Asbestosis is a chronic lung disease which leads to long-term respiratory complications and is caused by the inhalation of asbestos fibres. Symptoms due to long exposure to asbestos usually appear 10 to 40 years after initial exposure and include shortness of breath, cough, weight loss, clubbing of the fingers and chest pain. Typical chest X-ray findings include diffuse lung infiltrates that cause the appearance of shaggy heart borders.

The diaphragm and external intercostals are muscles of inspiration as they increase the volume of thoracic cavity and reduce the intrathoracic pressure. Muscles of expiration include abdominal muscles and internal intercostals.

Acute (or adult) respiratory distress syndrome (ARDS) is a life-threatening lung condition characterised by a non-cardiogenic pulmonary oedema that leads to acute respiratory failure. The most common risk factors for ARDS include trauma with direct lung injury, sepsis, pneumonia, pancreatitis, burns, drug overdose, massive blood transfusion and shock. Acute onset of dyspnoea with hypoxemia, anxiety and agitation is typical. Chest X ray most commonly demonstrates bilateral pulmonary infiltrates. Histological changes include the exudative, proliferative and fibrotic phase. ARDS is mainly a clinical diagnosis.

Pulmonary embolism (PE) is a blockage of an artery in the lungs by an embolus that has travelled from elsewhere in the body through the bloodstream. The change in cardiopulmonary function is proportional to the extent of the obstruction, which varies with the size and number of emboli obstructing the pulmonary arteries. The resulting physiological changes may include pulmonary hypertension with right ventricular failure and shock, dyspnoea with tachypnoea and hyperventilation, arterial hypoxaemia and pulmonary infarction. Consequent alveolar hyperventilation is manifested by a lowered pa(CO2). After occlusion of the pulmonary artery, areas of the lung are ventilated but not perfused, resulting in wasted ventilation with an increased ventilation/perfusion ratio – the physiological hallmark of PE – contributing to a further hyperventilatory state. The risk of blood clots is increased by cancer, prolonged bed rest, smoking, stroke, certain genetic conditions, oestrogen-based medication, pregnancy, obesity, and post surgery.

Acidosis with high p(CO2) and normal standard bicarbonate indicates respiratory acidosis, commonly seen in acute worsening of COPD patients. Respiratory acidosis occurs due to alveolar hypoventilation which leads to increased arterial carbon dioxide concentration (p(CO2)). This in turn decreases the HCO3 –/p(CO2) and decreases pH. In acute respiratory acidosis, the p(CO2) is raised above the upper limit of normal (over 45 mm Hg) with a low pH. However, in chronic cases, the raised p(CO2) is accompanied with a normal or near-normal pH due to renal compensation and an increased serum bicarbonate (HCO3 – > 30 mmHg).

According to Bohr’s equation, VD/VT = (pA(CO2) − pE(CO2))/pA(CO2), where pE(CO2) is mixed expired CO2 and pA(CO2) is alveolar CO2pressure. Normally, the pa(CO2) is virtually identical to pA(CO2). Thus, VD/VT = (pa(CO2)) − pE(CO2)/pa(CO2). By Fowler’s method, VD/VT= 0.25. In the given problem, (pa(CO2) − pE(CO2)/pa(CO2) = (40 − pE(CO2)/40 = 0.25. Thus, pE(CO2) = 30 mmHg. If there is a great perfusion/ventilation inequality, pE(CO2) could be significantly lower than 30 mm Hg, and the patient’s physiological dead space would exceed the anatomical dead space.

In patients suspected of having chronic obstructive pulmonary disease, pulmonary function testing (PFT) is useful to confirm airway obstruction, to quantify its severity and reversibility, for following disease progression and monitoring response to treatment. These tests include:

FEV1 – volume of air forcefully expired during the first second after a full breath

Forced vital capacity (FVC) – total volume of air expired with maximal force and flow-volume loops. The hallmark of airway obstruction is reduction of FEV1, FVC and the ratio of FEV1/FVC, with a concave pattern in expiratory tracing on the flow-volume loop. FEV1 and forced vital capacity (FVC) are easily measured with office spirometry and are useful to assess the severity of disease. Other parameters include increased total lung capacity, functional residual capacity and residual volume, which can help distinguish chronic obstructive pulmonary disease (COPD) from restrictive pulmonary disease where these values are lower than normal. Along with these, other tests are decreased vital capacity; and decreased diffusing capacity for carbon monoxide (DLCO). DLCO is non-specific and can be low in other disorders that affect the pulmonary vascular bed, such as interstitial lung disease. DLCO is however useful to distinguish COPD from asthma, in which DLCO is normal or elevated.

Pulmonary functional residual capacity (FRC) is = volume of air present in the lungs at the end of passive expiration.

Obstructive diseases (e.g. emphysema, chronic bronchitis, asthma) = an increase in FRC due to an increase in lung compliance and air trapping.

Restrictive diseases (e.g. pulmonary fibrosis) result in stiffer, less compliant lungs and a reduction in FRC.

Acute or adult respiratory distress syndrome (ARDS) is a reaction to several forms of lung injuries and is commonly associated with sepsis and SIRS (systemic inflammatory response syndrome), severe traumatic injury, severe head injury, narcotics overdose, drowning, pulmonary contusion, and multiple blood transfusions. There is an increase in risk due to pre-existing liver disease or coagulation abnormalities. It results due to indirect toxic effects of neutrophil-derived inflammatory mediators in the lungs. ARDS is defined by the 1994 American–European Consensus Committee as the acute onset of bilateral infiltrates on chest X-ray, a partial pressure of arterial oxygen (pa(O2)) to fraction of inspired oxygen Fi(O2) ratio of less than 200 mmHg and a pulmonary artery occlusion pressure of less than 18 or the absence of clinical evidence of left arterial hypertension. ARDS is basically pulmonary oedema in the absence of volume overload or poor left ventricular function. This is different from acute lung injury, which shows a pa(O2)/Fi(O2) ratio of less than 300 mmHg. Pathogenesis of ARDS starts from damage to alveolar epithelium and vascular endothelium, causing increased permeability. Damage to surfactant-producing type II cells disrupts the production and function of pulmonary surfactant, causing micro atelectasis and poor gas exchange. There is a decrease in lung compliance and increase in work of breathing. Eventually, there is resorption of alveolar oedema, regeneration of epithelial cells, proliferation and differentiation of type II alveolar cells and alveolar remodelling. Some show resolution and some progress to fibrosing alveolitis, which involves the deposition of collagen in alveolar, vascular and interstitial spaces.

To determine compliance of the respiratory system, changes in transmural pressures (in and out) immediately across the lung or chest cage (or both) are measured simultaneously with changes in lung or thoracic cavity volume. Changes in lung or thoracic cage volume are determined using a spirometer with transmural pressures measured by pressure transducers. For the lung alone, transmural pressure is calculated as the difference between alveolar (pA; inside) and intrapleural (ppl; outside) pressure. To calculate chest cage compliance, transmural pressure is ppl (inside) minus atmospheric pressure (pB; outside). For the combined lung–chest cage, transmural pressure or transpulmonary pressure is computed as pA – pB. pA pressure is determined by having the subject deeply inhale a measured volume of air from a spirometer. Under physiological conditions the transpulmonary or recoil pressure is always positive; intrapleural pressure is always negative and relatively large, while alveolar pressure moves from slightly negative to slightly positive as a person breathes.