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Respiratory Alterations and Management 365

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risk factor for the development of COPD. Continued
Overlap of bronchitis, emphysema and asthma
within chronic obstructive pulmonary disease smoking accelerates the decline of respiratory function in
(COPD) susceptible individuals. 71,72 However, less than 15% of
smokers actually develop clinically-significant COPD 68,73,74
suggesting that other factors are also involved, including
Chronic environmental and occupational pollutants, genetic pre-
bronchitis Emphysema disposition, hyper-responsive airways and respiratory
infections. 68,75-79 Disease progression in susceptible indi-
viduals is most likely to be dependent on the synergistic
effects of these factors.
COPD
Ventilation abnormalities in COPD result from airway
inflammation, bronchoconstriction, increased mucus
Airflow secretion and oedema. Perfusion abnormalities arise
from hypoxic-induced vasoconstriction of the capillary
obstruction
beds. Pulmonary ventilation/perfusion (V/Q) abnormali-
ties, and hyperinflation contribute to increased pulmo-
nary vascular resistance (PVR), and respiratory muscle
fatigue. Increased PVR and hypoxaemia require the
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heart’s right side heart to work harder, over time resulting
Asthma in hypertrophy, remodelling and cor pulmonale. 81,82 The
incidence of right ventricular hypertrophy approximates
40% for patients with moderate levels of COPD (i.e. FEV 1
This non-proportional Venn diagram shows the overlap of chronic 60
bronchitis, emphysema and asthma within COPD. Chronic <1000 mL). The left ventricle may also be compromised
bronchitis, airway narrowing and emphysema are independent by hyperinflation, which generates an increased work
effects of cigarette smoking, and may occur in various of afterload. Heart disease is therefore a frequent
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combinations. Asthma is, by definition, associated with reversible concomitant condition with COPD 84-86 (see Chapter 11
airflow obstruction. Patients with asthma whose airflow obstruction
is completely reversible do not have COPD. In many cases it is for further discussion). Impaired ventilation and perfu-
impossible to differentiate patients with asthma whose airflow sion leads to hypoxaemia and mechanical dysfunctions,
obstruction does not remit completely from persons with chronic with the primary cause of adverse lung mechanics being
bronchitis and emphysema who have partially reversible airflow hyperinflation.
obstruction with airway hyperreactivity.
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Hyperinflation has two components: static and dynamic.
FIGURE 14.2 Overlap between asthma, emphysema and bronchitis. Loss of elastic recoil (static hyperinflation) and incom-
60, p. S10
plete expiratory airflow (dynamic hyperinflation) leads to
expert guidelines 60,61 depict this overlap between condi- air trapping and a reduced inspiratory capacity. 87,88 The
tions. It is not uncommon for people with an obstructive effects of incomplete and prolonged expiration accounts
lung disease to share clinical characteristics for more than for increased work of breathing, dyspnoea and reduced
one respiratory condition, although the dominant clini- exercise tolerance experienced by people with COPD. 89-95
cal symptom is usually indicative of the underlying con- Severity of COPD promotes hyperinflation of the lungs,
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dition. It is however important to differentiate between and hyperinflation is a catalyst for hypoventilation. 96
COPD and asthma as they have different management COPD is also a systemic condition that has an effect on
and illness trajectories. 56
the skeletal muscles, the intercostals and diaphragm. 97-99
PATHOPHYSIOLOGY Bloodflow is diverted from lower limb muscles to meet
the oxygen requirements of these respiratory muscles; a
Asthma is a complex syndrome influenced by genetic and phenomenon referred to as circulatory steal. Use of
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environmental factors. Altered airway physiology and supplemental oxygen to hypoxaemic patients with
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airway wall remodelling in asthma are consequences of COPD has been found to reduce dynamic hyperinflation,
inflammatory processes. While initial symptoms can dyspnoea and improve exercise tolerance; 88,97 reduce
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occur at any age, most patients exhibit episodes of wheez- PVR; 76,86,100 reduce ventilatory requirements and circulat-
ing and obstruction before the age of six. 65,66 The increas- ing lactate levels. The systemic limitations that arise
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ing incidence of disease burden in children may be with COPD are therefore profound and complex. These
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attributable to a greater awareness and diagnosis of the inter-relationships are illustrated in Figure 14.3.
condition, with the overall differences in global preva-
lence now becoming less. 67 CLINICAL MANIFESTATIONS
In contrast, COPD is a systemic, permanent and progres- With asthma and COPD, a patient may present with
sive condition with a number of mechanisms involved in wheeze, cough and/or dyspnoea. History and physical
its development. Smoking is the cardinal risk factor and assessment are fundamental to determining the severity
continuation is the most significant determinant for of presentation. Presence of diminished or silent breath
disease progression. 60,68 The concept of ‘pack years’ is sounds, central cyanosis, an inability to speak, an altered
used to quantify smoking, and is independent of whether level of consciousness, an upright posture and diaphore-
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an individual is a current or reformed smoker. A history sis indicate a life-threatening case. Chest pain or tight-
of more than 20 pack years of smoking is a significant ness may be present. Underestimation of severity is