autoregulation: myogenic or metabolic
• neural
• local.
CBV CVR
CBF
060
Fig. 13.1 Graph illustrating control of cerebral blood
flow (CBF). The range of autoregulation is at a CPP
of 60–160 mmHg. Flow is maintained by changes in
the cerebrovascular resistance (CVR) with increasing vasoconstriction at high CPP and vasodilatation
at low CPP. The effect of CVR can also be seen to
affect cerebral blood volume (CBV): vasodilatation
increasing CBV and vasoconstriction decreasing it.
(From McGeown JG. Physiology, 2nd edn. Churchill
Livingstone, Edinburgh, 2002, with permission.)
160
259
260
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SECTION II Physiology
Autoregulation
Myogenic
• e brain will maintain a remarkably similar cerebral
blood ow over a wide range of blood pressures: this is
known as autoregulation.
• Myogenic autoregulation occurs when the cerebral
blood vessels constrict or dilate to maintain adequate
cerebral perfusion.
• When the blood pressure rises, the vessels constrict,
thus decreasing ow; when the blood pressure falls, the
cerebral vessels dilate in order to increase ow.
• Autoregulation has a limit to which it can compensate.
At a cerebral perfusion pressure (CPP; see below) of
around 50 mmHg, the dilatation of cerebral vessels will
fail to maintain ow, and at a CPP of 150–160 mmHg,
the cerebral vessels will begin to fail to regulate ow –
indeed, at this point, they become abnormally permeable, causing cerebral oedema.
• ese same mechanisms are responsible for maintaining cerebral ow in patients with head injuries.
• In patients with severe head injuries the amount of perfusion the brain is receiving is dependent upon the intracranial pressure resisting ow within the cranial cavity:
Cerebral perfusion pressure CPP
mean arterial pressure MA
intracranial pressure ICP
• When CPP falls below 50 mmHg then cerebral ischaemia
results; when it falls below 30 mmHg then death occurs.
• ese changes occurring during cerebral autoregulation
can be seen in Fig. 13.1:
• autoregulation occurs over the range 50–150 mmHg
• to maintain ow over this range you can see from the
graph that CVR (cerebral vascular resistance) falls as
CPP falls; this reects the vasodilatation of cerebral
vessels
• as the CPP rises then CVR increases; this reects the
vasoconstriction of cerebral vessels
• as the CVR varies so does the CBV (cerebral blood
volume); as vessels vasodilate the CBV rises, and as
CVR increases the CBV decreases.
• Myogenic autoregulation can be impaired by a number
of factors, such as:
• hypoxia
• ischaemia
• trauma
• cerebral haemorrhage
• tumour
• infection.
Metabolic
• e activity of certain areas of the brain will differ depending on the task being performed; as a
( PP
)
consequence, these areas will require additional blood
ow.
• e increased activity results in a decrease in PaO2 and
increase in PaCO2 and H+, the changes resulting in
local vasodilatation of cerebral blood vessels and thus
increased perfusion.
Neural Control of Cerebral Blood Flow
• e cerebral circulation does receive some sympathetic
vasoconstrictor and parasympathetic vasodilator innervation, but their eect is very weak and their precise
role, if any, is unclear.
Local Control of Cerebral Blood Flow
• Cerebral blood ow is sensitive to changes in the arterial
PaO2 and PaCO2.
• Increases in PaCO2 are associated with an increase
in CBF due to marked cerebral vasodilatation; however, just as hypercapnia results in vasodilatation,
then a fall in PaCO2 (hypocapnia) results in cerebral
vasoconstriction.
• e eect that CO2 has on cerebral blood ow is particularly important in head injury patients; maintaining a
low–normal CO2 prevents increases in ICP due to cerebral vasodilatation. Equally it must be remembered that
overzealous ventilation to low CO2 levels can be equally
detrimental due to vasoconstriction and consequent
cerebral ischaemia.
• The effect of changes in PaO2 is not as marked;
hypoxia has a significant effect only when it falls
below 8kPa. Below this level then CBF may increase
dramatically.
• Increases in PaO2 can cause mild cerebral vasoconstriction; indeed hyperbaric oxygen therapy can reduce CBF
by 20–30%.
• ese normal responses to PaO2 and PaCO2 can be
aected by a number of factors, such as:
• head injury
• cerebral haemorrhage
• shock
• hypoxia.
Cerebrospinal Fluid
• Cerebrospinal uid (CSF) lies in the subarachnoid
space; the total volume is 130–150 mL (40 mL in the
cerebral ventricles and 100 mL around the spinal cord).
• e rate of production of CSF is approximately
500 mL/day.
• e normal CSF pressure is approximately 0.5–1kPa;
obstruction to the ow of CSF leads to an increase in
this pressure, i.e. hydrocephalus.
• CSF is produced by the choroid plexus in the lateral,
third and fourth ventricles.
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