Respiratory insufficiency is the failure of the lung to perform at an optimal level. When we breathe, we inhale oxygen for energy and exhale carbon dioxide (CO2). Obviously, we obtain oxygen from the environment, but how does the CO2 get there? Well, CO2 is produced as a waste byproduct of cellular respiration, where cells use incoming oxygen for the conversion of biochemical energy from nutrients, and produce CO2, which needs to be eliminated from the body. We achieve this through exhalation.
“The respiratory system is concerned with the delivery of an adequate amount of oxygen to and elimination of a corresponding amount of carbon dioxide from the cells of the body and maintenance of normal acid-base balance in the body. Proper supply of oxygen and elimination of carbon dioxide from various tissues of the body depends on the optimal functioning of various parts of the respiratory system like chest wall and respiratory muscles, airways and lungs, CNS (including medullary respiratory centers), spinal cord, CVS, and endocrine system. A disorder in any portion of these systems can lead to respiratory failure. During respiratory failure, there is an inability to keep the arterial blood gases at normal level, while breathing air at rest at sea level, and the partial pressure of oxygen is usually below 60 mmHg with or without partial pressure of carbon dioxide above 49 mmHg in arterial blood.”1
“The respiratory system can be said to consist of two parts: the lung, i.e. the gas-exchanging organ, and the pump that ventilates the lungs. The pump consists of the chest wall, including the respiratory muscles, the respiratory controllers in the central nervous system (CNS) and the pathways that connect the central controllers with the respiratory muscles (spinal and peripheral nerves). Failure of each part of the system leads to a distinct entity (fig. 1). In general, failure of the lung caused by a variety of lung diseases (e.g. pneumonia, emphysema and interstitial lung disease) leads to hypoxaemia with normocapnia or hypocapnia (hypoxaemic or type I respiratory failure). Failure of the pump (e.g. drug overdose) results in alveolar hypoventilation and hypercapnia (hypercapnic or type II respiratory failure). Although there is coexistent hypoxaemia, the hallmark of ventilatory failure is the increase in Pa, CO2. Undoubtedly, both types of respiratory failure may coexist in the same patient, as, for example, in patients with chronic obstructive pulmonary disease (COPD) and carbon dioxide retention, or in those with severe pulmonary oedema or asthmatic crisis, who first develop hypoxaemia and, as the disease persists or progresses, hypercapnia appears.”2
The cardiovascular system is the one responsible for distributing oxygen molecules to all systems, as well as transporting diluted CO2 in the blood to the lungs for exhalation. Hence, by measuring the levels of both O2 and CO2 in the blood, physicians can tell when there is an imbalance of gases. Respiratory insufficiency is an alteration that affects the exchange of gases, where oxygen (O2) levels in the blood drop dramatically while the levels of carbon dioxide (CO2) increase.
The causes are extremely varied. As a general characteristic, the patient begins to feel tired and short of breath. It can also present slight sweating and a bluish coloration in different areas of the skin. Other symptoms include high blood pressure along with an increase in heart beats per minute (bpm).
“A history, physical examination and investigations are required to identify the underlying disease process causing the acute respiratory failure. A full review of the presentation of all the underlying causes is beyond the scope of this article. Careful clinical examination and blood gas analysis will assist in diagnosis of the underlying condition by identifying the type of respiratory failure. Type I respiratory failure – patients with type I respiratory failure usually have impaired gas exchange with a low Pa O2, a low functional residual capacity (FRC) and reduced pulmonary compliance. Minute ventilation increases in response to lung juxta-capillary receptor stimulation, metabolic acidosis and severe hypoxaemia, reducing the Pa CO2. There is a mechanical advantage to breathing rapidly, with small tidal volumes when the lungs have are stiff and the FRC is reduced. Patients with type I respiratory failure are therefore hypoxic, hypocarbic and tachypnoeic, and take small breaths. Type II respiratory failure – patients with pure ventilatory failure are hypercarbic and hypoxic, with a low respiratory rate although patients with neuromuscular disease or chest wall injury may be tachypnoeic with small tidal volumes. They may experience extreme dyspnoea before their blood gases deteriorate. Mixed respiratory failure – the two types of respiratory failure may occur together to produce a mixed picture.
Pulmonary parenchymal disease will initially cause acute hypoxaemic respiratory failure, because of V/Q mismatch and shunt. As a result of the increased work of breathing (due to reduced pulmonary compliance), the respiratory muscles then become fatigued and ventilatory failure develops. Arterial Pa CO2 rises, giving a picture of mixed respiratory failure. Ventilatory failure may also be complicated by the development of pulmonary parenchymal disease. These patients often have a poor cough, are unable to take a deep breath and are at risk from retained secretions, alveolar collapse and nosocomial infection. A reduced level of consciousness, with exhaustion and hypercapnia, also increases the risk of aspiration pneumonitis.”3
We can differentiate two types of respiratory insufficiency:
- Acute: The disorder develops in a short period of time. Symptoms appear spontaneously and severely.
- Chronic: In this case, the disease progresses gradually throughout the patient’s life.
The triggers of this disorder vary depending on the subtype of insufficiency that the patient presents.
Acute Respiratory Insufficiency
“Acute Respiratory Failure (ARF) was defined as the inability of the respiratory system to exchange gases and to oxygenate the blood adequately. We can distinguish two mechanisms at the basis of ARF: 1. Failure in pulmonary ventilation (pump failure); 2. Failure in gas exchanges (lung failure). The first one is due to neuromuscular diseases, chest wall deformities, obstructive pulmonary diseases.
The second mechanism (mismatch in blood gas exchanges) is due to the following different pathologies:
- Adult acute respiratory distress syndrome;
- Neonatal respiratory distress syndrome;
- Acute cardiogenic pulmonary edema;
- • Severe status asthmaticus;
- • Pneumonia;
- • Airspace collapse (atelectasis);
- • Pulmonary embolism.
The clinical signs and symptoms of patients with ARF, refer to the two main manifestations of pulmonary diseases: arterial hypercapnia and hypoxemia. The pathophysiology of hypercapnia is based on four main mechanisms: Increase in CO2 production (for instance, parenteral feeding with high doses of carbohydrates; high body temperature, etc.) Deterioration in gas exchanges as the increase in alveolar death space ventilation (for instance in Chronic Obstructive Pulmonary Disease – COPD –, because of mismatch in ventilation/perfusion ratio, and in pulmonary embolism); Deterioration in respiratory mechanics that involves a huge effort, an increase in respiratory work and the development of a rapid shallow breathing ↑ CO2; Alteration in the mechanism of control of the ventilation (for instance, in chronic hypercapnia, we observe a decrease in ventilatory drive with an increase in tolerance threshold to CO2; it happens in metabolic alkalosis too).
The hypoxemia is due to different pathophysiological mechanisms:
- Alteration in gas diffusion;
- Mismatch in ventilation/perfusion ratio;
- Pulmonary shunt.
Which are the clinical signs and symptoms of hypoxemia and hypercapnia? The first one shows with shortness of breath, tachycardia, mental confusion, changes of personality, restlessness, cyanosis, hyper/hypotension, arrhythmias and palpitations. Hypercapnia, instead, shows with sleepiness, mental confusion, cephalea, convulsions, arrhythmias, miosis, papilledema, peripheral vasodilation, hypotension and coma. The first goal of the initial diagnostic evaluation is to understand the underlying causes, and so to do differential diagnosis among all pathologic conditions that showed the most important clinical symptom of this illness: dyspnea.”4
Causes of Acute Respiratory Insufficiency
May appear if the patient has any of the following problems:
- Sleep apnea. During this complication, the person stops breathing for a variable period of time while sleeping. As a general rule, being overweight is a risk factor because the chest is burdened with that extra weight, especially when the patient is in a horizontal position. “Sleep involves a complex pattern of physiological processes which, though felt to be restorative and beneficial in nature, may also have potential adverse effects, particularly in subjects with underlying disease. One of the main areas of interest in sleep physiology has been the control of respiration, due largely to the discovery of a defect of respiratory control during sleep, namely sleep apnea. This condition is now recognized to be very common, affecting 1–4% of adults. However, it has also long been recognized that sleep may have adverse effects on respiration and gas exchange in patients with underlying disease, and such patients may develop profound hypoxemia during sleep, which may predispose to nocturnal death”5
- Crisis of asthma. “Severe asthma, although difficult to define, includes all cases of difficult/therapy-resistant disease of all age groups and bears the largest part of morbidity and mortality from asthma. Acute, severe asthma, status asthmaticus, is the more or less rapid but severe asthmatic exacerbation that may not respond to the usual medical treatment. The narrowing of airways causes ventilation perfusion imbalance, lung hyperinflation, and increased work of breathing that may lead to ventilatory muscle fatigue and life-threatening respiratory failure.”6
“Asthma is a chronic inflammatory disease of the airways. Patients with asthma are predisposed for developing exacerbations, leading to respiratory failure. Recognizing patients at risk, careful assessment, and rapid institution of appropriate treatment is of paramount importance for favorable outcome.”7
- “Bronchitis is an inflammation of the bronchial tubes, causing excessive swelling and mucus production. Cough, increased expectoration of sputum and shortness of breath are the main symptoms of bronchitis. Bronchitis can be either acute or chronic. Acute bronchitis is caused by the same infection that causes the common cold or influenza and lasts about few weeks. Chronic bronchitis is defined as a cough that occurs every day with sputum production that lasts for at least 3 months 2 years in a row. Second-hand environmental tobacco smoke (ETS), malnutrition, overcrowding, reduced ventilation, lack of fresh running water, wood smoke, and obesity are known risk factors for bronchitis”8
- Trauma or injury that affects the lungs or any part of the respiratory system in any way.
- Excessive consumption of toxic substances such as alcohol, drugs, or tobacco.
- Alveolar alterations. There are certain viral infections that can modify the membrane of these functional units.
- Inhalation of liquids and foreign bodies that obstruct the bronchi or bronchioles.
- Cardiovascular problems related to blood clots, emboli or myocardial failure.
Chronic Respiratory Insufficiency
It can develop for a number of different reasons. The main one is from a chronic consumption of tobacco, alcohol, and other toxic substances. Asthma, tuberculosis, pulmonary emphysema (destruction of the walls that conform the alveoli), surgical interventions, and infections can all cause chronic respiratory insufficiency. Infections can be particularly tricky because they can make their way into the patient’s spinal cord, creating complications of the nervous system. For example, paralysis and atrophy of different muscles, including involuntary muscles involved in gas exchange in the lungs.
Respiratory insufficiency can also be the result of pulmonary fibrosis. In this case, the tissue that forms the lungs begins to deteriorate, but instead of healing by the development of normal lung cells, it’s substituted by fibrous processes instead. This modification produces alterations in the normal breathing of the patient.
Treatment may vary depending on the underlying cause. For acute respiratory insufficiency, oxygen therapy is administered in the most serious clinical cases. Whereas in chronic respiratory insufficiency, the use of medications is usually recommended along with the application of oxygen. “The rationale behind supplemental oxygen in the acute setting has been to increase oxygen delivery to the ischemic heart, brain, or other organs. In the hypoxemic patient (hypoxemia defined as oxygen saturation >90%), this approach seems reasonable. However, most of the patients today are not hypoxemic at baseline, and supplying oxygen therapy to normoxemic patients (normoxemia defined as oxygen saturation ≥90%) may not only be unnecessary but might even involve risks.”9
There are many causes of respiratory failure, so the patient’s treatment is always personalized and it is intended to act on the process responsible for the disease. This way, it’s very possible to improve the symptoms and the quality of life in an effective way.
(1) Singh, C. P., Singh, N., Singh, J., Brar, G. K., & Singh, G. (2001). Oxygen therapy. Journal, Academy of Clinical Medicine, 2(3), 178. Available online at http://medind.nic.in/jac/t01/i3/jact01i3p178.pdf
(2) Roussos, C., & Koutsoukou, A. (2003). Respiratory failure. Respiratory Journal, 22(47 suppl), 3s-14s. Available online at https://pdfs.semanticscholar.org/cf19/560384127f47cc44c2dc9719db1004bc50f1.pdf
(3) Gunning, K. E. (2003). Pathophysiology of respiratory failure and indications for respiratory support. Surgery (Oxford), 21(3), 72-76. Available online at http://m-learning.zju.edu.cn/G2S/eWebEditor/uploadfile/20121022112355188.pdf
(4) Forte, P., Mazzone, M., Portale, G., Falcone, C., Mancini, F., & Silveri, N. G. (2006). Approach to respiratory failure in emergency department. European review for medical and pharmacological sciences, 10(3), 135. Available online at https://www.europeanreview.org/wp/wp-content/uploads/382.pdf
(5) McNicholas, W. T. (1997). Impact of sleep in respiratory failure. European Respiratory Journal, 10(4), 920-933. Available online at https://www.researchgate.net/publication/14068888_Impact_of_sleep_in_respiratory_failure
(6) Soubra, S. H., & Guntupalli, K. K. (2005). Acute respiratory failure in asthma. Indian Journal of Critical Care Medicine, 9(4), 225. Available online at http://www.bioline.org.br/pdf?cm05035
(7) Papiris, S., Kotanidou, A., Malagari, K., & Roussos, C. (2001). Clinical review: severe asthma. Critical Care, 6(1), 30. Available online at https://www.ncbi.nlm.nih.gov/pubmed/11940264
(8) Karunanayake, C., Rennie, D., Ramsden, V., Fenton, M., Kirychuk, S., Lawson, J., … & Dosman, J. (2017). Bronchitis and Its Associated Risk Factors in First Nations Children. Children, 4(12), 103. Available online at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5742748/
(9) Hofmann, R., & James, S. K. (2018). Routine Oxygen Supplementation in Acute Cardiovascular Disease: The End of a Paradigm?. Circulation, 137(4), 320-322. Available online at https://www.ahajournals.org/doi/pdf/10.1161/CIRCULATIONAHA.117.031664