Case Presentation
You respond to the home of a 62-year-old female presenting with shortness of breath, which increases on exertion. The patient’s daughter informs you that her mother has a history of coronary artery disease, congestive heart failure (CHF) and chronic bronchitis. She also reports a long history of orthopnea, which requires her to sleep propped up on four pillows.”ž
The patient is unable to speak more than a few words at a time and appears to be weakening. Vitals: HR 118, RR 26 and shallow, BP 160/104, with a room air oxygen saturation of 88%. You observe jugular venous distention and obvious accessory muscle use. Auscultation of the lungs reveals diminished tidal volume and crackles in the bases of the lungs bilaterally.
You quickly place her on supplemental oxygen, while your partner readies equipment to deliver continuous positive airway pressure (CPAP). Shortly after CPAP is initiated, the patient reports improvement and appears to be breathing more comfortably, although she remains in severe distress.
During transport, her blood pressure remains elevated, so you administer repeated doses of nitroglycerine at 0.4 mg sublingual and 4 mg of morphine sulfate intravenously. On arrival at the local hospital, the emergency department (ED) staff removes the patient from CPAP and places her on a device that delivers biphasic positive airway pressure (BiPAP) and continues with nitroglycerine and morphine sulfate. They also administer diuretics and nebulized albuterol. As you leave the ED, you wonder why the hospital switched your patient from CPAPÆ’which worked well during transportÆ’to BiPAP.
Introduction
Utilization of CPAP is increasing in the prehospital setting, but it isn’t always the best choice of non-invasive positive pressure ventilation (NPPV). To understand why, we must first understand the related anatomy and physiology, mechanisms of action and indications for treatment.
NPPV can be effectively used in the prehospital environment and improves emergency management of patients with acute respiratory failure due to chronic obstructive pulmonary disease (COPD) and cardiogenic pulmonary edema. It has been shown to improve alveolar ventilation and gas exchange while decreasing preload and afterload, improving lung compliance, increasing functional residual capacity and decreasing breathing work. When used with other therapies, it’s effective in the treatment of acute respiratory failure in the emergency setting.
Because as many as 19% of intubated patients must be re-intubated, which is an independent predictor of death, avoiding intubation whenever possible benefits our patients. Further, with the increased incidence of pneumonia and other complications, associated endotracheal intubation can be avoided through use of NPPV. With increased utilization and development of NPPV techniques, intubation of these patients may become obsolete and outcomes for these patients can improve.
The Basics of Breathing
Cardiogenic pulmonary edema and COPD are the two disease states leading to acute respiratory failure that necessitate the use of NPPV in the prehospital environment. Thus, it’s important for emergency caregivers to understand the basic concepts surrounding the anatomic and physiologic aspects of breathing in both the healthy and diseased lung.”ž
The primary purpose of the lungs is to facilitate gas exchange via the 300 million alveoli in the normal adult lung. This number of alveoli provides 70à80 square meters of surface area in close contact with a meshwork of tiny capillaries that carry carbon dioxide and exchange it for oxygen. The lungs receive essentially 100% of the cardiac output and contain up to 12% of the body’s total blood volume at one time.
The lungs are ventilated through a bellows-like system or ventilatory pump. Anyone who has observed a dissection or autopsy has seen how the chest expands and the lungs contract when the thorax is dissected. This action demonstrates the natural tendency of the chest wall to move outward and the lungs to recoil inward.
As compared to the chest, the lungs are the more compliant; that is, they yield to force. In this case, the force is provided by the ventilatory pump, which consists of the chest wall, diaphragm and pleura.
Normal lungs are flexible because they’re made up of large amounts of elastin and collagen. Surface tension within the 300 million alveoli also contributes to the lungs elastic recoil. COPD, pulmonary edema and asthma damage the lung’s elastic airways and the alveoli themselves, causing a loss of surface tension. The combined effect is that the lungs become much stiffer, as occurs with pulmonary edema, making it more difficult for the ventilatory pump to expand the lungs, especially during exacerbations of the illness.
The diaphragm and other respiratory muscles within the chest wall are considered the only skeletal muscles essential to life. Fatigue of the respiratory muscles is a common cause of respiratory failure.
Respiratory muscles become fatigued when there’s an increased ventilatory demand, increased work of breathing or inadequate energy production by the muscles themselves. These conditions often result from disease states, such as COPD, asthma and CHF.
Inspiration is an active process. Muscles need to work and expand the pump so air moves into the lungs. Exhalation is a passive process in the normal healthy lung. It becomes an active process when air becomes trapped by mucus or collapsed airways in the presence of certain diseases, such as COPD. This effect increases the likelihood of muscular fatigue.
The diaphragm is the primary muscle of ventilation and moves downward to draw air into the lungs. When the lungs are already hyperinflated due to emphysema, the diaphragm is limited because it’s already low and flat. With severe hyperinflation, the contraction of the diaphragm causes an expiratory effect during inhalation because the lower portion of the ribs are pulled in rather than pushed out.
Mucociliary clearance provides one of the primary defenses of the lungs. Ciliated epithelia (little hairs) within the airways transport deposited materials from the level of the terminal bronchioles to the larynx where they’re coughed out or swallowed. The cilia are capable of moving particles at a rate of 3 mm per minute, allowing for 90% of deposited particles to be cleared every two hours.
Many diseases, including asthma and COPD cause a loss of cilia, impairing this defense mechanism. Particles become trapped in mucus secreted by goblet cells. Two layers of mucus and a thick top layer of gel trap material, while the cilia are housed in the thin sol layer (see”žFigure 1).
Chronic bronchitis results in a thickening of mucus due to the proliferation of mucus-secreting goblet cells. This impairs the ability of the cilia to function normally.
Another defense mechanism present in the lungs is the lymphatic drainage system. The lymphatic system can remove an estimated 10à20 mL of fluid per hour in the healthy lung. Under severe stress, this capability is exceeded, resulting in fluid accumulation and interstitial edema. The interstitium of each lung can hold more than 500 mL of fluid. When this volume is exceeded, tight junctions of the alveolar epithelium become damaged and the fluid floods into the alveolar air spaces, interfering with surface tension and gas exchange.
Patients in Respiratory Failure
Although cardiogenic pulmonary edema and COPD are two completely different conditions, they can both result in respiratory failure. It may develop over time, or it may appear suddenly with little or no warning.
Chronic obstructive lung disease (COLD) includes a group of disorders that cause chronic airflow obstruction. These disorders include emphysema and chronic bronchitis. COLD affects 5% of the adult population in the U.S.
The incidence and mortality of COLD is rising worldwide due to the increased prevalence of smoking in women and children. COLD is characterized by progressive, permanent destruction of the lung’s parenchyma. Although bronchodilators and anti-inflammatory agents do help, they can’t reverse the damage.
Chronic bronchitis is accompanied by narrowing of the airways due to inflammation and hypertrophy of mucus glands, along with excessive mucus secretion. The tissue of terminal airways and alveoli become fibrotic and stiff. Remodeling of the pulmonary vasculature results in a back pressure that causes the patient’s liver to enlarge, ankles to swell and neck veins to distend. These patients tend to be overweight, edematous and cyanotic.
Emphysema is characterized by permanent alveolar enlargement and alveolar wall destruction without fibrosis. Emphysema patients are frequently thin and barrel-chested due to the enlarged alveoli. They’re often pink due to excessive production of red blood cells, called polycythemia.
The Difference Between CPAP & BiPAP
It should be noted that there’s disagreement among the literature as to whether CPAP is a form of NPPV. CPAP provides oxygenation but not ventilation, which is the actual movement of air into the lungs. CPAP augments ventilation, which should qualify it as a form of NPPV. For the purpose of this discussion, CPAP and BiPAP will both be considered as forms of NPPV.
CPAP is a continuous pressure provided above ambient pressure, which helps prevent alveoli from collapsing and augments ventilation. This pressure remains relatively constant through each phase of the respiratory cycle, varying only slightly as the patient breathes (see”žFigure 2, p. 80).
Because the pressure is the same throughout all phases of the respiratory cycle, the patient must overcome the pressure during expiration. CPAP is limited by the patient’s ability to breathe and would be ineffective in those who can’t generate a strong enough tidal breath on their own.
BiPAP also provides CPAP, but it also detects the patient’s inspiratory effort and delivers greater pressure during inspiration (see”žFigure 2). This is similar to squeezing the bag while assisting a patient with breathing. At the end of the inspiratory phase, the pressure drops back to the preset level of CPAP.
The term Ë™BiPAPà“ is actually the trade name for the biphasic positive airway pressure device developed and sold by Respironics. Today, however, it’s commonly used to describe biphasic positive airway pressure. Other names include bilevel (or biphasic) airway pressure, bilevel (or biphasic) positive pressure, bilevel (or biphasic) CPAP, bilevel (or biphasic) pressure support, among others.
CPAP machines are generally capable of delivering only CPAP, whereas BiPAP machines can deliver either CPAP or BiPAP. Respiratory care practitioners and emergency physicians report that BiPAP provides a greater level of control than CPAP. So it’s not uncommon for a patient to be removed from the prehospital CPAP device and placed on a device capable of BiPAP. Usually the patient is kept on CPAP until blood gases are obtained. Once blood gas measurements are evaluated, BiPAP is initiated at settings that will provide the best gas exchange and optimum cardiopulmonary performance.
A 1997 study suggests that BiPAP improves ventilation and vital signs more quickly than CPAP. So in systems where transport times are long (e.g., rural areas), it may be beneficial for patients to be placed on BiPAP rather than CPAP. Improvements in ventilation and vital signs would occur sooner and can be maintained for the duration of the transport. However, the study also revealed an increase in the incidence of myocardial infarction in those patients placed on BiPAP. Thus, it’s necessary for the provider to reassess the patient frequently.
Benefits & Drawbacks
BiPAP and CPAP are beneficial because they decrease the need for endotracheal intubation, thereby lessening the complications associated with intubation. These include pneumonia, upper-airway injury and prolonged ICU and hospital stays. Additionally, although the use of NPPV is recommended for relaxed, non-combative patients, the use of these forms of NPPV doesn’t generally require sedation.”ž
Complications of BiPAP and CPAP are typically minor and include injury to tissues where the mask makes contact with the face. This risk is especially true for older patients who typically have thinner skin.
Other complications include gastric distention, aspiration pneumonia, hypotension and pneumothorax. For these reasons, NPPV shouldn’t be used on patients who have undergone recent facial surgery, have excessive secretions, are experiencing gastrointestinal bleeding or don’t have the ability to protect their own airways.
Conclusion
There’s significant support for NPPV in the emergency management of patients suffering from acute respiratory failure due to cardiogenic pulmonary edema and COPD. Although CPAP and BiPAP are both gaining popularity, BiPAP is sometimes preferable considering transport times and environment. Unfortunately, BiPAP machines are significantly more expensive, making CPAP the more common form of NPPV used in the field.
In the case presentation, the patient was removed from the CPAP device and placed on a BiPAP device. This therapy provided the hospital staff greater control once arterial blood gases were determined. The patient was kept on a CPAP mode until these values were determined, at which point inspiratory pressure support was initiated using BiPAP modes.
NPPV will likely be increasingly used by prehospital providers in the treatment of respiratory failure, and it’s critical for us to understand when and how to apply this therapy for the best possible outcome for our patients.
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