BY STEVEN KANARIAN
The clock reads 1:45 a.m. as Carl opens his eyes with the uneasy feeling of not being able to catch his breath. Once awake, he realizes he also has tightness in his chest. He begins to cough up pink-tinged white phlegm.
Carl’s wife (awakens): “Carl, you are very pale and sweaty. Are you okay?”
Carl (grunting): “I … I ... don’t ... know.”
Carl’s wife: “I told you not to eat all the food at the wedding last night.”
Carl (stammering): “How often ... does ... your ... niece get married, dear? My chest really hurts, honey.”
Carl’s wife calls 911.
At the Station
At 1:53 a.m., the tones sound.
“Ambulance 1, Engine 14, a Delta response to 55 Dutch Hills Lane for a 65-year-old male, conscious and alert with severe respiratory distress.”
Ambulance 1 acknowledges, responding.
As the experienced crew of this rural ambulance responds to the call location, personnel begin reviewing the dispatch information. Kevin and Don know several things. First, at this time of night, this is probably a real call. Second, it is straight out 45 minutes to the nearest hospital. Thankfully, the valley pass will not be icy tonight. As Ambulance 1 glides over the suburban roadway moving closer to the call, First Responder Engine Company 14 arrives by Carl’s side with oxygen and an automated external defibrillator (AED).
Engine 14: “Engine 14, advise Ambulance 1 we have a 65-year-old male with acute shortness of breath, blood pressure (BP) 160/110, pulse 124, respirations 30, O2 sat 88 percent on a nonrebreather. Ambulance 1, read direct.”
Kevin: “Ambulance 1, thanks for the update; we are eight minutes out.”
AMBULANCE 1 ARRIVES AT HOUSE
On arrival, the crew of Ambulance 1 finds Carl in a tripod position leaning on the edge of his bed, pale in color, his undershirt dripping with sweat. The engine company has administered oxygen by nonrebreather mask at 12 liters per minute and is assisting Carl with self-administration of a second tablet of his prescribed nitroglycerin.
Kevin: “Good morning, Lieutenant, what do you have?”
Lieutenant: “Carl is a 65-year-old male complaining of shortness of breath for about 15 minutes. He is coughing up pink-tinged sputum and is also complaining of tightness in the chest.
Kevin: “Thanks, Lieu.”
The senior partner then asks Carl’s wife the history of present illness and past medical history.
Partner: “How long has he been short of breath? What brought on this episode? Has this ever happened before? Does he sleep flat or with his head elevated on pillows?”
Meanwhile, Don speaks to Carl.
Don: “Anything else bothering you besides the trouble breathing?”
Carl: “Heavy.” (He rubs his sternal area.)
Don: “Have you ever experienced pain like this before?”
Carl’s wife (in annoyed tone): “Yes. He’s had heart failure with fluid in his lungs three times and still doesn’t learn to eat right.”
Don checks the fire department pulse oximeter attached to Carl, which now reads 86 percent.
Firefighter (as he finishes taking vitals): “He has a BP of 170/110, pulse 130, lungs are filled with rales halfway up.”
Kevin: “He has a history of type II diabetes, high BP, and had a stent placed for unstable angina a year ago. He takes Diabinese®, nitro as needed, and hydrochlorothiazide. Shortness of breath woke him out of his sleep 20 minutes ago; breathing is worse when he lies down, chest pain mid-sternal tightness. Sounds like pulmonary edema.”
Don: “Let’s call for advanced life support (ALS).”
Kevin (calling dispatch): “Ambulance 1, we have a 65-year-old male with pulmonary edema; requesting you advise on availability of ALS.”
Dispatch: “Ambulance 1, I have been checking; no ALS available at this time.”
Kevin and Don package Carl and carry him out to the ambulance with the first responder engine company.
In the ambulance, Carl’s vital signs are reassessed: BP is 182/118, pulse is 130, respirations are 32, with intercostal retractions.
Don: “He is working harder to breathe. I think we should call Medical Control for CPAP.”
Kevin contacts Medical Control as Don prepares the CPAP device.
Kevin: “Ambulance 1 to Valley Medical Control.”
Valley: “Valley Hospital, go ahead 1.”
Kevin: “We have a 65-year-old male who awakened with shortness of breath 30 minutes ago. The patient has a productive cough of white, blood-tinged sputum and substernal chest tightness, nonradiating. History of hypertension, diabetes, and a stent one year ago. The patient has JVD, rales all the way up on both sides, and 2+ pedal edema to the pretibial area. We are requesting permission to administer CPAP.”
Valley: “Go ahead, Ambulance 1; sounds like pulmonary edema. Administer CPAP, and assist the patient in taking one nitro every five minutes as long as the blood pressure is above 130 systolic. Monitor respiratory effort, and assist ventilations if necessary. What is your ETA?”
Kevin: “We are 45 minutes out.”
Valley: “We will be expecting you, Ambulance 1.”
Don and Kevin apply the CPAP device to Carl’s face, reassuring him that it may be uncomfortable at first, but it will help him breathe.
AT THE HOSPITAL
On arrival at Valley Medical Center, Carl is breathing with less exertion, his lungs are only one-third full with rales, and he is calmer.
In fact, Carl received the very same standard of care from his BLS providers as an ALS unit would have delivered, if one had been available: nitroglycerin administration and CPAP. This level of care not only shortened his hospital stay, but it also avoided intubation and days of mechanical ventilation in an intensive care unit; it also likely helped him to survive the 45-minute ride to the hospital.
PATHOPHYSIOLOGY OF PULMONARY EDEMA
The function of the respiratory system is to bring oxygen into the lungs through ventilation. From the lungs, oxygen diffuses into the bloodstream. Respiration begins with the contraction of the diaphragm, which expands the volume of the chest, thereby lowering pressure in the lungs, which causes air to rush into the lungs to equalize the pressure. As air fills the lungs, oxygen travels through the trachea, the bronchi, and the bronchioles to the alveoli. The alveoli are single-cell structures encased in capillaries that allow for the transfer of oxygen and carbon dioxide.
During respiration, oxygen-rich air is brought into the alveoli and diffuses into the alveoli, binding with hemoglobin. Carbon dioxide diffuses from the blood stream into the alveoli, where there is a lower pressure of CO2 gas. The exchange of oxygen and CO2 in the bloodstream by diffusion is essential to cellular oxygenation. Without oxygenated blood to transport oxygen and remove CO2, cells would become hypoxic and acidotic. Several disease processes can interfere with ventilation and diffusion of oxygen, causing shortness of breath and hypoxia.
RESPIRATION VS. VENTILATION
Diseases may limit expansion of the chest and control of breathing, obstruct flow of air into the lungs, or delay the diffusion of oxygen into the lungs. Pulmonary edema delays the absorption of oxygen into the blood through the alveoli by filling the alveoli with fluid. Pulmonary edema is caused by a weakened left ventricle, resulting in backup of fluid in the pulmonary veins and vasculature of the lungs or by an overload of fluid in the body. As pressure in the pulmonary veins increases, fluid seeps into the lungs, filling alveoli and small bronchioles at the bases of the lungs. As fluid continues to build, other areas of the lungs become filled, causing a shunting of nonoxygenated blood back into the circulatory system. As pulmonary edema increases, hypoxia and anxiety increase. Patients with pulmonary edema feel short of breath and often have a sensation of drowning in their own fluid. As hypoxia increases, the left ventricle becomes increasingly strained, causing ischemia of the heart muscle. The combined effects of a weakened left ventricle, lungs filling with fluid, and hypoxia cause increased CO2 retention, respiratory acidosis, and a downward spiral effect of patient deterioration.
Pulmonary edema can be caused by gradual progression of heart failure over a prolonged period. The patient history would typically include increased shortness of breath on exertion and sudden shortness of breath that awakens the patient from sleep (called paroxsysmal nocturnal dyspnea, or PND). Pulmonary edema can also be caused by increased permeability of the capillaries in the lungs caused by carbon monoxide poisoning, inhalation of chemicals, or sepsis.
WHAT IS CPAP?
Continuous positive airway pressure (CPAP) applies positive pressure through all phases of the respiratory cycle. The positive pressure opens collapsed alveoli. Pulmonary edema, pneumonia, and pulmonary embolism are medical problems that may cause collapsing of the alveoli. You may remember from anatomy class that alveoli are the one-cell terminal ends of the bronchioles where gas exchange takes place between inspired air in the lungs and the hemoglobin in a patient’s blood. The collapse of alveoli is referred to as “atelectesis.” “Atelectesis is the loss of lung volume caused by inadequate expansion of air spaces. It is associated with shunting of inadequately oxygenated blood from pulmonary arteries into veins.”1 The effect of many alveoli collapsing in a section of the lung is the inability to exchange gas. Similar to a train that passes through a station unable to unload or take on new passengers, blood passes through the lungs unable to release carbon dioxide or pick up oxygen, thereby passing through the lungs without oxygenating. The extent of shunting depends on whether a lobe or an entire lung is filled with fluid.
Prehospital care of pulmonary edema by paramedics traditionally includes the acronym LMNOP:
Lasix®, a diuretic, is used to increase the elimination of excess fluid through urination.
Morphine and Nitroglycerin are used to facilitate the pooling of blood in the distal veins to reduce the preload on the left ventricle (preload is the amount of blood the left ventricle receives and must pump out during systole).
Oxygen is used to increase the concentration of available oxygen in the lungs, thereby maximizing the concentration of oxygen in the blood.
Positioning a pulmonary edema patient in an upright position of comfort causes fluid to rest in the bases of the lungs, opening more lung surface area in the upper lobes for oxygen to pass into the bloodstream.
CPAP has been successful in reducing the use of endotracheal intubation in pulmonary edema2-3 and is easy and effective for EMTs to use. (3)
EMTs and paramedics must understand when administering CPAP that it provides additional pressure during inspiration but cannot ventilate an apneic patient. It is not a ventilation system (photo 1). CPAP, when used with a mask, provides positive pressure with a patient’s respiratory effort but not enough pressure to inflate the chest. When using CPAP, providers must diligently monitor the patient’s respiratory status and level of consciousness. When respiratory failure is present, respirations must be assisted with BVM attached to high-flow oxygen. Respiratory failure is detected by monitoring adequate chest rise, skin color, level of consciousness, and oxygen saturation.
(1) A typical prehospital CPAP unit. (Photos courtesy of Emergent Respiratory Products, Inc., Irvine, California.)
HOW TO APPLY CPAP
CPAP can be beneficial to your patient when your assessment reveals pulmonary edema and sufficient respiratory effort. Treat patients who meet criteria for CPAP in accordance with your local protocols with CPAP equipment following the manufacturer’s recommendations for your particular delivery system. When administering CPAP, have a BVM with high-flow oxygen and a suction unit with a rigid large-bore suction catheter available in case your patient deteriorates during CPAP administration.
CPAP is secured by elastic straps that encircle the head and secure the mask tightly over the nose and mouth (photo 2). Some systems use nasal masks, which cover only the nose. Before placing the mask on your patient, explain the procedure and benefit to your patient. Be sure to explain that this mask fits tightly over his face because a tight seal is important to ensure pressure. Explain to your patient that the pressure will make breathing easier.
CPAP will not ventilate your patient. Once CPAP is applied and the patient has grown accustomed to the treatment, continually monitor and reassess the patient’s respiratory effort and level of consciousness.
SIDE EFFECTS OF CPAP
Pneumothorax and aspiration are two possible consequences of CPAP. “Problems with administering CPAP by mask include gastric insufflation ... aspiration of gastric contents can occur if the patient vomits while the mask is strapped to the face.”4 Programs using CPAP have not found pneumothorax to be a significant problem from EMS administration of CPAP.5 EMS providers who are effectively trained in assessment, CPAP application, and monitoring the patient’s respiratory status can successfully administer CPAP. An effective CPAP program necessitates training in respiratory assessment, CPAP administration, strong medical control, continuous quality control monitoring, and a CME component. Above all, providers must understand CPAP is not a substitute for artificial ventilation. When a patient’s respiratory effort is no longer effective, providers must cease CPAP use and ventilate the patient.
CPAP use has progressed from in-hospital to prehospital administration. It has proven effective in the treatment of pulmonary edema, reducing the number of patients who have to be intubated during the treatment of their pulmonary edema. The system’s medical director should evaluate CPAP use, considering the frequency of pulmonary edema patients seen in your system. CPAP use will continue to increase in regions where ALS is not available or is a scarce resource. Evaluation of CPAP use in EMS should continue as prehospital CPAP use increases.
1. Kumar, V, S Ramzi, S Robbins, MD. Robbins Basic Pathology. (Philadelphia, PA: Saunders), 2003, 454.
2. Hubble M, M Richards, T Jarvis, T Millikan, D Young, “Effectiveness of Pre-Hospital Continuous Positive Pressure in the Management of Acute Pulmonary Edema,” Prehospital Emergency Care; 2006, 10:430-439.
3. Marchetta M, M Resanovich, L Edmunds, “Pre-Hospital CPAP reduces the need for intubation in respiratory emergencies (abstract).” NAEMSP, 2006.
4.Scanlan, Wilkins, Stoller, Egan’s Fundamentals of Respiratory Care, 7th edition, (St. Louis, MO: Mosby-Year Book), 1999.
5. Wesley, Keith, MD, “The ‘Basic’ Skill of CPAP,” Journal of Emergency Medical Services; 2007, 32:10, 21-22.
STEVEN KANARIAN, MPH, is the instructor coordinator for the LaGuardia Community College Paramedic Program in Queens, New York. He is also a lieutenant with the Fire Department of New York, EMS Command and chairs the National Association of EMS Educators (NAEMSE) Research Committee.