Pneumology: difference between type 1 and type 2 respiratory failure
To fully understand the differences between type 1 and type 2 respiratory failure, we must first start with some simple basics of human physiology
The respiratory system is the set of organs and tissues deputed to breathing, the term ‘breathing’ being understood to mean the incessant action that the bronchi and lungs perform in transferring a sufficient amount of oxygen (O2) present in the air we breathe to the blood (air is made up of about 20% oxygen and about 80% nitrogen, while the amount of carbon dioxide is insignificant), which is carried to all the body’s cells by the network of blood vessels and capillaries, while at the same time eliminating the excess carbon dioxide (CO2) produced in the course of the cells’ metabolic processes from the blood in an inverse pathway to oxygen.
Respiratory insufficiency is therefore defined as the inability of the respiratory system to remain effective in carrying out this dual exchange of respiratory gases, namely oxygen in one direction and carbon dioxide in the other.
Any condition or disease that prevents an adequate supply of oxygen to the blood and cells (hypoxia), with or without a simultaneous adequate elimination of carbon dioxide (hypercapnia), causes respiratory insufficiency.
How many types of respiratory failure are there?
Taking into account what was said earlier, two types of respiratory failure are recognised:
- Pure hypoxaemic respiratory failure (type I): corresponds to oxygen deficit in arterial blood only (partial pressure of O 2 in arterial blood less than 60 mmHg) with normal carbon dioxide (CO2)
- Hypoxaemic-hypercapnic respiratory failure (type II): corresponds to the simultaneous presence of an O2 deficit associated with an excess of CO2 in arterial blood (partial pressure of CO2 in arterial blood greater than 45 mmHg)
Depending on the time it takes for respiratory insufficiency to develop, a distinction is made:
- Acute respiratory failure: corresponds to the onset of respiratory failure with sudden onset in a subject with hitherto normal respiratory function
- Chronic respiratory insufficiency: corresponds to the presence of respiratory insufficiency that has been persistently present for some time in patients with chronic respiratory diseases capable of causing it. Both hypoxaemia and hypercapnia are often present in association.
- Acute on chronic respiratory insufficiency: this corresponds to an aggravation of a chronic respiratory insufficiency that can no longer be compensated for by oxygen therapy and ongoing drug therapy due to an occasional aggravation of the already present chronic respiratory disease caused by an additional acute infectious or inflammatory condition.
What are the causes of respiratory insufficiency?
Countless causes can be responsible for respiratory insufficiency.
The simple presence of an oxygen deficit in the air breathed, as happens for example by breathing air at high altitude with an oxygen content even much lower than that usually present at lower altitudes, is sufficient to generate acute respiratory insufficiency, which is why climbers are used to supplementing the oxygen content intended for the lungs by breathing in oxygen from pressurised oxygen cylinders in a mask.
Any suffocation crisis (accidental inhalation of a foreign body in the respiratory tract, homicidal suffocation, paralysis or functional insufficiency of the respiratory muscles due to curare-based poisons or neuro-muscular diseases, etc.) results in the interruption of the correct supply of oxygen to the blood and the adequate elimination of CO2, and consequently becomes a cause of hypoxaemic and hypercapnic acute respiratory failure (type II).
Many diseases of the bronchi, lungs and pleura are the source of acute and chronic respiratory failure and can be said to be the final outcome of almost all respiratory diseases in the final stages of severity of their natural course.
What are the consequences and symptoms of respiratory failure?
Respiratory failure can lead to severe functional impairment of all organs, progressing over time to the death of the affected individual.
Such damage is secondary to:
- insufficient amount of O2 in the blood (hypoxemia), with difficulties in concentration, attention and memory and ideational and cognitive deterioration, easy fatigability, dyspnoea, cyanosis, increased respiratory rate, nausea, lack of appetite and anorexia, weight loss and loss of muscle mass, development of pulmonary hypertension with increased respiratory discomfort and right heart failure, hyperglobulia (increased blood viscosity), leading to hypoxic coma
- excess CO2 (hypercapnia), which tends to accumulate to the point of becoming toxic to the body, initially leading to headache on awakening, reddened eyes and psychic and motor slowdown, tremors and muscle tremors, to worsen to coma in more advanced stages (as hypercapnic)
How is the diagnosis made?
Suspicion of respiratory failure is confirmed by performing a simple test called arterial haemogasanalysis, which consists of taking arterial blood from an artery in the wrist.
This makes it possible to determine the amount of the two gases O2 and CO2 present in the arterial blood and to make a diagnosis of insufficiency based on the criteria outlined above (O2 < 60 mmHg – CO 2 > 45 mmHg).
Alternatively, and only for oxygen deficiency (it is not possible with this method to measure CO2), it is possible to measure the amount of oxygen present in the blood by measuring haemoglobin saturation with an instrument called an oximeter or saturation meter, by simply attaching a dedicated clamp to the patient’s finger without having to take blood.
The advantage of this measurement lies in its practicality and the possibility of carrying out the check even at the home of the patient undergoing oxygen therapy.
What is oxygen therapy?
The therapy of respiratory insufficiency obviously consists of treating the many diseases that cause it or removing the acute causes that lead to it.
In relation, however, to changes in O2 and CO2 in arterial blood alone, it includes:
- type I respiratory insufficiency therapy (O2 deficiency only): this consists of oxygen therapy, i.e., the administration of compressed pure medical oxygen (99.9%) through nasal cannulae (CN) at a flow rate set by the pulmonary specialist, or with a Ventimask-type facial mask with a variable and adjustable O2 percentage as required. The advantage, compared to administration through nasal cannulae, is that in this way the percentage of oxygen in the gas mixture inhaled by the patient is perfectly known, which is impossible to determine with administration through nasal cannulae. As an alternative to compressed gaseous oxygen, it is possible to use liquid oxygen, which can deliver much smaller volumes of gaseous oxygen than the volumes of compressed oxygen (more convenient to transport and manage at home). The quantity, timing during the day and overall duration of oxygen therapy are determined by the pulmonologist, especially with regard to the proper management of long-term home oxygen therapy (O2-LTO) in patients with chronic respiratory diseases (COPD, pulmonary emphysema, pulmonary fibrosis, lung cancer treated at home, etc.). The patient requires careful monitoring of the amount of oxygen to be administered and scheduled specialist checks aimed at the correct management of the numerous practical and clinical problems that oxygen therapy entails, including those arising from imperfect humidification of inhaled oxygen, increased susceptibility to respiratory infections in treated patients (pneumonias) and the risk of a dangerous increase in CO2 in the patients.
- type II respiratory insufficiency therapy (O2 deficiency associated with excess CO2): this consists of the use of special ventilators for non-invasive ventilatory therapy (NIV), capable of avoiding recourse to the patient’s orotracheal intubation, associated with all that has already been described with regard to oxygen therapy.
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