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
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.
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
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
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.