Introduction
Acute respiratory failure (ACR) is a pathological condition in which the external respiratory apparatus cannot provide the body with sufficient oxygen and perform carbon dioxide elimination with average energy expenditure. ACR can shorten lives, so practicing physicians and nurses need a complete understanding of how pathophysiological mechanisms work and how to normalize them. This paper aims to analyze acute respiratory failure concepts that will allow us to recognize the pathology and quickly help the patient.
Pathophysiology of Acute Respiratory Failure
The main pathogenetic factors of external respiration disorders are impaired lung ventilation, impaired diffusion of gases through the alveolar-capillary membrane, impaired pulmonary blood flow, and respiratory regulation. Alveolar hypo- and hyperventilation, pulmonary hypertension, and impaired gas exchange with increased working breathing are commonly considered to be the predominant processes that occur during acute respiratory failure (Swenson, K. E., & Swenson, E. R., 2021). In addition, pulmonary edema in the first stages causes compression and cessation of normal ventilation.
Ventilatory Pulmonary Damage
Alveolar hypoventilation is a decrease in alveolar ventilation per unit time below that the body requires under given conditions. A distinction is made between obstructive and restrictive types of hypoventilation, each of which may be characteristic of ARF depending on the cause of the pathology. The obstructive type is associated with decreased airway patency and increased air resistance (Swenson, K. E., & Swenson, E. R., 2021). As a result, the respiratory muscles are forced to work hard during exhalation and energy expenditure increases. Lung elasticity decreases, hypoxemia, and hypercapnia are observed; blood analysis demonstrates acidosis and a rightward shift in oxyhemoglobin dissociation. Restrictive alveolar ventilation is associated with limitation of lung expansion due to intrapulmonary and extrapulmonary causes. Inflammatory processes develop in the pleura, and hydrothorax and hemothorax occur, which interfere with the average hemoglobin affinity for oxygen (Faverio et al., 2018). Alveolar hypoventilation and hypoxia cause spasms of the arterioles of the small circle of circulation, limiting blood flow through poorly ventilated lung areas and preventing discharge of venous blood in the great cycle.
Alveolar hyperventilation increases the volume of alveolar ventilation per unit time compared to that required by the body under given conditions. It is characterized by hypocapnia and respiratory alkalosis, which leads to a shift of the oxyhemoglobin dissociation curve to the left. Hypocapnia results in decreased excitability of the respiratory center and cerebral vasospasm (Swenson, K. E., & Swenson, E. R., 2021). The damage to the respiratory center is thought to be the major obstacle to the cure of ARF because it mediates nerve plexus lesions.
Inflammation
Inflammatory processes are the main features of irregular breathing regulation in ARF. Inflammatory processes begin immediately after introducing a pathogen that disrupts regular lung tissue activity. It is expressed by receptor binding to pathogens, which serve as danger signals. Through cellular signaling, information is transmitted, and anti-inflammatory processes are triggered, leading to the increased release of cytokines and chemokines (Matthay et al., 2019). As a result of increased production of these mediators, endothelial injury can occur, resulting in worsening lung damage.
Disruption of Respiratory Regulation
Disruption of respiratory regulation develops as a result of increased permeability of the epithelium, which leads to the formation of sticky compounds capable of creating large globules that interfere with the passage of oxygen through the alveoli. The alveolar epithelium is damaged, so there is a decrease in the production of surfactant that would allow the lungs to maintain their elasticity (Swenson, K. E., & Swenson, E. R., 2021). Instead, the lungs become more vulnerable and incapable of eliminating the preceding inflammation. As a result of the fluid clearance of pulmonary edema increased sodium and chloride transport into the interstitium, there is an artificial gradient for water resorption.
Methods of Patient Evaluation
The main clinical manifestations of ARF are hypoxia and hypercapnia; in ventilation disorders and hypoxia without hypercapnia in alveolar-capillary diffusion disorders. ARF developed with insufficient blood supply to tissues due to low cardiac output is manifested by hypoxemia with normo- and hypocapnia (Kassirian et al., 2020). Depending on the severity of pathophysiological shifts, respiratory acidosis develops. The main laboratory tests widely used are blood gas tests and blood pH-metric, oxy- and carbometric monitoring with non-invasive methods. Taking into account the clinical data and additional forms of research, one classifies ARF by severity.
In addition to the laboratory tests, general picture assessment is used: the first clinical symptom of ARF is often the feeling of shortness of breath (dyspnea). Breathing becomes at first deep, then rapid (Fernando et al., 2021). In upper airway obstruction, dyspnea is predominantly aspiratory; in bronchial obstruction, it is expiratory. Depending on whether hypoxemia with hyper- or hypocapnia is observed, there are three stages in which the patient’s condition gradually worsens (Ervin et al., 2020). In combination with hypercapnia, there is hyperexcitability with bilious and crimson body covering and persistent tachycardia. The state is also agitated in various hypocapnia, and convulsions and cyanosis are observed.
Medical Management
The medical management of a patient with ARF begins with a primary assessment and then referral to the intensive care unit. In the ICU, the patient’s lung function is maintained, and the underlying cause of the pathology is gradually treated. First, respiratory and airway patency tests are performed (Ergan et al., 2018). In the first minutes, vital functions are maintained, and infusion therapy is started to normalize the cardiac output (Griffiths et al., 2019). Then medications are prescribed to prevent blood clots and sedatives from relieving pain. For this purpose, narcotic analgesics and heparin are used (in addition to pain relief, they reduce hypercatecholamineemia and improve the rheological properties of blood) (Fernando et al., 2021). Finally, patients are shown activity and breathing exercises to prevent fluid stasis in the lungs and preserve respiratory muscle function.
Care Plan
A plan of care may consist of the following steps:
- Assessment of subjective and objective data.
- Creating an optimal position in bed while maintaining motor activity readings (Ergan et al., 2018).
- Performing a complete respiratory evaluation and administering supplemental oxygen if necessary (Kassirian et al., 2020).
- Nutritional support.
- Educating the patient and relatives: teaching stimulating spirometry, breathing exercises, and taking medication.
In addition to the above, it is recommended to resort to other ways of treatment and support patients with ARF. These include conservative pain management, extracorporeal membrane oxygenation, and the use of steroids (Griffiths et al., 2019). In addition, continuous suctioning of lung fluids and avoiding contact with other liquids to prevent complications are recommended (Ervin et al., 2020). Overall, care should be aimed at maintaining existing average values and improving those in critical values through medication, timely tests, and optimal respiratory support.
Conclusion
Thus, acute respiratory failure is a severe pathology that can lead to significant lung damage. The pathophysiological process consists of the gradual suppression of respiratory centers with the connection of hypo- or hyperventilation of alveolar nature and the development of lung epithelium damage. Management of patients with ARF consists of immediate transfer to the intensive care unit using clot-dissolving drugs and pain management. The nursing care plan aims to organize the patient’s space, diet, and medication adherence.
References
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