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7
General Physiology
HOMEOSTASIS
Homeostasis = maintenance of a constant internal
environment.
e composition of extracellular uid (ECF), and therefore
the cellular environment, is maintained in a constant state
through homeostatic mechanisms that monitor and regulate the functions of:
• circulatory system
• alimentary system
• respiratory system
• renal system.
Monitoring and regulation are co-ordinated through the
nervous and endocrine systems, requiring:
• receptors
• central integration
• eectors.
Homeostatic mechanism = a regulating mechanism, triggered by an alteration in a physiological property or quantity,
acting to produce a compensatory change in the opposite
direction. is requires:
• Receptors: specialized to detect alterations in certain
variables, e.g. osmoreceptors, chemoreceptors.
• Eectors, e.g.
• circulatory system, carrying O2 to cells and removing
waste products of metabolism
• alimentary system, providing nutrients
• respiratory system, carrying out gaseous exchange
• renal system, excluding waste products.
• Co-ordinating and integrating systems:
• nervous
• hormonal.
Nervous System
• Aerent bres link receptors to co-ordinating systems
in brain and spinal cord.
• Eerent bres carry information from co-ordinating
systems to eector organs.
• Somatic nervous system uses skeletal muscle as eectors
for purposeful behaviour and reex actions.
• Autonomic nervous system sends eerent bres to
glands, heart, hollow organs and blood vessels.
Hormonal System
• Endocrine glands secrete hormones to eect function of
target cells.
• Actions generally slower than those of nervous
system.
• Under control of nervous system via hypothalamic–
pituitary axis with negative feedback.
Thermoregulation
ermoregulation = balance between heat gain and heat
loss. It is controlled by the nervous system.
Body temperature is altered by:
• small adjustments by altering skin blood ow
• large adjustments by shivering and sweating.
Heat Production
• Increased voluntary muscle eort.
• Shivering.
• Controlled via hypothalamus.
Heat Loss
• Controlled by sympathetic nervous system.
• Controlled from hypothalamus.
• Altering skin ow alters thermal conductivity.
• Sweating increases heat loss by increasing evaporation.
Regulation of Body Temperature
Temperature-sensitive receptors are found in the anterior
hypothalamus:
• Activation of heat-sensitive neurons causes:
• skin vasodilatation
• sweating.
• Activation of cold-sensitive neurons causes:
• inhibition of heat-sensitive neurons
• vasoconstriction
• shivering.
171
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SECTION II Physiology
Peripheral Thermoreceptors
• Respond to warm and cold
• Connect centrally to cortex (conscious sensation and
hypothalamus).
Reflex Vasoconstriction
Direct contact with a cold stimulus on a limb leads to vasoconstriction on ipsilateral and contralateral sides.
• Aerent neuron: cutaneous nerve.
• Centre: hypothalamus and spinal cord.
• Eerent neuron: sympathetic nerves.
Reflex Vasodilatation
Reex vasodilatation occurs when radiant heat is applied to
part or the whole of a body.
• Aerent neuron: cutaneous nerve.
• Centre: above C5 of the spinal cord.
• Eerent pathway: sympathetic nerves (reduced activity).
Receptors on Internal Surfaces
• Respiratory and gastrointestinal tracts possess thermoreceptors.
• Inhalation of cold air leads to shivering during inspiration.
• Hot food causes sweating and vasodilatation.
Body Temperature
e body does not have the same temperature throughout.
Core Temperature
• Temperature of thoracic, abdominal contents and brain.
• Must be kept at optimal temperature.
• Usually measured as rectal temperature.
• 0.5°C higher than mouth and axilla.
• Shows diurnal variation: higher in evening than in early
morning.
• Varies during menstrual cycle: 0.5°C higher in latter
half.
Peripheral Temperature
• Less than core temperature, heat being lost from surface
to environment.
• Heat is lost from the body via:
• conduction and evaporation from skin to air
• convection from skin due to air movement; from
lungs via convection of tidal air ow
• radiation from naked skin (and to some extent
between layers of clothing).
Abnormal Temperature Regulation
e core temperature is maintained between 36°C and
37.5°C. It is thought that there is a set-point temperature
around which the core temperature is regulated by the
hypothalamus. If the set-point temperature is raised then
the hypothalamus activates mechanisms leading to increasing core temperature and vice versa.
Fever (Pyrexia)
• Fever may be caused by:
• illness
• exercise
• heatstroke
• anterior hypothalamic lesions, e.g. neoplasia, ischaemia, surgery
• hyperthyroidism
• malignant hyperpyrexia (abnormal muscle response
to anaesthetics)
• failure of heat-loss mechanism, e.g. dehydration.
• Set-point temperature is increased; therefore, the body
feels cold as the core temperature is lower.
• As a result the hypothalamus activates responses to
increase body temperature:
• vasoconstriction
• piloerection (‘goose esh’)
• shivering.
• Aspirin returns set-point temperature to normal and
therefore patient feels hot, as core temperature is higher
than set-point temperature.
• Hypothalamus then responds to increase heat loss by:
• activating vasodilatation
• activating sweating.
Heatstroke
• Occurs with body temperature above 41°C.
• Unacclimatized individuals undertaking exercise in hot,
humid conditions.
• Symptoms:
• nausea
• vomiting
• weakness
• headache
• skin feels hot
• circulatory failure
• cerebral oedema
• hepatic failure
• renal failure.
Hypothermia
• Core temperature (rectal) below 35°C.
• If temperature is <30°C, temperature regulatory mechanism fails completely.
• erefore no response occurs to elevated temperature.
• Oen fatal if temperature is <32°C.
• Symptoms:
CHAPTER 7 General Physiology
173
• shivery and feeling cold at 32–35°C
• bradycardia, hypotension, respiratory depression,
muscle stiness, metabolic abnormalities at <32°C
• death occurs from cardiac arrhythmias, especially
ventricular brillation.
Factors Affecting Thermoregulation
• Anaesthetics:
• depress hypothalamic function
• vasodilatation with increased heat loss
• lack of shivering
• consequent drop in body temperature.
• Exercise:
• increases body temperature
• hypothalamus cannot launch responses that result in
loss of heat faster than its production from muscle
metabolism.
• Circulatory shock:
• reduced tissue perfusion
• reduced cellular metabolism and heat production
• results in decreased body temperature
• compensatory mechanisms include vasoconstriction, piloerection and increased secretion of catecholamines
• skin feels cold
• exception is septic (endotoxic) shock, where there is
vasodilatation and skin feels hot.
• Spinal injuries:
• thermoregulatory mechanisms lost below level of
injury
• vasoconstriction lost; therefore, heat loss increased
• patient unable to shiver
• sweating in relation to hyperthermia lost below level
of lesion
• quadriplegics tend to assume temperature of
environment.
• Hyperthyroidism:
• increased basal metabolic rate (BMR)
• increased O2 consumption
• patient hyperactive
• all of above contribute to increased temperature
• patient intolerant of heat and feels hot.
• Hypothyroidism:
• opposite eects to hyperthyroidism
• patient feels cold, intolerant of cold weather
• body temperature low
• Neonates and premature babies:
• large surface area to body weight ratio
• inability to shiver
• less insulating fat
• temperature regulating mechanisms less developed
• therefore predisposed to increased heat loss.
FLUID BALANCE AND FLUID
REPLACEMENT THERAPY
Body Water
In healthy adults water constitutes approximately 60%
of the body weight. Body water is partitioned into two
components:
• intracellular
• extracellular.
Extracellular component may be divided further into:
• intravascular
• extravascular (interstitial).
For a 70-kg man there would be approximately:
• 25 L of intracellular water
• 19 L of extracellular water.
• Of the extracellular water:
• 3 L is in blood plasma
• 15 L is interstitial uid
• 1 L is transcellular uid, e.g. CSF, peritoneal uid,
intraocular uid.
Functions of the Kidney
See Chapter 11.
DIURESIS
ere are two types of diuresis:
• water
• osmotic.
Water Diuresis
• Occurs when water is ingested or administered in excess
of body’s requirements.
• Antidiuretic hormone (ADH) secretion is suppressed.
• Collecting ducts become relatively impermeable to water
and excess water is lost without solute.
• e kidney can therefore adjust to excretion of water
without markedly aecting its handling of solutes.
Osmotic Diuresis
is results when more solute is presented to the tubules
than they can reabsorb.
Examples of osmotic diuresis include:
• Diabetes, where the concentration of glucose in the
plasma rises so that the ltered load exceeds the tubular
maximum.
• e administration of mannitol, which is ltered but is a
non-reabsorbable solute.
• Inhibition of tubular function, e.g. by drugs that block
reabsorption of sodium chloride in one or more parts of
the tubule.
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SECTION II Physiology
WATER BALANCE
Normally body water remains constant over a 24-h period;
therefore, intake and loss of water must balance exactly.
Intake comprises drinking uids, solid food (which may
contain as much as 1 L of uid in 24 h), and the water of
oxidation of metabolites (about 300 mL in 24 h). Water is
lost in the following ways:
• evaporation via the respiratory system: 500 mL
• skin (insensible): 400 mL
• faeces: 100 mL
• urine (obligatory): 500 mL
• total = 1500 mL.
Urine water loss is variable. About 600 mosmol of solutes must be excreted each day in the urine. e maximal
achievable urinary osmolality is about 1200 mosmol/L and
therefore the obligatory volume of urine is about 500 mL
per day. In practice, water intake is such that 1.5 L of urine
is excreted each day.
Regulation of Total Body Water
Although the movement of certain ions and proteins
between the various compartments is restricted, water is
freely diusible. Consequently the osmolality of all components is identical, being maintained within a narrow range
of 285–295 mosmol/L. Control of osmolality occurs by two
mechanisms:
• adjustments in secretion of ADH
• thirst-mediated water intake.
If water loss exceeds gain there is a reduction in total
body water content and the osmolality of the body uid
increases. is has two eects:
• thirst, resulting in ingestion of water
• release of ADH so that water is retained by the kidneys.
Conversely, excess intake of water dilutes the body uids,
reducing osmolality. is eliminates thirst and inhibits the
release of ADH, thus allowing diuresis and consequent
removal of excess water.
In health, both thirst and ADH release are determined
by the osmolality of plasma-perfusing nuclei in the hypothalamus. e receptors indicating thirst have an osmotic
threshold of about 10 mosmol higher than that of the
osmoreceptors involved in ADH release. Under normal circumstances therefore, thirst is not experienced until ADH
release has ensured that ingested water is retained by the
kidneys.
Other mechanisms are available for the stimulation of
thirst and ADH release. ese are important in conditions
where circulating blood volume falls. ey include:
• reduced arterial blood pressure (signals via carotid and
aortic baroceptors)
• reduced central venous pressure (signals via atrial low
pressure receptors)
• increased angiotensin II in the brain.
DISTURBANCES OF TOTAL BODY WATER
CONTENT
Changes in total body water aect the concentration of solutes in all the body compartments.
Water Depletion
Pure water depletion is rare in clinical practice. More usually it is associated with sodium depletion. Pure water
depletion usually results from decreased water intake.
Causes of water depletion include:
• Diminished oral intake:
• exhaustion
• inability to swallow, e.g. comatose
• restricted intake aer gastrointestinal surgery.
• Loss of uid from the lungs.
• Hyperventilation with unhumidied air.
• Diabetes insipidus.
• Diuretic phase of acute renal failure.
Pure water deciency is reected biochemically by
hypernatraemia. is is associated with:
• increase in plasma osmolality
• concentrated urine
• a low urine sodium concentration despite the hypernatraemia.
Clinical manifestations are usually due to the hypernatraemia, which can depress the central nervous system (CNS),
leading to lethargy or coma. e sodium plasma level is
usually in excess of 160 mmol/L. Treatment consists of
administration of water intravenously as 5% dextrose in
wate r.
Water Intoxication
is is more common in clinical practice. It occurs with
the administration of excessively large amounts of water
in patients who are unable to excrete it. It is dicult to
produce water intoxication in health, the kidneys having
a maximal excretory rate of about 750 mL water per hour.
Causes of water intoxication include:
• Impaired renal excretion of water, e.g.
• renal failure with excessive intake
• excessive administration of 5% dextrose in the post-
operative period when ADH secretion is high
• ADH-secreting tumours.
• Cardiac failure.
• Liver disease.
• Hypoalbuminaemia.
TABLE 7.1 Disturbances of Body Water
Osmolality of Body Fluid Compartment Affected Clinical Manifestation
Water Excess
Primary Reduced
Secondary to Na+ ↑
Water Depletion
Primary Increased
Secondary to Na+ ↓
Normal
Normal
ICF ↑, ECF ↑
ECF ↑
ICF ↓, ECF ↓
ECF ↓
CHAPTER 7 General Physiology
Water intoxication
Oedema
Thirst
Circulatory collapse
175
e commonest cause of water intoxication in surgical
practice is excessive uid administration in patients with
compromised renal function.
Pure water excess is reected by:
• peripheral oedema
• raised central venous pressure (CVP)
• pulmonary oedema.
Treatment depends on the degree of overhydration. If it is
associated with gross pulmonary oedema and is life-threatening, dialysis or continuous veno–venous haemoltration
is indicated. With less severe causes and previous normal
renal function, water restriction and the administration of
a diuretic will suce. If cardiac failure is present, digitalization may be indicated. A summary of the disturbances of
body water is shown in Table 7.1.
ELECTROLYTE DISORDERS
Sodium
• Major cation in the ECF.
• 100–300 mmol Na+ are consumed daily in a typical diet.
• Almost all this is absorbed from the gastrointestinal
tract, only about 5–10 mmol daily being lost in faeces.
• Excretion of sodium is chiey renal, the only other route
in health being from the skin as sweat.
• Loss of Na+ in sweat is extremely variable.
• Each litre of sweat contains 30–50 mmol Na+; loss of a
few litres of sweat can cause a signicant loss of sodium
from ECF.
Regulation of Sodium
is occurs by both:
• renal mechanisms
• extrarenal mechanisms.
Renal
• 99% of the ltered sodium is reabsorbed: 65% in the
proximal tubule, 25% in the loop of Henle, and approximately 10% in the distal tubules and collecting ducts.
• Regulation of sodium balance in the kidney is determined by:
• glomerular ltration rate (GFR)
• renin–angiotensin mechanism
• several prostaglandins.
• Angiotensin II has two important intrarenal eects:
• stimulates Na+ reabsorption in most nephron
segments
• constricts the glomerular arterioles.
• Above two factors favour Na+ retention and restoration
of ECF volume.
Extrarenal
• Renin–angiotensin mechanism via aldosterone.
• Atrial natriuretic peptide (ANP).
• Circulating angiotensin II stimulates release of aldosterone from zona glomerulosa of adrenal gland.
• Aldosterone promotes sodium reabsorption in the
distal tubule and collecting ducts as well as in colonic
epithelium and the ducts of salivary and sweat glands.
• ANP is released from the cardiac atria in response to
stretch.
• ANP increases the excretion of Na+:
• by increasing GFR
• inhibiting Na+ reabsorption in the collecting
ducts
• reducing the secretion of renin and aldosterone.
Sodium Excess
Hypernatraemia is usually a sign of water depletion, but
other causes may be apparent. ese are shown in Box 7.1.
With sodium retention:
• e osmolality of ECF increases.
• is results in the release of ADH and retention of water
in distal tubule.
• is increases the volume of ECF and restores osmolality to normal.
• Sodium excess presents with dependent oedema, increase
in body weight and eventually pulmonary oedema.
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SECTION II Physiology
BOX 7.1 Causes of Hypernatraemia
Sodium excess
• Excessive intravenous sodium therapy, especially
postoperatively
• Conn’s syndrome (primar y hyperaldosteronism)
• Cushing’s syndrome
• Steroid therapy
• Chronic congestive cardiac failure (CCF)
• Cirrhosis of the liver
Water depletion
• Reduced water intake, e.g. coma, confusion
• Renal, e.g. osmotic diuresis, diuretic phase of acute
renal failure, post-relief of obstructive uropathy,
diabetes insipidus
• Others, e.g. fever, burns, diarrhoea, fistulae
• Treatment of sodium excess is aimed at a reduction of
intake together with treatment of the underlying cause,
e.g. the use of spironolactone in Conn’s syndrome or liver
disease, or digitalization in congestive cardiac failure.
• If hypernatraemia is a reection of water depletion then
increase in water intake by intravenous administration
of 5% dextrose will usually suce.
Sodium Depletion
• Hyponatraemia may be the result of:
• water retention
• sodium depletion.
e causes of sodium deciency are shown in Box 7.2.
BOX 7.2 Causes of Sodium Deficiency
• Low intake:
• saline-free intravenous solutions
• reduced oral intake, e.g. coma, dysphagia
• Excessive loss via gastrointestinal tract
• diarrhoea
• intestinal obstruction
• fistulae
• paralytic ileus
• Excessive sweating, e.g. fever
• Burns
• Drainage of ascites
• Addison's disease
• Diuretics
• Inappropriate secretion of ADH:
• bronchogenic carcinoma
• head injury
Sodium depletion initially results in:
• decrease in osmolality of ECF
• as long as osmoregulation continues, loss of Na+ leads to
loss of water at a rate of 1 L per 150 mmol of Na
+
• water loss is shared between plasma and extravascular
ECF
• consequences are more serious for the circulation than
those of primary water depletion since ECF and plasma
are chiey aected by the water deciency
• chief manifestation of depletion of body Na+ is peripheral circulatory failure. Treatment involves:
• hyponatraemia due to ECF depletion: usually
treat ed with isotonic saline, as sodium loss is invariably accompanied by water loss. Infusion of normal
saline requires close monitoring with checking of
serum electrolytes and measurement of urinary
sodium, which increases with adequate sodium
repletion
• hyponatraemia: an apparently normal or high ECF vol-
ume should be treated by water restriction. Avoidance
of a diuretic is advisable since this may remove nearly
as much sodium as water
• severe hyponatraemia (<119 mEq/L) with clinical
symptoms such as ts, confusion or coma, should be
treated with hypertonic saline.
Potassium
Potassium is the chief intracellular cation, 98% of it being
within cells. e intracellular concentration (150 mmol/L)
is not critical but a two- to threefold increase or decrease
in the extracellular concentration can paralyze muscle or
cause cardiac arrest. Rapid loss of 5% of intracellular K+
into the ECF would be lethal.
Factors aecting plasma potassium include:
• aldosterone: increases renal excretion by eects on distal tubule
• insulin: promotes entry of K+ into cells
• acid–base balance: acidosis results in increased plasma
K+ due to reduced entry into cells and reduced urinary
excretion. Alkalosis causes the opposite eect
• hydration: K+ is lost from cells in dehydration and
returns when the patient is rehydrated
• catabolic states, e.g. trauma, major surgery, infection: K+
is lost from the cells.
Hyperkalaemia
Hyperkalaemia is a potentially fatal condition of insidious
onset. e causes are shown in Box 7.3.
Clinically, signs may be dicult to detect and sudden
cardiac arrhythmia with cardiac arrest may be the rst sign.
Laboratory tests will conrm high serum K+ with acidosis.
Electrocardiogram (ECG) changes include:
CHAPTER 7 General Physiology
pH
HCO
HCO
[]
[]
23
pH
HCO
CO
2
×
−
003
[]
. P
[]/PCO
2
HCO
−
177
BOX 7.3 Causes of Hyperkalaemia
• Excess administration of potassium, especially
rapidly
• Renal failure
• Haemolysis
• Crush injuries
• Tissue necrosis, e.g. burns, ischaemia
• Metabolic acidosis
• Adrenal insufficiency (Addison’s disease)
• peaked T-waves
• loss of P-waves
• widening of the QRS complex.
Urgent treatment of hyperkalaemia is required. e following methods are available:
• infusion of calcium gluconate
• infusion of glucose and insulin
• ion-exchange resins, e.g. resonium
• haemodialysis.
Hypokalaemia
Potassium depletion is usually the result of abnormal losses
from:
• gastrointestinal tract
• renal tract.
e causes are shown in Box 7.4.
BOX 7.4 Causes of Hypokalaemia
Inadequate intake
• Potassium-free intravenous fluids
• Reduced oral intake:
• coma
• dysphagia
Excessive loss
• Renal:
• diuretics
• renal tubular disorders
• Gastrointestinal:
• diarrhoea
• vomiting
• fistulae
• laxatives
• villous adenoma
• Endocrine:
• Cushing’s syndrome
• steroid therapy
• hyperaldosteronism (primary and secondary)
e following are features of hypokalaemia:
• clinical fatigue and lethargy with eventual muscle weakness
• low serum K+ together with alkalosis
• ECG changes include low broad T-waves in the presence of U-waves
• treatment is by correction with oral supplements, or in
severe cases slow intravenous replacement with careful
monitoring.
ACID–BASE BALANCE
During the course of daily metabolism, approximately
70mEq of hydrogen ion is released into the body uids. A
large amount of carbon dioxide is produced, which combines with water to form carbonic acid (H2CO3). Methods
to eliminate this acid are necessary, otherwise the pH of the
body uids would fall rapidly.
e following are important buer systems in the body:
• proteins
• haemoglobin
• phosphate
• bicarbonate.
e bicarbonate system is important in that:
• CO2 is excreted in the lungs and can be regulated by
changes in ventilation
• bicarbonate excretion is also regulated in the kidney.
Carbonic Acid–Bicarbonate System
The carbonic acid–bicarbonate system (H2O + CO2 ⇋
−
H2 CO
The Henderson–Hasselbach equation is derived from
⇋ HCO
3
this, i.e.
e pK for the HCO
acid is more usually expressed in terms of carbon dioxide,
and the equation then becomes:
where 0.03 is the solubility of CO2 expressed in mmol/L.
mmHg and PCO2 in mmHg.
e equation makes it clear that pH depends on the
ratio of [HCO
controlled slowly by the kidneys while CO2 is controlled
rapidly by the lungs.
If the CO2 rises so will the bicarbonate to keep the
3
Similarly, if bicarbonate falls there will be a fall in PCO2
to prevent a change in pH. If the primary change is an alteration in CO2 it is called a respiratory acidosis or alkalosis;
−
) is catalysed by carbonic anhydrase.
3
log
3
3
= pK
+−log
−
/H2CO3 system is 6.1. e carbonic
3
= 6.1
+
−
] to PCO2, i.e. the buer pair. [HCO
3
ratio constant.
−
] is
3
178
pH
kidney function
lung function
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SECTION II Physiology
if it is a primary change in [HCO
acidosis or alkalosis.
−
] it is called a metabolic
3
A simple way of looking at the Henderson–Hasselbach
equation is:
= constant
+
Basically, the regulation of pH is achieved through control of:
• excretion of H+ and re-absorption of [HCO3−] by the
kidneys
• excretion of CO2 by the lungs through regulation of
alveolar ventilation
• buering of H+ by other buering systems within the
body.
Disturbances of Acid–Base Balance
• Primary respiratory disturbances cause changes in
PCO2 and produce corresponding eects on blood
hydrogen ion concentration.
• Primary metabolic disturbances aect the plasma
bicarbonate.
• Whether the disturbance is primarily respiratory or metabolic, some degree of compensation occurs in either
numerator or denominator of the Henderson–Hasselbach
equation to limit or negate the change in blood pH.
• Changes in PCO2 from respiratory disturbances are compensated for by renal tubular handling of bicarbonate.
• e metabolic disturbances are compensated for by
appropriate respiratory change.
Respiratory Acidosis
e causes are shown in Box 7.5.
• Caused by CO2 retention due to inadequate alveolar
ventilation.
• ↓pH ↑PCO
• Compensation occurs by:
• ↑HCO3− by bicarbonate buer system
• ↓H+ by kidneys.
• In acute respiratory acidosis there is little time for bicarbonate to increase as a consequence of raised arterial
CO2; therefore, bicarbonate may be normal.
• In chronic CO2 retention, although CO2 levels may
be high, the pH is not so depressed, because kidneys
compensate by retaining bicarbonate in response to
increased PCO2.
Respiratory Alkalosis
e causes are shown in Box 7.6.
• Occurs when carbon dioxide is lost via excessive pulmonary ventilation.
• ↑pH ↓PCO2.
2.
BOX 7.5 Causes of Respiratory Acidosis
(Any Cause of Hypoventilation)
Respiratory depression
• CNS depression:
• head injury
• drugs, e.g. opiates, anaesthetics
• coma
• cerebrovascular accident (CVA)
• encephalitis
• Neuromuscular disease:
• myasthenia gravis
• Guillain–Barré syndrome
• Skeletal disease:
• kyphoscoliosis
• ankylosing spondylitis
• flail chest
• Artificial ventilation (uncontrolled and unmonitored)
• Impaired gaseous exchange:
• thoracic injury, e.g. pulmonary contusions
• obstructive airway disease (acute and chronic)
• alveolar disease e.g. pneumonia, ARDS
BOX 7.6 Causes of Respiratory Alkalosis
(Any Cause of Hyperventilation)
Stimulation of respiratory centre
• High altitude (hypoxia)
• Pneumonia
• Pulmonary oedema
• Pulmonary embolism
• Fever
• Head injury
• Metabolic acidosis (overcompensation)
Increased alveolar gas exchange
• Hyperventilation, e.g. hysteria, pain, anxiety
• Artificial ventilation (uncontrolled)
• Compensation occurs by:
• ↓HCO3− by bicarbonate buer system
• ↑H+ by kidneys.
• Acute hyperventilation lowers the PCO2 without concomitant changes in plasma HCO
• In chronic hyperventilation HCO
−
.
3
−
is reduced.
3
Metabolic Acidosis
e causes are shown in Box 7.7.
• Results from increased production of hydrogen ion
from metabolic causes or from excessive bicarbonate
losses, leading to a decrease in pH and a compensatory
decrease in PCO2.
CHAPTER 7 General Physiology
179
BOX 7.7 Causes of Metabolic Acidosis
Excessive production of H
• Diabetic ketoacidosis
• Lactic acidosis secondary to hypoxia
• Septicaemia
• Starvation
Impaired excretion of H
• Acute renal failure
• Chronic renal failure
Excess loss of base
• Diarrhoea
• Intestinal, biliary and pancreatic fistulae
+
+
BOX 7.8 Causes of Metabolic Alkalosis
Excess loss of H
• Vomiting
• Nasogastric aspiration
• Gastric fistula
• Diuretic therapy (thiazide or loop)
• Cushing’s syndrome
• Conn’s syndrome
Excessive intake of base
• Antacids, e.g. milk–alkali syndrome
• ↓pH ↓HCO
• Compensation occurs by:
+
−
.
3
• ↓PCO2 by hyperventilation
• ↓H+ by kidneys (unless renal failure).
Metabolic Alkalosis
Causes are shown in Box 7.8.
• Results from primary disturbance of an increase in
• ↑pH ↑HCO
• Compensation occurs by:
−
HCO
or a decrease in H+.
3
−
.
3
• ↑PCO2 by hypoventilation (limited by hypoxia)
• ↓HCO
−
by kidneys.
3
Mixed Acid–Base Disorders
• In many situations mixed disorders occur.
• Commonest example in surgical practice is a combination of a metabolic acidosis and respiratory
alkalosis.
• is may occur in:
• renal failure
• sepsis
• septic shock.
• As the two acid–base disorders tend to cancel one
another out, the disturbance in H+ is usually small.
• Respiratory acidosis and metabolic acidosis may occur
together in:
• adult respiratory distress syndrome (ARDS)
• cardiac failure
• cardiorespiratory arrest.
• Respiratory alkalosis and metabolic alkalosis in combination is rare, but may occur when over-ventilating a
patient with chronic respiratory acidosis.
A summary of disturbances of acid–base balance is
shown in Table 7.2.
Interpretation of Acid–Base Changes
A blood gas analyser usually prints out the variables shown
below (normal values).
• temperature: 37°C
• pH: 7.35–7.45
• PCO2: 4.6–5.8kPa (35–44 mmHg)
• PO2: 10–13kPa (75–100 mmHg)
• HCO
• total CO2: 24–28 mmol/L
−
(actual): 22–28 mmol/L
3
• standard bicarbonate: 22–26 mmol/L
• base excess: −2 to +2 mmol/L
• standard base excess: −3 to +3 mmol/L
• O2 saturation: >95%
• Hb: 11.5–15.5 g/dL.
As the patient’s acid–base status varies, three factors are
changing at the same time:
• pH
• PCO
• HCO
2
−
.
3
TABLE 7.2 Disturbances of Acid–Base Balance
Abnormality Primary Disturbance pH Base Excess Compensatory Mechanism
Metabolic acidosis
Respiratory acidosis
Metabolic alkalosis
Respiratory alkalosis
−
[HCO
] ↓ ↓ −ve PCO2 ↓
3
PCO2 ↑ ↓ [HCO
−
[HCO
] ↑ ↑ +ve PCO2 ↑
3
PCO2 ↓ ↑ [HCO
−
] ↑
3
−
] ↓
3
180
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SECTION II Physiology
Blood gas machines measure PO2, pH and PCO2 directly.
Bicarbonate is calculated from the Henderson–Hasselbach
equation. e standard bicarbonate is a value obtained aer
correction of the PCO2 to 40 mmHg (5.3kPa). is correction is required in order to remove any respiratory component. In other words, it indicates what the bicarbonate
would be if there was no respiratory disturbance.
• e normal standard bicarbonate is 22–26 mmol/L.
• Values above this range indicate metabolic alkalosis.
• Values below this range indicate metabolic acidosis.
Interpretation of blood gas analysis should be performed systematically:
1. First the pH should be noticed; this indicates whether
the patient is acidotic or alkalotic.
2. Next, the PCO2 is noted; this will indicate the respira-
tory component, i.e. it will be elevated in respiratory
acidosis and decreased in respiratory alkalosis.
3. Next, the standard bicarbonate or base excess is noted;
both give the same information, i.e. metabolic acid–
base status aer correcting for the PCO2.
4. Serum electrolytes should be checked and the anion gap
calculated.
Anion gap
• Normally between 10 and 19 mmol/L.
• Reects the concentration of those anions present in
the serum but not routinely measured, e.g. phosphates,
organic acids.
• For electrochemical neutrality of the ECF, the number
of anions must equal the number of cations.
• Normally only Na+, K+, HCO
the laboratory.
• When the normal values of these are added they do not
balance, i.e. Na+ (140) + K+ (5)=145; and HCO
Cl− (105)=130.
−
and Cl− are measured in
3
−
(25) +
3
• e dierence, 15 mEq/L, is known as the anion gap
and represents anions that are not usually measured.
• With excessive bicarbonate loss, e.g. diarrhoea, stulae,
decrease in plasma HCO
serum Cl− so that the anion gap remains around normal
−
is matched by an increase in
3
level.
• Metabolic acidosis resulting from an increase in pro-
duction of acid is associated with an increased anion
gap, e.g. lactic acidosis secondary to hypoxia, ketoaci-
dosis of diabetes and renal failure.
FLUID BALANCE AND FLUID
REPLACEMENT THERAPY
An average adult normally loses between 2.5 and 3 L of
uid in 24 h, approximately 1 L being lost from the skin
and lungs (insensible losses), 100 mL in the faeces and the
remainder in the urine. About 100–150 mmol of Na+ and
50–100 mmol K+ are lost in the urine each day. is is usually balanced by normal dietary intake.
Fluid Balance in the Uncomplicated Patient
• Requires 2.5–3 L intravenous uid containing 150 mmol
of Na+ and 60 mmol of K+ per day.
• A suitable uid regimen for 24 h would therefore be as
follows:
• 500 mL 0.9% sodium chloride + 20 mmol KCl
• 500 mL 5% dextrose
• 500 mL 5% dextrose + 20 mmol KCl
• 500 mL 0.9% sodium chloride
• 500 mL 5% dextrose + 20 mmol KCl
• 500 mL 5% dextrose.
Each bag of uid is given over 4 h.
Change in Fluid and Electrolyte Requirements in
Response to Surgery and Trauma
Following surgery or trauma, certain physiological responses
occur in the body:
• catecholamines are released
• stress stimulates the hypothalamo–pituitary–adrenal axis
with an increased secretion of cortisol and aldosterone
• these hormones produce conservation of sodium and
water by the kidney, resulting in a reduction of urine
volume and urine sodium concentration
• if renal perfusion falls, e.g. due to haemorrhage or uid
loss into other spaces, the renin–angiotensin–aldosterone mechanism is activated
• this promotes reabsorption of sodium and water, and
more potassium is lost in the urine
• ADH secretion from the posterior pituitary also leads to
water conservation
• despite loss of potassium in the urine, serum K+ does not
usually fall but may even rise, due to release of potassium
from tissue damage caused by trauma or surgery or administration of stored blood containing excessive potassium.
ese factors must be taken into account when prescribing
intravenous uids, particularly in the rst 24 h aer major
surgery. e regimen described above for an uncomplicated patient may not be appropriate, and an appropriate
regimen for the rst 24 h postoperatively is as follows:
• 500 mL 0.9% sodium chloride
• 500 mL 5% dextrose
• 500 mL 5% dextrose
• 500 mL 5% dextrose.
Each bag of uid is given over 6 h.
Fluid and Electrolyte Problems in
Surgical Patients
e common causes of uid and electrolyte loss in surgical
patients are shown in Box 7.9.
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