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Approach to the patient in respiratory distress (Proceedings)

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Aug 01, 2010

Patients presenting with severe respiratory distress have minimal respiratory reserves, so stress during physical evaluation and treatment must be minimized. Quick evaluation of the patient with minimal additional stress (i.e. radiographs, blood draws) is ideal so that accurate therapy can be instituted without delay. Once the problem is localized, proper emergency treatment can be instituted prior to subjecting the patients to stressful or lengthy diagnostic tests, minimizing the risk of respiratory arrest.

Respiratory anatomy

The main function of the lungs is gas exchange, moving oxygen into the blood and carbon dioxide out. The air passages are made up of conducting airways, whose primary purpose is to move air into and out of the lungs, and the respiratory zone, where gas exchange occurs. Conducting airways are made up of the trachea, right and left main bronchi, lobar bronchi, segmental bronchi, and terminal bronchioles. These airways contain no alveoli and take no part in gas exchange thereby functioning as an anatomic dead space.

The respiratory zone is made up of respiratory bronchioles with occasional budding alveoli, and the alveolar ducts completely lined with alveoli. The respiratory zone makes up most of the volume of the lung.

The physiology of breathing

During inspiration the volume of the thoracic cavity increases, and air is drawn into the lung. Contraction of the diaphragm and intercostals increases the cross sectional area and draws air down to the terminal bronchioles. During expiration elastic recoil passively returns lungs to pre-inspiratory volume. This is a low-pressure system and requires little work in normal patients. Oxygen and CO2 move between air and blood by simple diffusion, as the blood-gas barrier is exceedingly thin with an enormous surface area.

Respiratory pathology

The location of respiratory disease may include the upper airways (laryngeal paralysis, upper airway obstructing foreign body or mass, pharyngeal/laryngeal airway swelling, hemorrhage, brachycephalic airway syndrome, collapsing trachea, nasopharyngeal polyps); lower airways (asthma, bronchopneumonia); lung parenchyma, including the interstitium and alveoli (pneumonia, edema, infiltrative disease, cardiogenic or non-cardiogenic edema, contusions); or may be extra-pulmonary, such as the pleural space (pneumothorax, pleural effusion, pleural space occupying masses, diaphragmatic hernia), thoracic wall, CNS or PNS, or systemic disease.

Respiratory failure may be a failure of ventilation, oxygenation, or both. Ventilation failure manifests as an increase in CO2 tension (hypercapnea). This is always accompanied by hypoxemia unless the patient is receiving supplemental oxygen. Ventilation failure can result from central or peripheral nervous system disease (cervical spinal cord injury, polyradiculoneuritis, central respiratory depressant drugs, etc.), chest wall trauma (flail chest), or pleural space disease (pneumothorax, diaphragmatic hernia, etc.).

Oxygenation failure manifests as hypoxemia. Causes of oxygenation failure can include decreased inspired oxygen (i.e. high altitude), ventilation-perfusion mismatch, a true shunt, hypoventilation, or diffusion impairment.

Ventilation-perfusion mismatch is the most common cause of oxygenation failure and occurs when there is an uncoupling of appropriately matched regional alveolar ventilation and blood flow. Examples of diseases that lead to ventilation-perfusion mismatch include pneumonia, inhalant lung injury, COPD, asthma, and cardiogenic or non-cardiogenic edema.

A true shunt or venous admixture results in the addition of un-oxygenated venous blood to the arterial system. Shunts may be extrapulmonary (congenital cardiac defects—VSD, PDA, and ASD) or intrapulmonary (lung consolidation or complete atelectasis resulting in blood flow to un-ventilated lungs). True shunts are rarely oxygen responsive.

Hypoventilation is always associated with elevated PaCO2 as well as hypoxemia. Addition of oxygen may correct the hypoxemia but will not correct the ventilatory problem.

Diffusion impairment results in a lack of equilibration of oxygen from alveolar gas to the blood. This usually results from a thickened blood-gas barrier with interstitial diseases (pulmonary fibrosis, interstitial neoplasia, severe edema). Oxygen supplementation often overcomes diffusion impairment.

Localization of respiratory pathology can be based on the respiratory rate and pattern of respiration. Two classic breathing patterns can be induced by alterations in the work of breathing. Obstructive diseases obstruct movement of air into or out of the lungs and are usually associated with increases in airway resistance. This typically results in a slower and deeper respiratory pattern than normal. Examples include chronic bronchitis/bronchiolitis, compressive tracheobronchial lesions, extraluminal compression, foreign body, neoplasia, and laryngeal diseases.

Restrictive diseases restrict the expansion of the lungs or chest wall. This is usually associated with decreases in compliance with stiffer lungs or chest wall. Restrictive diseases result in a faster and shallower respiratory pattern. Examples of restrictive diseases include pleural effusion, pneumothorax, diaphragmatic hernia, chest tumors, pulmonary fibrosis, edema, pneumonia, hemorrhage, embolism, severe abdominal distension, and severe obesity. These patient's lungs operate at smaller volumes.