Respiratory failure is one of the common reasons for majority of the ICU admissions. Usually, these conditions act as a pointer to either an underlying condition in the patient's body, which is being complicated by the lungs failing, or as a primary problem of the lungs itself.

Let's assume that we have a 54-year-old gentleman with a week’s history of high grade fever with chills, and progressively worsening breathlessness. Physical examination reveals that he is febrile, has a high respiratory rate, is unable to finish his sentences, and has fine crepitations over the lower lobe of right lung; investigations show high white blood cell count, low oxygen levels on the arterial blood gas analysis, and a chest X-Ray showing a consolidated patch in the lower zone of the right lung.

This is the typical picture of pneumonia. But what we need to focus on here is his arterial blood gas report.

Low arterial oxygen levels (PaO2) with normal levels of carbon dioxide (PaCO2).

This is the defining criteria for Type-1 Respiratory Failure.

In order to understand how this happens, let's try and look at how gas exchange occurs in the alveoli.

When we inspire, air from the atmosphere, predominantly containing nitrogen and oxygen, reaches the alveoli in our lungs. This inspired air, interacts with the blood across the alveolar membrane, which is made up of alveolar epithelial cells and the capillary endothelium. The oxygen from the inspired air attaches to the hemoglobin inside the RBC while the carbon dioxide does the opposite journey and eventually gets expired out to the atmosphere; all this by simple diffusion across the alveolar membrane, within the blink of the eye.

This is when everything is normal; but in the setting of any disease, like pneumonia or in any other condition affecting the membrane separating this blood-gas interface, like acute respiratory distress syndrome (also known as hyaline membrane disease) or an interstitial lung disease like hypersensitivity pneumonitis, this gas exchange is compromised. We will be able to inspire normally, but since there is a pathology in the area where the actual exchange of gases occur, the oxygen doesn’t get transferred to the hemoglobin; this is reflected by low PaO2 levels.

This, however, isn’t the case with the carbon dioxide that is brought to the lungs via the blood. By nature, carbon dioxide is a highly permeable gas; so this thickened interface doesn't make a difference. CO2 diffuses across and gets expelled out of the lungs by the act of expiration; thus there is a normal level of carbon dioxide (PaCO2) in cases of type-1 respiratory failure.

The deoxygenated blood flowing to the lung to get oxygenated fails to get oxygenated; goes back to the systemic circulation in the deoxygenated state, producing the so called “physiological shunt phenomenon”, which essentially forms the basis of all problems in Type-1 Respiratory Failure.

The premise of Type-1 Respiratory Failure is that the physical act of respiration is normal, so that with every breath, the carbon dioxide gets expired out and doesn’t stay long enough at the blood-gas interface to interact with the hemoglobin any further.

But there are conditions where the act of breathing itself is impaired, as in hypoventilation due to obesity or neuromuscular diseases like Guillain-Barre syndrome. The retained carbon dioxide diffuses back to circulation producing hypoxemia (low PaO2) and hypercarbia (elevated PaCO2); this is Type-2 Respiratory Failure.

When there is atelectasis, or collapse of the alveoli, there is a reduction in the effective area available for respiration which compromises the amount of oxygen entering circulation; carbon dioxide being an easily diffusible gas, as explained earlier, doesn't build up. So there is low PaO2 and normal PaCO2; this is seen very commonly in patients who have undergone a surgical procedure under general anesthesia; this is called “Perioperative Respiratory Failure” or Type-3 Respiratory Failure. This is a self-limiting condition and such patients respond very well to positive pressure ventilation and conservative measures like physiotherapy.

The muscles used for respiration are diaphragm, the intercostal muscles and the accessory muscles like the sternocleidomastoid and the scalenes. In quiet breathing, inspiration is the active process, and expiration is passive, brought about by the elastic recoil of the lungs.

Normally, 5% of our cardiac output (about 250ml/min) is required for these muscles. In conditions where there is hypoperfusion to these muscles; either due to increased demand (as a result in increased work of breathing, thus involving the accessory muscles) or reduced supply to these muscles (in cases of hypovolemic shock), a picture similar to Type-2 Respiratory Failure develops; this is Type-4 Respiratory Failure. Treatment of this involves supportive measures to reduce the work of breathing while treating the cause of the hypoperfusion.

Why does this assume importance?

Respiratory failure, unless identified promptly and managed, can lead to unwarranted complications; while giving enough time for us and the patient to treat the cause. All it requires is 2ml of an arterial blood sample, a functioning and calibrated ABG analyser, a little bit of clinical acumen and lot of common sense.