CPAP is a form of non-invasive positive pressure ventilation. There are several variations seen in the prehospital setting, however the 2 most common are CPAP and BIPAP. Both are essentially the same, with the exception being that BIPAP produces different airway pressures during the inspiratory and expiratory phases of ventilation.
So, how does CPAP work, and who is it for?:
CPAP works by increasing the end expiratory pressure in the airway, creating a similar effect to that which occurs by exhaling through pursed lips. This increased pressure prevents alveolar and bronchiole collapse, which commonly occurs in the setting of COPD, particularly emphysema. With this in mind, we can see obvious applications in treating COPD exacerbation in patients who do not respond to other ventilation strategies. A patient with a mild to moderate exacerbation, who responds to an increase in home oxygen flow, or the application of bronchodilators and corticosteroids, probably doesn’t need CPAP. However, a patient who is in pending respiratory failure may have their trajectory reversed by including CPAP in your frontline treatment. CPAP essentially allows us to splint the airways open, and to increase the partial pressure of oxygen across the alveolar membrane. This means we allow for greater surface area for gas exchange, and assist in overcoming respiratory acidosis. This can greatly reduce the need for emergency intubation, and placement on a ventilator. There is a caveat to this however, as these patients must be conscious and able to sit upright for CPAP to work properly. In unresponsive patients, PPV with a BVM is still best practice.
The other population who benefit from CPAP are those with cardiogenic pulomonary edema. These patients have fluid accumulation in the alveoli, reducing oxygen exchange to the blood. CPAP works by displacing the fluid and making available more area for gas exchange. When used in conjunction with Nitroglycerine, which reduces fluid accumulation by dropping pressure in the pulmonary vasculature, there can be significant improvement in patient oxygenation.
What are the risks with CPAP:
There are some considerations that we need to know about. First, CPAP causes an increase in intra-thoracic pressure. This causes pressure on the heart itself, and the vena cava, and can reduce preload and cardiac output, leading to hypotension. Anyone getting CPAP needs to be normotensive from the beginning. Barotrauma is another concern. There is a risk, especially with patients with existing degenerative pathologies such as COPD, that an increase in pulmonary pressure may lead to a pneumothorax. This can be mitigated by monitoring vitals and patient complaints closely. Our other concern is patient compliance. A combative or uncooperative patient cannot likely tolerate CPAP.
How to use it:
Depending upon local protocols, initiation and final settings may vary, however, the general consensus is to start low and gradually titrate to effect over several minutes. VERY IMPORTANT: Once CPAP is on, IT STAYS ON. As the patient’s body adjusts to the effects of CPAP, the various compensatory mechanisms that have been maintaining oxygenation gradually stop occurring. This means that sudden discontinuation of CPAP leaves the patient in a state where they are no longer able to compensate for their pathology. CPAP needs to gradually be titrated down in hospital.
So, thats it. Pretty simple, and super effective.
Comments