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CHAPTER 7 General Physiology
181
BOX 7.9 Causes of Fluid Loss in Surgical
Patients
Blood
• Trauma
• Surgery
Plasma
• Burns
Gastrointestinal
• Nasogastric aspiration
• Vomiting
• Diarrhoea
• Intraluminal:
• intestinal obstruction
• paralytic ileus
• Fistulae
• Stomas
Exudate in peritoneal cavity
• Peritonitis
• Acute pancreatitis (also into the retroperitoneum)
• Septicaemia
Excess insensible loss
• Fever
• Sweating
• Hyperventilation
Blood and Plasma
• Blood loss may be rapid, the loss of 1 L causing hypotension and hypovolaemic shock.
• Blood is normally replaced by blood, but initially plasma
expanders such as gelatin solutions are used until crossmatched blood is available.
• Less rapid haemorrhage allows time for the loss to be
replaced from the extracellular extravascular compartment.
• Greater volumes may be lost slowly before the circulation is compromised.
• Plasma lost from severe burns is replaced by plasma, the
anticipated losses being replaced according to a standard formula.
Gastrointestinal Losses
• 6–10 L of electrolyte-rich uid are secreted in the upper
GI tract daily (Table 7.3).
• Most of this is reabsorbed lower down in the intestine.
• Abnormal uid losses must be measured or estimated
as accurately as possible.
• With sequestration of uid in the bowel lumen, e.g. in
ileus, only an estimate can be made, but with stulae
the amount can be measured accurately and its electrolyte content assessed.
• As a general rule, gastrointestinal uid loss should be
replaced with normal saline with the addition of potassium as necessary.
• Regular assessment of serum electrolytes will provide
information regarding their requirements.
Intraperitoneal Fluid Loss
• Peritonitis and acute pancreatitis will result in loss of
uid into the peritoneal cavity.
• In pancreatitis, uid is also lost into the retroperitoneum.
• ese losses should be made good by plasma substitutes
and normal saline.
Septicaemia
• Septic shock associated with peripheral vasodilatation
causing relative hypovolaemia.
• Large increase in capillary permeability results in extensive loss of protein and electrolytes into the extracellular
space.
• is loss combined with peripheral vasodilatation results
in collapse and shock.
• Fluid replacement is with plasma expanders and normal
saline.
• Exact uid loss is dicult to estimate but should be
monitored by:
• urine output
• blood pressure
TABLE 7.3 Normal Daily Gastrointestinal Secretion Volumes and Electrolyte Composition
Secretion Volume (L) Na+ (mmol/L) K+ (mmol/L) Cl− (mmol/L) HCO3 (mmol/L)
Saliva 1–1.5 20–80 10–20 20–40 20–160
Gastric juice 1–2.5 40–100 5–10 120–140 0
Bile 0.5–1.5 140–200 5–10 40–60 20–60
Pancreatic juice 1–2 130 5–10 10–60 80–120
Succus entericus 2–3 140 5 variable variable
182
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SECTION II Physiology
• central venous pressure (CVP)
• pulmonary wedge pressure monitoring.
Excessive Insensible Fluid Loss
• Insensible uid loss may be greatly increased in the ill
patient.
• Pyrexia increases insensible losses by about 10% for
each °C rise in temperature.
• Loss is chiey from the lungs as expired water vapour.
• Excessive sweating causes loss of sodium-rich uid,
sweat containing about 50mEq Na+/L
• May be overlooked in the pyrexial patient in hot, humid
ward in summer months.
COLLOID AND CRYSTALLOID SOLUTIONS
Colloids are osmotically active particles in solution.
Types
• Albumin: human albumin solution.
• Dextran: dextran 70 in 0.9% saline or 5% glucose.
• Gelatin: polygeline (Haemaccel); succinylated gelatin
(Gelofusin).
• Hydroxyethyl starch: hetastarch (Hespan).
• Pentastarch (Pentaspan).
Uses
• Maintenance of plasma volume.
• Acute replacement of plasma volume decit.
• Short-term volume expansion (gelatin, dextran).
• Medium-term volume expansion (albumin, pentastarch).
• Long-term volume expansion (hetastarch).
• Interferes with coagulation (factor VIII↓; inhibits platelet aggregation).
• Relatively high incidence of allergic reactions.
Gelatins
• Prepared by hydrolysis of bovine collagen.
• Do not aect coagulation per se.
• Low incidence of allergic reactions.
• Small average particle size; therefore, stay in intravascular space shorter period of time.
• Polygeline (Haemaccel):
• contains K+; also contains Ca2+, which can cause
coagulation if mixed with citrated blood in giving set
• stays shorter time in circulation.
• Succinylated gelatin (Gelofusin):
• larger molecular weight than polygeline; therefore,
slightly longer eect
• does not contain calcium.
Hydroxyethyl Starch
• Longer half-life in plasma.
• 10% solutions hyperoncotic; hence increasing plasma
volume by more than volume infused.
• Hetastarch (Hespan):
• 6% in saline has largest molecular weight of any plasma
expander and therefore stays in circulation longer
• most useful in capillary leak
• may cause coagulopathy
• high degree of protection from metabolism.
• Pentastarch (Pentaspan):
• lower degree of protection from metabolism
• shorter-lasting eect than Hetastarch.
Albumin
• 5% and 20% human albumin solution.
• Used for replacement of plasma protein and expansion
of plasma volume.
• No evidence that maintenance of plasma albumin
levels, as opposed to maintenance of plasma colloid
osmotic pressure with artificial plasma substitutes, is
advantageous.
• 20% albumin used for replacement of plasma protein:
• in severe hypoproteinaemia in renal or liver disease
• aer large-volume paracentesis
• aer massive liver resection.
• Some leaks through capillary membrane (in patients
with capillary leak).
• Suppresses albumin synthesis.
Choice of Plasma Expanders
• Succinylated gelatin (Gelofusin) has most advantages in
acute hypovolaemia:
• short-acting
• useful until blood becomes available
• no calcium; therefore, does not cause coagulation if
mixed with citrated blood in giving set
• cheap.
• Hetastarch (Hespan):
• has most advantages in chronic (continuing) hypo-
volaemia
• longer-acting
• larger molecules better retained in circulation when
capillaries leaky, e.g. septic shock
• high degree of protection from metabolism.
Dextran
• Glucose polymers of dierent molecular weights.
• Dextran 70 formerly popular as plasma substitute.
• Interferes with cross-matching.
General Problems of Plasma Expanders
• Dilution coagulopathy.
• Allergic reactions.
CHAPTER 7 General Physiology
1/5
1/5
TABLE 7.4 Composition of Common Crystalloid Solutions
Hartmann's
mmol/L N Saline
+
Na
+
K
++
Ca
−
Cl
−
HCO
3
Osmolality (mosmol/L) 308 280 284 278 300
a
In the form of lactate which is metabolized to bicarbonate in the liver.
155 131 30 0 150
0 5 0 0 0
0 2 0 0 0
155 111 30 0 0
0 29
Solution
a
4% Dextrose/
N Saline
0 0 150
5%
Dextrose
183
Sodium Bicarbonate
(1.26%)
• Interfering with cross-matching (dextran 70).
• Persistence of colloid eect dependent on molecular
size and protection from metabolism.
• All articial colloids are polydisperse, i.e. there is a
range of molecular sizes.
Crystalloids
Crystalloids are salt ions in water.
Common Types
• Normal saline (0.9%).
• 4% dextrose/(
• Glucose, e.g. 5% glucose or stronger solutions.
• Sodium bicarbonate, e.g. 1.26%, 8.4%.
• Potassium chloride.
e content of these solutions is shown in Table 7.4.
Uses
• Provision of daily requirements of water and electrolytes.
• Plasma volume should be replaced with colloids, since
crystalloids are rapidly lost from plasma.
• Of a volume of crystalloid infused initially, one-third
stays in intravascular compartment and two-thirds
pass to ECF; therefore, risk of oedema if excessive
infusion.
• Advantage that ECF decit is replaced in shock.
• 5% glucose is used to supply intravenous water requirements, 50 g/L glucose being present to ensure an isotonic solution.
• Hartmann’s solution has no practical advantages over
0.9% saline for uid maintenance; however, may be useful if large volumes of crystalloid are exchanged (e.g.
during continuous haemoltration) to maintain acid–
base balance.
• Higher concentrations of glucose are used to prevent or
treat hypoglycaemia.
) normal saline.
• Sodium bicarbonate is used to correct metabolic acidosis.
• Potassium chloride is used to supplement K+ in crystalloid uids. Safety rules for giving K+ include:
• urine output of at least 40 mL/h
• not more than 40 mmol to be added to 1 L of uid
• infusion rate no faster than 40 mmol/h.
OEDEMA AND LYMPHATIC FUNCTION
Oedema is an increase in the volume of interstitial uid
above normal levels.
• A hydrostatic pressure difference across the capillary endothelium results in flow from vessel to tissue
space.
• Retention of plasma proteins within the vasculature is
an opposing force, i.e. the plasma oncotic pressure.
• e Starling equilibrium describes the relationship
between hydrostatic pressure, oncotic pressure (colloid
osmotic pressure) and uid ow across the capillary
membrane.
• e Starling equilibrium states:
• capillary hydrostatic pressure + tissue oncotic pres-
sure (pressure tending to drive uid out of the capillary) = interstitial uid pressure + plasma oncotic
pressure (pressure tending to hold uid into the
capillary).
e Starling equilibrium across the capillary is shown
in Fig. 7.1. Filtration is favoured at the arterial end of the
capillary, while absorption is favoured at the venous end of
the capillary. Any uid not reabsorbed from the interstitium by the capillaries is returned to the circulation by the
lymphatic system.
Causes of Oedema
Causes of oedema are:
• Increased capillary hydrostatic pressure:
184
Arterial end
Net hydrostatic
Interstitial
Interstitial
Interstitial
Venous end
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Fig. 7.1 Starling equilibrium across capillary.
SECTION II Physiology
Hydrostatic
pressures
(mmHg)
Colloid
osmotic
pressures
(mmHg)
and colloid
osmotic
pressures
(mmHg)
32 12
0 0
32 12
25 25
5 5
20 20
12 8
Filtration
Reabsorption
Blood
fluid
Blood
fluid
Blood
fluid
• chronic right heart failure
• venous obstruction
• increased uid volume (e.g. overtransfusion).
• Decreased plasma oncotic pressure due to hypoproteinaemia:
• starvation
• cirrhosis
• nephrotic syndrome.
• Increased capillary permeability:
• inammatory reactions
• allergic reactions.
• Increased tissue oncotic pressure:
• lymphatic blockage
• protein accumulation in burns.
Obstruction to Lymphatics
Lymphatics remove protein and excess uid that has been
ltered at the arterial end of the capillary and not reabsorbed at the venous end. If lymphatics are obstructed, then
this uid cannot return to the vascular system and accumulates behind the obstruction, causing oedema. Lymphatic
obstruction may occur due to lymph node pathology as a
result of:
• surgical removal, e.g. axillary clearance with mastectomy or block dissection
• metastatic tumours
• irradiation
• lariasis.
OSCE SCENARIOS
OSCE Scenario 7.1
A 64-year-old male is admitted for a right hemicolectomy
and is found to have a serum sodium of 120 mmol/L.
1. What are the possible causes of hyponatraemia in this
patient?
2. Describe what investigations you would carry out in
order to identify the cause of the hyponatraemia.
3. How would you correct it?
OSCE Scenario 7.2
An 82-year-old male is transferred to ITU following a
Hartmann’s procedure for perforated diverticular disease.
He has been anuric for 3 h. A number of uid challenges
have been given, achieving a BP of 120/90, pulse of 87 and
a CVP of 10. ABG analysis shows a pH of 7.2 and U&Es
reveal serum potassium of 7.1 mmol/L.
1. What are the possible causes of hyperkalaemia in this
patient?
2. What are the ECG changes associated with hyper-
kalaemia?
3. What would be your possible treatment options for this
patient? Explain how each works to lower the serum
potassium.
OSCE Scenario 7.3
A 56-year-old male is admitted with severe dehydration
and vomiting. His urea came back raised at 15 mmol/L and
his creatinine level was at 215µmol/L. A blood gas analysis
shows the following abnormalities – pH 7.55, PO2 10.9kPa,
CO2 6.9kPa and HCO3 is 21.
1. What type of metabolic abnormality is this patient
displaying?
2. How has it occurred?
3. e patient has a ‘sucussion splash’ on examination.
What is the diagnosis?
4. How would you manage this condition?
CHAPTER 7 General Physiology
185
OSCE Scenario 7.4
A 35-year-old female patient with weight of 70 kg underwent
uncomplicated appendicectomy. As she arrives back to the
ward, the nurses ask you to prescribe her intravenous uids for
the next 24 h as she is unable to eat and drink due to nausea.
1. What are the volumes of the uid compartments of the
body?
2. In general, what are the average daily uid and electro-
lyte requirements?
3. What intravenous uids would you prescribe for the
looks very unwell and is in obvious pain and is very confused. He is wearing a medical alert bracelet informing you
he is diabetic. He has a temperature of 39°C and his blood
pressure is 90/50 with a heart rate of 110. He has a rather
strange smell of acetone or ‘pear drop’ sweets.
1. What is the diagnosis?
2. What would you expect his blood gases to show and
why?
3. How would you manage this patient, explaining which
electrolyte needs specic management?
next 24 h?
Answers in Appendix pages 444–446
OSCE Scenario 7.5
A 65-year-old male patient is brought to the Accident and
Emergency department with acute abdominal pain. He
Please check your eBook at https://studentconsult.inkling.com/ for more self-assessment questions. See inside cover for
registration details.
8
Airflow
e
−PP
R
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Respiratory System
INTRODUCTION
Components
e respiratory system is composed of:
• Nasal passages.
• Olfactory system.
• Conducting airways:
• nasopharynx
• larynx
• trachea
• bronchi
• bronchioles
• respiratory portions of the lung (alveoli).
Function
e functions of the respiratory system include:
• cleaning of inhaled air
• warming or cooling of inhaled air
• moistening of inhaled air
• respiratory gas exchange
• facilitation of olfaction and sound production.
Airway Function
e airways have three main functions:
• passage of inhaled gases
• protection against inhaled foreign material
• warming and humidication of inhaled gases.
• Passage of inhaled gases:
• the ow of gases depends on the pressure gradient
between the atmosphere and the alveoli
AlveoliAtmospher
(V )
=
V: rate of airow
P: pressure
R: resistance
• the smooth muscle within the bronchi and bronchioles can inuence airow
• bronchoconstriction, under parasympathetic control, leads to an increase in resistance (R) and thus a
decrease in airow
• bronchodilatation, under sympathetic control, leads
to a decrease in resistance (R) and thus an increase in
ai row.
• Protection against inhaled foreign material:
• inhaled air is ltered by the nasal hairs
• any particles passing through the nose become
trapped on the mucus coating the airways
• motile cilia lining the airways transport the mucus to
the pharynx, where it is swallowed
• the epiglottis closes during swallowing, thus preventing food matter from entering the airways
• if any food matter is inhaled, it stimulates a reex
cough that will expel the material.
• Warming and humidifying gases:
• as inhaled air passes through the respiratory system, it is warmed and saturated with water vapour;
this produces a water vapour pressure of 6.3 kPa
(47 mmHg) at 37°C.
MECHANICS OF VENTILATION
Pulmonary Ventilation
• At the beginning of inspiration the intrapleural pressure
is around −4 cmH2O.
• Contraction of the respiratory muscles increases the
volume of the chest; this decreases the intrapleural pressure to about −9 cmH2O.
• e change in intrapleural pressure causes the lungs
to expand, and thus generates a negative intra-alveolar
pressure as the alveoli are pulled open.
• As the atmospheric pressure is higher and air ows
from high to low pressure, air is inhaled (approximately 500 mL air during quiet ventilation).
• During exercise, other accessory muscles of respiration
are used and can generate more negative intrapleural
pressures, i.e. −30 cmH2O. Pressures of this magnitude
can lead to the inhalation of 2–3 L of air.
186
CHAPTER 8 Respiratory System
Inspiration
Pressure (cmH
O) Pressure (cmH
O)
Expiration
Volume (mL)
–20
187
• Expiration is a passive process due to the elastic recoil of
the chest wall.
• During exercise, contraction of internal intercostals and
abdominal muscles can generate intrapleural pressures
as high as +20 cmH2O to expel air more rapidly.
Lung Pressures (Fig. 8.1)
• ere are three forces acting on the lung:
• elastic nature of the lungs: under normal conditions
the lungs are stretched; this results in a force that
pulls inwards on the visceral pleura
• surfactant: lines the alveoli and exerts an inward or
collapsing pressure
• negative intrapleural pressure: opposes the above
two forces. is negative pressure is created by
the chest wall and diaphragm pulling the parietal
pleura outwards. As the two layers of pleura are
pulled in opposite directions, they generate a negative pressure.
• e pressure in the alveoli equals the atmospheric
pressure as they are both in direct contact via the airways; atmospheric pressure is zero and the intrapleural
4.0
3.5
3.0
Volume (L)
A
2.5
+2
Fig. 8.1 Graphs demonstrating the relationship bet-
ween (A) lung volume, (B) intrapleural, and (C) intraalveolar pressure during normal quiet respiration.
(From McGeown JG. Physiology, 2nd edn. Churchill
Livingstone, Edinburgh, 2000, with permission.)
0
–10
–2
–4
–6
–8
+1
0
–1
2
B
2
C
pressure is between −4 and −9 cmH2O. is produces
the transmural or transpulmonary pressure; it is this
that keeps the lungs distended.
Surfactant and Surface Tension (Fig. 8.2)
• Phase 1: it takes a considerable pressure increase before
there is a change in volume.
• Phase 2: expansion of the lung is proportional to the
increase in pressure.
• Phase 3: maximum capacity.
• Phase 4: in the initial stage the lung volume is maintained
until the pressure has fallen considerably (approximately
8 cmH2O).
• e unequal pressure needed to maintain a given
lung volume in inspiration and expiration is called
hysteresis.
• Surfactant is a phospholipid-rich detergent produced
by type II alveolar cells; it coats the luminal surface of
alveoli and produces a force called surface tension.
• Surface tension is present at all air–uid interfaces.
• Surface tension occurs because water molecules are
attracted more to each other than they are to gas molecules. When any liquid surrounds a gas, i.e. in the alveolus, this produces an inward pressure.
• Lungs inated with normal saline do not exhibit hysteresis; there is no air–uid interface, so there is no surface
tension; the only force opposing expansion is the elasticity of the lung parenchyma.
Inflation with
saline
200
150
100
50
0
0 –10
Phase 4
Phase 1
Pressure (cmH2O)
Fig. 8.2 Graph illustrating the differences in compli-
ance between the lungs inflated with air and the lungs
inflated with saline. The greater compliance in salinefilled lungs is explained by the lack of surface tension.
Inflation with
air
Phase 3
Phase 2
188
∆
T
r
Co
mL/cmHO
=
∆
100
2
Volume above FRC (L)
0.5
2
–10
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SECTION II Physiology
• In air-inated lungs the surface tension at the air–uid
interface opposes expansion; surface tension accounts
for almost two-thirds of the elastic recoil of the lungs.
• Surfactant has several other functions:
• by lowering the surface tension, surfactant increases
compliance and reduces the work of breathing
• prevents uid accumulating in the alveoli
• reduces the tendency of alveoli to collapse (alveolar
instability).
• Alveolar instability is related to changes in alveolar
diameter and can be explained by the law of Laplace:
0.4
0.3
0.2
0.1
Expiration
Compliance
Inspiration
• As alveoli decrease in size, the radius (r) will tend to
• As the alveolar radius decreases, then the concentration
Compliance (Fig. 8.3)
• Compliance is the ease with which the lungs can be
• Two principal factors govern compliance:
• Normal lungs have high compliance as the elastic tis-
• Conditions which decrease compliance include:
P ∞
ΔP: alveolar distending pressure
T: surface tension
r: radius
increase (assuming surface tension [T] remains constant). If surfactant were not present, this would mean
that pressure would be greater in small alveoli and lower
in larger alveoli; this would result in collapse of the alveoli as air moves from the smaller to the larger alveoli.
of surfactant increases and thus reduces surface tension
(T). erefore, surface tension and radius increase or
decrease in tandem and this results in very little change
in alveolar pressure.
inated:
mpliance
=
=
∆VP
500
5
cmHO
mL
2
ΔV: change in volume
ΔP: change in pressure
↑ compliance means lungs are easy to expand.
↓ compliance means lungs resist expansion.
• elasticity of the lung parenchyma
• surface tension.
sue is easily stretched and surfactant reduces surface
tension.
• scarring or brosis of lung parenchyma
0
–1 –2 –3 –4 –5 –6 –7 –8 –9
Pressure (cmH
O)
Fig. 8.3 Pressure–volume curve for a single respi-
ratory cycle. It represents the volume change if the
work of respiration was against elastic resistance
only. To the right of the compliance line represents
the additional pressure required to overcome airflow
resistance and other resisting forces. To the left of the
compliance line is the work required during passive
expiration. (From Pocock G & Richards CD. Human
Physiology: The Basis of Medicine, 2nd edn. Oxford
University Press, Oxford, 2004, with permission.)
• pulmonary oedema
• deciency of surfactant, e.g. premature babies
• decreased lung expansion, e.g. respiratory muscle
paralysis
• supine position
• mechanical ventilation (due to reduced pulmonary
blood ow)
• age
• breathing 100% O2.
• Conditions which increase compliance include:
• emphysema (due to destruction of elastic bres in
the lung parenchyma).
Respiratory Muscles
See Anatomy section (Chapter 1).
Work of Breathing (Fig. 8.4)
• Work of breathing is the work required to move the lung
and chest wall.
• During inspiration, work consists of two components:
• work needed to overcome the elastic forces of the
chest wall and lungs
• work needed to overcome non-elastic forces of the
chest wall and lungs.
CHAPTER 8 Respiratory System
1.0
resistance, friction and
189
Work against
elastic
elements
X
Volume above FRC (L)
2 0 –2 –4 –6 –8 –10
A
Change in pressure (cmH2O)
Y
Work against airways
inertia
X = Work of
expiration
X + Y = Work of
inspiration
• Non-elastic forces include:
• airway resistance (most signicant)
• frictional forces
• inertia of the air and tissues.
• One-third of airway resistance occurs in the upper airways
– nose, pharynx and larynx. is can be greatly reduced
by breathing through the mouth (e.g. during exercise).
• Two-thirds of the resistance is in the tracheobronchial
tree, mainly in the medium-sized bronchi (high ow but
low cross-sectional area).
• Resistance in the terminal bronchioles is very low due to
the high cross-sectional area.
• Resistance falls as the volumes of the lungs increase;
1.0
X
Y
the elastic parenchyma pulls open bronchioles and thus
resistance decreases.
Regional Variations in Ventilation (Fig. 8.5)
• In the upright position the lung is not evenly ventilated;
the upper parts are not ventilated as well as the lower
parts.
• ere are two reasons to explain this:
Volume above FRC (L)
• the weight of the lungs
• the compliance curve is sigmoid, and the upper and
lower parts of the lung lie on dierent parts of this
2 0 –2 –4 –6 –8 –10
B
Change in pressure (cmH
O)
2
curve.
• Transpulmonary pressure is the dierence between the
intrapleural pressure and the alveolar pressure.
• During phase 1, when the lung volume is near resid-
1.0
C
X
ual volume, the compliance is low, thus it takes a large
change in pressure to cause a change in volume.
• In phase 2, the compliance is at its maximum and lung
volume increases linearly with an increase in pressure.
• In phase 3, the compliance falls as the lungs become
fully expanded.
• e lower parts of the lungs lie on the diaphragm and
Volume above FRC (L)
are compressed, whereas the upper parts are already
stretched by their own weight; therefore, ination begins
further along the pressure–volume curve.
2 0 –2 –4 –6 –8 –10
C
Change in pressure (cmH
O)
2
Fig. 8.4 (A) Graph demonstrating the work of respira-
tion. The increasing volume above functional residual
capacity (FRC) is plotted against the change in intrapleural pressure. The work of inspiration is greater than
expiration. Energy for expiration is from the stretching of elastic lung tissue. (B) The increased pressure
required to move an equal volume of air with reduced
lung compliance. (C) The increased resistance to expiration and increased energy required to expire a similar volume of air in a patient with increased airways
resistance. (From Pocock G & Richards CD. Human
Physiology: The Basis of Medicine, 2nd edn. Oxford
University Press, Oxford, 2004, with permission.)
Clinical Physiology
Pneumothorax
ere are a number of types of pneumothorax:
Spontaneous (primary) pneumothorax
• Occurs in young males. e cause is unknown; there is
rarely any associated respiratory disease. Occasionally
the patient has Marfan’s syndrome with an associated
apical pleural bleb.
Spontaneous (secondary) pneumothorax
• Occurs in patients due to underlying respiratory pathology; causes include:
• asthma
• chronic obstructive pulmonary disease (COPD)
190
100
Transpulmonary pressure
% Lung volume
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SECTION II Physiology
90
80
70
60
50
40
30
20
10
FRC
0
X
0 15 30
V
P
V
P
O
cmH
2
Fig. 8.5 Pressure–volume curve for lung inflation and its influence on the distribution of ventilation during
inspiration from functional residual capacity (FRC).
• cancer
• lung abscess.
Traumatic (closed) pneumothorax
• Iatrogenic, e.g. mechanical ventilation or lung biopsy.
• Non-iatrogenic, e.g. stab wound or road trac
accident.
Tension pneumothorax
• A pneumothorax occurs when air enters the pleural
space due to the disruption of either the visceral (ruptured pleural bleb) or parietal pleura (stab wound).
• e air entering the pleural space leads to loss of the
negative intrapleural pressure and thus the lung collapses; this is the type of pneumothorax seen in spontaneous and traumatic closed pneumothoraces.
• In a tension pneumothorax the lung injury may form
Pulmonary Assessment
Lung Volumes (Table 8.1)
• Lung volumes can be measured using a spirometer.
• e denition of each lung volume is as follows:
• tidal volume (TV): the air taken in and exhaled during quiet breathing
• inspiratory reserve volume (IRV): the maximum volume
of air that can be inspired in excess of normal inspiration
• expiratory reserve volume (ERV): the maximum
amount of air that can be forcefully expired aer
normal expiration
• functional residual capacity (FRC): the volume of
gas le in the lungs aer expiration during normal
breathing
a valve in which air leaks into the pleural cavity during inspiration but closes during expiration; this leads
to a positive intrapleural pressure (can be as high as
20 cmH2O), and pushes mediastinal structures into the
opposite side of the chest.
Open pneumothorax or ‘sucking’ chest wound
• In an open pneumothorax there is a defect in the
chest wall, e.g. due to a gunshot wound; this allows
intrathoracic pressure to equalize with atmospheric
pressure. If the defect is greater than two-thirds of
the diameter of the trachea then air will preferentially
enter through the hole in the chest wall as this is the
path of least resistance; this leads to impaired ventilation and hypoxia.
TABLE 8.1 Values for Respiratory
Variables in a Healthy Adult Male
Lung Volume Value (L)
Total lung volume 6.0
Vital capacity 4.8
Residual volume 1. 2
Tidal volume 0.5
Functional residual capacity 2.2
Inspiratory capacity 3.8
Expiratory reserve volume 1. 0
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