Notes

Case Study
It is a cool winter morning when the tones go off for a respiratory call at the large senior apartment complex down the street from your station. It is that time of year where colds and flu are affecting the elderly population, and you have been responding frequently to the complex.

You arrive simultaneously with the paramedic engine company and make your way up to a third floor unit. You are met by a slender man who opens the door and invites you in. He has on a nasal cannula and is noticeably short of breath. Although calm, he is concentrating on his breathing.

The engine crew begins to obtain vital signs, and they place the patient on the cardiac monitor while you begin your assessment. You ask them to place the patient on capnography monitoring as well as pulse oximetry.

The man, who is 67-years-old, states that he came down with a persistent cough a few days ago, but last night became significantly more short of breath and experienced chest pain this morning when coughing. He says this is not his worst episode he’s ever had; he says one time before he was intubated and ended up on a ventilator for two weeks.

He says he thinks he might have a fever, notes green sputum production, and states his inhaler hasn’t been working. The chest pain is sharp in nature, located across the entire anterior surface of his chest and worsens with breathing, coughing, and palpation. He says he’s had a heart attack before and this doesn’t feel anything like it.

His medical history is significant for chronic obstructive pulmonary disease (COPD), cardiac stents, and gout. He is oxygen dependent (2 liters per minute), uses Albuterol and Atrovent inhalers, and is on corticosteroid therapy for his COPD. Additionally, he takes aspirin daily, Lotensin and spironolactone. He is allergic to codeine.

Your examination reveals the patient is alert and fully oriented. His skin is pale, slightly hot and dry. He is speaking in 3-4 word sentences. His lips are slightly pursed and perioral cyanosis is present. He has jugular venous distention and his trachea is midline. He is notably barrel chested and using accessory muscles to breathe. His lung sounds are diminished in all fields with inspiratory and expiratory wheezing noted, in addition to rhonchi in the lower fields. His abdomen is soft and non-tender, with no masses or guarding. He has strong and equal distal pulses, no neurological deficits. and noted clubbing of the fingernails.

The engine paramedic reports vital signs of 146/90, a heart rate of 130 corresponding with an EKG rhythm of sinus tachycardia with occasional unifocal PVCs, a respiratory rate of 28, pulse oximetry (on his 2L nasal cannula) of 78%, tympanic temperature of 100.4°F and end tidal capnography revealing a "shark fin" waveform and a reading of 62.

A 12 lead EKG reveals the sinus tachycardia with ectopy, a possible right bundle branch block, but no ST changes indicative of cardiac ischemia or infarct.
Noting the patient’s respiratory severity, you decide to begin aggressive treatment on scene. You begin CPAP with an inline Albuterol/Atrovent nebulizer, using caution with the pressure settings due to his preexisting pulmonary disease.

An 18g IV of .9% Normal Saline is started in the left antecubital and set at a TKO rate. You continue to monitor the patient for signs of deterioration or improvement, with the thought in the back of your mind that if he starts to become significantly fatigued, you will be presented with the decision of if you need to intubate the patient via RSI to manage his ventilations for him, despite the fact that COPD patients often have a tough time being weaned from mechanical ventilation.

As you prepare to transport the patient, you note some minor improvement and he says he is feeling slightly better, but is still having a tough time breathing and is now coughing more. His pulse oximetry is now 90%, ETCO2 is 50, and his respiratory rate remains 28 per minute. You get a quick set of lung sounds walking out to the ambulance, and note that they are slightly less diminished.

En route, you continue the treatment and consult with medical control on whether to give SoluMedrol. It is decided that due to the short ETA, you will hold off on steroids until the patient is reevaluated in the ER.

Introduction
Chronic obstructive pulmonary disease (COPD) is the third leading cause of death in the United States behind cancer and heart disease. In 2012, it was estimated that 15 million Americans had been diagnosed with COPD. There is a strong possibility that COPD is under diagnosed, implied by the 25 million Americans that have evidence of impaired lung function.1

Nearly 134,000 people died of COPD in 2009. Although the number of overall deaths has risen by 12% between 1999 and 2009, the biggest trend has been the increase in female deaths. The number of male COPD related deaths climbed by 5.1% during the same time frame, while the number of female deaths from COPD rose by 19.3%.2

Other demographic characteristics of COPD related deaths include the fact that whites (non-Hispanics) have the highest death rate from COPD, while Hispanics have the lowest death rates amongst major ethnic groups.2

Geographically, Kentucky and Alabama had the highest age-adjusted rate of COPD per population (9.7% and 9.4%, respectively), while Minnesota and Washington had the lowest (4.0% and 4.1%, respectively). Overall, rates of COPD tend to be higher in the Southeast and Midwest.2

Since cigarette smoking is far and away the leading cause of COPD, and cigarette smoking has been declining in the US for several decades, it stands to reason that the domestic incidence of COPD will eventually start declining. Sadly, the opposite is true in the global population. Currently, COPD is the sixth leading cause of death globally, however, that is projected to increase to the fourth leading cause by 2030. This increase in COPD occurrence is due to increased smoking rates in many countries, in conjunction with shifts in median population age.3

COPD is a costly and debilitating disease for the American healthcare system. An estimated 715,000 hospital discharges were reported in 2010 due to COPD. Of these, two-thirds of the patients were over 65 years of age.2

It is estimated that the national annual cost for COPD is $49.9 billion, of which $29.5 billion is actual health care expenditures. The remaining costs are indirect costs related to the morbidity and mortality of the disease.2

Other costs associated with the disease include an estimated $8.0 billion related to a loss of productivity due to the illness and another $12.4 billion in indirect mortality costs related to lost productivity due to early death.

COPD is one of the costliest diseases and is thus a major target for future healthcare reform. COPD causes nearly as much disability as strokes, and more than cancer or heart disease. As such, COPD patients are prone to receiving disability benefits due to their inability to work (approximately half of all COPD patients are under 65).4

It is estimated that over half of the costs of direct treatment of COPD relate to emergency room visits and hospitalizations, as opposed to chronic disease management. This places a need for focus on proper disease management and patient compliance with treatment plans. Adding insult to injury, there is an approximate 10% readmission rate (30 day) for COPD hospitalizations.4 The American Lung Association reports that the average COPD hospitalization costs $17,066 and lasts for over 4 days.2

Physiological Overview
The pulmonary system is responsible for the delivery of oxygen to the body and the exhalation of carbon dioxide. This system is a group of organs and structures that are required to sustain life. While it may seem like a simple, subconscious process that occurs throughout a person’s life, the process of breathing is highly complex and that serves to maintain adequate pH, oxygenation and cardiovascular function.

Blood Gasses/Respiratory Drive
Peripheral chemoreceptors, located in the carotid and aortic arteries, serve to stimulate respiratory activity based on blood oxygen, carbon dioxide, and pH levels. As carbon dioxide builds up in the blood in concert with falling oxygen levels, chemoreceptors "fire" to stimulate ventilation. In a healthy human, hypercapnia (high carbon dioxide levels) is the primary catalyst in increasing ventilation.

The most precise levels of measurement for proper pulmonary gas exchange in the bloodstream are arterial partial pressures of oxygen and carbon dioxide. The respective abbreviations are PaO2 and PaCO2. These two measurements, in conjunction with measures of blood acidity, pH, and HCO3, provide a comprehensive view of the state of perfusion within the human. Additionally, they allow insight into whether a pH imbalance is likely caused by respiratory or metabolic causes. These values are achieved via arterial blood gas draw.

An arterial blood gas (commonly referred to as "ABG") draw involves a thin needle usually inserted at the radial artery, directly perpendicular to the arm so that an arterial blood sample can be drawn. This is the most common site for an arterial blood gas to be performed. This test is often performed by a respiratory therapist, however, a phlebotomist, nurse, or physician may also perform the test.

In a healthy adult patient at sea level, the normal ranges for the arterial blood gas levels are5:

PaO2 75-80 to100 mmHg

PaCO2 35 to 45 mmHg

pH 7.35 to 7.45

HCO3 22 to 26 mEq/L

Mechanics of Ventilation
Inspiration (inhalation) is the active phase of ventilation. This involves the diaphragm contracting and a decreased pressure in the thoracic cavity occurring. This draws air into the lungs.

Air passes through the superior airway (nose and mouth) until it reaches the larynx ("voice box"). Once air has passed the larynx on inspiration, it passes into the trachea. The trachea is a cartilaginous structure that extends from approximately the level of the sixth cervical vertebra, down to the carina. The carina is the bifurcation at the distal end of the trachea, and it leads to right and left main stem bronchi. The left main stem bronchus is narrower, longer and turns at a sharper angle laterally. The structural differences between the right and left bronchi correspond to the underlying difference in the right and left lung due to the presence of the heart on the left side. The right lung has three lobes and the left lung has two.

After the main stem, these bronchi further segment, becoming progressively narrower, more numerous, and shorter until they reach the terminal bronchioles. At the end point of a bronchiole are the alveoli. The alveoli are elastic sacs that maximize surface area to support gas exchange. The elasticity of the alveoli is highly important to normal function. The alveolar capillary membrane is where a majority of gas exchange takes place between the blood supply and the inhaled air.

There are two systems of blood supply to the pulmonary system. The first is the bronchial blood supply. This accounts for only 1% of left ventricular cardiac output and serves to supply the tissues of the lungs themselves with the required oxygen. The lungs are living tissues that need a steady supply of oxygenated blood.

The second system of blood supply is the pulmonary vascular system, which serves to accommodate the blood flow to the lungs that allows for gas exchange to occur. This is how the body receives oxygen from inspired air and how carbon dioxide is disposed of.

Definition
COPD is the name given to the disease process that patients with emphysema or chronic bronchitis suffer from. These two disease processes commonly co-exist. The term "obstructive" refers to the progressive narrowing of the airways in chronic bronchitis, or the reduction in surface area of the alveoli. In either condition, a disease process is hindering the normal passage of airflow and is thus inhibiting proper gas exchange.

Emphysema is a disease caused by the damage and destruction of tissue of the lungs that is vital to proper respiration and gas exchange. The destruction is particularly focused around the alveoli and the alveolar septa. The alveolar septa separate individual alveoli that are next to each other; thus, when emphysema causes destruction of these septa, pulmonary function is adversely affected. The damage to the alveoli causes a loss of elasticity and shape and leads to air trapping and a decrease in alveolar surface area. This air trapping causes a build-up of carbon dioxide (hypercapnia). These factors also prevent proper gas exchange and air movement, ultimately leading to a potentially chronic hypoxic condition.

This is what causes the well known shift in respiratory drive from hypercapnic to hypoxic. These patients can have chronic hypercapnia as the disease progresses, and therefore would not have the normal hypercapnic impulse to cause respiratory drive. Therefore, a physiologic change occurs in which oxygen chemoreceptors began to have more influence in creating the impulse for respiration, as the body becomes dependent on using falling blood oxygen levels to drive respiration since there are chronic elevated CO2 levels at all times.

Chronic bronchitis, which frequently accompanies emphysema, is a condition of chronic inflammation of the terminal bronchioles. In more detail, chronic bronchitis can be caused by cellular changes to the bronchioles including bronchial wall thickening, smooth muscle hyperplasia (an increase in the number of cells), and atrophy. Accompanying the inflammatory process of chronic bronchitis, are secretions that develop and are obstructive. Managing these secretions is a significant problem for chronic bronchitis patients.

Clinically, chronic bronchitis refers to a persistent cough and sputum production for at least three months of the year.6 It is often initially dismissed as a "smoker’s cough" by the patient. The cough is usually worse in the morning and the sputum produced is often colorless. Exertional dyspnea is often a later sign of the disease and is more prevalent with advanced age. Wheezes may or may not be present.

Both chronic bronchitis and emphysema cause a ventilation perfusion ("V/Q") mismatch. This term refers to the scenario where the respiratory rate (V) and the expected perfusion (Q) that should occur with that respiratory rate do not match up expectedly.

For example, if a patient is tachypneic and breathing 26 times per minute, it would be expected that there would be an abundance of oxygen in the bloodstream and lower carbon dioxide levels (as is the case with an anxiety induced hyperventilation). When a patient is tachypneic, but profoundly hypoxic and/or hypercapnic, he or she would have a ventilation perfusion mismatch.

Chronic bronchitis causes a ventilation perfusion mismatch. The patient will be tachypneic, however, oxygenation will not be occurring due to the inflammatory process. The body attempts to correct this imbalance by increasing cardiac output and ventilatory rate will not increase. Carbon dioxide will become elevated (hypercapnia), and eventually a respiratory acidosis will develop. The lung is considered poorly ventilated due to the obstructive process preventing proper air flow during ventilation.

The ensuing hypercapnia and respiratory acidosis will cause vasoconstriction of the pulmonary arteries, affecting the right side of the heart. This condition is known as cor pulmonale. The term "blue bloaters" was coined as a euphemism for these patients due to their presentation of edema and cyanosis.

Cor pulmonale refers to a disease or dysfunction of the right ventricle due to pulmonary circulation abnormalities. This usually relates to pulmonary hypertension, which can be caused by chronic bronchitis/COPD. In a healthy pulmonary circulatory system, there is minimal resistance and a high flow of blood to the right side of the heart. When vasoconstriction and chronic lung disease occur to alter this normal pulmonary circulation, cor pulmonale can develop.

Emphysema has an opposite scenario where the lung is well oxygenated, however, proper gas exchange with the blood cannot occur due to damage of the alveoli. The body reacts opposite of how it responds to chronic bronchitis and attempts to increase ventilation, while decreasing cardiac output. They are thus termed "pink puffers" due to their presentation of short pursed breaths and retained oxygen.

Although not official medical jargon, the terms "blue bloaters" and "pink puffers" have a long history as medical nicknames for patients with chronic bronchitis and emphysema, respectively.

While either of these disease processes alone is a significant obstacle for proper oxygenation, the combination of the two (as is often present in COPD patients) creates the potential for severe, chronic systemic difficulties for the patient to maintain normal oxygenation and acid/base balance.

Far and away, smoking is the leading cause of COPD. Smoking may be the cause of as much as 90% of COPD cases. Alternately, 15% of smokers will develop diagnosable COPD.7 Cigarette smokers have an annual decline in lung volume (FEV: forced expiratory volume) which is more than triple the rate of non-smokers.

COPD does occur in those that do not smoke. Studies differ in their results; however, it is likely that air pollution and chronic smoke from indoor cooking, may both be contributory.5 Additionally, industrial exposures can be contributory to a wide variety of pulmonary disease, including COPD.

Other causes of COPD include a deficiency of a certain genetic lung surface protectant known as AAT (Alpha1-antitrypsin). This accounts for less than 1% of all cases of COPD in the U.S. Patients with COPD that do not have a readily identifiable cause (i.e. tobacco use, toxin exposure), may be screened for Alpha1-antitrypsin deficiency.

AAT deficiency may also manifest itself as idiopathic liver disease, and irreversible asthma. The most likely treatment option for the deficiency is intravenous infusion of the protein. It is derived from human plasma donation.

Intravenous drug use can cause emphysema. Approximately 2% of persons who use intravenous drugs develop emphysema. This is due to damage to the pulmonary vasculature from fibers such as cornstarch and talc that are insoluble and commonly used in cutting IV drugs of abuse. Additionally, intravenous use of heroin and/or cocaine can result in the formation of cysts in the lung tissue.

HIV (human immunodeficiency virus, the precursor to AIDS) and connective tissue disorders, can all cause pulmonary damage resulting in COPD. Marfans syndrome and Ehlers-Danlos syndrome are both connective tissue disorders with a variety of symptomology, but both have shown to produce patients with higher rates of COPD than the general population. Salla disease is a very rare genetic disorder that can cause localized acidosis. Lung damage in these patients can lead to COPD.

Clinical Presentation
Initial diagnosis of COPD is made primarily by testing lung function via spirometry. The inability to meet 70% of the predicted forced expiratory volume in one second is clinically significant for COPD. There is no single blood test (biomarkers) that specifies the presence of COPD or not, however, arterial blood gasses can play an important factor in gauging the systemic perfusion of the COPD patient.

COPD severity is graded in four categories based on their percentage of expected lung capacity (FEV1/FVC)5 (See below).

Stage I (mild): FEV1 80% or greater of predicted.

Stage II (moderate): FEV1 50-79% of predicted.

Stage III (severe): FEV1 30-49% of predicted.

Stage IV (very severe): FEV1 less than 30% of predicted, or less than 50% and chronic respiratory failure.

Depending on the degree of distress that is present, a clinician will also expect some degree of hypoxia to be present and hypercapnia may accompany depending on extremis. Hypercapnia is normally not present in cases of mild COPD.

As severity increases, these patients will trend towards being in a respiratory acidotic state, but this can progress to a metabolic alkalosis. In the hospital, arterial blood gasses are needed to gauge these values.

A healthy patient expels most carbon dioxide through proper ventilation and respiration. This removal of carbon dioxide via expiration is part of the complex system of maintaining a proper blood pH in the human body (7.35 – 7.45). When carbon dioxide begins to build up, either due to a respiratory rate that is too low, or in the case of a COPD patient, hypercapnia, the blood begins to become acidic.

In the presence of developing respiratory acidosis, the body’s acid/base balance system will begin cellular buffering by releasing bicarbonate into the blood. This mechanism, although effective, is limited in its capabilities of managing an acute respiratory acidosis.

If ventilation levels rise and carbon dioxide is effectively removed, the elevated bicarbonate can lead to a metabolic alkalosis. The alkalosis is deemed metabolic because it is no longer related to an elevated carbon dioxide level and ineffective ventilation. It is now due to a metabolic condition (elevated blood bicarbonate presence).8

The complexity of this process is why such attention is paid to the ongoing status of a COPD patient’s condition, particularly during an acute exacerbation of the disease.

Electrolyte values may be abnormal due to multiple causes. COPD patients tend to retain sodium, and other medications they may be on (diuretics, theophylline, etc.) can act to lower potassium.

Chest radiography will show the telltale signs of the disease including hyperinflation, and can assist in determining if there is an infectious process present.

COPD patients often have other comorbid factors due to their tobacco use. These can include hypertension, coronary artery disease, and congestive heart failure.

Prognosis and mortality from COPD varies depending on several factors. A four point scoring system was devised known as the BODE index to determine expected four year survival rates for COPD patients.

The BODE index rates COPD patients on four criteria: body mass index, obstruction, dyspnea, and exercise capacity. The index gives a score on a 10-0 scale, with 0 as the best possible score. Those patients that score above 2 points have an 80% survival estimate versus patients that score higher than 7 whom only have an 18% estimated chance of four year survival.8

The perfect score in the BODE index would be for a patient to have a body mass index below 21, a respiratory capacity of 65% of predicted capacity, the ability to undergo strenuous exercise without dyspnea, and the ability to walk for six minutes without suffering oxygen desaturation.

Differentiating between chronic bronchitis and emphysema can be difficult, especially since they often occur together. However, below is a list of signs and symptoms that align with each of the respective syndromes.6

Chronic bronchitis patients may be obese, have a frequent cough with sputum production, use accessory muscles, may have coarse rhonchi and wheezing on auscultation, and may have signs of right sided heart failure including peripheral edema and cyanosis.

Patients with emphysema, however, may present differently. Physically, emphysema patients may have the classic barrel chest (increased anterior posterior diameter of the chest), be very thin, have no sputum production or cough, breathe in tripod position with pursed lips, wheezing on auscultation and distant heart sounds. These are the patients that have more of the "Classic" COPD presentation to them.

Barrel chest in the COPD patient is due to the chronic overinflation of the lungs. This leaves the chest and the muscles of ventilation in a chronic state of expansion, creating this recognizable symptom of emphysema.

Treatment
COPD is not a reversible condition. The goal of treatment is to maintain the best pulmonary function possible through eliminating risk factors for COPD exacerbation and maintaining a high quality of life for patients. Aside from lung transplantation, there is no clinically proven therapy to decrease mortality in COPD patients.

Clinicians aim to treat COPD exacerbations early to prevent hospital admission and the worst-case scenario, intubation and mechanical ventilation. Indications for admission are impending respiratory failure, respiratory acidosis, progressive hypoxia, and changes in mental status.

Proactive management of chronic conditions is based on the degree of severity of the patient’s underlying disease and can follow the Stage I (mild) to Stage IV (very severe) scale referenced prior in the article.9

Stage I treatment is focused on risk reduction such as influenza vaccine. A short acting bronchodilator is to be used as needed. As severity of disease increases to Stage II, long acting bronchodilators may be added into the treatment plan, along with cardiopulmonary rehabilitation therapy.

In the case of severe disease (Stage III), inhaled glucocorticoids are added to the Stage II treatment plan. Stage IV COPD patients will usually have long term oxygen therapy and may be considered for surgical options including lung transplantations.

Attention is paid to the systemic health of the patient as well, as they often have comorbid factors or lifestyle modification needs. Nutritional support for COPD patients is an important part of their overall health. They are often underweight or overweight and need to have their diets modified.

Another major treatment goal for any COPD patient is smoking cessation. This seems intuitive; however, it can remain one of the more challenging goals of COPD management. These patients often have smoked for decades and are greatly affected by the addictive powers of nicotine. Some might not see any hope in quitting smoking at an advanced age or disease state; however, it is highly necessary to prolong survival from COPD.

Acute exacerbations of COPD are very common for moderate to severe COPD patients. The average moderate to severe COPD patient will have 1.3 events per year on average.6

Bronchodilators are the primary medications used to combat COPD exacerbation (regardless of whether mild or severe). They work by decreasing airflow resistance by opening (dilating) the airways. It is important to recognize that these medications combat symptoms and short term exacerbation, but do not halt disease progression long term.

Beta2 agonists such as Albuterol have long been considered the first line defense for COPD exacerbation. These medications act by relaxing smooth muscle in the airways. Side effects are manageable and may include tachycardia and tremors.

Additionally, anticholinergics such as Atrovent work to relax smooth muscle in the lungs; however, they achieve this through a different mechanism. Side effects may include prostate problems, dry eyes, and dry mouth.

Combination therapy using both Beta2 agonists and anticholinergics has been successful.

Theophylline is a potent medication that is part of the medication class known as phosphodiesterase inhibitors. Theophylline used to be widely utilized in the management of COPD, however, its narrow therapeutic window and potential severe reactions have largely led to it falling out of favor. Theophylline use requires monitoring of serum levels to prevent toxicity and could cause serious side effects including cardiac arrhythmia and seizure. Due to its high index of side effects, theophylline use is not a mainstay of COPD management any longer.

While inhaled bronchodilators and anticholinergics serve to decrease airflow resistance in the airways, the second goal of pharmacological treatment in moderate to severe cases of COPD is inflammation management.

Inhaled corticosteroid use proves effective in patients with repeat exacerbations of COPD. Unlike long-term oral steroid therapy, there are less side effects for this route. The most concerning side effect of oral steroids is an increased prevalence of pneumonia.10 Since the avoidance of respiratory infections is a major goal of ongoing COPD management, this side effect is not to be taken lightly. Inhaled corticosteroids are used in conjunction with a bronchodilator and not alone.

Glucocorticoids, of which most inhaled steroids are, are a class of steroids that act to suppress immune response and thus have an anti-inflammatory response. It is this same mechanism of action though, that can present an increased risk of infection with patients receiving the medication. One of the more common infections these patients can develop is thrush, a yeast infection on the tongue. Examples of inhaled steroid medications that may be seen are Advair, Aerobid, Azmacort, Flovent, Pulmicor, Symbicort and Qvar.

While steroid therapy itself can be highly effective, the long-term use of oral steroids is generally discouraged due to a wide spectrum of unwanted side effects. These side effects can include bleeding, osteoporosis/fractures, difficulty in managing blood glucose, and hypertension.

COPD patients are particularly prone to chronic infections of the lower airways. These infections can progress to life threatening events for these patients that are already having difficulty with oxygenation. Antibiotic therapy is common and is effective with these patients; however, they must be monitored for improvement. The risk of ventilator associated pneumonia for the intubated patient is a particularly significant risk for the COPD patient.

Long term home oxygen therapy is a very important issue for consideration for these patients. Hypoxemia is an inevitable side effect of the worsening COPD patient, and ultimately, the decision to place the patient on oxygen will have to be made by the treating clinician. The oxygen may be prescribed for activity only, for certain times of day, or for 24 hour a day use. Several studies have shown that long term oxygen therapy for appropriate COPD patients, can double their survival.11

While there are several clinical conditions to consider when deciding whether to place a COPD patient on long term oxygen, generally a COPD patient with a PaO2 less than 55mmHg or pulse oximetry of 90% or below, is considered hypoxemic enough that he or she will benefit from oxygen therapy.12

Every EMS student has learned to be very cautious when placing oxygen on a COPD patient for fear of blunting their respiratory drive. This relates to the hypoxic drive of a COPD patient, versus the primarily hypercapnic drive of a non-COPD patient. It is now believed and verified through multiple studies, that this fear of over oxygenating COPD patients has been exaggerated.

No matter what, a hypoxic patient will benefit from oxygen. Never withhold oxygen from a hypoxic COPD patient for fear of the side effect of inhibiting respiratory drive. It is appropriate to titrate oxygen on these patients. In hospital with the availability of arterial blood gas testing, the oxygen should be titrated to PaO2 of 60-65mmHg.6

Ambient air has approximately 21% oxygen in it and each additional liter of oxygen administered to the patient adds approximately 4% additional oxygen (FiO2) to the total oxygen concentration of the air the patient is inhaling. Therefore, placing a patient on 5L/min via nasal cannula, would nearly double (40% FiO2) the available oxygen for the patient.

Early recognition and aggressive treatment are critical in preventing the COPD exacerbation from deteriorating into complete respiratory failure. Intubating the patient and having him or her on mechanical ventilation should be the last resort for these patients as they can be extremely difficult to wean off mechanical ventilation.

Generally, mechanical ventilation is not required until there are changes in mental status, continuously worsening acidosis, or the continued decline in oxygenation despite therapy.

Intubation and ventilation is associated with tracheal injuries, ventilator associated pneumonia ("VAP"), and the previously mentioned difficulties in weaning these patients off of the ventilator.

Non-invasive ventilation, namely BIPAP or CPAP provides an intermediate step of ventilator support between relying solely on the patient’s ventilatory efforts and the severity of intubation/mechanical ventilation.

Prehospital, CPAP (continuous positive airway pressure) is generally used, and in hospital BIPAP (bi-level positive airway pressure) is predominantly used.

CPAP is applied using a mask covering the patient’s nose/mouth that mechanically supplies a constant level of airway pressure to the patient, while he or she uses his or her own ventilatory effort to breathe. This procedure can increase residual capacity and can assist in "splinting" open the terminal airways in patients with pulmonary obstructive diseases.13

BIPAP is also supplied via a similar mask to CPAP and usually uses a traditional hospital ventilator. BIPAP functions by issuing a higher inspiratory pressure than expiratory pressure, versus the constant pressure of CPAP.

Studies have shown that the use of BIPAP reduces the need for intubation and possibly improves mortality rates.14

Pharmacological interventions for COPD exacerbation mirror that of chronic disease management. Aggressive use of nebulized bronchodilators, the use of IV steroids (SoluMedrol is frontline), and close attention to the need for airway management via CPAP/BIPAP or intubation.

A common initial nebulizer regimen will include a single or double dose of Albuterol, mixed with Atrovent. Continuous nebulizing treatment is generally maintained. The half life of Atrovent is longer than Albuterol, and therefore, additional Atrovent doses do not need to be added with the same regularity as Albuterol.

There are several beta agonist bronchodilators in use for COPD management. Often the duration of action is one of the major factors in selecting a specific bronchodilator. Short acting bronchodilators used for emergent management of COPD exacerbation include: Albuterol, Xopenex (levalbuterol), and Maxair (pirbuterol). Longer acting beta2 agonists include Serevent (salmeterol), Foradil (formoterol) and Brovana (arformoterol). Prehospital, Albuterol is the predominant beta2 agonist used.

In addition to Atrovent, other anticholinergics that may be used in hospital include: Spiriva (tiotropium). Its pharmacological properties are very similar to Atrovent, although the duration of action is longer.

Subcutaneous/intramuscular epinephrine may be considered for cases of refractory COPD exacerbation, however, the common comorbid factors and advanced age, make this a situation not without significant risk.

Magnesium sulfate sometimes plays a secondary role in the management of COPD exacerbation. Magnesium acts as a smooth muscle relaxant, and in studies, has been shown to be somewhat effective when given intravenously after initial bronchodilator therapy. Magnesium has also been nebulized with some limited success in the treatment of COPD patients. As there are slight variations in COPD treatment based on regional location, always follow local protocol for treatment of COPD patients.

Prehospital recognition of COPD may be easily and readily apparent or can be more difficult due to the presence of multiple conditions. Respiratory distress may be due to congestive heart failure, pneumonia, COPD, pneumothorax, and anxiety amongst several other syndromes.

A thorough assessment including inquiring about fever, chest pain, orthopnea, pedal edema, sputum production, and progression of symptoms, can assist in narrowing down the etiology. Regardless, the focus on maintaining airway, a thorough assessment and taking steps to maintain proper oxygenation are the hallmarks of all respiratory distress calls.

Treatment of COPD in the field specifically focuses on bronchodilation and treating hypoxia. In hospital, the focus continues on to include managing any underlying causes (infection), decreases in inflammation and secretion production and correction of underlying metabolic abnormalities.

Increasingly, capnography has become a standard of care prehospital for respiratory distress patients. In addition to pulse oximetry, capnography can help paint a picture of the respiratory status of the patient.

Waveform capnography produces a graphic tracing of the patient’s ventilation, which can be divided into five phases. This waveform shows the amount of carbon dioxide being exhaled by the patient. This presents a literal picture of the rate and quality of breathing in conjunction with the balance of gases that are exchanged during normal respiration.

The waveform of a COPD patient may present with the classic "shark fin" appearance associated with obstructed airways (also seen in asthmatics). Quantitative ETCO2 readings can help monitor the degree of air "trapping" and CO2 retention associated with emphysema.

Conversely, a patient in congestive heart failure (absent of COPD) will have decreased carbon dioxide levels expired and will not have the "shark fin" of a COPD/asthmatic patient.

Capnography provides a nearly instantaneous evaluation of pulmonary gas exchange of the patient. This tool allows providers to assess severity, and more importantly, trending of the patient’s acuity and response to treatment.

For example, if a COPD patient with worsening dyspnea is placed on a nasal cannula with supplemental oxygen, the prehospital provider would be able to monitor whether this was proving effective in improving the condition, or if further treatment (CPAP, nebulizer) was warranted.

Prehospital, one of the most pivotal roles is the frequent reassessment of the patient to determine if the patient is starting to decompensate despite treatment and may need more aggressive airway management.

Conclusion
When you check up on the patient later after another transport, you are disappointed to find him on a ventilator. You check in with the emergency physician who says he is also disappointed that it ended up that way.

The physician says that he continued the prehospital treatment for another hour, added Solumedrol and even tried nebulized magnesium sulfate, but the patient continued to be hypercapnic, tachypneic, and became fatigued. Rapid sequence induction was used and the patient was intubated to facilitate correcting his respiratory status. He will be admitted to the ICU and the physician says he hopes that they can get the patient off the ventilator soon.

As you leave the hospital, your partner and you discuss how COPD exacerbation can be a difficult disease process to manage and doesn’t always have the desired outcome. Fortunately, you find out from your QA coordinator that the patient was ultimately discharged home without deficit after a week on a ventilator and antibiotic therapy for pneumonia.

A home health specialist will be coordinating the patient’s at home post admission therapy, to ensure compliance with the treatment regimen, as well as looking for any signs of disease exacerbation.