Common Respiratory Conditions

Chronic Obstructive Pulmonary Disease (COPD)

This condition is a common cause of death and disability in the UK.


  • Shortness of breath- this is typically worse on exertion, of a prolonged duration, and worsens over time. In advanced stages the breathlessness is present even at rest and it is this which can result in a poor quality of life for those affected.
  • Cough- a chronic cough is often the first symptom to occur. Its presence for more than three months a year for more than two years, along with increased sputum production is often used as a definition for chronic bronchitis.
  • Sputum- the amount of sputum can change over hours to days.

The prime cause of COPD is smoking. Of those who smoke approximately 20% will develop COPD and if you are a lifelong smoker this increases to about 50%. Women are more susceptible to the effects of smoke than men.

Air pollution such as that from poorly ventilated cooking fires leading to indoor air pollution are one of the most common causes of COPD in developing countries. Those living in large cities have a higher rate of COPD compared to those in rural areas.

Prolonged exposure to workplace dusts, chemicals and fumes increase the risk of COPD.





Due to the large number of alveoli and their pocket like structure the normal healthy lung as a very large surface area across which diffusion of gases can occur. If the lung were to be spread out this is often compared to the size of a tennis court.

The smoking and pollutants in the lung cause inflammation, which then causes the release of elastases, an enzyme which breaks down the elastic fibres within the lung. This causes reduction of the elastic fibres in the bronchioles and the alveoli, which makes the airways narrower causing obstruction and reduces the surface area in the alveoli.

The loss of elasticity also has a another consequence on the lung. In the normal lung there is a constant balance between the elastic fibres pulling the lung inwards and the chest wall pulling the lung outwards. If those elastic fibres are damaged there is less force pulling the lung inwards so the balance has changed.

This means that the total lung capacity will increase resulting in a barrel chest, hyperinflation and a flattened diaphragm on chest x-ray.



In order to diagnose COPD spirometery is used. This technique can measure the volumes of air in the lungs.

Forced vital capacity (FVC) is the total amount of air that the patient can expire in one breath.

Forced expiratory volume in one second is the volume of air that can be expired over this period of time and is commonly referred to as FEV1.

These two values help develop the ratio as shown;

FEV1/FVC      ratio = 0.70

So if you cannot exhale more than 70% of your forced vital capacity in one second then you are considered to have some obstructive disease.

The lower the FEV1 the worse the obstruction.

Low oxygen levels and, eventually, high carbon dioxide levels in the blood can occur from poor gas exchange due to decreased ventilation from airway obstruction, hyperinflation and reduced desire to breathe.




Reversible airway obstruction.


  • Breathlessness
  • Tight chest
  • Wheezing
  • Attacks triggered by exercise, exposure to allergens and other triggers
  • Coughing, particularly at night and early morning.




 The smooth muscle in the bronchioles is served by two types of receptors, beta receptors which cause smooth-muscle relaxation and muscarinic receptors which cause smooth-muscle contraction.

Asthma has many known “triggers,” including physical exertion, allergens, medications, occupational infection, emotions and stress.

In response to contact with a triggering substance or mechanism, mast cells of the immune system, which are found in loose connective tissue, are responsible for releasing vasoactive (action on vessels) chemical mediators, including histamine, bradykinin, leukotrienes, cytokines and prostaglandins.

These target the respiratory system and cause bronchoconstriction, vascular congestion, vasodilation, increases in capillary permeability, mucosal oedema, impaired mucociliary action (removal of mucus and contaminants within the bronchial tree by movement of the cilia inside the bronchioles), and increased mucus production, which leads to an increase in airway resistance.

Mucus plugging may also occur in the smaller bronchioles. These pathophysiologic factors produce the typical clinical presentation of asthma, including wheezing and respiratory distress.



Acute Respiratory Distress Syndrome (ARDS)

Acute, or adult respiratory distress syndrome is where injury has occurred to the lung which then causes increased permeability of pulmonary micro- vasculature causing leakage of fluid across the alveolar capillary membrane.

The inflammatory agents, such as cytokines injure both the epithelium and endothelium of the lung. These inflammatory insults can occur locally in the lung (primary ARDS) or be part of a systemic inflammatory syndrome (secondary ARDS).

The consequences for the patient are initially a severe oxygenation defect, reduced lung compliance, bilateral pulmonary infiltrates, leak of protein rich oedema fluid in interstitial and air spaces in the acute phase and more chronically

XRAY ARDS can result in persistent low lung compliance and increasing dead space ventilation, extensive pulmonary fibrosis, obliteration of normal alveolar architecture and widespread emphysema and discreet bullae.

The current consensus requires these three to exist:

  • Acute onset: 20-50% of acute lung injury patients will develop ARDS within seven days.
  • CXR shows bilateral infiltrates.
  • Refractory hypoxaemia: acute lung injury is present when the ratio PaO2:FiO2 <300; ARDS is present when PaO2:FiO2 <200.


The most common risk factors include;

  • Sepsis
  • Massive trauma with shock and multiple transfusions
  • Hypovolaemic shock
  • Pneumonia
  • Gastric aspiration.


Pneumonia is usually caused by an infection either by viruses or bacteria. It can also be caused by certain drugs and some autoimmune diseases. It is an inflammatory condition affecting the alveoli in the lungs.



A combination of physical signs and a chest x ray. Symptoms as in the above diagram. On examination there may be added crackles when listening to the chest with increased dullness on percussion. Chest x ray may show increased opacities over the affected area, however this is not always present.


Pulmonary Embolism


This is a clot in one of the blood vessels running through the lungs. These clots can originate from any other part of the body but often come from the deep veins in the legs, commonly referred to as deep vein thrombosis.


This clot travels around the body and when it enters the veins in the lung becomes lodged in one of them as they become smaller. This means that the veins beyond the clot are denied any blood, preventing gas exchange from taking place in those areas.

This clot in the pulmonary vasculature will also cause a back pressure making its way back to the right side of the heart which will then lead to some of the other symptoms of a P.E.

Signs and symptoms

 Shortness of breath.

Chest pain.


Circulatory instability

Low grade temperature

Raised JVP.



 After consideration of the other signs and symptoms and the possibility of risk factors the diagnosis of pulmonary embolism is often based upon scoring systems such as the Wells score.

 The Wells score

  • clinically suspected DVT — 3.0 points
  • alternative diagnosis is less likely than PE — 3.0 points
  • tachycardia (heart rate > 100) — 1.5 points
  • immobilization (≥ 3d)/surgery in previous four weeks — 1.5 points
  • history of DVT or PE — 1.5 points
  • heamoptysis — 1.0 points
  • malignancy (with treatment within 6 months) or palliative — 1.0 points

The presence of a deep vein thrombosis can be confirmed using ultrasound on the suspected limb and the presence of a pulmonary embolism can be confirmed using CT pulmonary angiography.





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