I. CPAP & CHF
The primary goal of CPAP is to decrease the work of breathing so the patient doesn’t deteriorate, doesn’t require intubation—which is associated with increased mortality—and doesn’t suffer respiratory arrest. Patients who are intubated are as much as seven times more likely to die than those who are not.(1)
Several studies have demonstrated that instituting CPAP in the field reduces the
need for intubation by as much as 60%.(1,2)
In this article, we examine some of the many indications for CPAP use, including congestive heart failure (CHF), asthma/COPD, drowning, carbon monoxide (CO) poisoning and pulmonary infections, and discuss some of the physiological responses that make CPAP beneficial.
CPAP & Heart Failure
The primary cause of respiratory distress with heart failure is increased work of breathing.
The underlying cause: In heart failure, the heart cannot efficiently pump the blood delivered to it. In some cases, the patient is volume overloaded, but in the majority of cases the patient’s total blood volume is normal. For whatever reason, the heart fails to pump blood efficiently, and pressure in the pulmonary veins rises. Blood does not actually “back up,” but the rise in pressure makes movement of blood through the lungs more difficult.
As the pressure rises, the blood, primarily the serum, moves out of the capillaries and into the tissue space between the capillaries and the alveoli. Eventually, the fluid migrates into the alveoli, causing them to collapse and become unable to exchange gases, similar to the collapse of alveoli in COPD. To counteract this, the patient must breathe out through pursed lips (a process called auto-PEEP) in an attempt to keep the alveoli open.
Unfortunately, the heart failure patient isn’t accustomed to this type of reflexive breathing; as a result, their work of breathing increases quickly.The role of CPAP in the treatment of heart failure is twofold:
1. The PEEP helps keep the alveoli open during exhalation, and inspiratory pressure helps to open additional alveoli, relieving the work of breathing;
2. The pressure generated by CPAP helps move fluid back into the vascular system.
To facilitate this second action, it’s critical that the underlying myocardial dysfunction be corrected. The best method to reduce the elevated pressure in the pulmonary vasculature is the administration of nitrates.(3,4) Once the pressure in the pulmonary arteries and veins is decreased, CPAP will be better able to move the fluid out of the lungs and into the circulatory system.The use of diuretics in heart failure has come under scrutiny, and current recommendations are to avoid their use during initial treatment. Note: Some studies suggest that high-dose diuretic use for acute CHF increases mortality.(5,6)
When and if diuretics are used, they will be effective only if the pulmonary interstitial fluid is in the circulatory system. This is where CPAP comes into play. Even in the absence of nitrate administration, CPAP can move fluid out of the lungs. Combined with the decrease in work of breathing, this can lower the sympathetic tone of the patient and encourage diuresis.
Therefore, by reducing the work of breathing and relieving pulmonary congestion, CPAP buys time for other treatments, such as nitrates and diuretics, to work.
Contraindication to CPAP
If left untreated, heart failure deteriorates into cardiogenic shock with profound hypotension from low cardiac output. One side effect of CPAP, particularly at high pressures (greater than 10 cm H2O), is that intrathoracic pressure is increased, which can result in lowering of venous blood return to the right side of the heart.
If the patient is on the verge of cardiogenic shock, this increased pressure may tip the scales. Therefore, it’s best to avoid the use of CPAP in heart failure if the patient is already hypotensive.(7) Instead, the administration of dopamine is indicated. Once the pressure is stabilized, CPAP can be started. If, after starting CPAP on the hypertensive patient, the patient becomes hypotensive, it’s not likely the effect of CPAP, but instead the onset of cardiogenic shock.
Time Is Crucial
When using CPAP for heart failure, time is of the essence, and you must aggressively treat the underlying cause. If there’s a new onset of rapid atrial fibrillation, slow it down with a calcium channel blocker. If the patient is hypertensive, administer nitrates. Don’t forget to obtain a 12-lead ECG and deliver the patient to a percutaneous coronary intervention center if a ST-elevation myocardial infarction is suspected.
CPAP has been the mainstay of heart failure treatment in the emergency department for years. The data now shows that it’s just as safe and effective in the field.
1. Hubble MW, Richards ME, Jarvis R, et al. Effectiveness of prehospital continuous positive airway pressure in the management of acute pulmonary edema. Prehosp Emerg Care. 2006;10:430–439.
2. Masip J, Roque M, Sanchez B, et al. Noninvasive ventilation in acute cardiogenic pulmonary edema: Systematic review and meta-analysis. JAMA. 2005;294:3124–3130.
3. Levy P, Compton S, Welch R, et al. Treatment of severe decompensated heart failure with high-dose intravenous nitroglycerin: A feasibility and outcome analysis. Ann Emerg Med. 2007;50:144–152.
4. Mebazaa A, Gheorghiade M, Piña IL, et al. Practical recommendations for prehospital and early in-hospital management of patients presenting with acute heart failure syndromes. Crit Care Med. 2008;36[Suppl.]:S129–S139.
5. Cleland JG, Coletta A, Witte K. Practical applications of intravenous diuretic therapy in decompensated heart failure. Am J Med. 2006; 119(12A):S26–S36.
6. Hasselblad V, Gattis Stough W, et al. Relation between dose of loop diuretics and outcomes in a heart failure population: Results of the ESCAPE trial. Eur J Heart Fail. 2007;9:1064–1069.
7. Collins SP, Mielniczuk LM, Whittingham HA, et al. The use of noninvasive ventilation in emergency department patients with acute cardiogenic pulmonary edema: A systematic review. Ann Emerg Med. 2006;48:260–269.
II. CPAP in asthma & COPD
It may seem counterintuitive that external pressure support (e.g., CPAP) would improve ventilation and oxygenation in an asthmatic patient, but the improvement in respiratory function offered by CPAP is impressive.
The fundamental pathophysiological change that occurs with acute exacerbation of asthma is the obstruction of expiratory air flow, leading to air entrapment, acute pulmonary distention and decreased functional reserve capacity. Secondarily, an inspiratory obstructive component may be present.
This significant increase of obstruction in inspiratory and expiratory air flow in both large and small airways is caused by inflammation, bronchoconstriction and intraluminal mucus, with development of mucous plug formations resulting in heterogeneous pulmonary ventilation. This may result in an auto-PEEP of up to +20cm H2O and a loss in the V/Q ratio in different areas of the lung.
Under these conditions, breathing is labored. The increase in inspiratory resistance determines the need for more negative pleural pressure, which creates differential pressure between capillary and interstitial tissue, leading to interstitial and peribronchial edema and, thus, worsening ventilatory functions. Expiratory resistance makes active exhalations more laborious, with a further increase in the work of breathing.
During the initial decompensatory phase in asthma, hypoxemia and hypocapnia occur. In patients who are nonresponsive to traditional therapy, the condition can lead to a mixed acidosis due to CO2 retention and lactic acidosis due to the increased work of breathing.
The improvement seen following CPAP administration most likely occurs through a combination of 1) decreased work of breathing and reduction of fatigue; 2) recruitment of alveoli and improved oxygenation; and 3) splinting of larger airways, bronchiolar and bronchial to reduce airway collapse and mucous plugging. Current CPAP systems may allow intermittent or continuous administration
A variety of modalities exist to administer CPAP: nasal masks and partial- and full-face masks. Sedation may be necessary in some patients, but asthmatics seem to respond well to coaching and emotional support while they hold the mask on their face. Thus, CPAP may be a BLS skill when ALS isn’t available or has extended response times.
To qualify for CPAP, patients must be conscious, cooperative and hemodynamically stable (relative). The following would indicate CPAP application:
• Moderate or severe asthma/COPD;
• Respiratory failure and muscular fatigue;
• Poor response to medical treatment;
• Increased end-tidal (Et) CO2 and/or decreased SpO2;
• Use of accessory respiratory muscles;
• Ability to wear the face mask; and/or
• Not being in obvious need of intubation.
The following patients exhibit exclusion criteria:
• Obvious respiratory failure who require immediate intubation;
• Decreased level of consciousness who cannot cooperate with (tolerate) the CPAP system;
• Cardiovascular instability (SBP less than 90 or on vasopressors; relative);
• Morbid obesity (more than 200% over ideal weight; relative); and/or
• Acute abdominal processes, recent gastro-esophagus surgery, or recent facial or ENT surgery, facial deformities or facial trauma.
Discontinue CPAP if the patient exhibits the following symptoms:
• Deteriorating mental status, becomes lethargic with worsening hypercapnia or agitated with hypoxemia;
• Inability to tolerate mask due to pain
• Inability to improve respiratory function;
• Hemodynamic instability;
• Electric instability (with ischemia or malignant V arrhythmia); and/or
• Suspicion of pneumothorax.
Note: The patient may also request discontinuation.
Complications following CPAP may include abdominal distention, barotraumas, hypotension, secretion retention, facial necrosis caused by pressure and/or increasing fatigue and respiratory failure.
As discussed above, CPAP noninvasive positive pressure has a long history in acute heart failure and now asthma. It has also proved beneficial in COPD and other forms of respiratory failure.(1,2) The improvement is based on the following important principles:
1. Reduction of inspiratory muscle recruitment and, therefore, avoidance of muscular fatigue. This effect can be observed in a slowing of respiratory rate and an increase in tidal volume. CPAP should counteract the effects of intrinsic PEEP.
2. Early improvement of gas exchange. This is due to an increase in ventilation and to a greater tolerance to higher oxygen concentrations (without hypoventilation). The shunt effect and the ventilation-perfusion mismatch secondary to CPAP also decrease.
3. Hemodynamic effects. These may be beneficial or harmful. In patients with fluid overload and a decrease in systolic function performance, an increase in intrathoracic pressure caused by CPAP produces a decrease in right ventricular preload and afterload. To avoid this adverse affect, avoid application of CPAP to patients with a systolic pressure below 105 mmHg. If hypotension occurs, either discontinue CPAP or use a lower pressure.
The Bellingham (Wash.) CPAP Experience
The primary BLS/ALS service for Bellingham and Whatcom County is Whatcom Medic One. Because of its population distribution and ALS response times, transports can take 20 minutes or more.
Approximately six years ago, Medic One trained its ALS providers to use CPAP. The initial indication was suspected acute heart failure with respiratory distress. It quickly became apparent that differentiating acute heart failure from COPD, asthma, and other forms of respiratory distress wasn’t easy. Because the literature strongly suggested that CPAP provides significant respiratory support and assistance to patients with COPD, asthma and other forms of respiratory distress, those conditions were included for CPAP use.
Most of these patients would normally require significant sedation or paralysis to maintain intubation. In COPD, intubation may lead to air trapping, with subsequent barrow traumas. Even with improved oxygenation, EMS providers need to understand the long-term effect intubation has in this acute and chronic disease.
In asthma, intubation rarely treats the primary problem, which is bronchial and bronchiolar in nature. Intubation is usually only indicated to provide relief for profound fatigue with secondary respiratory failure. Issues and concerns with intubation in these patients are obviated with the use of CPAP. Thus, CPAP has allowed us to reduce intubation in all types of acute respiratory disease by two-thirds or more.
By the numbers: Medic One has now treated more than 600 patients with CPAP—65% for presumed acute heart failure, 25% for COPD, and 20% for asthma as well as other forms of presumed respiratory distress. Sedation was needed in approximately 30% of patients, but most patients responded to coaching during CPAP use.
In spite of sedation and coaching, approximately 15% could not tolerate or failed CPAP. Only 20% of the patients who failed CPAP proximately or subsequently went on to acute intubation. In spite of these numbers, it’s hard to quantify the outcome in these patients except to look at reductions in the number requiring intubation.
The overall number of patients intubated in all of these categories treated with and without CPAP fell to 30% of those intubations performed prior to the introduction of CPAP.
Clearly, CPAP has been, and continues to be, an important modality for EMS. It’s generally considered as a “non-invasive” airway device and should qualify for BLS use where appropriate. It has and will continue to make a significant impact on EMS.(3,4,5)
1. Masip J. Noninvasive ventilation in acute cardiogenic pulmonary edema. Curr Opin Crit Care. 2008;531–535.
2. Mattu A, Lawner B. Prehospital management of congestive heart failure. Heart Fail Clin. 2009;19–24, v.
3. Warner GS. Evaluation of the effect of prehospital application of continuous positive airway pressure therapy in acute respiratory distress. Prehosp Disaster Med. 2010;25:87–91.
4. Taylor DM, Bernard SA, Masci K, et al. Prehospital noninvasive ventilation: A viable treatment option in the urban setting. Prehosp Emerg Care. 2008;12:42–45. Erratum in: Prehosp Emerg Care. 2009;13:151.
5. Hubble MW, Richards ME, Jarvis R, et al. Effectiveness of prehospital continuous positive airway pressure in the management of acute pulmonary edema. Prehosp Emerg Care. 2006;10:430–439.
III. Additional indications for CPAP
The literature supporting the use of CPAP in the prehospital environment is almost exclusively limited to acute respiratory distress secondary to cardiogenic pulmonary edema or COPD exacerbation. Although most EMS protocols limit CPAP use to these two primary indications, it’s valuable to consider other possible applications that can impact morbidity and mortality.
Given the demonstrated benefit of CPAP in cardiogenic pulmonary edema, it’s particularly important for medical directors to consider how CPAP could be employed as an adjunct for managing patients with noncardiogenic pulmonary edema conditions, such as saltwater drowning or altitude-associated pulmonary edema, to achieve the same physiological effect.
Likewise, given the demonstrated ability of CPAP to clinically improve patients with COPD exacerbations, we believe EMS systems should consider application of CPAP in cases of acute lung injury that are also associated with hypoxia and hypercapnia and increased work of breathing. Even if your system isn’t ready to advocate for the use of CPAP in all of these conditions, these areas are still important to monitor for new developments as well as conditions in which judiciously applying CPAP in carefully selected patients may be justified.
Toxic Inhalation Injuries
Many prehospital patient care protocols for hazmat feature CPAP as an important adjunct to the management of toxic inhalation injuries, particularly those associated with lower airway injury and pulmonary edema. Irritant gases are a good example of the type of agents that can cause these injuries. When these gases are inhaled, they dissolve in the water of the respiratory tract and cause inflammation and injury. Irritant gases with high water solubility dissolve quickly, with their effects typically limited to the eyes and upper airway.
However, those gases with intermediate water solubility, such as chlorine, affect both upper and lower airways, and gases with low water solubility predominantly affect the lower airways. Lower airway injury symptoms may be delayed and can include bronchorrhea, bronchospasm and noncardiogenic pulmonary edema. The use of CPAP in these types of lower airway injuries may relieve respiratory distress, improve oxygenation and decrease the need for intubation.(1)
Other toxic inhalations have also been suggested as candidates for CPAP. For example, smoke inhalation injuries in the early phase are associated with bronchospasm, bronchorrhea, decreased compliance and ventilation-perfusion mismatches. It has been suggested that CPAP may be an appropriate supportive measure that can help prevent the deterioration of oxygenation and intrapulmonary shunting. This concept has been demonstrated in a canine model of smoke inhalation injury where CPAP improved pulmonary function and oxygenation.(2)
Carbon Monoxide Poisoning
The primary treatment for CO poisoning is the application of 100% oxygen and, in significant cases, the use of hyperbaric oxygen that requires the use of a hyperbaric chamber to place the patient under two to three atmospheres of pressure. Both treatments displace CO from hemoglobin.
No data suggests that CPAP mimics a hyperbaric chamber, but it does enhance the elimination of CO by providing 100% oxygen (if the device is so designed) via a tight-fitting mask that is superior to loosely applied 100% nonrebreather masks.
Exposure to organophosphates, such as the nerve agent sarin gas or certain herbicides, results in a cholinergic crisis with the classical SLUDGE (salivation, lacrimation, urination, defecation, gastrointestinal upset and emesis) presentation. When exposed to organophosphates, pulmonary edema can also occur. Therefore, it would be reasonable to presume that CPAP administration would be useful in this toxic exposure. But CPAP wouldn’t take the place of the administration of antidotes, such as atropine and 2-PAM chloride, which reverse the effects of the agents.
There are numerous case reports supporting the use of CPAP in the management of submersion injuries.(3,4) Patients suffering from near-drowning in freshwater have pulmonary injuries that are associated with atelectasis and altered surface tension in the alveoli. This sets up a ventilation perfusion mismatch leading to hypoxia.
Patients suffering from near-drowning in saltwater are more likely to develop pulmonary edema as the inhaled hypertonic solution pulls plasma into the alveolar cavity.
In both of these cases, the application of CPAP provides an excellent way to improve oxygenation in patients who are awake and spontaneously breathing. The physiological disorders—atelectasis in the case of fresh water drowning—and pulmonary edema in the case of salt water drowning, are both reversed by the application of positive pressure breathing.
The physiological cause of high-altitude pulmonary edema (HAPE) remains controversial. The typical HAPE patient will have a history of rapid ascent to altitudes of 8,000 feet or greater, with the development of pulmonary edema and hypoxia within one to four days. It is thought that hypoxia leads to leaking of the alveolar capillary membrane.
This may be the result of areas of vasoconstriction in the pulmonary vasculature, which causes over-perfusion and hydrostatic pulmonary hypertension in other areas of the pulmonary vasculature, ultimately leading to pulmonary edema. The application of CPAP along with supplemental oxygen has proven effective in these patients.
The management of patients with traumatic flail chest from blunt trauma is both challenging and controversial. These patients occasionally need endotracheal intubation and ventilator support. However, prolonged mechanical ventilation in these patients is associated with numerous complications, such as pneumonia and poor outcome. More recently, the role of CPAP by face mask with good pain control has been explored as an alternative first line of treatment for flail chest caused by blunt thoracic trauma.(5,6) In one randomized in-hospital study of CPAP compared to intubation and mechanical ventilation, the CPAP group had fewer cases of pneumonia and higher survival rate.(7)
Although the concept of “pneumatic stabilization” with CPAP is promising, it’s not without its own concerns. The biggest concern likely to be raised is that of creating a pneumothorax with the positive pressure of CPAP in the setting of rib fractures. Given the relatively small numbers of cases reported in the literature in which CPAP has been used in this situation, we have to conclude that the incidence of pneumothorax is largely unknown, but it’s not likely to be greater than that of mechanical ventilation in the same scenario.
It’s important to note that although there may be value for CPAP use in traumatic chest injuries, the FDA currently lists such injuries as a contraindication to CPAP administration.
It’s well known that pulmonary infections, such as community-acquired pneumonia (CAP), are associated with the complications of hypoxia and acute respiratory dysfunction. Because the infections alter alveolar structure and function, supplemental oxygen alone may not be enough to correct the hypoxia in these patients.
In one “proof-of-concept” type study of CPAP in CAP, patients with moderately severe respiratory failure showed rapid improvement in oxygenations with CAP.(8) It’s hypothesized that CPAP improves gas exchange by recruiting collapsed alveoli, decreasing “flooding” in the interstitial space and alveoli associated with inflammation, and ultimately decreasing the ventilation perfusion mismatch.
CPAP has been used successfully in other pulmonary infections, too—most notably Pneumocystis carinii pneumonia. There are also numerous case studies claiming clinical improvement with the use of CPAP in respiratory failure from H1N1 influenza and case controlled studies showing improved outcomes in pediatric patients with bronchiolitis that receive CPAP as compared to intubation.(9)
CPAP has been used successfully in hospital and prehospital settings for CHF, asthma/COPD, drowning, CO poisoning, pulmonary infections and other conditions. It helps avoid the need for intubation and may, therefore, reduce mortality. If your EMS agency has not yet purchased CPAP devices and is invested in training your providers, you should consider it now.
1. Miller K, Chang A. Acute inhalation injury. Emerg Med Clin North Am. 2003;21:533–557.
2. Davies LK, Poulton TJ, Modell JH. Continuous positive airway pressure is beneficial in treatment of smoke inhalation. Crit Care Med. 1983;11:726–729.
3. Dottorini M, Eslami A, Baglioni S, et al. Nasal-continuous positive airway pressure in the treatment of near-drowning in freshwater. Chest. 1996;110:1122–1124.
4. Gonzalez-Rothi RJ. Near drowning: Consensus and controversies in pulmonary and cerebral resuscitation. Heart Lung. 1987;16:474–482.
5. Pettiford BL, Luketich JD, Landreneau RJ. The management of flail chest. Thorac Surg Clin. 2007;17:25–33.
6. Tanaka H, Tajimi K, Endoh Y, et al. Pneumatic stabilization for flail chest injury: An 11-year study. Surg Today. 2001;31:12–17.
7. Gunduz M, Unlugenc H, Ozalevli M, et al. A comparative study of continuous positive airway pressure (CPAP) and intermittent positive pressure ventilation (IPPV) in patients with flail chest. Emerg Med J. 2005;22:325–329.
8. Cosentini R, Brambilla AM, Aliberti S, et al. Helmet continuous positive airway pressure vs. oxygen therapy to improve oxygenation in community-acquired pneumonia: A randomized, controlled trial. Chest. 2010;138:114–120.
9. Javouhey E, Barats A, Richard N, et al. Non-invasive ventilation as primary ventilatory support for infants with severe bronchiolitis. Intensive Care Med. 2008;34:1608–1614.
1. Oherrick MR. Prehospital use of continuous positive airway pressure: Implications for the emergency department. J Emerg Nurs. 2009 Jul;35(4):326–329. Epub 2008 Jul 15.
2. Pettiford BL, Luketich JD, Landreneau RJ. The management of flail chest. Thorac Surg Clin. 2007;17:25–33.
3. Hubble MW, Richards ME, Wilfong DA. Estimates of cost-effectiveness of prehospital continuous positive airway pressure in the management of acute pulmonary edema. Prehosp Emerg Care. 2008;12:277–285.
4. Deis JN, Abramo TJ, Crawley L. Noninvasive respiratory support. Pediatr Emerg Care. 2008;24:331–338.
This article originally appeared in the January 2011 JEMS supplement “CPAP: The push for rapid relief” as “The Many Benefits of CPAP: Indications for continuous positive airway pressure.”