Respiratory Failure

supplemental oxygen, bronchodilator therapy, corticosteroids, antibiotics, and sometimes assistance with ventilations. Most of the time, the cause of the exacerbation is unknown, although smoking, air pollution, bacterial infections, and viral infections can all play a role.

The uncomplicated patient can be managed as an outpatient. Those with other comorbidities, prior respiratory failure, respiratory acidosis, deteriorating respiratory function, or a new arrhythmia will require an ICU admission. Oxygen should be given, even if it worsens the hypercapnia because it minimizes the ventilation/perfusion mismatch. If hypercapnia is leading to respiratory failure, nasal prongs or a Venturi mask should be considered to better regulate the oxygen intake.

Besides oxygen, the first treatment for a COPD exacerbation should be a short-acting beta-agonist, such as albuterol. Anticholinergics, like ipratropium, can also be inhaled. Interestingly, metered dose inhalers with spacers are just as good as nebulizer treatment. All but the mildest of cases should be treated with IV or oral corticosteroids. If there is purulent sputum, antibiotics should be given. The most effective initial antibiotics are trimethoprim/sulfamethoxazole, amoxicillin, and doxycycline, although sicker patients should be treated with a fluroquinolone, second generation cephalosporin, amoxicillin/clavulanate, or extended spectrum macrolides, such as clarithromycin or azithromycin.

RESPIRATORY FAILURE

There are two kinds of respiratory failure. The first is acute hypoxemic respiratory failure, which involves severe hypoxemia that does not resolve with supplemental oxygen. The main cause is shunting of blood in areas of the lungs that are not aerating. The main causes of this are left ventricular failure, which fills the alveoli with fluid, increased permeability of the capillaries as in ARDS, or consolidation or blood in the alveoli, which keep them from aerating.

In ARDS, there is inflammation of the lungs or systemically along with the release of cytokines that recruit inflammatory molecules and other factors that damage the capillary endothelium, disrupting the respiratory membrane so that the alveoli fill with

fluid. The alveoli and airways collapse and there is severe ventilation/perfusion mismatching. The cause may be from a direct lung injury or to indirect inflammation of the lungs from an extra-pulmonary source.

The patient with ARDS will have restlessness, anxiety, altered level of consciousness, tachypnea, diaphoresis, tachycardia, and dyspnea. Crackles will be heard in almost all lung fields. A chest x-ray and ABGs will clarify the diagnosis. Figure 2 shows what ARDS typically looks like on chest x-ray:

Figure 2.

While oxygenation will not reverse the hypoxemia, it should be given. The rest of the treatment is directed at identifying and treating the underlying cause. Identify if the patient is hypervolemic and has high-pressure ARDS or low-pressure ARDS, as would be seen in pneumonia or sepsis.

The treatment may involve mechanical ventilation, if other ways of ventilating the patient are not possible. Positive pressure ventilation or PEEP will help reduce the ventilation/perfusion mismatch and will improve the oxygenation. The goal is to keep the airways open and the alveoli oxygenating so as to enhance oxygenation while the underlying process is treated.

The other cause of respiratory failure is failure of ventilation, which leads to hypercapnia. There can be a decreased minute ventilation or an increase in dead-space ventilation that is not compensated for by increasing the ventilatory rate. There can be neuromuscular incompetence or excessive loads on the respiratory system that cannot be overcome by the patient’s respiratory drive.

Hypercapnia from ventilatory failure causes respiratory acidosis. If this is severe, there will be vasoconstriction of the pulmonary arteries, vasodilation of the systemic vasculature, hyperkalemia, hypertension, decreased myocardial contractility, and increased risk of arrhythmias. For patients who are head injured, the cerebral vasculature will dilate, which will increase the intracranial pressure. If the kidneys do not have time to compensate, the acidosis can be severe.

There are many possible causes of this type of ventilatory failure. Anything that affects neuromuscular transmission or muscle strength will contribute to failure. Impaired respiratory drive, increased chest wall elastic loads as is seen in obesity or pneumothorax, increased lung elastic loads, or increased resistance to airway flow can all contribute to ventilatory failure.

Most patients will exhibit some type of dyspnea with an increase in use of accessory muscles, anxiety, gasping breathing, tachycardia, tachypnea, diaphoresis, poor tidal volume, and anxiety. There will be CNS changes, such as significant confusion, decreased level of consciousness, and coma.

The patient should have a chest x-ray, confirmatory arterial blood gases, and continued pulse oximetry. Acidosis and elevated CO2 levels confirm the diagnosis. The patient with neuromuscular failure may not have any signs of dyspnea until they suffer an arrest. The treatment is directed at managing the underlying disorder and ventilating