A Synopsis of Respiratory Diseases

156 Pages·1964·2.984 MB·English

by  J. Smart (Auth.)

A SYNOPSIS OF
RESPIRATORY DISEASES
BY
J. SMART
M.A., M.D., F.R.C.P.
Physician, London Chest Hospital, Brompton Hospital, and Connaught Hospital
BRISTOL: JOHN WRIGHT & SONS LTD.
1964
© JOHN WRIGHT & SONS LTD., 1964
PRINTED IN GREAT BRITAIN BY
JOHN WRIGHT & SONS LTD., AT THE STONEBRIDGE PRESS, BRISTOL
PREFACE
THE late Dr. Letherby Tidy's Synopsis of Medicine was a book
which was written in note form covering all medical subjects, and
was particularly useful to students and postgraduates, enabling
them to obtain in a concentrated form the essential features of
medical conditions, including differential diagnoses. Since his
death the work of revision of the book was found to be difficult
for one person to undertake in view of the rapid advances in
certain branches of medicine. The publishers therefore felt that
it would be wiser to republish in the form of a series of books
dealing with various subjects.
In A Synopsis of Respiratory Diseases I have maintained the
original character of Dr. Letherby Tidy's synopsis, that is to say,
it is largely written in note form and reduced to a minimum.
Where the book was accurate the original text has been main-
tained, and this includes, particularly in tuberculosis, the acute
type of case which is seldom seen in this country, including the
differential diagnoses. These have been retained because such
cases are still quite common in other parts of the world and the
diagnosis, prognosis, and differential diagnoses are still important.
A completely new chapter on 'Pulmonary Physiology' and the
conception of the basic principles of this subject is introduced as
this is essential to the understanding of pulmonary diseases.
There is also a brief section referring to congenital lesions which
had not previously been mentioned.
No radiograph reproductions have been included because of
the difficulty of illustrating adequately the various conditions
without showing many radiographs, but a few diagrams have
been introduced to demonstrate some of the important features
which, it is hoped, will be of value to the reader.
January, 1964 J. SMART
A SYNOPSIS OF
RESPIRATORY DISEASES
CHAPTER I
PULMONARY PHYSIOLOGY
In recent years the importance of pulmonary physiology in the
understanding of chest diseases has been recognized. This chapter
has therefore been included although it does not deal with any
disease process within the lungs.
Essential Function of the Lungs.—To absorb 0 from
2
atmosphere; transfer to haemoglobin; eliminate CO from
a
blood.
Transfer of Gases.—
1. VENTILATION.—Maximum breathing capacity was test
originally used, but this found to be difficult in dyspnoeic
patients. Tiffneau curve therefore introduced as measure
of ventilation, patient giving one 'blow' only. From this
the one-second forced expiratory volume (F.E.V.) and the
forced vital capacity (F.V.C.) can be measured and volume
of air expired in 1 sec. expressed as percentage of total
F.E.V. percentage. Normal F.E.V. percentage = 75-80 per
cent of F.V.C. In bronchitic patients both fall, F.E.V. falling
much more rapidly than F.V.C, F.E.V. percentage often
being only 30-35 per cent. In dyspnoea due to cardiac
disease F.E.V. and F.V.C. fall together, F.E.V. percentage
remaining approximately normal (60 per cent or over). In
pulmonary fibrosis and allied conditions both figures may
fall, but ratio always normal. Alternative simple test using
Wright's Peak Flow Meter—figure obtained from this is the
peak velocity of expired air, figure correlating approxi-
mately with F.E.V.
2. MIXING OF GASES.-—Smaller bronchioles and alveoli not
ventilated by breathing, gaseous exchange taking place
by mixing of gases. Rate can be assessed by breathing
air with 10 per cent helium in a closed circuit. If volume in
container and lung volume known, then rate of mixing of
gases can be determined by estimating time taken for
percentage of helium in closed circuit to fall to steady
figure.
2 PULMONARY PHYSIOLOGY
Transfer of Gases, continued
Note,—This test satisfactory in people with normal
lungs, but unsatisfactory in dyspnoeic patients because of
different rate of ventilation in various parts of lungs, serial
reading therefore not giving same result.
Uneven distribution of inspired air to alveoli (more to
some, less to others) may contribute to respiratory
insufficiency. The pulmonary nitrogen emptying rate is the
simplest test of this. Patient breathes 100 per cent O for
a
7 min., then breathes out forcefully and nitrogen concentra-
tion in last portion of expired air is measured. Normally
this should contain less than 2-5 per cent nitrogen.
Ventilation uneven if nitrogen concentration much above
this.
3. DIFFUSION OF GASES.—Diffusion of gases from alveoli
into blood-stream and Hb difficult to estimate, depending
on difference of partial pressure of gases in alveoli and
blood-stream, thickness of mucous membrane and alveoli.
4. VENTILATION PERFUSION RATIO.—By this is meant
the relationship between alveolar ventilation and capillary
blood-flow to alveoli. If alveolar ventilation poor and
circulation in capillaries good, desaturation occurs. If this
involves a number of alveoli, hyperventilation is unable
fully to saturate blood, because unsaturated and saturated
blood will be meeting in pulmonary vein.
Note.—Ventilation perfusion ratio may vary in different
parts of lung.
Because of difficulty in estimating mixing of gases within
lungs, diffusion of gases through mucous membrane, and
ventilation perfusion ratio, a simple test which approxi-
mates to the summation of those mentioned above can be
used, i.e., the carbon monoxide diffusion capacity test This
entails patient breathing air from a gasometer with non-
return valve containing known percentage of CO, expired
air being collected in a Douglas bag. Volume of air
inspired, time taken, and CO percentage in Douglas bag are
measured. From these figures the percentage of CO taken
up is estimated. CO having a solubility similar to that of
0 can be used in this way to record O uptake as there is
2 a
no pCO in blood. The driving force is difference between
pCO in inspired gas and pCO in expired gas.
Blood Gas Analysis.—
1. OXYGEN SATURATION = content/capacity. Arterial
blood is taken, O content and capacity estimated by van
z
Slyke or Haldane method. Normal arterial saturation
= 96 per cent. Important factor is partial pressure of 0
2
as this is the force which drives 0 through tissues. At
2
PULMONARY PHYSIOLOGY 3
96 per cent saturation (normal) = 88 mm. Hg; at 90 per
cent = 64 mm. Hg; at 80 per cent = 45 mm. Hg; at 70 per
cent = 37 mm. Hg.
2. ARTERIAL BLOOD pC0.—This is measured directly
2
from arterial blood, or indirectly by measuring pC0 in
2
alveolus, which is equivalent to that of mixed venous blood
(Campbell rebreathing method). Arterial pC0—6-7 mm.
2
Hg—lower than that of mixed venous blood, this amount
being subtracted from alveolar ^?C0. Normal pC0 =
2 2
35-45 mm. Hg.
Control of Respiration.—Rate and volume of respiration con-
trolled by two factors: (1) Arterial O level; (2) CO level.
a a
Anoxia will always cause increase in volume and rate of
respiration by stimulating carotid body, to which patient
does not become acclimatized. Increased C0 level causes
2
increase in rate and volume of respiration, but gradual
increase in C0 level does not change rate or volume of
2
respiration, as patient becomes acclimatized to slowly rising
C0 level.
2
Examples of Evaluation of Dyspnoea by Physiological
Means.—
1. CHRONIC BRONCHITIS AND EMPHYSEMA.—
VENTILATION.—F.E.V. very low. F.V.C. low. Ratio: often
down to 30-35 per cent.
ARTERIAL SATURATION.—Normal until disease advanced,
then under 90 per cent. May fall steeply with acute
respiratory infection.
pC0.—High normal or raised.
2
2. HEART FAILURE.—
VENTILATION.—F.E.V. low. F.V.C. low. Ratio: reduced to
approx. 60 per cent.
ARTERIAL SATURATION.—Slightly reduced, over 90 per cent.
pC0.—Normal.
2
3. INTERSTITIAL FIBROSIS.—
VENTILATION.—F.E.V. low. F.V.C. low. Ratio: normal.
ARTERIAL SATURATION.—Reduced, approx. 90 per cent.
pC0.—Low, due to hyperventilation in attempt to improve
2
arterial saturation, which results in 'blowing off' of C0.
2
Differential Lung Function.—0 absorption per minute, tidal
2
volume, and vital capacity of each lung obtained by passing
a catheter, such as a Carlen's double catheter, which separates
air coming from the two lungs (Fig, 1). Two tubes from
catheter connected to recording spirometer, one opening of
catheter being 3 cm. shorter than other, the longer being
curved so that tip automatically passes into left main
bronchus. Small rubber cuff close to tip inflated so that
gases from left lung pass up tube. Further rubber cuff above
4 PULMONARY PHYSIOLOGY
Differential Lung Function, continued
opening of second catheter, at lower end of trachea, blown up,
thus excluding trachea, hence gases from right lung pass up
other catheter. From tracing obtained, O absorption,
a
ventilation, and vital capacity of each lung demonstrated.
Br
Fig. 1.—Carlen's catheter. A, Opening of double catheter.
Bu Opening of catheter into trachea. B2, Opening of catheter into
left main bronchus. Clt Tracheal cuff. C2, Left main bronchial
cuff. D, Tubes for inflating cuffs. E, Hook which engages over
carina enabling catheter to be correctly positioned blindly.
MODERN TECHNIQUES IN PHYSIOLOGY OF THE
LUNG.—By mass spectrometry function of each lobe can
be assessed. Fine sampling tube passed into each lobe,
continuous record then taken of gases within lobes. Partial
pressure of 0 , C0 , and N recorded. Ventilation assessed
2 2
by use of inert gas, such as argon.
PULMONARY PHYSIOLOGY 5
RADIOACTIVE GASES.—Radioactive O and CO have been
a a
used experimentally in differential lung function. One
breath of radioactive gas inhaled; rate of elimination
estimated by Geiger counters placed over each lung, first
at apex then at base. This gives function of upper and
lower zones of each lung, rate of clearance being associated
with ventilation and pulmonary artery blood-flow.
Physiological Events leading to CO2 Narcosis.—Occurs in
chronic bronchitis when pulmonary reserve low and ventila-
tion poor, resulting in low arterial saturation, approx.
80-85 per cent, and high pC0, over 60 mm. Hg. Inter-
2
current infection causes ventilatory obstruction which in
turn reduces pulmonary reserve with further fall of arterial
saturation, often to 70 per cent or less. Anoxia causes increase
in respiration rate, which prevents further rapid increase in
pC0 despite reduced pulmonary function. If O given for
2 a
relief of anoxia, arterial 0 saturation rises, stimulus to
2
respiration thereby being removed. Respiration rate and
volume fall, CO consequently retained. CO may rise to a
a a
level sufficient to produce coma.
Physiological Events leading to Cor Pulmonale.—Sequence
to chronic bronchitis and emphysema, which give rise to
poor ventilation and pulmonary function with low arterial
saturation and raised pC0. Associated with this, increased
2
resistance in pulmonary vascular bed resulting in (1) unequal
capillary perfusion, (2) impaired diffusion capacity, (3)
pulmonary hypertension. Intercurrent infections lead to
further reduction in arterial saturation, thus increasing
respiration rate and depth, resulting in increase in 'work
done' because of rapid breathing and further obstruction to
ventilation caused by recent infection. It has been calculated
that 0 required for increase in respiratory 'work' often
2
exceeds 0 absorbed by increased ventilation, O saturation
2 a
thereby falling further, hence vicious circle established.
Increased 'work' of respiration, high pulmonary pressure,
and increased resistance in pulmonary vascular bed associ-
ated with marked cardiac anoxia result in congestive failure.
Acute Respiratory Failure.—Tracheostomy, with or without
controlled respiration, has become recognized way of treating
acute respiratory failure over last 10 years. To understand
this form of treatment, subject will be discussed under
headings of: (1) Causes; (2) Indications; (3) Care of the
patient; (4) Types of ventilators.
1. CAUSES.—
a. Interruption of nervous control of respiration, e.g.,
poliomyelitis.
6 PULMONARY PHYSIOLOGY
Acute Respiratory Failure—Causes, continued
b. Damage to thoracic cage preventing adequate ventilation,
e.g., crush injury of chest.
c. Bronchitis and emphysema with gross impairment to
ventilation, with big physiological dead space.
2. INDICATIONS.—
a. Neurological conditions, poliomyelitis, head injuries,
myasthenia gravis, polyneuritis, encephalomyelitis,
encephalitis.
b. Trauma, especially crush injuries of chest causing multiple
rib fractures, whereby portion of chest becomes flail,
giving rise to contra-selective movements.
c. Acute medical emergencies—neurological conditions as
above, tetanus, status epilepticus, amyotonia congenita
(rare).
d. Major surgical cases—some cardiac cases, removal of
thymus for myasthenia gravis.
e. Acute and chronic pulmonary lesions—treatment of these
patients usually involves tracheostomy, but with acute
failure supervening on chronic failure, i.e., chronic
bronchitis and emphysema, value not yet fully deter-
mined. Treatment by Bird's respirator should be first
attempted.
3. CARE OF THE PATIENT.—
a. Constant nursing care required, therefore specialized unit
necessary.
b. Blood gas analysis, fluid intake and output, control of
electrolytes, humidification of inspired gases, antibiotics
to combat infection, sedatives.
c. Frequent bronchial lavage and sucking out of secretions
with sterile catheter, often every 20 min.
d. Deglutition often disturbed and feeding by Ryle's tube
necessary.
e. Physiotherapy to remove tenacious mucus and secretions
from bronchi.
/. Psychological aspect important—reassurance.
4. TYPES OF VENTILATORS.—
a. Bird's Respirator—simple triggered respirator whereby O
a
and air mixture blown in as soon as patient starts to
inspire to a predetermined pressure. Only suitable in
early stages when patient conscious and co-operative.
Intravenous nikethamide and aminophyllin give in-
creased depth of respiration and relieve bronchial spasm.
b. Volume Cycled Respirator—designed to give known
volume of air or O and air at predetermined rate. Not
a
controlled by patient, particularly suitable for neuro-
logical group and chest injuries.
PULMONARY PHYSIOLOGY 7
c. Pressure Cycled Respirator—designed to deliver air or 0
2
and air up to a certain pressure as opposed to a known
volume, either automatically or triggered so that change
in pressure as patient inspires activates respirator.
More complex machine, not suitable if patient cannot
breathe, i.e., neurological cases and flail chest.
d. Combination of types (b) and (c)—recent modifications
have produced mechanical ventilator in which both
these processes can be combined. This may prove to
be superior.
With all mechanical respiration, volume of air must be
adequate. For average adult, ventilation should be at
least 8 1. per min. Pressure must be controlled so that
lung is not underventilated, which may give rise to
collapse of segments, not overventilated, which may
damage alveoli. Pressure usually necessary = approx.
16-20 cm. water.