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Shortness of Breath

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CONTINUING EDUCATION FROM EMS

     This CE activity is approved by EMS Magazine, an organization accredited by the Continuing Education Coordinating Board for Emergency Medical Services (CECBEMS), for 1.5 CEUs. To earn your credits, go to www.rapidce.com, or to print and mail a copy, download the test here. The deadline to take the test is August 31, 2009.

OBJECTIVES

  • Review respiratory and cardiac anatomy
  • Discuss cardiac causes of shortness of breath
  • Discuss respiratory causes of shortness of breath
  • Review patient assessment

An ALS ambulance responds to a report of shortness of breath. Upon arrival, the EMS crew finds a female in her mid-40s complaining of difficulty breathing. She is sitting on a chair in the tripod position and says she has never felt like this before.

     Physical assessment reveals that the patient is conscious and oriented with pale, sweaty skin. Her heart rate is 142, sinus tachycardia, with a respiratory rate of 40 and blood pressure of 146/62. Breath sounds reveal expiratory wheezes in all fields. She is able to speak in complete sentences, says she has had a nonproductive cough for three days, and she smokes one pack of cigarettes a day. She denies any other complaints. The remainder of her assessment is unremarkable.

     The EMS providers initiate treatment. Supplemental oxygen is administered and an intravenous line is established. An albuterol breathing treatment is administered via nebulizer and the patient indicates that it is helping. During transport to the hospital, the patient's color improves, her respiratory effort decreases, and she has less wheezing. Vital signs are repeated as the crew arrives at the hospital.

     As illustrated above, EMS frequently responds to requests for assistance due to difficulty breathing. This article provides an overview of respiratory and cardiac anatomy, as well as examples of conditions that can result in shortness of breath.

RESPIRATORY ANATOMY

     Breathing involves the movement of air through the mouth, nose, trachea and lungs. The trachea divides into the left and right main bronchi, which lead to the bronchioles and alveoli. Gas exchange occurs in the alveoli along the alveolar-capillary membranes. Waste products, such as carbon dioxide, are transported to the lungs by venous circulation to the alveoli, where they are removed when an individual exhales.1-3

     The process of breathing involves the interaction of several systems, including the diaphragm, intercostal muscles and brain stem. The diaphragm is a layer of muscle that extends along the bottom of the thoracic cavity, separating it from the abdominopelvic cavity. When relaxed, it has a dome shape. When contracted, it flattens and increases the size of the chest cavity by making it longer. This results in negative pressure within the thoracic cavity and contributes to inhalation. The air within the thoracic cavity is passively released when the diaphragm relaxes.1-3

     When the intercostal muscles of the rib cage contract, they pull the rib cage upward, expanding the chest wall and stretching the lung. Negative pressure is created in the thoracic cavity, resulting in inhalation as air is drawn through the respiratory tract.1-3

     Breathing is also influenced by the brain stem, which has a respiratory center that is sensitive to the presence of gases in the blood. For example, when sufficient amounts of carbon dioxide (CO2) are in the bloodstream, the brain stem responds by triggering a breath. This helps to remove the CO2.1-3

     Each breath, or respiration, involves inhalation and exhalation. In most cases, exhaling is passive. During exhalation, the intercostal muscles relax, the diaphragm returns to its rested curved shape, and the chest cavity and lungs return to a resting size. Air is then compressed into a smaller thoracic cavity. When this occurs, air pressure in the lungs is usually greater than that of the atmosphere. Air is then passively released from the respiratory system, often without using any muscles.1-3

     During strenuous activity, exhaling may become an active process. Abdominal wall muscles contract, pushing the diaphragm upward, while contraction of the intercostal muscles pulls the rib cage downward, accelerating expulsion of air.1-3

     Exhalation may be an active process in the presence of certain medical conditions like emphysema. This can be the result of numerous factors, including changes of the respiratory anatomy or obstruction of the airways. A classic example of active exhalation is the "pursed lip breathing" that is sometimes observed in emphysema. In this situation, the respiratory system must actually assist with exhalation due to air trapping in the alveoli.1-3

CARDIAC ANATOMY

     The heart's right side is comprised of the right atrium and ventricle; the left side includes the left atrium and ventricle. The right side receives blood flow from the venous system; the left side feeds the systemic circulation through the arterial system.4-7

     Each chamber of the heart contains valves that promote smooth myocardial function. The tricuspid valve is located between the right atrium and ventricle; the mitral valve is between the left atrium and left ventricle. The pulmonary valve is between the right ventricle and pulmonary artery; the aortic valve is between the left ventricle and aorta.4-7

     The heart's function and effectiveness are influenced by electrical and mechanical activity. The conduction system is responsible for transmitting signals throughout the myocardium. In general, the electrical pathway begins in the sinoatrial node (SA node), passes through the atrioventricular (AV) junction and then follows the Purkinje's fibers. Electrical signals are sent throughout the myocardium with the goal of triggering muscle contraction. In the prehospital setting, electrical activity of the myocardium can be monitored by an electrocardiogram (EKG), while mechanical activity is assessed by the presence of a pulse.4-7

     Although presented as separate systems, the respiratory and cardiovascular systems complement and influence each other. Fluctuation in one may trigger a response in the other. If an individual experiences an abnormality in either system, such as a heart attack or bronchitis, he may experience "shortness of breath." The remaining discussion provides an overview of select cardiac and respiratory conditions that may result in shortness of breath.4-7

CARDIAC CAUSES

MYOCARDIAL INFARCTION

     A myocardial infarction (MI) involves cardiac necrosis that results from an imbalance in oxygen supply and demand. In the United States, it is estimated that MIs are responsible for a half-million deaths annually.4,5

     A common cause of MI is atherosclerosis (narrowing of blood vessels) that results from plaque build-up and the subsequent plaque rupture leading to partial or complete occlusion of a vessel, then myocardial necrosis. Nonatherosclerotic causes include cocaine use, an infected heart valve, acute anemia and trauma.4,5

     Primary symptoms of an MI can include chest discomfort, described as tightness, pain, squeezing or pressure. The discomfort may radiate to the jaw, shoulder, neck, back or both arms. Dyspnea may also be reported. The patient may experience shortness of breath without any chest pain or discomfort. Nausea, vomiting, anxiety, lightheadedness, cough and diaphoresis may be present.

     A myocardial infarction can also present without symptoms, referred to as "silent MI." An MI can be described based on assessment findings, such as ST-elevation MI (STEMI), non-ST-elevation MI (NSTEMI) and unstable angina. Elderly and diabetic patients may exhibit more subtle symptoms, including lightheadedness, fatigue, weakness or syncope.4,5

CONGESTIVE HEART FAILURE

     Congestive heart failure (CHF) is a condition where the heart's ability to pump oxygen-rich blood does not meet the body's needs. It affects over 2 million people in the United States, with 500,000 new cases diagnosed each year. More than 1 million involve individuals under age 60.8-12

     CHF has numerous causes, including myocardial ischemia, valvular heart disease, cardiomyopathies and myocarditis. In general, any disease that weakens or causes stiffening of the heart muscle and/or leads to increases in oxygen demand that exceed the heart's ability to deliver can result in CHF.8-12

     In CHF, excess fluid accumulates behind the affected heart chamber. In left ventricular failure, excess fluid develops in the lungs, resulting in pulmonary edema or congestion and often shortness of breath.8-12

     The symptoms associated with CHF vary and depend on right side versus left side heart involvement. Some symptoms may be nonspecific, such as fatigue, while others like edema of the ankles, legs and/or abdomen are more obvious in right-side CHF. In left-side CHF, the patient may report shortness of breath that becomes more severe with physical exertion or while supine. Nausea may develop due to the accumulation of fluid in the liver and intestines. Coughing and breathlessness may also be reported.8-12

     A common symptom of left-side heart failure is dyspnea, particularly with exertion. When pulmonary pressures reach high levels, fluid moves into the lungs and compresses the alveoli, which results in increased resistance to airflow and increases the work of breathing.

     Additional symptoms like orthopnea (the sensation of breathlessness while lying flat) and paroxysmal nocturnal dyspnea (PND) may develop. PND results from gradual reabsorption of lower extremity edema after lying down and can result in severe breathlessness that awakens the patient from sleep. Other symptoms may include fatigue and altered mental status.8-12

RESPIRATORY CAUSES

CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)

     CODP is a group of disorders, such as bronchitis and emphysema, that are characterized by airway obstruction. In COPD, the obstructed airflow tends to be progressive and may be partially reversible. It is estimated that 14 million Americans have diagnosed COPD. COPD and asthma together represent the fourth leading cause of death in the U.S.5,7

BRONCHITIS

     Acute bronchitis involves inflammation of the tracheobronchial tree, including the trachea and bronchi. The inflammation can be temporary and mucus may develop. A majority of cases are the result of a virus. Chronic bronchitis differs from acute bronchitis, both in duration and ruling out of other disease processes. In the field, it is not always possible to differentiate between the two, and prehospital treatment may not depend on the differentiation.13-17

     Causes include infectious pathogens; allergens and irritants such as influenza A and B, parainfluenza, adenovirus, rhinovirus and respiratory syncytial virus; cigarette smoking or exposure to cigarette smoke; and exposure to dusts, noxious gases and air pollution.13-17

     Symptoms of bronchitis can include a productive cough, rhinorrhea (runny nose), nasal congestion, sore throat, wheezing, dyspnea and chest tightness or pain. Myalgia (muscle pain), arthralgias (joint pain), fever and malaise may be present. Breath sounds may be normal or slightly diminished. Rhonchi or wheezes may be present. Gas exchange can be impaired and may lead to increased carbon dioxide production, resulting in irritability, decreased mental status and headache.13-17

EMPHYSEMA

     Emphysema is the abnormal and permanent enlargement of air spaces within the lungs, characterized by the gradual progression of airway collapse. When mild, bronchiolar changes are responsible for airflow restrictions. With increased severity, elastic recoil is lost and vascular changes may develop. This can result in chronic cough and sputum production. The airflow obstruction in emphysema may be irreversible; however, bronchoconstriction may be reversed through aggressive treatment.5,7,18

     Cigarette smoking is cited as a significant risk factor for emphysema and may play a role in up to 90% of cases. Additional factors include respiratory infections, occupational exposures, intravenous drug use, air pollution and exposure to second-hand smoke.5,7,18

     The most common initial symptom is the progressive development of dyspnea. Breathlessness and exertional dyspnea may be reported with moderate exertion. A cough is common and tends to be worse in the morning, producing small amounts of colorless sputum. Wheezing may occur, especially during exertion and exacerbation. As the disease progresses, the intervals between acute exacerbations become shorter. Cyanosis and right heart failure may develop. Severe disease progression can involve tachypnea and respiratory distress with moderate or even minimal physical activity.5,7,18

     Be attentive for signs and symptoms of respiratory distress. This can include tachypnea, accessory muscle use and the paradoxical in-drawing of lower intercostal spaces. In later stages of emphysema, cyanosis, increased jugular venous pressure (JVP) and peripheral edema may develop. Hyperinflation (e.g., barrel chest), decreased breath sounds, wheezing, hyperresonance on percussion and prolonged expiration may be involved (Table I).5,7,18

Table I: Emphysema and Bronchitis Comparison
SYMPTOMS EMPHYSEMA PREDOMINANT (PINK PUFFER) BRONCHITIS PREDOMINANT (BLUE BLOATER)
Major complaint Dyspnea after age 50 Chronic cough, production of sputum, may present in 30-40-year-olds
Appearance Think recent weight loss, appear uncomfortable with accessory muscle use to breath Tend to be overweight, cyanotic, appear comfortable at rest
Breath sounds Chest tends to be quiet, peripheral edema uncommon Chest noisy, rhonchi present, wheezing may be present

ASTHMA

     Asthma involves inflammation of the airways and is characterized by hyperresponsiveness of the tracheobronchial tree to various stimuli. The inflammation may be acute, subacute or chronic. Edema and mucus secretion contribute to airflow obstruction and bronchial reactivity. There are several forms, such as exercise-induced asthma (EIA).19,20

     Asthma affects as much as 10% of the U.S. population. More than 1.5 million emergency department evaluations occur annually due to asthma. It is the most common chronic disease of childhood. Trends suggest an increase in prevalence and morbidity of the disease, especially among individuals younger than age 6. Influencing factors include urbanization, air pollution, passive smoking and changes in exposure to environmental allergens. Most acute attacks are reversible and improve spontaneously or within minutes to hours with proper treatment.19,20

     Causes of asthma usually involve stimuli that are known to produce an acute episode and can range from environmental agents (e.g., animal hair) to certain medications (e.g., beta blockers).

Table II: Causes of Asthma

  • Environmental (animal, cockroach, fungi)
  • Viral respiratory infections
  • Hyperventilation
  • Gastroesophageal reflux disease (GERD)
  • Nonsteroidal anti-inflammatory drug hypersensitivity
  • Use of beta-adrenergic receptor blockers
  • Occupational exposure
  • Perinatal factors (prematurity, increased maternal age)
  • Exercise
  • Sinusitis or rhinitis
  • Tobacco smoke
  • Emotional factors

     Others: insects, plants, latex, gums, anhydrides, wood dust, and fluxes.

     When assessing the asthmatic patient, consider all possible causes in an effort to provide optimal care (Table II).19,20

     When a triggering source like pollen is encountered, several events occur. The body releases histamine, which leads to bronchoconstriction, bronchial edema and a reduction in expiratory airflow.19,20 If the initial phase continues, a second sequence of events may occur. Immune system reactions contribute to additional edema and restrictions throughout the respiratory system. Airway hyperresponsiveness and bronchial hyperreactivity also occur.19,20

     Airflow obstruction in asthma can be influenced by a variety of factors, including acute bronchoconstriction, airway edema and mucus plug formation. Airway edema can develop as long as 24 hours or later following an allergen exposure. When mucus plugs and congestion develop, it may take several weeks to resolve.19,20

     Symptoms can range from mild shortness of breath to cardiopulmonary arrest. A triad of symptoms includes dyspnea, wheezing and cough (Table III). Note that lack of wheezing in an asthmatic patient might indicate that the airways are so narrow as to not allow passage of any air. Because of this, do not depend primarily on the presence of wheezing to initiate treatment for asthma. For example, the asthmatic patient who complains of shortness of breath, is agitated and/or combative (e.g., refusing oxygen) and has no wheezing, yet appears ill, should be considered to be in severe exacerbation or asthma until proven otherwise. This is sometimes referred to as "air hungry." The patient is short of breath but is unable to effectively breathe due to hyperinflation of the airways.19,20

Table III: Signs and Symptoms of Asthma

  • Cough
  • Wheezing
  • Dyspnea
  • Chest tightness
  • Shortness of breath
  • Tachypnea
  • Speech dyspnea (need to take a breath to complete a sentence)
  • Pulsus paradoxus: 10 mm Hg or greater decrease in systolic blood pressure with inspiration
  • Accessory muscle use
  • Minimal air movement with chest auscultation
  • Tachycardia

PULMONARY EMBOLISM

     A pulmonary embolism (PE) involves blockage of a pulmonary artery. This is frequently caused by a thromboembolism, which occurs when a blood clot becomes dislodged from its site of formation and travels to the arterial blood supply of one of the lungs. Deep vein thrombosis (DVT) is the source of PE in up to 90% of cases.5,21

     A potentially lethal event, PE has an incidence of more than 650,000 cases per year, with over 200,000 deaths. Up to one-third of the deaths occur within the first hour, and many patients die despite prompt recognition and treatment. The diagnosis may be missed because patients often present with nonspecific signs and symptoms and as many as half may be asymptomatic. In patients who survive, prompt diagnosis and therapy can impact long-term morbidity and mortality. 5,21 Treatment with anticoagulants decreases the mortality rate to less than 5%. The risk of PE is increased in pregnancy and during the postpartum period.5,21

     The pathways of pulmonary emboli are complex. Three key factors that lead to their formation include venous stasis (reduced blood flow), injury to the intima (damaged vessel) and changes in the blood's coagulation (ability to clot).5,21 Pulmonary emboli often arise from the thrombi that originate in the deep venous system of the lower extremities. They may also occur in the pelvic, renal or upper extremity veins and the right heart chambers. After traveling to the lung, thrombi can lodge at any location within the pulmonary system.5,21

     Occlusion of a larger vessel can lead to immediate hemodynamic compromise, resulting in acute shortness of breath, tachycardia and profound hypotension. Occlusion of smaller vessels is more likely to produce less specific findings.5,21

     There is no typical presentation of PE. In the prehospital setting, providers may be called to assess a complaint of dyspnea, pleuritic chest pain, cough or hemoptysis. It may be unclear as to what is causing the patient's symptoms. Hospital-based diagnostic assessments may be required to determine the exact pathology.5,21

     Symptoms of pulmonary embolism may range from mild dyspnea to sudden hemodynamic collapse. The presentation can be categorized into different classes based on the acuity and severity of pulmonary arterial occlusion (Table IV). Pulmonary embolism should be considered in patients with respiratory symptoms that are unexplained by an alternate cause, such as asthma or bronchitis. Because the symptoms of a PE can be nonspecific, a high index of suspicion is required, particularly when a patient has risk factors like recent surgery or immobility. Consequences include increased alveolar dead space, pneumoconstriction, hypoxemia, hyperventilation and pulmonary infarction.5,21

     The development of a PE can increase pulmonary vascular resistance and may lead to right heart failure. Pre-existing cardiopulmonary disease increases the potential impact a PE may have, but patients without pre-existing disease can still experience devastating effects. Tachypnea is present in over 90% of PE, while tachycardia occurs in less than 50%. Localized wheezes are suggestive of PE, but are not a common finding.5,21

Table IV: Examples of Physical Assessment Findings of Pulmonary Embolism
PATHOLOGY SYMPTOMS
Massive pulmonary embolism: large emboli impact pulmonary circulation leading to circulatory shock Hypotension, poor perfusion to extremities, tachycardia, tachypnea, pale, sweaty, altered mentation
Acute pulmonary infarction: peripheral occlusion of pulmonary artery leading to parenchymal infarction Acute onset pleuritic chest pain, dyspnea, hemoptysis, local tenderness, reduced chest wall movement, pleural friction rub, may mimic ischemic chest pain
Acute embolism without infarction Nonspecific symptoms that may be confused with other disease processes, tachypnea, tachycardia, local wheeze, dyspnea and substernal discomfort
Multiple pulmonary emboli or thrombi Two different patterns may be seen
1. Repeated episode of pulmonary emboli over time; eventually present with symptoms of pulmonary hypertension and cor pulmonale.
2. No previously document pulmonary emboli but have obstruction of pulmonary system with clot. Tend to present with dyspnea, exertional chest pain, pulmonary hypertension.
ADDITIONAL SIGNS AND SYMPTOMS
Seizures Syncope New onset atrial fibrillation
Rales Tachycardia Chest wall tenderness, with or without a history of trauma
Fever Tachypnea

PNEUMONIA

     Pneumonia can be a complication of a pre-existing condition or the result of an infection. It may also be triggered when the defense system is weakened, as in the case of a viral upper respiratory tract infection or influenza. Pneumonia is a common medical problem accounting for more than 600,000 hospitalizations every year.5,22

     Pneumonia is often caused by inflammation of the lung as a result of a bacterial or viral infection. Individuals considered to be at high risk include the elderly, the very young and those with underlying health problems, such as COPD, diabetes mellitus, congestive heart failure and sickle cell anemia. Patients with diseases like AIDS that impair the immune system, those undergoing cancer therapy or organ transplantation, and patients with other chronic illnesses are also at risk.5,22

     The classic presentation involves dyspnea with fever, rigors and sputum production. There is, however, wide variability in both symptoms and physical findings. Pulmonary findings can include bronchial congestion, such as rhonchi and wheezing, rales or decreased breath sounds.5,22

     Symptoms vary, depending upon factors like the patient's age, underlying health and severity of the episode. Overall, symptoms of viral pneumonia are similar to those of influenza and include fever, dry cough, headache, muscle pain, weakness, fever and increasing breathlessness. Bacterial pneumonia symptoms can vary from gradual to acute. The patient may experience shaking/chills, chattering teeth, severe chest pains, sweating, a cough that produces rust-colored or greenish mucus, tachypnea, tachycardia and/or cyanosis. Older patients may present with a change in mental status, with or without respiratory symptoms.5,22

Table V: Examples of Medications for Shortness of Breath
MEDICINE MECHANISM/CLASS OVERVIEW
Epinephrine Bronchodilator Subcutaneous
Betamethasone Corticosteroid Inhaler
Prednisone Corticosteroid Oral
Albuterol (Proventil, Ventolin) Bronchodilator Administered via nebulizer
Isoetharine (Bronkosol) Bronchodilator Administered via nebulizer
Alupent Bronchodilator Administered via nebulizer
Terbutaline (Brethine) Bronchodilator Metered dose inhaler or subcutaneous injection
Aminophylline Smooth muscle relaxant, bronchodilator Intravenous infusion
Methylprednisolone (Solu-Medrol) Anti-inflammatory Intravenous or intramuscular

PATIENT ASSESSMENT

     On arrival, look at both the patient and his surroundings, noting any indications of treatment for shortness of breath such as oxygen supplies, respiratory medications, ventilators and other medications.6,7

     Is the patient conscious? If so, is he exhibiting any signs or symptoms of respiratory distress? Is he in a tripod position? Can audible lung sounds, such as wheezing or rales, be heard? What is the patient's skin color: pink, pale, cyanotic, ashen or gray? Is his skin warm and dry or cool and moist? Look for other clues. Edema of the feet or legs may indicate fluid retention and possibly a cardiac component. Jugular vein distention may indicate fluid overload or heart failure. A patient with a barrel chest may have pre-existing respiratory conditions.6,7

     Can the patient speak in complete sentences? Does he use accessory muscles to breathe? This can be seen as intercostal retractions, nasal flaring, suprasternal retractions or diaphragmatic breathing. Does he appear to be tiring, or is he easily agitated? A restless patient who is experiencing difficulty speaking and complains of shortness of breath should be considered potentially critical.6,7

     Reassess respiratory rate, breath sounds, heart rate and blood pressure every 10 minutes, or more frequently as needed. Use pulse oximetry, capnometry and cardiac monitoring (EKG) when available.6,7

     If the airway is at risk, provide manual support with a bag-valve-mask or endotracheal intubation. Administer oxygen to any patient complaining of shortness of breath. Liter flow rate and route of administration will depend on the patient's condition and provider judgment.6,7

     Because some patients with shortness of breath may be dependent on a hypoxic respiratory drive, administration of oxygen may decrease respiratory drive and lead to significantly reduced ventilations. As a result, be prepared to intervene and support the patient's breathing as necessary. However, this potential should never be a reason to avoid or reduce oxygen administration in any patient complaining of respiratory symptoms. Never withhold oxygen from the dyspneic patient.6,7

     Establish intravenous access as soon as possible. While aggressive fluid administration may not be required, having intravenous access may prove invaluable if the patient needs intravenous medications. Consider establishing the IV line at a "keep-open" rate.6,7

     Medication administration will vary with each scenario. An asthmatic patient may benefit from oxygen and a bronchodilator. A patient with a suspected PE and pleuritic chest pain may need oxygen and close monitoring. A patient in CHF who is short of breath may benefit from preload and afterload reduction (typically with nitroglycerin). Administration of medications should be guided by factors like the patient's medical history, physical assessment findings, local protocols and the treatment (if any) that has already been provided (see Table V).6,7

     Treatment may also include the use of heliox—most commonly provided in a specific compressed mixture of helium and oxygen and delivered through a standard oxygen mask. In the past, it has been used for upper respiratory obstruction, COPD and croup, as well as treatment of refractory asthma as an adjunct to traditional treatments. It is considered a bridging therapy until other therapies, such as bronchodilator and anti-inflammatory agents, take effect.23-25

     Heliox has no bronchodilator or anti-inflammatory effects; however, the oxygen-helium gas mixture is less dense than air, which results in smoother airflow and requires less effort by the patient to breathe while promoting air exchange in the lower airway. Heliox-driven albuterol therapy has shown to be a beneficial adjunct for older patients with severe asthma exacerbations.23-25 While heliox does not produce significant side effects, its benefit has not been conclusively proven and routine use is debated.23-25

     Intubation is a valuable lifesaving tool in some patients with shortness of breath. Be aware, however, that certain patients, particularly those with moderate to severe COPD or asthma, may have better outcomes if intubation can be avoided. Consider intubation as a treatment option while also allowing time for other treatments to take effect.6,7

     Additional management options include the use of continuous positive airway pressure (CPAP) and bilevel positive airway pressure (BiPAP). These techniques are noninvasive and do not require endotracheal intubation. They may be used in the prehospital setting for a variety of medical conditions, including COPD, CHF and asthma. 26-29

     The concept of CPAP is to apply a tight-fitting mask with high-flow oxygen to the patient in an effort to support constant airway pressure. By providing pressure, it is more likely that fluids will not be allowed to interfere with pulmonary gas exchange and ventilation. CPAP essentially opens and supports the alveoli and assists in avoiding alveolar collapse. This can contribute to improved lung compliance, promotes greater functional residual capacity, and may reduce the patient's respiratory effort. It also decreases preload and afterload for the myocardium.26-29

     BiPAP provides CPAP but also has the ability to sense when inhalation is occurring. When the patient inhales, the BiPAP system delivers high-pressure airflow. When the high pressure stops, airflow pressure returns to a predetermined level. With BiPAP, the positive pressure wave that occurs during inhalation helps to reduce the diaphragm's level of work during each breath.26-29

CONCLUSION

     EMS providers are likely to encounter a litany of cases involving "shortness of breath." Having a thorough understanding of shortness of breath pathology is essential to providing adequate care.

References

     1. The Franklin Institute, Resources for Science Learning. Oxygen Delivery System. http://sln.fi.edu/biosci/systems/respiration.html.

     2. Ohio State University Medical Center. Anatomy of Respiratory System. http://medicalcenter.osu.edu/patientcare/healthinformation/diseasesandconditions/respiratory/about/anatomy/.

     3. Wikipedia. Thoracic Diaphragm. http://en.wikipedia.org/wiki/Thoracic_diaphragm.

     4. Fenton D, Stahmer S. Myocardial Infarction. www.emedicine.com/EMERG/topic327.htm.

     5. McPhee S, Papadakis M. Current Medical Diagnosis & Treatment. New York: McGraw Hill, 2007.

     6. Stiell I, Spaite D, Field B, et al. Advanced life support for out-of-hospital respiratory distress. New Engl J Med, 2007.

     7. Bledsoe B, Porter R, Shade B. Paramedic Emergency Care. Upper Saddle River, NJ: Brady Prentice Hall, 1997.

     8. Wrongdiagnosis.com. Prevalence and incidence of congestive heart failure. www.wrongdiagnosis.com/c/congestive_heart_failure/prevalence.htm.

     9. Kulick D, Lee D. Congestive Heart Failure. www.medicinenet.com/congestive_heart_failure/page2.htm.

     10. Cardiology Channel. Congestive Heart Failure. www.cardiologychannel.com/chf/.

     11. MedicineNet, Inc. Congestive Heart Failure. www.medicinenet.com/congestive_heart_failure/article.htm.

     12. U.S. Department of Health and Human Services. Healthier You. Congestive Heart Failure in the United States: A New Epidemic. www.healthieryou.com/chf.html.

     13.Ong S. Bronchitis. www.emedicine.com/emerg/topic69.htm.

     14. Mayo Foundation for Medical Education and Research. Bronchitis. www.mayoclinic.com/health/bronchitis/DS00031.

     15.Wenzel R, Fowler A. Acute bronchitis. New Engl J Med. http://content.nejm.org/cgi/content/full/355/20/2125.

     16. American Family Physician. Chronic Bronchitis. www.aafp.org/afp/20040515/2445ph.html.

     17. Hueston W, Mainous A. Acute bronchitis. American Family Physician. www.aafp.org/afp/980315ap/hueston.html.

     18. Sharma S. Emphysema. www.emedicine.com/med/topic654.htm.

     19. Morris M. Asthma. www.emedicine.com/med/topic177.htm.

     20. National Heart, Lung, and Blood Institute. What Is Asthma? www.nhlbi.nih.gov/health/dci/Diseases/Asthma/Asthma_WhatIs.html.

     21. Sharma S. Pulmonary Embolism. www.emedicine.com/med/topic1958.htm.

     22. American Lung Association. Pneumonia Fact Sheet. www.lungusa.org/site/pp.asp?c=dvLUK9O0E&b=35692.

     23. Reuben A, Harris A. Heliox for asthma in the emergency department: A review of the literature. Emerg Med J. http://emj.bmj.com/cgi/content/abstract/21/2/131.

     24. Krass J, Terregino C. The effect of heliox in acute severe asthma: A randomized controlled trial. Chest. www.chestjournal.org/content/vol116/issue2/index.shtml.

     25. Lee D, Hsu C, Lee H, et al. Beneficial effects of albuterol therapy driven by heliox versus by oxygen in severe asthma exacerbation. Acad Emerg Med. www.aemj.org/cgi/content/abstract/12/9/820.

     26. Sullivan R. Prehospital use of CPAP. EMS 34:8, 120-126, 2005.

     27. Rappard S. Use of CPAP and BiPAP in Acute Respiratory Failure. www.theberries.ns.ca/archives/CPAP.html.

     28. Macon County, North Carolina. CPAP use and operation. www.maconnc.org/ems/CPAP.html.

     29. Poponick J, Renston J, Bennett R, et al. Use of a ventilatory support system (BiPAP) for acute respiratory failure in the emergency department. Chest, Vol. 166. www.chestjournal.org/cgi/content/abstract/116/1/166.

     Paul Murphy, MA, MSHA, EMT-P, has clinical and administrative experience in healthcare organizations.

     Chris Colwell, MD, is medical director for the Denver Paramedic Division and Denver Fire Department, and attending physician in the emergency department at Denver Health Medical Center.

     Gilbert Pineda, MD, FACEP, is medical director for the Aurora Fire Department and Rural/Metro Ambulance (Aurora, CO), and an attending physician in the emergency department at The Medical Center of Aurora and Denver Health Medical Center.

     Tamara Bryan, BS, EMT-P, has more than a decade of healthcare experience, including clinical and project management roles.

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