Non-invasive pressure-support ventilation (NIPSV), a method of assisting a patient’s respiration without intubation, was first reported in the 18th century. Used in the 1930s for patients with pulmonary edema and in the 1950s for those with polio, NIPSV is currently delivered through CPAP or bi-level positive airway pressure (BiPAP) devices.
Prior to the advent of CPAP and alternative or rescue airways, EMS providers administered ventilatory support in the field with bag-valve masks (BVMs) or the invasive intervention of intubation. CPAP helps prevent the need for mechanical ventilation and intubation by delivering positive end-expiratory pressure (PEEP) while decreasing the incidence of barotrauma and volutrauma. It also helps EMS providers avoid complications from intubation-related sedation or paralysis, in addition to such unexpected difficulties as hypoxia, lethal dysrhythmia, tissue trauma, aspiration and undetected esophageal intubation.
Provider use of CPAP helps patients avoid mandatory admission to an intensive care unit (ICU), reducing the increased morbidity and mortality associated with ventilator-acquired pneumonia (VAP) and such nosocomial infections as Methicillin-resistant Staphylococcus aureus (MRSA) and Klebsiella. Read “CPAP & VAP“ on p. 22 for more about how CPAP devices reduce the instances of VAP.
If CPAP isn’t in your toolbox now, stay tuned because it’s coming soon. But whether it’s on the horizon or already in your BLS and ALS scope of practice, every EMS provider should understand the physiology of breathing and how CPAP works, so they can properly use this therapy to treat patients in respiratory distress.
Physiology of Ventilation
To understand how CPAP works, providers should begin with an understanding of the physiology of the pulmonary system. The lower airways resemble an inverted tree extending from the trachea through the bronchi to the alveolar sacs.
Alveoli form the primary constituent of lung tissue. An average adult has 300—600 million alveoli, each of which measures about 1/3 mm in diameter. Alveolar walls consist of a single layer of cells and elastin fibers that permit stretching and contracting during ventilation.
The internal surface of each alveolus is covered by a thin film of fluid containing surfactant that decreases surface tension and keeps alveolar walls from collapsing and sticking together on expiration. This reduces the work of reopening them with each breath.
Surfactant production diminishes when lungs are hypoperfused and hypoxic. Without adequate surfactant, alveoli collapse and atelectasis develops. The lungs become stiff, and alveoli ultimately fill with fluid.
The alveolar-capillary surface area available for gas exchange is about 1 sq. meter/kg of body weight in the average adult. Normally, the blood-gas barrier is one cell thick. Every red blood cell circulating through the lungs spends about one second in the pulmonary capillary network. During that time, it goes through two to three alveoli and picks up its full complement of (O2) in one-fifth of a second.
The brief time each red blood cell spends in the pulmonary capillary network is normally sufficient for adequate gas exchange. However, this isn’t the case in states of disease, such as emphysema and lung cancer, when the gas exchange surface area is reduced by more than two-thirds and the membranes are thicker, or interstitial or alveolar fluid is present. In this situation, O2 diffusion will be inadequate to meet the body’s demands at rest, and carbon dioxide (CO2) won’t be adequately eliminated.
The relationship between pressure inside the pulmonary system and atmospheric pressure determines the direction of airflow, and the amount of air moved into the lungs depends on airway resistance and lung compliance.
Several factors determine airway resistance. These include airway diameter, motor nerve impulses, the length of the airway, lung volume, tissue resistance, compliance and work of breathing. We’ll discuss each here.
Airway diameter: If the airway radius is narrowed by half, the resistance through it increases by 16. There’s a reduction in airflow to the fourth power. Airway diameter is affected by receptors in the trachea and large bronchi that are activated by irritants or immune system responses.
Motor nerve impulses: Resistance may greatly increase due to airway secretions or bronchial constriction. The vagus nerve constricts bronchioles and sympathetic stimulation dilates bronchioles. Release of histamine causes constriction of smooth muscle resulting in bronchoconstriction.
Length of the airways: If length doubles, resistance doubles.
Lung volume: Diminished lung volume results in increased airway resistance. Small airways may close completely. Patients with increased airway resistance often breathe at high volumes to help decrease airway resistance.
Tissue resistance: Tissue resistance accounts for about 20% of the total airway resistance in young patients, although it may be increased with some diseases.
Compliance: This is the ability of the lungs and thorax to expand easily with inhalation. Good compliance means easy expansion. A normal breath of 500 mL requires a distending pressure of less than 3 cm of water (H2O). A child’s balloon may need a pressure of 300 cm of water for the same change in volume.
***To demonstrate and appreciate compliance, chew some bubble gum. See how easy it is to blow a bubble after only a minute of chewing. This is great compliance. Compare that to the difficulty in blowing a bubble after an hour when gum elasticity has diminished. This demonstrates poor compliance.
Work of breathing: In healthy persons, the energy required for normal quiet breathing is small (only 3% of the total body expenditure). Loss of surfactant, increased airway resistance, decreased compliance, airflow obstruction and lung hyperinflation increase the work of breathing. As lungs become “stiffer,” respiratory muscles become fatigued, resulting in ventilatory failure. Anything that increases functional reserve capacity (FRC) will improve lung mechanics and enable more work to be generated for the same effort.
Although work of breathing is difficult to measure at the bedside, it’s easy to appreciate clinically. EMS providers can do this by observing the patient for tripoding, use of accessory muscles and retractions. O2 consumption increases as ventilatory reserves decrease. As the amount of O2 needed becomes excessive, the body becomes hypoxic. See Table 1 for symptoms and diseases that increase work of breathing.
How CPAP Works
Patients who benefit from CPAP frequently present with a chief complaint of dyspnea. Dyspnea can be caused by cardiac, pulmonary, neuromuscular, psychologic/social/spiritual etiologies or any combination of them. The severity varies widely among patients. EMS providers should get a good baseline assessment to trend improvement. See Table 2 for a modified Borg Dyspnea Scale, which rates the intensity.
CPAP gets many patients with severe inspiratory muscle fatigue through their acute crisis without the need for intubation. CPAP delivers a constant positive pressure to the airways of a spontaneously breathing patient during inspiration and expiration through a noninvasive mask. CPAP raises inspiratory pressure above atmospheric pressures and then applies PEEP to exhalation.
Intrinsic PEEP (auto-PEEP) is usually about 5 cm water. It must be overcome before negative pressure can be generated to inhale more air. If one exhales against resistance, smaller, dependent airways are “splinted” open at the end of expiration, and small bronchi and alveoli don’t collapse.
Keeping these structures open on exhalation allows the muscles that were working to keep them open (the ones exerting auto-PEEP) to be recruited into inspiration. When alveoli stay open, inspiratory effort doesn’t have to be expended to reinflate them. This reduces inspiratory work, relieves respiratory muscle fatigue and decreases work of breathing.
Increased pressure in the airways also allows for better distribution of gases, which leads to an increase in alveolar pressure and reexpansion of collapsed alveoli. This reverses micro-atelectasis. In addition, maintaining inspiratory and expiratory pressures above normal levels results in improved functional reserve capacity, better lung compliance and bronchodilation. This positively affects the ventilation/perfusion (V/Q) ratio.
As alveoli stay open, gas-exchange time can double. This increases oxygen levels in the blood and decreases CO2 levels–as long as respiratory diffusion and pulmonary perfusion dynamics work properly. This reduces hypoxia and reverses hypercarbic ventilatory failure.(1)
CPAP changes alveolar/hydrostatic pressure dynamics. An increase in alveolar pressures will counterbalance interstitial or capillary hydrostatic pressures and will slow or stop movement of fluid into the alveoli. Positive airway pressure pushes fluid out of the alveoli in pulmonary edema and will stop further influx.
It also improves cardiac output. When pulmonary capillary wedge pressures (PCWP) are less than 23, cardiac output is determined by preload (venous filling pressures). Thus, increased preload equals increased cardiac output.
In cardiogenic pulmonary edema due to heart failure, PCWP is already maxed out. If greater than 23, cardiac output is dependent on afterload. CPAP increases pressures throughout the thorax, including pressure surrounding the left ventricle (LV). This makes it easier to eject blood out of the heart. Similarly, pressure surrounds the thoracic cavity but not the abdominal aorta, giving the impression of reduced LV afterload outside of the thoracic cavity. This will increase cardiac output unless PEEP levels are too high. High intrathoracic pressures greatly reduce preload to the right heart and will reduce the blood pressure.
CPAP produces an increase in tidal volume with a subsequent reduction in the work of breathing. Stabilization of minute ventilation with an increase in FRC should improve ventilation-perfusion relationships and potentially reduce oxygen requirements. This allows for an increase in available O2 for tissue perfusion and a decrease in CO2 levels.
If CO2 elimination from the lungs decreases, CO2 levels in the blood will rise. This condition, called hypercarbia, occurs with respiratory depression or hypoventilation, which can be caused by airway obstruction, respiratory muscle impairment or pulmonary obstructive diseases, among other pathologies. EMS providers should correct hypercarbia by increasing ventilation and attempting to correct the underlying cause. Improved ventilation and gas exchange are major benefits of CPAP.
Prehospital crews have been without the capabilities offered by CPAP and had to watch dyspneic patients decline, requiring intubation. Patients who are still awake during intubation often experience anxiety and discomfort and need to remain sedated. They can’t talk with the tube passing through their vocal cords, and the aspiration risk is high with open cords. Intubated patients are also more susceptible to VAP, MRSA and Klebsiella than non-intubated ones.
Consideration of these complications, as well as the cost of equipment and a mandatory ICU admission, makes avoiding intubation by administering CPAP an attractive option.
CPAP should be the first line of respiratory therapy in carefully selected patients based on local protocols. It relieves symptoms but should be used in concert with appropriate medications in patients with asthma, chronic obstructive pulmonary disorder (COPD) and heart failure. This will address specific underlying pathology.
Remember, CPAP isn’t a ventilator. Patients must be monitored carefully (vital signs, SpO2, capnography and clinical responses) after CPAP application to detect improvement in condition or lack of improvement that may indicate the need for intubation and assisted ventilations, as well as for signs of complications that may signal the need to remove the CPAP mask.
1. Kallio T, Kuisma M, Alaspaa A, et al. The use of prehospital continuous positive airway pressure treatment in presumed acute severe pulmonary edema. Prehosp Emerg Care. 2003;7:209—213.
“¢ EAST Practice Management Workgroup for Pulmonary Contusion-Flail Chest. www.east.org/tpg/pulmcontflailchest.pdf
“¢ Eisenman A, Rusetski V, Sharivker D, et al. Role of the Boussignac continuous positive pressure mask in the emergency department. Israeli J Emerg Med. 2008;8:6—11.
“¢ Respiratory Disease. www.pathguy.com/lectures/resp.htm
“¢ Hastings D, Monahan J, Gray C, et al. CPAP. A supportive adjunct for congestive heart failure in the prehospital setting. JEMS. 1998;23:58—62.
“¢ BLS CPAP: Improving breathing in the prehospital setting. www.fireengineering.com/index/articles/display/331568/articles/fire-engineering/fire-ems/medical-info/2008/06/bls-cpap-improving-breathing-in-the-prehospital-setting.html
“¢ Mistovich JJ, Karren KJ. Respiratory emergencies: In Prehosp Emerg Care (9th Ed.). Brady: Boston. 540—548, 2010.
“¢ Moritz F, Brousse B, Gellee B, et al. Continuous positive airway pressure versus bilevel noninvasive ventilation in acute cardiogenic pulmonary edema: A randomized multicenter trial. Ann Emerg Med. 2007;50:666—675.
“¢ Lightner L, Brywczynski J, McKinney J, et al. Shortness of Breath: Prehospital treatment of respiratory distress. JEMS. 2010;35:56—63.
This article originally appeared in the January 2011 JEMS supplement “CPAP: The push for rapid relief” as “Positive Pressure: The physiology of respirations with CPAP.”