There are inconsistent data on the percentage of EMS calls involving pulmonary emergencies. A search of the literature reveals respiratory calls make up approximately 11% to 15% of all EMS requests.1,2 Few publications actually define the types of calls and concomitant demographics of those patients. After the terrorist attacks of 9/11, there was an increase in “syndrome surveillance” across the country primarily in an attempt to discover aberrant trends in the incidence of pulmonary disease. Despite attempts to classify the number of disease presentations, including using EMS/9-1-1 call records, the information remains scarce.3
Nevertheless a patient with a pulmonary emergency is an anxiety-provoking situation for both the patient and the prehospital provider.
Discuss demographics of respiratory disease pertaining to EMS, including percent of EMS calls, the incidence and increase of acute and chronic lung disease, as well as fatality data from respiratory distress.
Understand and be able to integrate knowledge about normal respiratory physiology including normal versus positive pressure ventilation, mechanics of gas exchange, and the CNS control of respiratory drive.
Discuss and list common causes of respiratory illness including pathophysiology, presentation, and treatment for asthma, COPD, CHF, and lung malignancy.
Describe differences between acute and chronic respiratory conditions including chronic and acute phases of respiratory failure.
Discuss and list causes, presentation, and treatment for other acute medical causes of respiratory distress including PE, pneumonia, pulmonary edema, croup, and epiglottitis.
List and discuss other nonmedical causes of respiratory distress including asphyxiants, respiratory toxins, and foreign body airway obstruction.
Describe the indications for prehospital endotracheal intubation.
Discuss the use of supraglottic airway devices and their role in prehospital care.
Describe the physiology and indications for use of prehospital noninvasive positive pressure ventilation.
Discuss and understand the RSI process including indications and medications.
According to the CDC, in 2007 the number of visits to ambulatory cares sites in the United States, including physician offices, hospital outpatient, and emergency departments for chronic and unspecified bronchitis, as a primary diagnosis, was 11.7 million, and for other chronic obstructive pulmonary disease conditions, as a primary diagnosis, was 6.1 million.4
Health statistics provided by the CDC for US adults in 2009 reveal the number of noninstitutionalized adults diagnosed with chronic bronchitis as 9.9 million or 4.4% of the US population. The percent of noninstitutionalized adults who had been diagnosed with emphysema was 4.1 million (2.2%) of the population. The number of deaths in the United States from chronic/unspecified bronchitis per 100,000 population is 0.2. The number of deaths per 100,000 population from emphysema is 4.2 and for other chronic lower respiratory diseases excluding asthma per 100,000 population is 36.8.5
These statistics reveal that COPD is responsible for a significant economic burden on society and a significant medical burden on EMS responders.
Two conical lungs, whose inferior borders overlie the diaphragm and have apices that extend above the first ribs, are covered with a visceral pleura. This pleura is in close proximity to the parietal pleura, which covers the inside of the pleural cavities. Only a thin layer of pleural fluid separates the parietal and visceral pleura. The parietal layer secretes 2400mL of fluid daily, which is reabsorbed by the visceral layer. The pleura are a dynamic layer protecting the lung and pleural cavity from infection while transmitting the forces of respiration without damage to the underlying lung parenchyma.6,7
The trachea bifurcates at the carina, forming the right and left mainstem bronchi. Each side continues branching multiple times eventually down to a terminal bronchiole, which enters an acinus or the beginning of the respiratory zone. The acinus has several generations of branching and ultimately ends in the terminal alveolar sacs (Figure 40-1).
A: pulmonary anatomy. B: the terminal bronchioles with the alveolar sacs where gas exchange takes place across the air-alveolar capillary interfaces. (Reproduced with permission from Barrett KE, Barman SM, Boitano S, Brooks HL. Ganong's Review of Medical Physiology, 23rd ed. New York, NY: McGraw-Hill; 2010. Figure 35-1.)
Pulmonary circulation consists of mixed venous blood from the pulmonary arteries whose origins are in the right ventricle. After passing through the pulmonary capillary beds, where carbon dioxide is discharged and oxygen gas is absorbed via diffusion, the blood returns via the bronchial veins to the pulmonary veins and ultimately the left atrium. Pulmonary circulation is a low-pressure system with typical pulmonary artery pressures of 20mm Hg systolic and 12mm Hg diastolic.8,9
The graph shown in Figure 40-2 gives a visual conception of the common lung volumes and measurements used in pulmonary physiology. One can see from the graph that there is always a residual amount of volume in the lungs even after a forced expiration. A typical adult will have a tidal volume of approximately 0.5 L but volumes depend on height, weight, age, gender, and disease status. Females may have a decrease in vital capacity of up to 25% of a typical male. Children typically have much smaller volumes and any calculations for respiratory interventions should be based on weight (Figure 40-2).
Lung volume is depicted in milliliters of air. Notice the sine wave of normal tidal volume as one breathing at rest interrupted by a forced inspiration, a forced expiration and then a combined maximum inspiration with forced expiration. (Reproduced with permission from Hall JE, ed. Guyton & Hall Textbook of Medical Physiology, 13th ed. Philadelphia: Elsevier; 2016. Figure 38-6. Copyright Elsevier.)
GAS EXCHANGE IN THE LUNGS
In order to understand the basic respiratory physiology, in the following discussion, a few definitions need to be introduced:
Minute ventilation: the total amount of new air moved into the respiratory passages each minute. On average this is approximately 6 L/min
Alveolar ventilation: the amount of air reaching the alveoli per minute.
Anatomic dead space: the amount of air in the respiratory anatomy that does not participate in gas exchange (trachea, bronchi, etc).
Tidal volume: the amount of air that moves into the lungs with each breath.
Ventilation: movement of air into lungs. When discussing gas exchange, it refers to the movement of CO2 out of the lungs.
Perfusion: movement and distribution of blood through the pulmonary circulation.
Diffusion: movement of O2 and CO2 across the air-blood barrier or alveolar capillary membrane. O2 and CO2 are exchanged via simple diffusion and passively move down a partial pressure gradient. For most individuals, the arterial blood becomes fully saturated with oxygen early in inspiration, and the rate of uptake of oxygen depends on capillary blood flow.
The diffusion capacity depends on the thickness of the alveolar wall, the area available for gas exchange, and the partial pressure difference between the two sides. If the thickness of the wall increases (pulmonary edema), or the alveolar complex is destroyed (emphysema), the diffusion capacity is lower.
CNS CONTROL OF RESPIRATORY DRIVE
The pacemaker activity for respiration is in the respiratory control centers of the brain. It is primarily an involuntary process influenced not only by neural control, but also by chemical control, some voluntary control, body temperature, drugs, pain, emotion, sleep, baroreceptors, and proprioceptors. Neural control of respiration includes factors responsible for alternating inspiration/expiration, rhythm, factors that regulate rate and depth of ventilation (vagal nerve input), and factors that modify respiratory activity, both voluntary (speech) and involuntary control (sneeze, cough).
The medullary rhythmicity area is the respiratory control center of the central nervous system located in the medulla. The medullary respiratory control center is the primary control center and provides output to the respiratory muscles.
The respiratory control center can be divided into the inspiratory center and the expiratory center. The inspiratory center spontaneously controls the diaphragm and intercostal muscles responsible for inspiration. Two other centers in the pons, the apneustic center and the pneumotaxic center influence medullary respiratory output.
Molecules such as oxygen, carbon dioxide, and hydrogen influence respiration. Deviation from the normal concentrations of these molecules will change the rate, depth, or rhythm of respiration as sensed by chemoreceptors located in the medulla, carotid arteries, and the aortic arch (eg, elevated CO2 or hypercapnia decreases blood pH and is sensed by chemoreceptors in the medulla). The medulla then increases the rate and depth of respiration (hyperventilation) to blow off CO2 during expiration to return the pH to a normal or near normal range. Conversely, if CO2 and hydrogen levels fall below the baseline level, hypocapnia may result. Hypocapnia results in slow, shallow breathing called hypoventilation. Likewise, when oxygen levels fall and carbon dioxide and pH remain normal, respiratory rate will increase until oxygen levels return to normal.
To some extent, respiration can be controlled voluntarily because of neural pathways between the cerebral cortex and the respiratory control center (eg, hyperventilation). Respiration may increase with hyperthermia and decrease in response to hypothermia. Certain drugs and medications can affect respiration. For example, narcotics such as Demerol and morphine can reduce the rate and depth of breathing while adrenaline, amphetamine, and cocaine typically have the reverse effect.
Pain and emotions often increase respiration. Emotions such as crying are controlled by the hypothalamus and limbic system that, in turn, stimulate the respiratory center and increase respiration. When the pain or emotion subsides, respiration returns to normal. Baroreceptors are pressure receptors located in the carotid and aortic sinuses that sense changes in blood pressure. Changes in respiration are inversely proportional to changes in blood pressure. For example, when blood pressure increases, respiration decreases. Proprioceptors are receptors located in muscles, tendons, and joints that sense movement. During exercise, these receptors transmit signals to the respiratory center that increase the rate and depth of respiration.
COMMON CAUSES OF RESPIRATORY DISTRESS
In this section, common medical causes of respiratory distress will be presented. For each, this section will highlight the pathophysiology (causes) as well as the typical clinical presentation and general treatment.
COPD AND ASTHMA PATHOPHYSIOLOGY
The prevalence and incidence of asthma is very high in the Western world.10 The number of people with asthma continues to grow. One in 12 people (about 25 million, or 8% of the population) had asthma in 2009, compared with 1 in 14 (about 20 million, or 7%) in 2001.11
Asthma is a disease that is reversible and episodic. It is characterized by a chronic inflammatory disorder of the airways coupled with airway hyperresponsiveness that leads to recurrent episodes of wheezing, shortness of breath, chest tightness, and coughing. Children will often be awakened from a sound sleep with an episode and it may consist primarily of coughing (cough variant asthma). These episodes are associated with reversible airflow obstruction and between acute attacks, the patient often returns to a normal respiratory pattern. Patients with persistent inflammation may have lung remodeling over time, which eventually leads to a loss of lung function. Asthma patients tend to be younger patients and are more likely to have an allergy trigger or a strong family history.
Obstructive lung disease can be classified into two categories: chronic bronchitis and emphysema. Patients with COPD have significant fixed airway obstruction that remains, even when the disease in under control. Both diseases cause chronic cough and shortness of breath. Chronic inflammation causes structural changes and irreversible airflow limitation. This can be caused by an increase in resistance of the conducting airways or an increase in compliance due to destruction of the airway walls or both. Destruction of the lung parenchyma, also by inflammatory processes, leads to the loss of alveolar attachments to the small airways and decreases lung elastic recoil; in turn, these changes diminish the ability of the airways to remain open during expiration. Often, COPD patients have right heart failure and chest remodeling. Cigarette smoking is a primary cause of COPD. Other environmental and genetic factors can cause COPD including exposure to air pollution, second-hand smoke, occupational chemicals, and a history of childhood respiratory infections.12
Chronic bronchitis is characterized by chronic cough and sputum production. A working definition of chronic bronchitis can be defined as a chronic, productive cough for 3 months during two successive years in which other causes for chronic cough have been excluded.13
Emphysema is destruction and irreversible enlargement of the air spaces distal to the terminal bronchioles. The destruction of the alveoli reduces expiratory flow by decreasing the elastic recoil present in healthy lung parenchyma. Destruction of the airspace walls is found upon histologic examination. Bullae, radiolucent areas larger than 1cm in diameter that indicate severe local destruction, may be seen in macroscopic examination and on radiographs.
One must be cautious in diagnosing COPD in the field as other disease states may also present with breathlessness, wheezing, and sputum production. Remembering the adage, “All that wheezes is not asthma,” may help keep a broadened differential.
Clinically, patients have chronic difficulty breathing that persists daily and is acutely exacerbated by an inflammatory stimulus such as an infection, allergens, or noncompliance with medications, etc. Differentiating asthma from COPD is sometimes difficult and the patient's age, medical and social history are typically helpful. Asthma patients may be younger at age of onset but that is variable. Most COPD patients will be older and may be thin, have pursed lip breathing (exhalation), as well as clubbed or stained fingertips from long-term smoking. However, many patients have both asthma and COPD. Both diseases will present with increased work of breathing, and variably cough and wheezing. Wheezing is the clinical hallmark of bronchospasm and a diagnostic sign in COPD and asthma that patients will benefit from bronchodilator therapy. However, be warned that in severe cases, patients may not be able to move enough air through the lungs to generate wheezing. Quiet lungs in the setting of respiratory distress is an ominous sign. Vital signs will commonly show an increased heart and respiratory rate as well as decreased oxygen saturations. Asthmatics can typically compensate and maintain near normal oxygenation until severe, whereas COPD patients are typically chronically hypoxic and may have low oxygen saturations at baseline.
Chronic treatment of both conditions involves inhaled bronchodilators and also the use of steroids to reduce chronic inflammation. Treatment in the acute setting is similar. The ABCs should be managed first and supplemental oxygen given. For patients at risk for immediate respiratory failure, assisting ventilations or intubation should be considered. In alert patients a trial of CPAP or BiPAP may be appropriate.14,15 In asthma, high flow oxygen can be utilized liberally. However, in mixed disorders or COPD, oxygen should be titrated to keep pulse oximeter readings between 92% and 95%. Prolonged high flow oxygen in COPD can suppress the hypoxic respiratory drive and has been linked to worsened long-term outcomes.
Bronchodilators such as albuterol (Ventolin) and levalbuterol (Xopenex) are the mainstays of prehospital treatment and can be given in a range of dosing based on severity from a “unit dose,” typically 2.5mg of albuterol to continuous nebulizer treatments lasting 30 minutes or more and delivering 10 to 20mg of albuterol in some cases. Providers should remember that in addition to bronchodilation, β-agonists have activity on the heart and can produce significant tachycardia and hypertension which can be harmful in some patients with cardiovascular disease. The patient should be monitored for high heart rate, significant hypertension, or signs of cardiac ischemia such as chest pain or ECG changes. Ipratropium bromide (Atrovent) is a nebulized medication adjunct that can be combined with. Atrovent works by reducing airway secretions and synergizing bronchodilatory medications. Atrovent is used primarily in the prehospital and ER setting and has been less effective in the inpatient chronic care setting.
Steroids and IV fluids are also a mainstay of treatment and can be given in a variety of doses and ranges. Chronic therapy is usually delivered via inhaled steroids. For acute treatment, methylprednisolone (Solu-Medrol) and dexamethasone (Decadron) are common choices. Whether administered orally, IV, or IM, these medications take around an hour or more for onset of action and do not offer immediate benefit. Additionally, IV volume replacement is an important consideration as most patients with respiratory distress are volume depleted from increased respiratory losses and reduced oral fluid intake.
Severe COPD and asthma that do not respond to conventional treatment may require other β-agents such as subcutaneous epinephrine, terbutaline, or in some cases an IV infusion of those medications. Again, this carries a risk of significant increases in cardiac demand.
Lastly, the patient with complete respiratory failure and severe alterations in mental status will require intubation. However, intubation should be considered the last resort for obstructive lung disease patients. Mechanical ventilation of COPD and asthma patients is difficult and perilous. Responders must remember that air trapping continues to occur and ventilation requires more time for exhalation. Normal intubated patients require approximately 1 second for inhalation and 2 seconds for exhalation, thus a 1:2 ratio. COPD and asthma patients may benefit from a ratio of 1:3 or more requiring slower ventilation rates and making oxygenation difficult. Continue aggressive treatment for bronchospasm even after intubation with in-line β-agonist nebulizer treatments and continued IV medications.16
PULMONARY EDEMA AND CHF PATHOPHYSIOLOGY
Just as gases can diffuse across the thin alveolar membrane in the lungs, so can fluids. However, in the case of fluids this is typically due to hydrostatic or osmotic forces. Any fluid, excluding pus/blood, in the lungs can be termed “pulmonary edema” although the term is classically used to describe fluid that enters the alveoli from the capillary circulation. Pulmonary edema has many causes ranging from heart failure to alveolar injury (such as in ARDS, inhalation injury, burns, etc) or overly aggressive resuscitation with IV fluids. Congestive heart failure (CHF) is a common cause of pulmonary edema encountered by EMS. The right heart pumps blood into the pulmonary circulation and an impaired left heart is unable to “pump out” blood from the right heart. The high pressure in the pulmonary circulation causes fluid to shift into the alveoli. Left-sided heart failure produces pulmonary edema and symptoms whereas right heart failure produces the peripheral signs of heart failure, leg swelling, etc. Most patients have impairment of both sides of the heart and left-sided heart failure in the United States is most commonly due to ischemic heart disease (CAD).
EMS providers may encounter patients with new onset or existing CHF. Exacerbations may come on abruptly or gradually worsen over several days. Patients with CHF may give a worsening history of the disease as well as weight gain or increased peripheral edema in the time period preceding the trouble. Frequently, poor adherence to medications, diuretics, or excessive fluid or salt intake can cause CHF exacerbations. Patients will typically appear with increased work of breathing and distress. Coughing may be present and may produce classic “pink frothy” sputum, giving them a nickname of “pink puffer.” Vital signs are highly variable depending on how poor the patient's cardiac function is. Heart rate and blood pressure can range from high to low. And oxygen saturations may be low or normal. The most complicated CHF patient is one who has significant respiratory distress paired with hypotension and bradycardia. This is a clear sign of a very sick heart and contraindicates many mainstays of treatment for CHF. The lung examination classically reveals coarse crackles in the lung bases, formally called rales. This sound is produced from fluid in the small airways.
The goal for CHF and pulmonary edema is fundamentally simple—get the fluid back into the circulation and out of the alveoli. The ABCs must be managed and if airway or breathing adequacy is questioned, CPAP, BiPAP, or intubation may be indicated.17,18 For pulmonary edema from a non-CHF source, that is, IV fluids, altitude, irritants, etc, treatment involves stopping the offending agent and using positive pressure ventilation. Every CHF patients should have supplemental oxygen and positive pressure ventilation via NIPPV. For the “warm” CHF patient—those with adequate heart rate and blood pressure—the addition of nitrates is indicated. A common prehospital regimen is up to three sublingual nitroglycerin tablets followed by some nitroglycerin paste administration. For advanced providers, establishing a nitroglycerin IV infusion is also an option that allows rapid titration of treatment. Remember to ask all patients about use of erectile dysfunction drugs such as Viagra or Cialis. For the “cold” CHF patient—those with bradycardia or hypotension—treatment is far more difficult. Oxygen can still be used but nitrates must initially be avoided and CPAP is questionable based on its tendency to reduce venous return and lower blood pressure. Intubation should be performed if airway patency and breathing are not adequate and once done, hypotension may need to be treated initially with judicious IV fluid boluses if any suspicion of “intravascular” volume depletion is present (ie, recent hx of vomiting, diarrhea, etc). Vasopressors may be needed to support blood pressure. Dopamine is a good choice because of its positive effect on blood pressure, heart rate, and cardiac contractility as well. Once blood pressure and heart rate are corrected, CPAP and nitrates can carefully be administered to help mobilize pulmonary edema.19
LUNG MALIGNANCY PATHOPHYSIOLOGY
Cancer remains the second most common cause of death in the United States and lung cancer remains in the top five malignancies.20 At present, EMS providers render care to a large geriatric population with a significant incidence of lung malignancy. Lung malignancy is mentioned in this chapter because it presents with a variety of features that cause respiratory distress, ranging from acute to more chronic. Malignancy can cause bleeding, inflammation, physical obstruction, and mass effects that all reduce functional lung capacity or cause other problems such as pulmonary edema or pneumothorax.
For many patients, a nagging cough, worsening shortness of breath, or hemoptysis (coughing up blood) may be the first signs that lead to a diagnosis of lung cancer. For others, worsening disease may produce symptoms that mimic obstructive lung disease, CHF, or predispose the patient to recurrent infections like pneumonia. For patients with existing lung malignancy, the clinical presentation is highly variable. The above features may produce COPD or CHF type symptoms with wheezing, rales or rhonchi, and increased work of breathing. Decreased immune function in the lungs can lead to infection with a clinical picture of pneumonia with sputum, fever, and worsening shortness of breath. Also, unlike some other respiratory illness, the malignancy can erode structures within the lungs. Spontaneous pneumothorax or erosion into blood vessels producing massive bleeding or hemothorax is possible. Patients may have massive hemoptysis (bloody sputum) that cannot be controlled and compromises the airway.
Treatment of symptoms is the best approach. Supplemental oxygen provides a great deal of comfort for most patients with lung malignancy. Albuterol or other bronchodilatory medications should be used for wheezing and steroids may have some role in reducing inflammation. Pulmonary edema treatment is best accomplished with CPAP as other measures that would work on CHF-like nitrates and diuretics are less effective. IV fluids and pain medication should also be considerations but not in amounts that will depress or labor breathing further. Intubation is indicated for complete respiratory failure but the EMS provider should ensure that the patient does not have a DNR order or specific directive against mechanical ventilation. Intubation may also be required for massive hemoptysis if the airway cannot be kept clear. Evidence of pneumothorax should be treated with pleural decompression of the affected side. In lung cancer patients who request palliative treatment, oxygen, CPAP, and pain medication is the mainstay of treatment.
ACUTE AND CHRONIC RESPIRATORY CONDITIONS
A detailed list of causes of respiratory distress and the timeline associated with each is presented in Chapter 34. Related to this, the EMS responder must be able to differentiate between chronic stable disease and acute exacerbations. Asthma, COPD, and CHF patients all have baseline daily symptoms. This will include physiologic compensation mechanisms and routine medications for control of these disease processes. For all of these patients, the EMS provider must also differentiate between respiratory distress and respiratory failure in these patients.
Asthma patients with chronic disease may appear normal and have normal function outside of exacerbations. Asthma onset has a typical bimodal onset presenting either in early childhood or later in adult life. Most patients will develop symptoms such as coughing and wheezing, especially in response to allergens, infection, and exercise. Diagnosis is clinical with a history, physical examination, and pulmonary function testing (PFT) for confirmation if needed. Asthmatics may have a family history or also suffer from other common ailments such as allergies, eczema, or other inflammatory conditions such as arthritis and irritable bowel syndromes. Daily therapy with long-acting bronchodilators and inhaled steroids produce good symptom control for many patients.
COPD although similar to asthma in clinical presentation has a different pathophysiology and course. Most patients develop COPD from chronic lung irritants, most commonly cigarette smoking in the United States. Some are from direct use and others from heavy second-hand smoke in households with smokers, etc. Others may have injury from workplace environmental exposures or chronic infections. A small portion of the population may have a condition called α1-antitrypsin (A1AT) deficiency where the elastic fibers surrounding the alveoli and bronchioles age and breakdown prematurely. This is genetic in nature and not related to exposure. Generally, COPD will present after the fifth to sixth decades of life and will continue to worsen if the person continues to smoke, etc. The exception is the A1AT patient who may have disease at a younger age. Chronic therapy involves the same as for asthma patients, but also with the addition of ipratropium bromide (Atrovent) inhalers and then typically requiring supplemental home oxygen at some point. Both asthma and COPD patients are extremely sensitive to any decreases in baseline lung function, with infection being one of the most common causes of deterioration and exacerbation from baseline.21
Congestive heart failure is also a slowly progressive and insidious disease that is typically encountered later in life. As a patient's left heart function declines either from heart disease, pulmonary disease, or other causes, pulmonary symptoms worsen. Depending on overall heart function and the ability to contract and eject blood, the ejection fraction (EF), patients will have variable needs and treatment. Mild CHF may produce minimal daily symptoms and may be controlled with oral diuretics and dietary fluid and salt restriction. Severe CHF may require numerous medications including aggressive diuretics, hormone modifying agents, and long-acting oral nitrates. Many patients will become oxygen dependent and have significant distress when trying to sleep, lying flat, etc. Many CHF patients may already use CPAP when sleeping, or in some severe cases, continually during the day. Acute CHF exacerbations may result from a variety of problems ranging from superimposed infection, worsening heart disease (such as silent MI, etc), or commonly medication and/or dietary noncompliance. Many EMS providers may answer calls for other complaints and find patients in CHF decompensated states.22 The most severe CHF patients in end-stage heart failure may require portable IV infusions of medications to increase heart rate and contractile function like Milrinone and some may have implanted portable ventricular assist devices like the LVAD. Patients with an LVAD or similar device have an implanted impeller or other pumping device in the left heart that is surgically implanted and connected to an external battery/control pack that is connected to wires externalized through the chest. These are typically installed in patients who have failed all other therapy and are end stage. Recent research has shown that LVADs may provide up to another year of life for end-stage CHF patients and that number continues to increase.23 Of note, patients with such devices may not have a palpable pulse due to the continuous flow of blood from the LVAD as opposed to the contractile flow normally produced by the heart. EMS responders should ask the patient or immediate family for help troubleshooting problems with the LVAD as they have been extensively trained by the manufacturer.
Remember that in cases of chronic disease, the human body can compensate for wide variations in disease and physiology given enough time. Acute illness finds the body unprepared to compensate and rapidly throws off body physiology, compensatory mechanisms, and defenses. When this happens, chronic respiratory conditions can turn into respiratory failure.
ACUTE AND CHRONIC RESPIRATORY FAILURE
Respiratory failure is a syndrome rather than a single disease process and the overall frequency of respiratory failure is not well known.24
The mortality rate associated with respiratory failure depends on the etiology. For acute respiratory distress syndrome, the mortality rate is approximately 45% in most studies.25 For an acute exacerbation of COPD, the mortality rate is approximately 30%.
Respiratory failure is situation whereby the system fails in oxygenation, ventilation, or both. In practice, respiratory failure is defined by a PaO2 of less than 60mm Hg or a PaCO2 of more than 50mm Hg. Respiratory failure may be acute or chronic. Acute respiratory failure may present with dramatic changes in acid-base status. It usually develops over minutes to hours and the pH is usually less than 7.3. Hypoventilation, V/Q mismatch, and shunt are the most common pathophysiologic causes of acute respiratory failure.
Chronic respiratory failure is found to have less dramatic acid-base changes. It usually develops over weeks or months and allows for renal compensation and an increase in bicarbonate retention with a less dramatic decrease in pH. Chronic respiratory failure may actually go undetected if careful observation is not included in your examination or review of previous health evaluations is not undertaken. The clinical presentation is important and chronic hypoxemia as manifested by polycythemia or cor pulmonale suggests a chronic nature.
Respiratory failure is classified as either hypoxemic or hypercapnic and may be acute or chronic. Type 1 respiratory failure, the most common form, is hypoxemic and is characterized by a PaO2 of less than 60mm Hg with a low or normal PaCO2. Cardiogenic or noncardiogenic pulmonary edema, pneumonia, and pulmonary hemorrhage are examples of acute lung disease that causes type 1 respiratory failure.
A PaCO2 of more than 50mm Hg characterizes hypercapnic respiratory failure, or type 2 respiratory failure. Hypoxemia is common in these patients. The acid-base status depends on the level of bicarbonate which, in turn, is dependent on the duration of hypercapnia. Drug overdose, neuromuscular disease, COPD, asthma, and chest wall abnormalities are common etiologies of this particular type of respiratory failure.
OTHER ACUTE MEDICAL CAUSES OF RESPIRATORY DISTRESS
Acute medical causes of respiratory distress are those that arise within minutes to hours to days and can be single in presentation or superimposed on chronic existing disease.
RESPIRATORY INFECTIONS PHYSIOLOGY
Pulmonary infections are one of the major causes of acute respiratory distress and involve all age groups, but again are more prevalent in the young and the old. Children and adults suffer from all manner of pathogens that affect the lungs including viruses (likely the most common) as well as bacteria and less commonly fungal infections. All are capable of causing lung inflammation, causing edema and swelling of the airways and causing pulmonary edema or secretions that block air exchange in the alveoli.
For viral respiratory infections, usually the triad of “cough, coryza (runny nose, watery eyes), and fever” are present. Cough is a uniform feature of almost all lung infections as inflammation promotes coughing and expulsion of mucus and other infectious debris in the lungs. Cough in children can be classified as “brassy,” “barky,” or sometimes having a “seal bark” type quality. A barky or seal bark cough is commonly associated with upper respiratory infections that inflame the larynx such as croup and respiratory syncytial virus (RSV). Viral respiratory infections are volatile and may present rapidly with many patients becoming ill in as little as 24 hours.
Bacterial lung infections are commonly termed pneumonia and in contrast may take days to progress in severity. There are numerous pathogens that affect human lungs and the disease course ranges from mild with recovery within a week to those that are uniformly fatal like Bacillus anthracis (anthrax). Clinically cough is still a major feature, deep and “chesty” in nature, often with production of thick foul smelling sputum. Patients will develop progressive symptoms of fever, malaise, and chills.
Fungal and other atypical lung infections tend to be less common and are usually confined to immunocompromised patients, such as those with HIV or diabetes. Also patients who have structural lung disease like chronic bronchitis or cystic fibrosis are at increased risk. Symptoms in these patients may be vague with fevers, cough, and malaise existing for weeks to months. Tuberculosis is one such infection caused by the organism Mycobacterium tuberculosis that has features of both a bacteria and a fungal organism. The incidence of tuberculosis in the United States continues to be very low, 3.8 cases per 100,000 persons in 2009, thanks to advanced surveillance and monitoring of cases. Foreign born or visiting persons from other countries where tuberculosis is prevalent may bring the disease to the United States. Immunocompromised patients are also at increased risk. Clinical symptoms include chronic cough with symptoms for weeks to months, night sweats, weight loss, and bloody sputum are all hallmarks (although this can present in many pulmonary diseases).26
Epiglottitis is a bacterial upper airway infection that affects mainly the epiglottis and larynx, causing swelling of the upper airway, epiglottis, and glottic opening. Previously seen mainly in children, the Hib and other vaccines have reduced the incidence and shifted this disease toward adults. Children may present with high fevers, malaise, severe sore throat, and a minimum of cough. They also fail to swallow saliva and airway secretions producing drooling. Most will sit up in a “tripod” fashion. Adults may have a similar complaint with a hoarse voice and complaints of severe sore throat.
Respiratory Infection Treatment
Treatment for patients with acute pulmonary infections remains the same regardless of the etiology. Protection of the rescuer is paramount. EMS providers should wear PPE that provides protection for contact/droplet and airborne pathogens such as a gown, gloves, and an N95 respirator mask. Every patient with a presumed infectious respiratory disease should be treated as hazardous until proven otherwise. Once the patient has been assessed, if their condition permits, it is simplest to place an N95 respirator mask on the patient as opposed to the entire crew. This also prevents droplet spread of infection to ambulance surfaces and at the receiving hospital.
Initial assessment should focus on ensuring that ABCs are intact. High flow oxygen can be provided and if assessment reveals impending respiratory failure, NIPPV or intubation should be considered. Low pulse oximetry readings should respond to high flow supplemental oxygen. Patients with hypoxia refractory to supplemental oxygen administration should be reassessed to ensure work of breathing and tidal volume is adequate, if not, again NIPPV or intubation should be considered. Breath sounds will frequently be coarse and reveal rhonchi or rales. In a patient with no history of CAD or heart failure, this frequently is due to secretions and mucus from the inflammatory process. If wheezing or stridor is present, an inhaled β2 agonist such as albuterol should be considered; the use of Atrovent may have benefit as well. IV fluids should be administered in boluses as needed for dehydration and hypotension. The use of steroids in the EMS setting is controversial and may not be beneficial. Some patients may benefit from steroids but their impact is generally in the inhospital setting over the total course of treatment. Steroids may be more beneficial in patients with superimposed asthma or COPD.
Patients, specifically children, with suspected epiglottitis or other upper airway inflammation are at high risk of airway compromise and have different treatment priorities. Excessive agitation and crying on part of the patient can cause laryngospasm or complete obstruction of the airway. Measures should be taken to keep these patients calm and comfortable and any treatment causing agitation or distress should be avoided. In patients with suspected epiglottitis, it is acceptable to calmly transport them in the parent's arms in a position of comfort. Supplemental humidified oxygen or β2- agonists can be provided via blow-by technique if this does not agitate the patient. However, in the background, the EMS provider should have an immediate plan in place for placement of a needle cricothyrotomy or a surgical airway in older patients should the airway become obstructed. The receiving hospital should be informed of the EMS provider's clinical suspicion so that personnel and equipment can be readied for any needed airway procedures. Adult treatment is similar to pneumonia as above.
PULMONARY EMBOLUS PHYSIOLOGY
A pulmonary embolus, commonly termed PE, is an obstruction that blocks blood flow to a portion of the lung's circulation ranging from severe to clinically insignificant. The blockage can be variable, most commonly being a “thrombus” or blood clot, but can also be an “embolus” such as dislodged cholesterol, air, or amniotic fluid. A PE can typically be found in the pulmonary arteries or the smaller pulmonary arterioles that carry deoxygenated blood to the heart. This obstruction, if large enough, causes a backup of blood flow into the right heart and prevents efficient oxygenation.
The patient's clinical symptoms are determined in large part by the size of the PE and the amount of blood flow that it obstructs. Patients may have tiny PEs that remain unnoticed whereas large PEs that obstruct the main pulmonary trunk frequently cause immediate death. Although PE is a great disease mimic with many presentations, patients classically present with sudden onset of shortness of breath and frequently chest pain, cough, and sometimes bloody sputum. PEs can also present with syncope, stroke-like symptoms, seizures, and other complaints that make PE diagnosis challenging. PE should always be on the EMS provider's differential for sudden onset shortness of breath. A good clinical history may reveal risk factors for increased blood clotting such as prolonged immobility or recent surgery, malignancy, smoking, use of birth control hormones, pregnancy, or a past history of blood clots or hypercoagulable state. Vital signs are typically abnormal with mild tachycardia being a major feature, often in addition to low oxygen saturations on pulse oximetry. Another feature is the 12-lead ECG. Although only present in up to 20% of patients, the “S1Q3T3” pattern may be noted with an S-wave in lead I, a pathologic Q-wave and an inverted or abnormal T wave in lead III. However, this is not sensitive or specific and the ECG is more valuable in ruling out other causes of symptoms such as acute MI or other arrhythmia. Lastly, patients with significant hypoxia will show a poor response to high flow oxygen with continued low oxygen saturations.
Treatment for Pulmonary Embolus
Treatment for patients with suspected pulmonary embolus is supportive. ABCs should be ensured and breathing can initially be supported with high flow oxygen or NIPPV if desired although it is not clear whether this is highly effective. Intubation may be required. Circulation is frequently an issue and both tachycardia and hypotension may be encountered. In most cases, the tachycardia is sinus and is compensatory; efforts at slowing the heart rate may be detrimental. Blood pressure can be treated initially with crystalloid IV fluid boluses taking care not to precipitate pulmonary edema and after adequate volume is restored. Vasopressors such as dopamine or norepinephrine may be required to support blood pressure. Limited prehospital treatment options are available for patients with severe PE. Rapid transport to the hospital is required for unstable patients where blood thinning agents such as heparin may be used, or more aggressive treatments such as clot lysis with tPA or endovascular procedures to “retrieve” the clot. EMS providers with routine long transport times and a tPA procedure for STEMI patients may want to discuss tPA options with their medical director for PE.27
MEDICAL, NONPULMONARY CAUSES OF RESPIRATORY DISTRESS
Not all patients with a subjective complaint of “shortness of breath” or with visible increased work of breathing have a pulmonary problem. Any variation in oxygen delivery, mechanical air movement, or circulation of blood will cause symptoms.
Any physical restriction on chest wall movement or cause that obstructs this process can cause shortness of breath and increased work of breathing. Commonly this can come from injury to the ribs with resultant pain and “splinting,” injury to the diaphragm muscle (either trauma or nerve innervation), or increased abdominal pressure. Any increased abdominal pressure will be translated up to the diaphragm, from either hiatal hernias, abdominal fluid–like ascites, or masses/bowel obstruction, etc. In small children, excessive crying and “air swallowing” can produce enough pressure and displacement to cause respiratory distress.
CIRCULATORY AND METABOLIC DYSFUNCTION
Patients with high metabolic demands will commonly have what appears to be respiratory distress or tachypnea. High metabolic states create wastes such as CO2 that must be eliminated. They body will increase the breathing rate to compensate. The best example of this is a patient with diabetic ketoacidosis (DKA). Fever is another cause, especially in children.
Abnormal pulmonary circulation can cause respiratory distress as well. Any factor that disrupts or shunts blood away from the pulmonary circulation will cause symptoms. Examples include pulmonary emboli that we have discussed already and other circulatory shunts where arterial and venous blood mixes together. An example of this is the dialysis patient who may form a large fistula allowing blood to mix and bypass the pulmonary circulation.
For most patients with nonrespiratory causes of shortness of breath, maximization of oxygenation is the main priority. Usually little can be done about things like shunts or hiatal hernias except to place the patient in a position of comfort and give high flow oxygen. If breathing and oxygenation are completely inadequate, mechanical ventilation should be considered.
FOREIGN BODY AIRWAY OBSTRUCTION
Foreign body airway obstruction affects all age groups but are most common in the small children and older adults. Small toys, pills, buttons, coins, and other small objects are frequently encountered by toddlers and small children and can readily turn into an acute airway obstruction. Elderly patients will commonly present with choking episodes during mealtime and may have a food bolus obstruction. Children may choke on food items as well and objects that fit snugly into the pediatric larynx and trachea may be difficult to remove. Examples are foods such as peanuts, grapes, and hot dogs. Parents should be cautioned to avoid these foods or cut them lengthwise to decrease the diameter. Dental appliances such as bridges and partial teeth are a common cause of choking in the elderly as well.
The clinical presentation typically usually involves a sudden onset of either complete airway obstruction, with apnea, cyanosis, and decompensation, or possibly the acute onset of coughing and stridor. Especially for children, the actual event may not be witnessed and the care provider may find the patient unresponsive or in extremis. In contrast, adult patients usually present with a history of eating or ingestion. Exceptions to these cases are intoxicated or impaired patients with disabilities who may not be able to summon help or give a history.
Management should follow the American Heart Association algorithm where the EMS provider must promptly analyze the situation and determine that a foreign body airway obstruction is likely to be present. For awake children and adults, age appropriate abdominal thrusts should be administered. The EMS provider should be prepared for the patient to decompensate and be ready to provide additional care. For the unresponsive patient, American Heart Association BLS CPR measures should be initiated. Advanced rescuers may try direct visualization of the foreign body under direct laryngoscopy with a laryngoscope and removal with Magill forceps. As a last resort, a surgical airway may be considered for obstructions that cannot be removed.28
TOXIC INHALATION AND ASPHYXIANTS
The EMS provider may encounter patients with respiratory distress due to toxic inhalations and either accidental or recreational exposure to asphyxiants. The complete range of toxic gases and inhalants is far too broad to be addressed in this book but can be classified into one of a few main categories. Simple asphyxiants cause harm by displacing oxygen but are relatively inert and pose no overall toxic role or cause physiologic damage. Good examples of these are the inert industrial gases such as helium, argon, nitrogen, and carbon dioxide. In high enough concentration, these all displace oxygen, causing respiratory distress, hypoxia, and eventually unresponsiveness and death.
Other gases are cellular asphyxiants that alter the way oxygen is used at the cellular level. Examples of this include the inhalation of products of combustion. Typically gases from a residential house fire contain both carbon monoxide and cyanide. Both of these agents prevent oxygen from being used by individual cells. Cell metabolism becomes anaerobic and generates large amounts of acidic waste, causing metabolic acidosis. Other gases react with the lining of the alveoli, damaging the surface for gas exchange. Examples of these gases are ammonia, chlorine, and phosgene. Many toxins affect multiple body systems and areas.
Regardless of the exposure, strict precautions must be observed and only trained rescuers should access and treat patients until proper decontamination has been done. Patients with toxic inhalations may continue to “off-gas” or exhale toxins even after being decontaminated externally. Adequate ventilation, in-line filters, or scrubbers should be used to deal with exhaled gases if indicated. Treatment for victims of simple asphyxiants involves immediate removal from the agent and supportive ventilation and oxygenation. The EMS provider must always suspect the presence of other gases or contaminants are involved until proven otherwise.
Patients exposed to cellular toxins such as cyanide may rapidly decline and become critically decompensated. Toxins may cause airway edema and swelling, necessitating early intubation. Aggressive ventilation, fluid, and blood pressure correction may be needed. If available, a toxin-specific antidote should be employed such as a cyanide kit or other tool to “reverse or block” the cellular effects of the toxin. The local HAZMAT authority or the Poison Control Center should be contacted in all of these cases for treatment information.
INDICATIONS AND STRATEGIES FOR AIRWAY MANAGEMENT
The decision to intervene on behalf of a patient and manage the airway is broad, ranging from clear indications for patients in cardiac arrest to other more difficult decisions for patients with a potential for deterioration. The actual techniques and considerations are discussed in Chapter 59; however, we will discuss the theory here of when to intervene and with what approach.
First and foremost, the decision to secure and manage a patient's airway is one that must be taken with great care and concern. Especially in the case of rapid sequence (RSI) or pharmaceutically assisted intubation (PAI), the EMS provider is making a decision to take away whatever spontaneous or self-initiated airway support and breathing the patient has and makes a commitment to replace that with what must be a secure, effective, and sufficient airway and ventilation strategy. This decision cannot be taken lightly.
NONINVASIVE POSITIVE PRESSURE VENTILATION
Noninvasive positive pressure ventilation (NIPPV), either bilevel positive airway pressure (BiPAP) or constant positive airway pressure (CPAP) has continued to revolutionize the treatment of respiratory distress. NIPPV is a very effective treatment adjunct for almost any patient with difficulty breathing provided that they are awake and alert, able to protect their own airway, and have a sufficient baseline level of spontaneous breathing.
Originally indicated for CHF, research about NIPPV has found it to be effective in patients with asthma, COPD, pneumonia, drowning, etc. CPAP or BiPAP fits over the patients' nose and/or mouth and provides a consistent level of airway pressure. Remember from the physiology section above, during end expiration and before active inhalation, airway pressures reach zero and then become negative. CPAP or BiPAP negates this pressure and keeps small airways and alveoli “propped” open, allowing more time for gas exchange and recruiting inactive or collapsed lung segments. Also, the pressure provides a positive gradient “pushing” fluid (water, serum, etc) back into the circulation.
It should be considered in any respiratory distress patient who continues to decline or worsen despite medical therapy and in most cases should be attempted before intubation as many times intubation can be delayed or avoided. NIPPV can be problematic in patients with hypotension as it worsens the venous return to the heart and may lower blood pressure but otherwise has few contraindications. Also, recall that any type of positive pressure ventilation will worsen pneumothorax. Chapter 59 discusses the mechanical properties and techniques for the use of NIPPV.29,30
INDICATIONS FOR INTUBATION AND MECHANICAL VENTILATION
In general, patients require mechanical ventilation due to failure to ventilate, failure to oxygenate, or airway problems. The decision to intubate is sometimes difficult and clinical experience is invaluable for those situations that do not have an immediate yes or no decision tree. Most patients who need to be intubated have one or more of the following indications:
Inability to maintain the airway patency or airway obstruction (eg, acute laryngeal edema, anaphylaxis, airway trauma, and epiglottitis)
Inability to protect the airway against aspiration (loss of gag reflex)
Anticipated loss of control of the airway (eg, deteriorating mental status, laryngeal edema, neck trauma, circumferential neck or facial burns, acute stridor, etc)
Inability to ventilate (inability to blow off CO2)
Inability to oxygenate
Inability to ventilate is characterized by reduced alveolar ventilation which manifests as an increase in the PaCO2 >50mm Hg. This may be due to neurological problems (including head injury, spinal cord injury, CVA, etc), myopathic disorders (including myasthenia gravis or an exacerbation of multiple sclerosis), structural or anatomical problems (flail chest, pleural effusions, pneumothorax or hemothorax, airway obstruction), or gas exchange problems (ARDS, pulmonary embolism, COPD exacerbation).
Inability to oxygenate, leading to hypoxemia, primarily occurs at the pulmonary capillary-alveolar interface. This can be due to diffusion defects, which interferes with gas exchange. This can be caused by thickening of the alveolar wall (pulmonary fibrosis) or increased extracellular fluid (pulmonary edema). Ventilation perfusion mismatch (V/Q mismatch or “shunting”) can also lead to the inability to oxygenate. Both “dead-space ventilation” (alveoli are perfused but not ventilated) and “shunt” (alveoli are ventilated but not perfused) can be found in the same lung. Inability to oxygenate can also occur at the cellular level, due to poisoning by hazardous exposures such as cyanide.
In addition, there may be a problem with oxygen delivery and utilization: if the cardiac output is low, if the patient is edematous, or if a specific pathology interferes with the normal processes. For example, an acute MI with resulting poor cardiac output would interfere with delivery and poor oxygenation would result.
Patients are usually intubated for controlled mechanical ventilation as an endotracheal tube or tracheostomy will provide a good seal for controlled ventilation: inspired volumes and pressures are consistent, compared with noninvasive methods.
Additionally, for the EMS provider, the EMS medical director may have a specific set of qualifications and standards for proceeding with intubation. This may include a checklist or a requirement to contact online medical control prior to proceeding. In general, the whole patient picture must be considered to time intubation effectively, and the key is to identify early signs of respiratory failure and intervene before complete failure occurs and cardiopulmonary arrest ensues.
INTUBATION AND VENTILATION MODALITIES
Once the decision has been made to perform advanced airway management, the modality becomes based on the certification level and skills set of the EMS provider. For EMT or ECA providers who are limited to “assisting ventilation” with a BVM only, this technique is difficult but can be effective with patient cooperation. The prevalence of CPAP and BiPAP has nearly replaced this technique.
EMS responders trained in endotracheal intubation can proceed once the patient has become obtunded, losing protective airway reflexes, or once the decision has been made to proceed with RSI/PAI.
For all providers, the use of the supraglottic airway has been in practice in EMS for some time. Products such as the Combitube, King airway, and other supraglottic products have traditionally been used as rescue airways for failed intubation but are now effective enough to find a place in the toolbox of many EMS providers. Many EMS medical directors grant authorization to EMT providers for placement of supraglottic airways. Although not the “gold standard” for tracheal isolation and prevention of aspiration, today's supraglottic airways have a proven track record for ease and rapidity of use as well as high success rates for ventilation. Remember that even in cardiac arrest, current trends are moving toward rapid placement of a supraglottic airway.
PHARMACEUTICALLY ASSISTED OR RAPID SEQUENCE INTUBATION
Rapid sequence (RSI) or pharmaceutically assisted intubation (PAI) is another tool the EMS provider has for treating respiratory emergencies. The use of RSI and in some literature endotracheal intubation in the prehospital setting is a topic of great debate. Certain EMS medical directors do not grant this right and other health care professional organizations believe that RSI and/or intubation is too specialized and complicated for prehospital use.31 In light of this, the EMS industry must be very judicious about when and how RSI is utilized. In well-trained hands, RSI is effective and may improve intubation rates.32 One can compare RSI to a game of “Russian Roulette” where a bullet is loaded into the chamber of a gun and the revolver chamber is spun randomly. When the EMS provider sedates and paralyzes a patient, removing all of their protective airway reflexes and any ability to spontaneously breathe, the gun is loaded and cocked. If the EMS provider is then unable to either place an airway or ventilate the patient, the result is as deadly as the proverbial “bullet to the head.” EMS providers with RSI privileges must be well trained, proficient, understand the mechanics and medications, and also know when not to use RSI techniques. If assessment of the airway and patient reveals a low probability for successful ventilation or intubation, it is best to consider another method.
RSI or PAI consists of one central theory—using pharmaceutical medications to remove consciousness, muscle tone, and in most cases, protective airway reflexes to allow the passage of an endotracheal tube on an otherwise awake patient. Usually a two-drug combination is used with the initial medication being the “induction” agent and the second being the “paralytic.”
The induction agent is typically a strong sedative or dissociative drug that at the intended dose produces unconsciousness, amnesia, relaxation, and in some cases, analgesia. Different medications can produce these results and some common ones are etomidate (Amidate), midazolam (Versed), Propofol, ketamine, and in some cases, high-dose opiates such as fentanyl or morphine. All of these medications at the intended doses produce relaxation, amnesia, and unconsciousness. However, only some have pain modulating properties. They all have side effects including variable amounts of respiratory depression, hypotension, and some cardiovascular side effects ranging from tachycardia to bradycardia. The choice of induction drug varies and can be selected based on the desired side effects or lack thereof. Etomidate and midazolam are some of the most common used medications in the prehospital environment.
The second medication is the paralytic that creates a blockade between the muscle cells and the innervating nerve cell, called the neuromuscular junction (NMJ). Two major classes exist, being depolarizing and nondepolarizing paralytics. Only one major depolarizing paralytic is in widespread use today, succinylcholine. This medication works by firing or “depolarizing” all of the skeletal muscle cells in the body and keeping them in a “refractory” state where they will not fire again until the medication wears off. Succinylcholine is well adapted to RSI because the onset of action is very rapid (15-60 seconds) depending on the dose and normally wears off within 10 to 15 minutes. This allows the intubation to occur and then if complications arise, usually the patient can be ventilated until the effects are gone. Succinylcholine, however, is complicated by a large side effect and contraindication profile; most of which relate to its tendency to elevate serum potassium. Thus it cannot be used in renal patients or other patients who might already have high serum potassium (hyperkalemia). The nondepolarizing paralytics also work by blocking the NMJ but do not cause the depolarization of the muscle cells. This eliminates the concerns about potassium release and does not raise the serum potassium level. There are many different types of nondepolarizing agents and selection is based mainly on the desired duration of action. The downside of many nondepolarizing agents is the slow onset of action (1-3 minutes) and the long duration of action (30 minutes-1/2 hours). Rocuronium (Zemuron) known quaintly as “rock” is a favored prehospital medication as at the proper dose, the onset of action is rapid and similar to succinylcholine. However, rocuronium does last two to three times longer than succinylcholine depending on the dose. It is important to know that there is no reversal agent for succinylcholine and few EMS services carry medications to reverse the nondepolarizing agents.
After intubation, the patient must be continued on an agent(s) that provide continued sedation and analgesia as the original RSI medications will wear off typically within 5 to 10 minutes. Favored regimens are a combination of versed/fentanyl or propofol. Patients should be secured to avoid inadvertent removal of the IV lines or the ET tube. In addition, judicious IV fluids should be continued as most RSI and sedation medications cause vasodilatation and hypotension.
COPD and asthma levy a significant burden on the EMS system and the health care system in general
COPD, which encompasses chronic bronchitis, emphysema, and asthma, is an obstructive pulmonary disease with an inflammatory component.
Emphysema and chronic bronchitis are irreversible, progressive diseases; asthma is reversible unless lung remodeling takes place.
The physiology of respiration is a complex process that has multiple structural, chemical, and neurologic controls.
Respiratory failure is situation whereby the system fails in oxygenation, ventilation or both.
The decision to intervene on behalf of a patient and manage the airway is broad, ranging from clear indications for patients in cardiac arrest to other more difficult decisions for patients with a potential for deterioration.
Noninvasive positive pressure ventilation (NIPPV), either bilevel positive airway pressure (BiPAP) or constant positive airway pressure (CPAP), has continued to revolutionize the treatment of respiratory distress.
NIPPV is a very effective treatment adjunct for almost any patient with difficulty breathing provided that they are awake and alert, able to protect their own airway, and have a sufficient baseline level of spontaneous breathing.
Originally indicated for CHF, research about NIPPV has found it to be effective in patients with asthma, COPD, pneumonia, drowning, etc.
Most patients who need to be intubated have one or more of the following indications:
Inability to maintain the airway patency or airway obstruction (eg, acute laryngeal edema, anaphylaxis, airway trauma, and epiglottitis
Inability to protect the airway against aspiration (loss of gag reflex)
Anticipated loss of control of the airway (eg, deteriorating mental status, laryngeal edema, neck trauma, circumferential neck or facial burns, acute stridor, etc)
Inability to ventilate (inability to blow off CO2)
Inability to oxygenate
EMS providers with RSI privileges must be well trained, proficient, understand the mechanics and medications, and also know when not to use RSI techniques.
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