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Applied Medicine
Clinical Examination and
Applied Medicine
Pulmonology Series
Volume II
Mushtaq Haroon
10 9 8 7 6 5 4 3 2 1
Keywords
history taking; respiratory examination; pulmonary clinical examination;
bedside assessment; pulmonary diseases; chest diseases; lung diseases;
pulmonology images; COPD; asthma; X-ray chest; pulmonary func-
tions; ABG; pulmonary investigations; pulmonary infections; chest dis-
eases; interstitial lung disease; tuberculosis; pulmonary embolism; pleural
diseases; lung tumor; obstructive airway disease; restrictive airway disease
Contents
Forewordxiii
Prefacexv
Acknowledgmentsxvii
TopicsPage
Section I 1
Pulmonary Investigations 1
Arterial Blood Gases (ABG) 4
Normal Values for ABG 5
Summary of Acid-Base Disturbances 6
Blood Gas Values and Nomenclature 7
Academia and Alkalemia 7
Metabolic and Respiratory Compensation 7
Simple Acid-Base Disturbance and Compensation 8
Examples of Mixed Acid-base Disturbances 8
Respiratory Acidosis 8
Respiratory Alkalosis 9
Metabolic Acidosis 11
Metabolic Alkalosis 12
Hypoxemia in Relation to the A-a Gradient 13
Pulmonary Function Tests (PFTs) 13
Common Indication of PFT 14
Types of PFTs 14
Utility of PFTs 15
FEV115
Obstructive disorders 16
Restrictive disorders 16
Walking test 17
Pulmonary diffusion capacity 17
Causes of Reduced TLco18
Causes of Increased TLco18
x Contents
Respiratory Failure 18
Section II 21
Radiology Section 21
Normal X-ray chest 21
Sequence of Examination 21
Classification of Opacities 23
Classification of Cavities 23
Causes of Pulmonary Cavitation 23
Simple cavity 23
Classification of Linear Shadows 24
Pulmonary nodules 24
Causes of Pulmonary Nodules 25
Evidence of Benign Nature 26
Evidence of Malignant Nature 26
Honeycombing26
Diffuse Miliary Pattern 27
Some Important X-rays 27
Acute chest syndrome 27
Acute respiratory distress syndrome (ARDS) 28
Aortic aneurysm 29
Aspergillosis30
Azygos lobe 31
Behcet’s disease 31
Bilateral infiltrates 31
Bronchiectasis33
Bronchogenic carcinoma 33
Bronchogenic cyst 34
Bronchopneumonia35
Cardiomegaly35
Cavitary lesions 36
Collapsed lung 38
Diaphragmatic pathologies 38
Emphysema39
Gas Under the Diaphragm 41
Heart failure 42
Hilar shadows 43
Contents xi
Hydatid disease 44
Lung abscess 44
Mediastinal lymphadenopathy 45
Mesothilioma46
Miliary shadowing 47
Pericardial effusion 48
Pleural effusion 49
Unilateral50
Subpulmonic50
Massive52
Pneumonia52
Pneumothorax53
Hydropneumothorax54
Tension pneumothorax 55
Pulmonary alveolar microlithiasis 55
Causes of Pulmonary Calcification 55
Pulmonary edema 56
Bedside chest ultrasound 56
Pulmonary embolism 58
Pulmonary hemorrhage 59
Causes of Diffuse Alveolar Hemorrhage 59
Pulmonary fibrosis 59
Pulmonary nodules 61
Retrosternal goiter 63
Sarcoidosis63
Silicosis65
Tuberculosis66
Latent tuberculosis 67
Section III 69
Picture Quiz, MCQs, with Applied Medicine 69
Acanthosis nigricans 69
Achalasia72
Ankylosing spondylitis 74
Digital clubbing 76
COPD79
Hypoxia and cyanosis 83
xii Contents
Guillain-Barré syndrome 86
Interstitial lung disease 89
Lambert-Eaton myasthenic syndrome 91
Lung abscess 94
Miliary tuberculosis 97
Pulmonary nodules 100
Pancoast tumor and Horner’s syndrome 103
Pectus excavatum 106
Pericardial disease 108
Pleural effusion 111
Pneumococcal pneumonia 114
Pneumonia117
Pott’s disease 121
Pulmonary hypertension 123
Pulmonary nodules 126
Pulmonary sarcoidosis 129
Pulmonary tuberculosis 132
Rheumatoid Lung 136
SLE139
Supraclavicular Lymphadenopathy 141
SVC Obstruction 144
Thoracic outlet syndrome 146
Tracheal Stenosis 149
Tuberculous Lymphadenitis 151
diagrams, figures, and photos has also been included to stimulate under-
standing and learning. As a further stimulus for learning, picture test and
MCQs with brief notes have been added.
The book is not a replacement for standard textbook on the subject,
but it is hoped that it would help the objective of transferring relevant
clinical knowledge with the arsenal to solve bedside problems of patients
efficiently and appear in undergraduate and postgraduate examination.
Dr. Mushtaq Haroon
MBBS (Pb); MCPS (Pak); MRCP (UK)
FRCP (London)
Acknowledgments
I am ever grateful to the Lord almighty, Allah Subhana wa Taala, for
granting me the knowledge and strength to reproduce what I have
learned through my teachers, colleagues, and students of Allama Iqbal
Medical College, Lahore; King Edward Medical University, Lahore; and
Quaid-i-Azam Medical College, Bahawalpur. I have found a conducive
and friendly environment at the Pakistan Kidney and Liver Institute,
Lahore, where I am presently working. The task would never have been
possible without the blessings of the Lord Almighty.
Section I
Pulmonary Investigations
The choice of investigations always depends on the differential diagnosis
and is tailored to the patient’s need. One must seriously question the
need of an investigation if it is not going to help in the diagnosis, assist
in prognosis, or follow-up or alter the management. Therefore, always
consider the cost and the need.
put the patient on BiPAP or ventilator support. A quick look at the pH,
PaCO2, and HCO3 will give good information about the acid base status.
ABG is normally done from the radial, brachial, or femoral artery. The
most dreaded complication of arterial puncture is ischemia distal to the
puncture site. Therefore, a proper evaluation of the site must be performed
before the procedure. After any arterial puncture, the site must be pressed
for more than five minutes. If an arterial sample cannot be obtained from
the radial (severe peripheral vascular disease, active R aynaud’s syndrome,
local infection, or other pathology) site, an alternative source may be
attempted or a venous sample taken. The procedure may be relatively con-
traindicated in severe coagulopathy (INR > 3 or APTT > 100 or platelet <
30,000 cmm) or when streptokinase has just been used.
In acute conditions, the pH correspondingly changes but in chronic
cases, there is respiratory or renal compensation resulting in minimal
change in pH (Figure 1). Any change in the pH primarily due to change in
bicarbonate is called metabolic, where the kidneys are usually responsible.
If a patient has low bicarbonate (metabolic acidosis), with time in chronic
cases, there is respiratory compensation by hyperventilation and lowering
of the pCO2. On the other hand, a patient with high bicarbonate (meta-
bolic alkalosis) with time in chronic cases will have respiratory compensa-
tion by hypoventilation, thus raising the pCO2. In acute metabolic acidosis
or alkalosis, there is more shift in the pH, while in the chronic condition,
the shift is less because it is associated with variable degree of compensation.
6 Clinical Examination and Applied Medicine
Compensatory mechanism of
acid base balance
CO2 HCO3
component.
Anion gap determines the source of acidosis from positive and negative ions.
Anion gap is calculated by (Na + K – {Cl + HCO3}) and is normally 10–15 mEq/L.
4. Upper airway problems: vocal cord and epiglottis problems, foreign body aspiration
5. Lung problems: severe pulmonary embolism and pulmonary vascular disease
There are various types of PFTs that can be ordered according to the
requirement.
Types of PFTs
Spirometry and pulse oximetry
Measurement of lung volumes
Diffusion capacity
Measurement of flow volume loops and maximum respiratory pressures
Exercise testing (e.g., six-minute walk)
Peak expiratory flow rate (PEFR) is the measure of the peak velocity
of air in the first 10 msec as the patient takes a very deep breath and blows
out as hard as possible into the PEFR meter. The measurement depends
on the caliber of the airways and patient cooperation (normal value is
about 4–6 liters/min).
Utility of PFTs
Decreased FEV1/FVC (< 70 percent) is seen in obstructive airway disease.
The ratio of FEV1/FVC (> 90 percent) is increased in restrictive airway diseases.
Increases in TLC and RV suggest hyperinflation (asthma or COPD).
Decreased TLC and VC suggest restrictive lung disease (fibrosis) or loss of lung volume.
Flow rates (FEV1 and PEFR) are diminished in COPD.
Diffusing capacity for carbon monoxide (DLCO) is low in emphysema, restrictive lung
diseases, pulmonary fibrosis, pneumonectomy, pulmonary hypertension, and recurrent
pulmonary emboli. A decrease in hemoglobin by 1 g diminishes DLCO by 7 percent.
DLCO is increased in the supine posture, after exercise, in polycythemia, in obesity, in
left-to-right shunt, and in some patients with asthma.
Maximal voluntary ventilation (MVV) tests airflow through major airways and muscle
strength.
ratio of FEV1/FVC is usually less than 65 percent in such cases (Figure 3).
In diseases that affect the lung parenchyma (restrictive airway diseases),
the airways are normal, the FEV1 is not reduced as much as FVC, the
ratio of FEV1/FVC is usually greater than 90 percent (Figure 3).
FVC
FEV1
Normal FEV1/FVC
200 ratio = 80 Percent
Seconds 1 2 3
FVC FV
FEV1
FEV1
sec. 1 2 3 sec. 1 2 3
TLCO is calculated from KCO and VA (alveolar volume), and a low value
indicates a low KCO and or VA. Cardiac output, hemoglobin level, and
heavy smoking affect KCO directly, and thus, TLCO.
Respiratory Failure
It is the inadequacy of the respiratory system to maintain blood gases and
is diagnosed by doing an ABG study. All such patients should also have
X-ray chest, ECG, pulmonary function tests, and sometimes, echocardio-
gram, but rarely require right heart catheterization.
It may be classified as Type I or hypoxemic, with PaO2 less than 60
mmHg and normal or low PaCO2, or Type II or hypercapnic with PaCO2
greater than 50 mmHg, which is usually associated with hypoxemia as
well. It can further be classified as acute (associated in minutes to hours
with severe metabolic derangements and symptomatic patient) or chronic
(associated over days or weeks with some compensation by the kidneys,
and therefore, milder metabolic changes and less symptomatic patient
who may also have polycythemia and cor pulmonale).
Pulmonary Investigations 19
Type I respiratory failure is more frequent and seen with any acute
pulmonary disease associated with dysfunctional alveoli (e.g., pneumonia
cardiogenic or non-cardiogenic pulmonary edema or ARDS, p ulmonary
hemorrhage, high altitude, pulmonary embolism, atelectasis and pulmo-
nary fibrosis). There is hypoxemia (PaO2 usually less than 60mmHg) with
a normal or low PaCO2 and increased PA-aO2. There is ventilation and
perfusion mismatch or shunt.
In Type II respiratory failure, because CO2 is high, the pH is lowered
in acute conditions and compensated partially or fully by bicarbonate
accumulation in chronic cases. It is usually seen in conditions that effect
the chest wall, neuromuscular disease, drug overdose, and severe airway
disorders like COPD and severe asthma, upper airway obstruction, cen-
tral hypoventilation and obesity hypoventilation syndrome. The PaCO2
is greater than 45mmHg with accompanying hypoxemia and normal
PA-aO2. There is reduction in minute volume and or increased dead space
ventilation.
Type III respiratory failure is associated with perioperative respiratory
problems of increased atelectasis due to low functional residual capacity
(FRC) in the setting of abnormal abdominal wall mechanics. It may be
type I or type II. It is avoided by proper anesthetic or operative technique,
posture, incentive spirometry, proper analgesia and lowering the intra—
abdominal pressure.
Type IV respiratory failure is associated with intubated and ventilated
patients in shock.
Respiratory failure can also be acute, chronic or acute on chronic. On
examination one should look for clinical features of hypoxia and hyper-
carbia (see volume page 167). Investigations involve ABG, X-ray chest,
ECG, echocardiography, pulmonary functions, CT angiography, sleep
study as needed.
Index
A-a gradient, 13 Campylobacter jejuni infection,
ABG. See Arterial blood gas 86–87
Academia, 7 Cardiomegaly, 35
Acanthosis nigricans, 70 Cavitary lesions, 36–37
Achalasia, 72 Cavities, classification of, 23
Acidosis, 7 Central airway obstruction, 149
Acquired unilateral clubbing, 76 Chagas disease, 72
Acrocyanosis, 84 Chest, normal X-ray of, 21
Acute chest syndrome, 27–28 Chronic obstructive pulmonary
Acute respiratory distress syndrome disease (COPD), 78–81
(ARDS), 28–29 Clubbing, 76
Alkalemia, 7 Collapsed lung, 38
Alkalosis, 7 COPD. See Chronic obstructive
Ankylosing spondylitis, 74 pulmonary disease
Aortic aneurysm, 29–30 Cyanosis, 83–84
ARDS. See Acute respiratory distress
syndrome
Diaphragmatic pathologies, 38–39
Arterial blood gas (ABG)
Diffuse alveolar hemorrhage, 59
acid–base balance and
Diffuse military pattern, 27
compensatory mechanisms, 6
Diffusion capacity, 15
acute conditions, 5
metabolic acidosis, 11–12 Digital clubbing, 76–77
metabolic alkalosis, 12–13 DLCO. See Pulmonary diffusion
metabolic and respiratory capacity
compensation, 7 Dressler’s sign, 109
normal values for, 5
overview of, 4–5 Emphysema, 39–41
respiratory acidosis, 8–9
respiratory alkalosis, 9–11 FEV1. See Forced expiratory volume
Aspergillosis, 30 in 1 second
Axial spondyloarthritis, 74 Forced expiratory volume in 1 second
Azygos lobe, 31 (FEV1), 15
Forced vital capacity (FVC), 15
Beck’s triad, 109 FRC. See Functional reserve capacity
Bedside chest ultrasound, 56 Functional reserve capacity (FRC), 15
Behcet’s disease, 31 Funnel chest, 106
Bilateral infiltrates, 31 FVC. See Forced vital capacity
Bronchiectasis, 33
Bronchogenic carcinoma, 33–34 Gas under diaphragm, 41
Bronchogenic cysts, 34 GBS. See Guillain-Barré syndrome
Bronchopneumonia, 35 Gibbus, 121
158 Index