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Study Guide: National Registry Paramedic Exam: Airway, Respirations, Ventilation, and Respiratory Emergencies
Source: https://www.fatskills.com/paramedic/chapter/national-registry-paramedic-exam-airway-respirations-ventilation-and-respiratory-emergencies

National Registry Paramedic Exam: Airway, Respirations, Ventilation, and Respiratory Emergencies

By Fatskills Exam Guides Team — the exam nerds behind 28,500+ quizzes and 2.1M practice questions across 500+ global exams.

⏱️ ~59 min read

Objectives
- Describe the structures and functions of the airways and the respiratory system.
- Explain the physiological regulation of breathing.

Supporting breathing efforts and maintaining an open airway are the 2 most important life-saving treatments that a paramedic will ever perform. They are the bread and butter of the profession. When it comes to airway and breathing problems, the paramedic should be proactive and aggressive in treating the patient. Quick action when faced with a patient with a critical respiratory condition will go a long way in not only preventing the patient from getting worse but also shortening the hospital stay for the patient. In this guide, the anatomy and physiology of the respiratory system will be reviewed, and intricacies of airway management will be discussed. Medical knowledge will be linked with the practical examination whenever possible. Finally, the assessment, management, and treatment of patients with respiratory issues will be presented.
 

1. Anatomy and Physiology of Respiratory System
The respiratory system includes all the structures relating to the passage of air from the atmosphere to the lungs and associated structures responsible for the actions of breathing, including muscles and nerves. To begin our discussion of the airway, the pathway of air will be followed as it enters the system from the atmosphere during inhalation.

Structures of Breathing

Upper Airway

The upper airway includes the structures superior to and inclusive of the larynx. Air first enters the mouth or nose, but primarily enters the nose, during quiet breathing at rest, so our journey will begin there. Air passes through the nostrils and enters the nasopharynx. This area is lined with mucous membranes where the air is warmed and humidified, helping protect the body from heat loss and hypothermia. This area also is lined with tiny hairs called cilia. These hairs trap foreign particles, such as bacteria and dust, so that they do not make it to the lungs, helping prevent infection. The turbinates also are located within the nasopharynx and create turbulent flow of air, which helps warm the air and increases the mucosal surface air that further aids in warming and humidification.


Figure: Anatomy of the Respiratory System

If the patient is breathing through his or her mouth, air passes between the tongue and the palates. Forming the anterior portion of the roof of the mouth is the hard palate, with the soft palate forming the posterior portion. The focus of many jokes, the uvula marks the division between the mouth and the oropharynx and actually has a purpose: It prevents food from passing upward into the nasopharynx. At the back of the mouth, the oropharynx and the nasopharynx merge into the pharynx, a muscular tube that helps guide food into the esophagus. Humidification, warming, and filtration of air entering the mouth are less efficient because there is less surface area and no cilia until beyond the oropharynx. Finally, a poorly defined area that represents the most inferior portion of the pharynx is the hypopharynx. Here, the trachea and the epiglottis are anterior, and the esophagus is posterior.


Figure: Upper Airway Structures

Lower Airway
The lower airway is defined as everything inferior to the larynx, so our journey to the lungs resumes there. The larynx is a rather complicated structure that houses the vocal cords.


Figure: Lower Airway Structures

The superior border to the larynx is essentially the epiglottis and the hyoid bone. The hyoid bone is the point of attachment of the tongue and the epiglottis. Anteriorly, the thyroid cartilage provides protection and is the anatomical reference point on the anterior neck, commonly known as the Adam’s apple. The Adam’s apple is typically more apparent in men than women. Posteriorly, the larynx is bordered by esophageal muscle. The inferior border of the larynx is marked by the cricoid cartilage. The cricoid cartilage is the only complete ring of cartilage in the trachea; all the others are C-shaped and open posteriorly to allow for easier transit of food through and contraction of the esophagus. The cricothyroid membrane is the midline groove palpable between the cricoid and thyroid cartilages on the anterior of the larynx. This is the site for surgical and nonsurgical airway placement, which will be discussed later in this guide.


Figure: Larynx, Anterior View

The narrowest part of the airway is the space between the vocal cords called the glottis or the glottic opening. A vocal cord forms each of the lateral sides of the glottic opening. The epiglottis is the superior border, and the inferior border consists of the cuneiform and corniculate cartilages, which, incidentally, are the superior division between the esophagus and the trachea. The epiglottis is a leaf-shaped flap of cartilage that is responsible for covering the glottic opening during swallowing so food does not enter the trachea. It is attached to the tongue, the thyroid cartilage, and the hyoid bone with 3 different ligaments; these attachments allow for the head tilt, chin lift, and jaw thrust maneuvers to effectively open the airway. The space that exists between the epiglottis and the tongue is called the vallecula and is important for certain intubation attempts, which will be learned later.


Figure: Glottic Opening, Superior View

Continuing past the larynx, air enters the trachea, also known as the windpipe. This hollow tube of C-shaped cartilage rings leads from the larynx to the carina, where it bifurcates (divides) into the 2 main bronchi. The cartilage rings are necessary to support the shape of the trachea; without them, the trachea would collapse with each inhalation. The right bronchus is shorter and lies in more of a straight line with the trachea than the left bronchus, which makes a sharper angle with the trachea. Thus, an ETT that is pushed too far down will more often than not enter the right bronchus, resulting right main-stem intubation and decreased or absent breath sounds over the left lung fields.
The main-stem bronchi continue to divide into bronchioles of decreasing diameter until they reach the biological cul-de-sacs known as alveoli. The trachea, the bronchi, and the bronchioles are lined with sticky mucus secreting goblet cells and cilia that work together to trap and remove potential pathogens and dust from the lungs. The superficial layer of mucus called the gel layer rides atop the lower, watery layer called the sol layer. The contaminants stick to the gel layer of mucus, whereas the cilia sweep back and forth with each breath, continuously moving the mucus up and out of the lungs through a process called the mucociliary escalator system. Unknowingly, humans swallow much of the mucus that our bodies produce each day, which is removed from the lungs or drained from the nose. Beta-2 adrenergic receptors also are present in the linings of the trachea, the bronchi, and the bronchioles. When stimulated, these receptors signal the smooth muscle in these tubes to relax, causing the tubes to dilate, which allows in more air for easier breathing.

Clinical Correlate

Mucociliary Escalator

In smokers, paralysis of the cilia leads to the inability of the lungs to clear debris from the lungs. This failure of the mucociliary escalator leads to congestion and, eventually, bronchitis. It contributes to the breathing problems of long-time smokers.


Figure: Gas Exchange in the Alveolus

Two types of cells make up each alveolus. The 1st type, appropriately named type I pneumocytes, is basically empty, which allows for faster gas exchange. Type I pneumocytes lack any organelles that would allow them to reproduce or conduct cellular respiration (guide). The 2nd type, not surprisingly called type II pneumocytes, is tasked with making new type I cells and producing surfactant. Surfactant is a slippery, soap-like substance that reduces surface tension, keeps the alveoli open, and allows the tissues of the lungs to slide past each other. Without the surfactant, breathing would be at the very least painful and at worst impossible. Smoking, infections, and trauma can destroy type II cells, causing the alveoli to collapse, effectively killing them. This process is called atelectasis.


Alveoli
Healthy adult lungs can hold about 6 L of air and contain 5 distinct lobes: 2 in the left lung and 3 in the right lung. The lungs are covered by a tough membrane called the visceral pleura, and the inner chest wall is lined with a parietal pleura. In between these 2 membranes is more surfactant, allowing the lungs to slide along the inside of the chest wall nearly frictionlessly.

Tip: You can remember which lung has only 2 lobes because the heart takes up the space of the 3rd lobe and lies on the left of the chest. Therefore, the left lung has only 2 lobes.

 

2. Physiology of Breathing

The act of breathing requires several systems to work together. The musculoskeletal system must be intact and functioning, and nothing can inhibit the transfer of O2 from the atmosphere to the blood or inhibit CO2 wastes from reaching the lungs and being exhaled. In this section, the physiology behind how people breathe is presented.

Ventilation
Ventilation is the process of moving air into and out of the lungs and should always be 1 of the highest priorities in the treatment plan for any patient. Ventilation can be divided into 2 parts: inhalation and exhalation. Inhalation is the act of moving air into the lungs and is regarded as the active phase of ventilation because the body must use energy to make muscles contract. The primary muscle of breathing is the diaphragm, a large sheet of muscle that separates the abdominal cavity from the thoracic, or chest, cavity containing the lungs. When this muscle contracts, it descends into the abdominal cavity, displaces abdominal organs, and creates negative pressure in the thoracic cavity, specifically the lungs. It is negative pressure because it is less than the surroundings. Atmospheric air then rushes into the lungs to quickly equalize the pressures. The intercostal muscles located between the ribs also are considered the primary muscles of ventilation and help generate this negative pressure. When they contract, the ribs are lifted anteriorly and superiorly, further increasing the thoracic cavity volume to allow for more air to rush in.
Except in special cases, everything diffuses along the concentration gradient. The chemical in question will diffuse across a permeable membrane from an area of higher concentration to an area of lower concentration. 
The concentration of gases is measured as the partial pressure of that gas; that is, the portion of the total pressure caused by that specific gas. Henry’s Law states that as the partial pressure of a particular gas present over a liquid decreases, so does the amount of that gas dissolved in the liquid. If that partial pressure of a gas present over a liquid increases, the amount of gas dissolved in a liquid will also increase. This law is at work in the lungs. 
In the lungs, O2 has a higher partial pressure in the alveolus than in the capillary, so O2 will move into the capillary according to Henry’s Law. The opposite is true for CO2 in the alveolar capillaries. Because the partial pressure of CO2 in the alveolus is less than that in the capillary, CO2 will preferentially diffuse out of the capillary and into the alveolus.
To help understand this, think about opening a brand new bottle of soda. When you twist the cap, you hear the rush of gas from the bottle and you immediately see bubbles form inside the liquid that percolate up to the top. This process will continue in an effort to reestablish the balance of partial pressures of CO2 in both the liquid and the space above the liquid. If you tightly seal the container again, this bubbling stops when the partial pressure of CO2 in the soda equals the partial pressure of CO2 in the space above the liquid.
You may have noticed that you do not breathe in the same amount of air each time. Sometimes, you may take a really big breath after a few minutes of quiet breathing. You may yawn, taking in even more air than usual. There are terms for this varying volume of air that the lungs can hold. First, during normal inhalation, the tidal volume is the tide of air in and out or, more formally, the volume of air moved in or out during a single breath. The tidal volume can be broken down further into 2 separate volumes: the alveolar volume and the dead space volume. The alveolar volume is the amount of air that actually reaches the alveoli, whereas the dead space volume is the amount of air in each breath that fills the portion of the lungs not involved with gas exchange. Physiologic dead space is the normal dead space plus the dead space resulting from atelectasis of any etiology.
With normal breathing tidal volume as a baseline, the volume of air a person can inhale with the deepest breath possible is called the inspiratory reserve volume. The amount of air a person can forcibly exhale after a normal exhalation is called the expiratory reserve volume. The inspiratory capacity is the total volume that can be inhaled, whereas the functional residual capacity is the expiratory reserve volume combined with the residual volume. The vital capacity is the sum of 3 volumes: the expiratory reserve capacity, the tidal volume, and the inspiratory reserve capacity. Even after forcing out as much air from the lungs as possible, air is still left in the lungs. This remaining air is called the residual volume. Residual volume plus the vital capacity gives the total lung volume.


Figure: Lung Volumes

Finally, when it comes to lung volumes and capacity, it often is more helpful to talk about these volumes during the span of 1 minute, rather than breath to breath as discussed previously. Minute volume is the amount of air that is moved through the lungs in 1 minute and can be calculated by multiplying the respiratory rate by the tidal volume. The alveolar minute volume is the tidal volume minus the dead space volume multiplied by the respiratory rate.
Unlike inhalation, exhalation in the healthy person is passive; it does not require the body to spend energy to expel the air from the lungs. As the muscles of inhalation discussed earlier relax, the pressure within the thoracic cavity increases, until it exceeds that of the atmosphere. At that point, air leaves the lungs without much effort. This becomes an active process in people with asthma or chronic obstructive pulmonary disease (COPD).

Regulation of Ventilation
Have you ever noticed that you cannot hold your breath for more than about 30 seconds to a minute? Or that you cannot keep your breath exhaled without being forced to take what ends up being a deeper breath than usual? Breathing is regulated primarily through chemical control and neural control, with chemical control being the most sensitive and complex. Chemoreceptors located throughout the body monitor all the body’s metabolic processes; the chemoreceptors concerned with respiration are located in the carotid arteries, the aortic arch, and the central chemoreceptor.
The aortic and carotid chemoreceptors monitor the partial pressure of carbon dioxide (PaCO2) dissolved in arterial blood to help it determine when to breathe. The central chemoreceptors are located near the respiratory centers in the brain and monitor the pH of cerebrospinal fluid (CSF). When the pH of CSF decreases, that is, CSF becomes more acidic, the central chemoreceptors send a signal to increase the rate and depth of breathing. These centers are not only important in driving respirations but also integral to holding the body’s pH and acid-base balance within a narrow range.
Under normal circumstances, breathing is regulated primarily by the methods described above: PaCO2 monitoring by the chemoreceptors in the carotid arteries and the aortic arch and by the pH in CSF. However, some patients, particularly those with COPD, live with an increased CO2 level and more acidic CSF because they have difficulty removing CO2 from the blood. Consequently, changes in CO2 level are not enough to drive respiration, so the chemoreceptors in the aortic arch and the carotid arteries begin to stimulate breathing based on a drop in the partial pressure of oxygen (PaO2) levels in the blood. This is called the hypoxic drive and is a fail-safe for the body to continue breathing under extreme circumstances. It is believed that giving patients with end-stage COPD excess O2 could override this hypoxic drive and cause them to stop breathing altogether.

The medical community has no consensus for this, so the best practice in these patients is to not deny O

Oxygenation and the Oxyhemoglobin Dissociation Curve
Ventilation is the act of moving air into the lungs. Oxygenation is specifically the loading of O2 onto the hemoglobin, the O2-carrying molecule in red blood cells. Oxygenation cannot occur without ventilation; however, ventilation can occur without oxygenation actually taking place. This can happen whenever the amount of O2 is not found in adequate concentrations in the inhaled air, such as at high altitudes or in confined spaces where another gas has displaced the O2.

- Nail polish may give a false high or low reading depending on color or prevent the machine from giving a reading at all.
- Cold extremity/poor perfusion: If the location of the sensor, typically a finger, a toe, or an earlobe is cold, blood may be shunted away from that area, resulting in a false low reading. Raynaud disease, wherein otherwise healthy people have cyanotic fingers in cool weather, is another example of poor perfusion.
- Low hemoglobin: This condition may be deceptive because the readout will likely indicate normal oximetry. Remember, this is the percentage of red blood cells that are carrying O2. For example, if normally 400 red blood cells pass by the sensor in a second, and 396 of them are carrying O2, the oximetry is 99%. The oximetry is the same if 200 red blood cells pass by a sensor and 198 of them are carrying O2. In the latter example, however, the person may still require O2 because he or she has a reduced carrying capacity. 

The oxyhemoglobin dissociation curve illustrates the relationship between the partial pressure of the O2 dissolved in arterial blood and the saturation of the hemoglobin molecules with O2: SpO2 if measured through pulse oximetry, and SaO2 if measured from an arterial blood gas (ABG) draw. Because paramedics typically do not have ABG results, only the SpO2 is referenced; however, paramedics should be aware that both exist. The Hb-O2 dissociation curve shows the oxyhemoglobin dissociation curve, and, under normal conditions, the PaO2 is about 105 mmHg when the SpO2 reads 98%. There is a steep drop-off of the partial pressure of O2 dissolved in the plasma when the SpO2 is <80%. When the blood reaches the tissues, dissolved O2 is taken up by the cells, first causing the PaO2 to drop. As this occurs, O2 bound to the hemoglobin detaches and dissolves in the plasma. In this way, O2 supply often far exceeds demand.


Figure: The oxyhemoglobin dissociation curve with left and right shifts.

Tip: Oxyhemoglobin curve mnemonic: CADET, face RIGHT! CO2, acidosis, 2,3-diphosphoglycerate, exercise, temperature moves the curve to the right. These are the conditions under which O2 is bound less tightly to the hemoglobin. Fortunately, they also are conditions common to tissues where O2 should be offloaded from the hemoglobin.

Respiration
Respiration is another term related to gas movement. Respiration is the process of exchanging O2 and CO2. The key here is the exchange of gases, which makes respiration different from oxygenation. The distinct forms of respiration are external respiration and internal respiration. External respiration is the exchange of gases at the alveolar level in the lungs. Internal respiration is where the cells of the tissues receive O2 and expel their waste CO2 into the bloodstream for removal. Internal respiration also is more frequently called cellular respiration. The cell uses O2 during aerobic metabolism within the mitochondria of the cell during the complete oxidation of glucose to CO2. Refer to this guide for more information on cellular metabolism.


Summary of O2 Transport-Related Terminology

Ventilation Process of Moving Air into and out of the Lung
Oxygenation Loading of O2 onto the hemoglobin
Perfusion Circulation at the cellular level, including the delivery of O2 and nutrients and the removal of wastes
Respiration Exchange of O2 and CO2 between blood and the alveoli (external respiration) or cells (internal respiration)

Tip: You can associate the word external with meaning external to the body to help you remember that this occurs in the lungs, and atmospheric air is external to the body.

Clinical Correlate

GERIATRIC CORNER
Many changes take place in the respiratory system as a person ages.

- The lungs become less elastic, and the portions of the ribs that are made of cartilage in youth ossify and become bone in the elderly. Combined with an overall weakening of the respiratory muscles, these lead to a reduction in vital capacity and an increase in residual volume.
- The PaO2 dissolved in the lungs declines from 90 mmHg at 30 years old to about 75 mmHg at 80 years old, which is caused in large part by changes in the distribution of pulmonary blood flow.
- The elderly are more likely to live with hypoxemia and hypercarbia (high blood CO2) because of decreasing sensitivity to minute changes in ABGs and pH in the central nervous system.

 

3. Airway Management and Suctioning

Getting O2 to the lungs is the single most important thing that the paramedic can ensure happens in every patient encountered. This section will discuss obstructions to the airway and how to relieve them and will conclude by discussing the airway adjuncts available to the paramedic, including BLS airways through surgical airways.

Airway Obstruction
Assessing airway patency in a person who is talking is about as easy an assessment a paramedic will ever make. If the person is talking, he or she has an airway. Check. But if the person is unresponsive, ensuring that the person has an adequate airway becomes a bit more of a challenge. When assessing the airway, listen for stridor. This upper airway sound will accompany any of the following causes and is sometimes the only clue to a narrowed airway passage. Let’s look at some of the common causes of airway obstruction.

- Tongue. In the person who is unresponsive, the tongue is the most common obstruction to the airway. In this group of patients, the muscles relax, and the tongue falls back against the posterior wall of the pharynx, effectively shutting off the airway.
- Foreign Body and Aspiration. Mama Cass (Cass Elliot) legendarily died of choking on a ham sandwich. Although not thought to be a factor in Mama’s untimely demise, choking often is associated with alcohol consumption, loss of a gag reflex in those with a stroke, and laughing or talking with food in the mouth.
- Laryngeal Spasm, Edema, and Injury. Laryngeal spasm occurs when the vocal cords close off the airway, which can happen from intubation attempts or can be a diver’s reflex. Edema is swelling and results from a fluid shift in the larynx that closes or nearly closes off the airway. Allergic reaction, trauma, or inhaling hot air or steam are common causes of laryngeal edema.

Patient Positioning and Manual Airway Maneuver
With some airway problems, simple repositioning of the head is all that is needed to relieve the obstruction and restore spontaneous breathing. Sometimes, however, more aggressive treatment is necessary to provide an airway for the patient. Any patient who has a CGS reading <8 or who is unresponsive should be immediately placed in a supine position if not found that way. This allows paramedics to quickly assess airway patency, breathing effort, and circulatory status with minimal difficulty.

- While at the patient’s side, place the hand nearest the head on the forehead.
- Place 2 fingers on the mandible, staying clear of the soft tissue under the chin.
- Simultaneously apply pressure to the patient’s forehead while lifting up on the mandible.

Jaw Thrust
Contraindications:None in unresponsive trauma. Otherwise, the head tilt/chin lift maneuver is preferred. This maneuver can be painful if performed on a person who is conscious.

- Position yourself superior to a supine patient’s head.
- Place your thumbs on the cheek bones of the patient and the tips of your first 2 fingers posterior to the angle of the jaw.
- Pull the jaw upward (anteriorly) using your thumbs on the cheeks for leverage. This position is difficult to maintain for long periods of time, so be sure to have a plan for inserting an airway adjunct.

Suctioning
Now that you have been introduced to the potential causes of airway obstruction and have learned how to open an otherwise occluded airway, it is time to discuss the active removal of debris in the airway with suctioning. The suction unit must be capable of generating 300 mmHg of vacuum force; have rigid-suction catheters, soft-suction catheters, large-bore noncollapsible tubing to connect the catheter with the suction unit; and include an unbreakable, disposable collection vessel to go along with a supply of water for rinsing the catheters after each suctioning run. The rigid-suction catheters, or Yankauer catheters, are ideal for suctioning the mouth of vomit and blood and are easy to control. The soft-suction catheters, or French catheters, are best suited for suctioning out the lumen of an ETT or a nasopharygeal airway.

- Select a rigid-suction (Yankauer) catheter.
- Measure from the corner of the mouth to the earlobe. This is the maximum depth of insertion.
- Open the mouth using the cross finger technique.- -

Procedure, ETT in place:
- Select a soft-suction (French) catheter.
- Observe sterile technique. Measure from the end of the ETT to the earlobe to the suprasternal notch. This is the maximum depth of insertion.
- Lubricate the tip of the catheter.- - - Ventilate or direct the ventilation of the patient.

Practical Point
On the NRPE, suction is tested only after intubation is successful through the ETT. Failure to preoxygenate the patient prior to suctioning (step 4) is a critical failure. Inserting any adjunct in a manner dangerous to the patient also is a critical failure. This could be selected if you fail to measure the length of the catheter and insert it too far into the tube. Suctioning in the Ventilatory Management—Adult station is worth up to 6 points.


4. Basic Airway Adjuncts

Although no adjunct can take the place of manual head positioning, adjuncts can help maintain an airway in patients who are unresponsive. They are designed to hold the tongue off the posterior wall of the pharynx.

Oropharyngeal Airway
Indications: The patient is unresponsive, breathing or not, without gag reflex.

- Measure the airway from the corner of the mouth to the earlobe.
- Open the mouth with the cross finger technique.
- Insert the airway upside down until the distal tip reaches the soft palate.

Nasopharyngeal Airway
Indications: Patients who are unresponsive and patients with an altered mental status who have an intact gag reflex and cannot tolerate an oropharyngeal airway.

- Measure the nasopharyngeal airway from the tip of the nose to the earlobe.
- Lubricate the tip with water-based lubricant.
- Select the larger nostril and apply gentle pressure posteriorly. A common error here is to aim the device superiorly, when the nasal passage is almost directly posterior to the nostril.

Tip: Oropharyngeal airways can be left in patients who have been intubated as a bite block. In the event the patient regains consciousness, seizes, or for some other reason experiences trismus (clenching of the jaw), this will prevent them from biting and crimping the ETT.

5. Advanced Airway Management and Adjuncts

It is worth repeating: BLS before advanced life support (ALS). This means that an advanced airway adjunct should be attempted only when any of the following conditions are met:

- After attempting and failing to establish a patent airway by 1 of the previously discussed methods.
- Prolonged airway management is required.
- Continued bleeding into the airway, excessive secretions, or vomiting require nearly continuous suctioning.
- Laryngeal fracture.

Before deciding to move to an advanced airway, evaluate the patient and anticipate and prepare for a difficult airway. If assessment reveals it will be difficult to successfully intubate the patient or current ventilation efforts are successful with minimal difficulty, sometimes it may be best to stay with what is working, rather than risk a bad outcome for the patient. A good mnemonic to assess for a difficult airway is LEMON, as follows:

- L, Look Externally. Look for things that may pose a problem, such as loose teeth or dentures. Short thick necks or severe overbite are clues that intubation may be difficult. - M, Mallampati. This scoring system evaluates the mouth opening by how much of the oropharynx is visible when the patient opens his or her mouth as wide as possible.
- O, Obstructions. Any other potential problem in the mouth that could inhibit intubation.

Figure: Mallampati Classification System

Orotracheal Intubation with Direct Laryngoscopy
The crowning achievement of any paramedic is walking into the emergency department with a successful intubation. Nothing feels better than when the resident or attending looks into the mouth and declares, “Yup! It’s in!” That sense of accomplishment can last the rest of the tour at least. To be successful at this, prepare for the procedure completely before making an attempt. Set out all the necessary equipment, including laryngoscope blades, the stylet, the water-based lubricant, the ETT, a 10 mL syringe, and suction. Put on gloves; because blood or bodily fluid splashing is possible, wearing a surgical mask with a face shield also is recommended.

- Prolonged ventilation expected (i.e., cardiac arrest, head injury)
- Absence of a gag reflex
- Anticipated airway compromise in respiratory failure, anaphylaxis, or airway burns
- A last resort for administering certain medications

Contraindications:
- Oral trauma
- Oral pathologies such as cancer, angioedema, and poor oral opening
- Inability to visualize glottic structures

Procedure:
- Preoxygenate the patient for 2–3 minutes prior to the intubation attempt. This helps elevate the PaO2 so that the patient can tolerate a minute or so without ventilation and oxygenation. -
- Insert the blade, displacing the tongue to the patient’s left. Insert the Miller (straight) blade all the way into the pharynx and lift straight up while controlling the epiglottis. If using a Macintosh (curved) blade, insert the blade by sliding it down the curve of the tongue and into the vallecula; lifting up on a curved blade will pull the tongue up directly and the epiglottis up indirectly because both are attached to the hyoid bone. This will reveal the rest of the glottic structures.
- Elevate the mandible with the laryngoscope. Remember, it is a lift of the laryngoscope along the axis of the handle, not a ratcheting movement using the upper teeth as a fulcrum. 
- Confirm tube placement by at least 1 additional method. Waveform capnography shows the amount of CO

Practical Point
The previous procedure follows the National Registry for EMT’s advanced level practical examination checklist for adult ventilatory management. Steps identified as a critical failure if not performed are failing to preoxygenate the patient prior to the attempt, allowing the stylet to protrude beyond the tip of the ETT, using the teeth as a fulcrum, failing to remove the syringe immediately after inflating the cuff, and failing to confirm tube placement by listening over the epigastrium and the bilateral lung fields.

Other methods of intubation exist and are frequently taught during paramedic classes. Because none of these methods or techniques have been tested, only their indications and contraindications will be discussed. A step-by-step procedural outline as done with other procedures that have been tested is not included here.

Other less commonly used intubation methods also exist in certain systems. Local protocols will indicate whether other alternate forms of intubation are available. First, a lighted stylet that illuminates the trachea internally and is visible through the skin externally when correct placement is achieved may be an intubation option. A 2nd option may be retrograde intubation, which involves inserting a large-bore intravenous catheter into the cricothyroid membrane in a cephalic direction and threading a guide wire through it until it is visible in the pharynx. The guide wire is then pulled out through the mouth, and an ETT is placed over it and slid directly into the trachea blindly. This very complex procedure should be performed only under the strictest of sterile techniques.


Alternative Airway Devices
While direct laryngoscopy is still currently the preferred method of securing an airway, other devices can be used in the event that orotracheal intubation is not possible or proves extremely difficult. In many cases, these devices and procedures should be used before attempting alternative intubation techniques, such as those discussed previously in this guide because placement of and successful ventilation with these techniques is often quicker than digital, nasal, or retrograde intubation will be.

Multilumen Airways
The Combitube is a preformed dual lumen plastic tube that is blindly inserted into a patient’s mouth and can be used for ventilation regardless of whether it is inserted into the esophagus or the trachea. This tube is expected to enter the esophagus but occasionally will enter the trachea, so, essentially, it cannot be misplaced.

- Wear gloves. A surgical mask with a face shield is recommended.-
- Position the patient supine and in the neutral or sniffing position.
- Open the mouth with the tongue/jaw lift maneuver.- - -

Supraglottic Airways

Laryngeal Mask Airway
The laryngeal mask airway (LMA) is designed to wedge itself into the hypopharynx and cover the entire glottic opening. Ventilation is then directed into the trachea after the cuff is inflated, sealing off the entire hypopharynx. Insertion for these types of airways is blind, similar to the Combitube. LMAs come in a variety of sizes and are not limited based on height, like the Combitube. A drawback for these devices, compared with the Combitube or the ETT, is that they do not completely prevent vomiting or aspiration.
Indications: An alternative to BLS airway when an ETT cannot be placed
Contraindications: Morbid obesity because the seal for these patients is not as tight as for others; patients with COPD may require higher airway pressures, which is not accomplished well with the LMA.

- Wear gloves. A surgical mask with a face shield is recommended.- - - - Secure the device with tape or a commercial tube holder.

King LT
The King LT is very similar to the Combitube, except that it is only a single lumen and must be inserted into the esophagus to work. Similar to the Combitube, it has a distal cuff that seals the esophagus and a pharyngeal cuff that seals the oropharynx; however, it has only 1 tube for ventilation. Unlike the Combitube, it comes in a variety of sizes and can be used in children as small as 12 kg.

- Wear gloves. A surgical mask with a face shield is recommended.
- Preoxygenate the patient prior to attempt.- - -
- Secure the device with tape or a commercial tube holder.

Surgical and Nonsurgical Cricothyrotomy
The surgical airway is not something that should be performed in the field. Severe bleeding during the incision of the trachea may occur if the thyroid gland is inadvertently lacerated. Because this procedure would be performed only if all the previously described procedures to establish an airway fail, it can safely be presumed that the airway in question is extremely difficult and could be made worse with excessive thyroid bleeding. In addition, this procedure should be performed only with operating room quality sterility, which is nearly impossible to effectively establish in the back of an ambulance or a helicopter. The nonsurgical or needle cricothyrotomy, on the other hand, is possible to successfully perform in the field and is the recommended method for establishing an airway when all else fails.
The needle cricothyrotomy is a life-or-death last resort for establishing airway patency. Ensure that local protocols allow this procedure to be performed; in many cases, online medical control needs to be contacted first to verify permission. This procedure is much quicker than a surgical airway and carries with it significantly less chance for bleeding or failure.

- Wear gloves. A surgical mask with a face shield is recommended. 

Special Patient Populations: Stomas and Tracheostomy Tubes
Some patients have a stoma or a tracheostomy tube and are in need of O2 or ventilatory assistance. Many of these patients need to be suctioned frequently and will sometimes have a sudden onset of severe respiratory distress until they are suctioned. Simply inserting a soft-suction catheter until resistance is felt but no more than 12 cm and suctioning only on the way out as described previously should clear up most respiratory issues. The patient will cough as the suction catheter is inserted, so use caution in case of airborne mucus.

After ensuring a patent airway, preferably by ensuring the patient can talk to you, evaluate and treat any breathing problems. Before exploring the variety of respiratory emergencies, this section reviews all the O2 administration methods that are available to the paramedic in the field. In addition, ventilatory support methods, including BVM techniques and continuous positive airway pressure (CPAP) will be presented. Finally, the section will conclude with a discussion on special patient populations who may present a challenge with breathing problems.

Designed for low concentrations of O2, nasal cannulas are typically used to deliver O2 to a breathing patient at a flow of 1–6 L per minute (LPM), providing a fraction of inspired oxygen (FiO2) of 24% to 45%. Remember, each liter per minute of supplemental O2 delivers 3% more O2 to the patient over the atmospheric concentration of 21%, so the equation to estimate FiO2 is FiO2 = 21 + (3 * liter flow). This can be used when a patient is unable to tolerate a non-rebreathing or simple face mask or does not require high concentrations of O2 to maintain adequate perfusion. It also is highly recommended that the patient be placed on nasal cannula O2 at 6 LPM during intubation attempts.

O2 humidifiers are designed to add moisture to the O2 being delivered to the patient. O2 delivered to a patient from a concentrator or a sealed bottle or cylinder is completely devoid of any moisture or humidity. Delivering dry O2 to a patient for extended periods can dehydrate the patient and the mucous membranes, which becomes an issue with long transport times, such as those on interfacility transfers, but not during a typical emergency where patient contact time is limited. 

Ventilatory Support
Normal ventilation is accomplished by creating negative pressure in the chest when the diaphragm contracts and descends into the abdominal cavity and the intercostal muscles contract and the rib cage raises anteriorly and superiorly to increase the volume of the thoracic cavity. This is important to the circulatory system as well. During the creation of negative pressure, not only is air drawn in but also blood is pulled up from the extremities and head, returning it in greater quantity to the heart. When artificial ventilation methods must be employed, however, the enhanced venous return is not only lost but also actually reduced because of the now positive pressures used to push air into the lungs. Finally, because positive pressures are used, the air that is squeezed into the chest enters the lungs; occasionally, if too much force is provided to deliver the breath, air will enter the stomach, a condition known as gastric insufflation or gastric distension.
As a patient’s breathing worsens, before the patient stops breathing altogether, the paramedic should begin assisting the patient’s existing respiration using a BVM device. This is a very difficult skill and requires almost complete concentration on the part of the paramedic to do it successfully. Losing concentration while assisting ventilations will inadvertently make the patient’s breathing and their already high anxiety worse.


Indications: Inadequate breathing based on fast rate or shallow depth
Contraindications: Patient’s increased anxiety when hands and the BVM are on the face

- Connect the BVM to an O2 source and explain the procedure to the patient.
- Place the mask over the patient’s mouth and nose.
- Observe the patient closely and squeeze the bag each time the patient initiates a breath. This will get easier as the squeezes get more in sync with the patient’s natural breathing rhythm. The patient will drive the exhalations. Do not try to force air in while the patient is trying to exhale. This will serve to only further worsen the patient’s apprehension.
- Slowly increase the volume delivered with each breath, which will do the most in attempting to control the breathing.

Artificial Ventilation
Multiple ways can be used to deliver a breath to a patient once he or she has stopped breathing; however, the most effective way is with 2 rescuers using a BVM. Mouth to mask with supplemental O2, as is taught in most CPR classes, is 2nd. Once a patient has stopped breathing, or is in respiratory arrest, paramedics need to breathe for them entirely. This is arguably the most important skill any prehospital provider can master at any level. There are no contraindications to this skill; even when there is massive facial trauma, still attempt to establish a seal with the mask to the face to deliver ventilations.

- Kneel superior to a patient’s head (assuming the patient is on the floor) and hyperextend the neck. If trauma is suspected, perform the modified jaw thrust maneuver instead and maintain the head in a neutral in-line position.
- Place the mask of the BVM over the patient’s mouth and nose and use both hands to simultaneously press the mask to the face with both thumbs and forefingers while pulling the patient’s jaw into the mask with the remaining fingers of both hands. Take care not to press on the patient’s eyes or the soft tissue under the jaw during this procedure. Establishing a seal and successfully ventilating may be difficult in patients with BONES: beard, obese, no teeth, elderly, snores.
- Connect the reservoir to O2 set to at least 15 LPM or higher. Connect the BVM to the mask if not already done. While holding the mask securely to the face, have a 2nd rescuer squeeze the bag with both hands enough to have visible chest rise. Squeezing the bag should be done slowly over 1–2 seconds to help minimize the chances of gastric distension. Repeat this 10–12 times per minute or give 1 breath every 5–6 seconds for the adult and 3–5 seconds for the infant and child. Ventilating faster than this will not be of any more benefit to the patient. If there are limited rescuers, use just 1 hand to secure the mask to the face using the E-C technique: the thumb and index finger form a C, and the other 3 fingers form a capital letter E under the jaw bone.

Practical Point
Although it may seem like an easy skill, ventilating a patient with a BVM is decidedly an underrated skill. This is a critical skill to practice and ensure that you are ventilating at the correct rate (10–12 per minute for an adult) and at the appropriate depth. Examiners pay particular attention to this skill.

Continuous Positive Airway Pressure
CPAP is essentially the same as the assisted ventilations described previously; however, it is controlled by a machine and does not require the provider to hold the mask to the face of the patient. It uses straps that fasten to the mask and wrap around the head. It has been shown to decrease the morbidity and mortality of patients with severe respiratory distress who, prior to the use of CPAP, would have been intubated. CPAP provides continuous pressure into the lungs and opens collapsed alveoli while preventing further atelectasis. It is not uncommon for patients who are found with respiratory rates in the 40s and oximetry readings <80% to dramatically improve with CPAP application to having a slowed respiratory rate and pulse oximetry reading approaching 100%.

- Connect the circuit (mask and tubing) to the CPAP device. Connect to the O2 source.
- With O2 flowing and the CPAP unit turned on, place the mask on the patient’s face, covering the mouth and nose.
- Have the patient breath normally. Connect the strapping system to 1 side of the mask first. Wrap the straps around the head and connect to the posts on the other side of the mask. Adjust for a tight, secure fit and check that it is comfortable for the patient.
- Continuously monitor the patient for decline in his or her status. Although CPAP often results in rapid improvement of the patient, it does not treat the underlying cause of why the patient began with respiratory distress in the first place; it treats only a symptom, and it also can be overpowered by a relentless disease process.

Gastric Distension
Any time artificial ventilation is used in the absence of an ETT, it is very likely that air enters the stomach in addition to the lungs, resulting in gastric distension. This presents the very real possibility of projectile vomiting as the stomach suddenly and spontaneously decompresses, further complicating the airway and respiratory problem at hand, not to mention creating a nightmare of a cleanup. Furthermore, as the stomach expands and pressure within it builds, it will become increasingly more difficult to ventilate the patient because the lungs can no longer expand into the abdominal cavity as they normally would.

Minimize the development of gastric distension by positioning the airway correctly and hyperextending the neck, delivering breaths slowly over 1–2 seconds, and allowing full exhalation before delivering the next breath. Even observing these suggestions will likely result in some distension. To relieve it, the paramedic can insert a nasogastric tube or an orogastric tube if protocols allow. The nasogastric tube is contraindicated in patients with facial fractures because the tube can enter the cranium through a fractured basal skull. The orogastric tube should be used only in the cases of facial fractures and in patients who are unresponsive and do not have a gag reflex. Because the orogastric tube is used only during these conditions, it is nearly always inserted after ETT placement and cannot be placed if any other advanced airway device is used. (It can be used with a Combitube if it was placed in the esophagus and the patient is being ventilated through blue tube number 1.)

- Explain the procedure to the patient while donning gloves and a face shield.
- Whenever possible, use a topical anesthetic spray to suppress the gag reflex and make the whole procedure a little more comfortable for the patient.
- Measure the tube for depth of insertion from the tip of the nose to the earlobe to the xiphoid process.- -

Orogastric tube placement procedure:

- Position the patient’s head in a neutral position.
- Measure the tube for depth of insertion from the corner of the mouth to the earlobe to the xiphoid process.
- Lubricate the tube with a water-based lubricant and insert it along the midline into the oropharynx. Advance it to premeasured depth.


6. Respiratory Emergencies

Respiratory emergencies are one of the most common reasons for a person to call an ambulance. The reasons can range from a foreign body airway obstruction to a severe asthma attack. Respiratory emergencies can affect patients of any age or medical history. The paramedic needs to be prepared for managing a wide variety of respiratory distress calls.

Pathophysiology of Breathing
Breathing can fail in a multitude of ways, such as a closed airway or obstructions in the alveoli, among other things. Hypoxia or hypoxemia is a state of low O2 levels in the blood that ultimately results in tissue and organ death if the condition is not quickly treated and reversed. Some tissues are more sensitive to hypoxic conditions than others. For example, the brain can tolerate a decline in blood O2 levels only for a few minutes; after 10 minutes without O2, irreversible brain damage occurs.

If ventilation can be performed without deficit, look at the issue of oxygenation and respiration. Because impairment to oxygenation also likely affects the transposition of CO2 from the blood into the alveolus, if 1 is affected, both are likely similarly hindered. As with ventilation, impairments to respiration come in both extrinsic and intrinsic flavors. An extrinsic factor affecting respiration is, for example, if the patient is in an environment where the concentration of O

Assessment
Any patient with a respiratory complaint must be assessed carefully because so many different factors go into successful breathing. The respiratory rate, the number of times a person breathes in 1 minute, is the easiest portion of the breathing assessment to ascertain. Immediately evaluate any person found breathing outside these ranges for respiratory problems because alveolar ventilation and tidal and minute volumes can start to be affected. It's essential to know the normal respiratory rates for adults, children, and infants. Assessing the remainder of the history and physical examination is more involved.

Normal Respiratory Rates

Age Range Respiratory Rate Range
Adult 12–20
Child 15–30
Infant 25–50


- General Information. In what position was the patient found? Is the patient tripoding? A patient in severe respiratory distress will not be lying down because it will worsen breathing. Assuming a tripod position—hands on the knees and back straight—will put the airways in line and allow for the least inspiratory resistance. As with every patient, remember to get a complete SAMPLE history, paying particular attention to the events leading up to the incident.

- Head and Skin. Are the nostrils flaring? Is there pursed lip breathing? Patients will flare their nostrils to create more space for air to enter with inhalation. When they exhale, they exhale almost exclusively through their mouth and purse their lips as if blowing out candles on a cake. This creates about 2 cm H2O of PEEP and helps keep the alveoli open. Assess the pupils for equality and reaction. This may indicate a neurological problem that could be the source of the patient’s respiratory problem. Remember that not all respiratory problems originate in the lungs. Check the skin for color, temperature, and texture. Findings of pale and sweaty or clammy skin could indicate shock, whereas flushed skin could be a clue for a fever, and hives indicate an allergic reaction.

- Neck. Is the patient using accessory muscles to breathe? Accessory muscles are most visible in the neck, and they stand out when in use. They are used to help elevate the rib cage. Is there jugular vein distension (JVD)? Is the trachea midline? JVD indicates increased intrathoracic pressure, commonly from CHF or pneumothorax, whereas a trachea that is displaced from the midline is a late finding in a pneumothorax.

- Chest.

- Are retractions present? Retractions form as a result of a combination of extremely high negative pressure in the thoracic cavity in an attempt to draw air in and a blockage, whether internal or external, in the airways. The following are locations for retractions: intercostal retractions (between the ribs), supraclavicular retractions (to the right and left of the neck), suprasternal retractions (above the sternal notch), and subcostal retractions (under the rib cage in the area of the epigastrium). Retractions indicate severe airway compromise.
- Are the rise and fall of the chest adequate? Equal? Unequal rise and fall of the chest indicates that the lung underneath is not getting ventilated with each breath. It often signals a pneumothorax. Paradoxical motion is the movement of a segment of the rib cage in the opposite direction of the rest of the ribs; on inhalation, a rib segment moves inward; on exhalation, the segment moves outward. This motion occurs in a flail segment and indicates chest trauma and broken ribs.
- Are there any adventitious breath sounds? Listen to the breath sounds of every patient. This can be done on either the anterior or posterior chest, but the bell of the stethoscope should always be placed directly against the skin for the best transmission of the clearest sound. More on breath sounds a little later.

Abnormal Respiratory Patterns

Type Description Pattern
Cheyne-Stokes respirations Periodic breathing with cycles of increasing rate and depth of breathing followed by gradual decrease in depth and rate of breathing in between periods of apnea that can last up to 60 seconds


 
Kussmaul respirations Continuous, deep sighing breaths with a rapid rate; usually >40 when the body is responding to metabolic acidosis


 
Biot’s (ataxic) respirations Irregular rate, rhythm, and depth with intermittent apnea


 
Apneustic respirations An ominous sign of a brain-stem injury, prolonged inhalation followed by short ineffective exhalation


 
Agonal respirations An ineffective form of breathing that is characterized by slow gasping breaths often seen in pulseless patients


 
Central neurologic hyperventilation Essentially the same as Kussmaul respirations but from a different cause—brain injury and increased intracranial pressure (ICP), resulting in respiratory alkalosis


 

 



Figure: End-Tidal CO2 Waveform Morphologies and Phases

- Upper Extremities. Is clubbing present on the fingers? Clubbing indicates chronic hypoxia.

Breath Sounds
Listening to lung sounds is an essential piece of the assessment puzzle in the patient with respiratory issues. It helps discern among the various pathologies that will be learned, which provides clues to the treatment that needs to be administered. When listening to breath sounds, it is important to listen on the same level, side to side, not up and down, first 1 lung and then the other. Look for equality of sound between the lungs at the same location, as well as the sound itself. Different volumes of sound in 1 lung versus the other lung at the same level could indicate that the diminished side is collapsing or filled with fluid, which indicates that air movement is not happening in that particular area. Remember to listen to all lung fields. This means listening to the following: listen to the apices by placing the stethoscope on the patient’s back just superior to the shoulder blade on each side; listen to the middle lung fields by listening between the shoulder blades and the spine on each side; listen to the lower lung fields by placing the stethoscope on the midaxillary line at about the level of the 5th rib. As a new paramedic, listen to as many “normal” lungs as possible so that it will be easier to differentiate subtle differences in lungs with adventitious breath sounds. Adventitious breath sounds are simply abnormal in some way. There are several lung sounds with which to be familiar.

End Tidal CO2 
A tool to help us evaluate patients’ respiratory status is the measurement of their EtCO2. It is measured as a patient exhales and can be done either with a colorimetric detector or as capnography that produces an actual numerical value and wave form on a monitor. Normal EtCO2 values range between 35 and 45 mmHg. Using a colorimetric detector is typically good only for a few breaths—until the litmus paper gets saturated with CO2 and no longer changes color from purple (unsaturated) to yellow (saturated). 
Waveform capnography is useful in cardiac arrest as well as respiratory distress. In cardiac arrest, a sudden jump in EtCO2 values could signal the return of spontaneous circulation. In a person with respiratory distress, high values indicate retention of CO2 and possibly acidosis as the body attempts to shift the reaction from guide to make more CO2. Low values could indicate hyperventilation or alkalosis. High values could indicate hypoventilation and CO2 retention or metabolic alkalosis.
The shape of the waveform can help us as well. Normally, it is more of a boxy shape represented as the dotted line. The expiratory upstroke, phase II, begins abruptly from the inspiratory baseline (phase I) and represents the start of the exhalation phase. Next, the flat part is the plateau phase, or phase III, which represents the ongoing exhalation and essentially consists entirely of alveolar gases. The EtCO2 value is read at the end of expiration, just prior to the expiratory downstroke. 
Finally, the expiratory downstroke, phase IV, represents the start of the next inhalation and a return to the baseline of atmospheric conditions. In cases of bronchospasm, as found in asthma and exacerbation of COPD, the waveform takes on the appearance of a shark’s dorsal fin. Following the solid line, the upslope is no longer abrupt, and there is an overall loss of the plateau phase. This provides a graphical representation of the difficulty a patient is having initiating his or her own exhalation. The distance from the start of the shark fin to the expiratory downstroke also tends to be longer and achieves a higher EtCO2 number in the patient with bronchospasm, illustrating the prolonged expiratory phase.

 

7. Conditions with a Complaint of Shortness of Breath

Many conditions will lead to a chief complaint from a patient of shortness of breath. This section will discuss those that are primarily caused by a problem with the respiratory system. Starting the discussion as done for the anatomy, the progression will be problems affecting the upper airway, followed by those affecting the lower airways and pulmonary circulation. Alternate causes of shortness of breath, such as diabetic ketoacidosis, myocardial infarction, and pulmonary contusion, among others, will be discussed later. With that in mind, when faced with a breathing complaint in the field, do not just focus on the respiratory issue. There may be a more insidious problem, such as diabetes or an aspirin overdose, at the root of the respiratory problem. As for all patients, always rule out other potential causes for the signs and symptoms found.

Upper Airway Pathologies

Foreign Body Airway Obstruction

Many everyday objects can cause a foreign body airway obstruction (FBAO), from the toys and small items that children explore with their mouths to accidentally inhaling a spicy shrimp while out to dinner at a fancy restaurant. The patient will be coughing if there is any air movement whatsoever. This is known as a partial FBAO because the patient can still exchange air in the lungs, albeit poorly. The patient may also have stridor during inhalation. The patient, in this case, will do a better job on his or her own of relieving the obstruction through forceful coughing without any intervention from a paramedic. As the responder, remain close to the patient in case the obstruction moves and causes a complete FBAO and be prepared to help the patient should he or she no longer be able to exchange enough air and pass out from the obstruction. Anticipation of patient need is key in this type of patient.


Figure: Magill Forceps

Swelling
Upper airway burns, anaphylaxis, croup, and Magill forceps are all possible causes for stridor and respiratory distress related to an upper airway problem. In most of these cases, getting a good history of the present illness from the patient or caregiver will help differentiate the likely reason and guide effective treatment. Aside from stridor, a complaint of difficulty breathing and, in most cases, an observable increase in the work of breathing, figure out which of these is the primary culprit and treat accordingly.

Croup
Croup is most commonly found in children between 6 months and 3 years old, although it can affect a person of any age. It is caused by swelling of the upper airways and is most commonly caused by a viral infection. It is often preceded by cold- or flu-like symptoms until the airway begins to swell. Croup’s hallmark sign is a barking seal-like cough that is unmistakable. The treatment for these children often is as simple as a change in environment; if the child is in a warm environment, having the child breathe cold air, such as outside during winter months or from a freezer, may help. If the child is already in a cool, dry environment, bringing the child into a steamy bathroom where a hot shower is running often can result in profound improvement. Although it is typically more scary because of the sounds the child is making, it is rarely life threatening, so manipulation of the airway with oral adjuncts or intubation is rarely needed. If the stridor persists after a change in environment, and the pulse oximetry is falling or remains low after blow-by O2 therapy, racemic epinephrine is the medication of choice. To administer racemic epinephrine, dilute 0.25–0.75 mL of a 2.25% solution in 2.0 mL normal saline and administer via a nebulizer for 5 minutes.

Epiglottitis is a severe and often life-threatening emergency characterized by swelling of the epiglottis caused by infection with the flu virus. In children, the epiglottis can swell to the point it completely closes off the airway. Adults, with larger airway diameters, rarely progress to that point; however, both populations present the same way. The typical presentation of a patient with epiglottitis includes sitting bolt upright to allow for the straightest pathway of air into the lungs. Because of a profoundly sore throat, these patients often will be drooling to avoid swallowing, and their voice will be hoarse. The best treatment practices include eliminating sources of anxiety for the patient and providing a calm environment. Be prepared to treat the patient aggressively should the airway close off but do not manipulate the airway in any way; this includes tongue depressors, oral airways, and attempts at intubation because the likelihood of causing more damage than actually remedying the situation is greater. Blow-by O2 should be provided as long as it does not create more agitation for the patient.

Anaphylaxis is swelling of the soft tissues of the mouth and throat, including the lips, tongue, hypopharynx, larynx, and vocal cords, as a result of a systemic release of histamine from exposure to any number of allergens. Interventions that involve manipulation of the airway should be performed only with extreme caution and should not include oral or nasal airways; any intubation attempt should be performed only by the most experienced provider available, if at all, and with a smaller tube than anticipated. 

Airway Burns
Airway burns are caused when superheated air or steam is inhaled and can occur even in the absence of fire. For example, a person can sustain airway burns when the oven is first opened and the air that first comes out is inhaled. The treating paramedic should be prepared for intubation and cricothyrotomy because the swelling will continue until the burning process is complete, which may not be for hours after the initial exposure. 
In summary, any severe upper airway problem should be treated with caution and preparations should be made to treat a difficult airway. Manipulation of the airway should not be performed prophylactically because it may precipitate worsening of the current condition and, in some cases, actually cause the airway to close.

Lung Tissue and Lower Airway Pathologies

Asthma

Asthma is a condition that affects millions of people in the United States and results in hundreds of thousands of hospital stays each year. Asthma is a collective term for a trio of lower airway issues that combine to cause dyspnea. First, there is bronchospasm, where the muscles in the bronchioles constrict, causing difficulty in exhaling air. The air becomes trapped in the alveoli, requiring increased pressure to exhale. This prolongs the exhalation time and causes normally passive exhalation to become an active process where muscle use is required. Second, increased mucus production further clogs already constricted airways. Finally, swelling in the lower air passages from infection or irritation can further worsen the breathing ability of the asthmatic. Any or all these issues may occur in varying degrees at all times during the life of an asthmatic and can worsen during an attack or exacerbation of the disease.
The patient with an exacerbation of asthma will be wheezing if there is sufficient air movement in the lower airways. The patient also may have diminished or absent breath sounds anywhere in the lungs if the airways are so tight that they are not allowing any movement. The patient may have had exposure to a trigger, such as smoke, animal dander, or mold that precipitated this attack. He or she often will be found in a tripod position trying to expand the lungs as much as possible and frequently will have taken multiple extra doses from an MDI or even a home nebulizer with little improvement. Inhaled beta-agonists treat only the bronchoconstriction piece of the asthma triad and do little to address edema or secretions.
The paramedic has many treatment options available for asthma and status asthmaticus.

The following therapies should be attempted in the order listed.

- Inhaled, nebulized beta-agonist such as albuterol. The usual dose is 2.5 mg in 3 mL saline nebulized with a flow of at least 8 LPM O2. The dose may be repeated as often as necessary during transport.
- Ipratropium bromide often is given concurrently with albuterol. The usual dose is 500 mcg (0.5 mg) inhaled.
- CPAP is recommended if the albuterol and ipratropium combination does not improve the patient’s status.-

Chronic Obstructive Pulmonary Disease
COPD is a name given to emphysema and chronic bronchitis. Patients with COPD often have a significant history of smoking and a barrel-shaped chest caused by the chronic collapse of alveoli and the trapping of CO2 in the bullae. People are able to live normally with COPD and tend to live in a constant state of shortness of breath. They will call the ambulance when the shortness of breath gets worse and when they can no longer control it with their rescue inhalers or daily medication regimen. A good question to ask these patients is, “What made it worse today to call the ambulance?” Patients with COPD may indicate that they have had a change in the amount or color of sputum, indicating that they may have a new onset of pneumonia.
The patient with COPD will present differently depending on what caused the exacerbation. If the patient’s overall condition is just worsening, he or she will likely present very similarly to the patient with asthma, with wheezes and tightness in the chest. If the patient is developing pneumonia, as these patients often do because of the increase in mucus and secretions in the lungs combined with the inability to move those secretions out, they may present with wheezes and ronchi as lung sounds; they also may have a fever and a change in the color of sputum. Remember, patients with pneumonia who do not have COPD will have a fever, a productive cough, and dehydration as well. Patients with COPD and pneumonia tend to be more difficult to manage and get pneumonia more often.
The treatment for these folks will be determined largely by identifying what is causing the exacerbation. Beta-agonists will help with bronchial constriction, and steroids will help with the bronchial edema as in asthma. Patients also may benefit from magnesium sulfate, as in asthma also. CPAP in these patients has been shown to work because it helps keep open the lower airways from the PEEP. The higher volume of air and the continuous pressure has the potential to cause barotrauma, especially in the delicate lungs of the patient with COPD. Administering O2 to a patient with COPD has always been a contentious point. Some believe that giving O2 will cause the patient to stop breathing because the patient has become so dependent on the hypoxic drive to breathe. If, however, the patient needs it, do not withhold it; if the patient stops breathing, not only is it likely that they would have anyway but also the complication can be managed.

Pulmonary Edema and Congestive Heart Failure
Generically, fluid building up within the lung tissues and alveoli, and eventually out into the bronchioles, is referred to as pulmonary edema. CHF is just 1 of many causes of the pulmonary edema. It is caused by dysfunction in either the right or left ventricle of the heart, resulting in the poor movement of blood through the lungs. As the pressure in the capillaries builds and the blood stagnates, the capillaries become leaky, causing plasma and sometimes red blood cells to seep into the lung tissues. If this continues long enough, eventually the level of the fluid rises from the bases to the apices of the lungs, causing a person to expel foamy sputum from the mouth that is blood streaked or tinged.
Other causes of pulmonary edema include the inhalation of toxic gases, high-altitude pulmonary edema (HAPE), and drowning. These are noncardiogenic and do not result from high pressure; they are a generalized increase in the permeability of the capillaries. Each of these noncardiogenic causes of pulmonary edema results in an irritation to the alveoli, which in turn causes the capillaries to swell and eventually leak, similar to the way an abrasion on the skin oozes plasma and blood.
Patients with pulmonary edema, regardless of the cause for the moment, will present with crackles in the dependent lung fields; in a person who can sit upright or stand, crackles would start in the bases and move superiorly until eventually filling the entire lung. Patients with noncardiogenic causes of pulmonary edema will have symptoms consistent with the specific cause. Patients with HAPE will have a history of recent mountain climbing with extended time at the higher altitude. Patients with toxic gas exposure may be among a group of patients with similar complaints or work with gases that could cause irritation, such as chlorine at a pool or ammonia at food processing plants. Pulmonary edema is a late finding in patients who are drowning, and the patient may have been treated and delivered to the emergency department long before the edema occurs. The treatment for these patients is largely dependent on the cause, but it centers on removing the patient from the environment if he or she is still in it and providing high-flow O2. CPAP is recommended to help increase intrapulmonary pressures and push the fluid back into the circulation. This also will help keep open alveoli that have collapsed and provide additional surface area for the exchange of gases.
Patients with CHF will have additional signs to look for in the physical examination, in addition to crackles in the lungs and information to gather (if possible) during the interrogation. The shortness of breath will have increased during the course of several days. The patient may no longer be able to sleep lying flat, using pillows to prop up or sleeping in a semi-seated position in a recliner. The patient may complain of associated chest pain. The patient often will be pale and very diaphoretic. Because of the failure of the pump to move blood around the body, JVD and swelling in the dependent areas of the body—feet, ankles, and lower extremities if the patient can sit or stand and the sacrum or hip area if the patient is bedridden—are common findings. The patient also typically has high blood pressure and tachycardia.
The treatment of a patient with pulmonary edema from CHF is 1 of the more intensive treatments that paramedics can complete. Delivering high-concentration O2 is the 1st priority. CPAP will be the best treatment for these patients as long as they can tolerate the mask. Next is the administration of large quantities of nitrates in the form of NTG. Before the CPAP mask is placed, administer 1 to 3 tablets of 0.4 mg NTG sublingually at once, depending on the patient’s blood pressure. Once the CPAP mask has been applied to the patient, removing it to administer additional doses of NTG can be difficult and is not recommended. Instead, if permitted in local protocols, apply a 1-inch strip of NTG paste to the patient’s chest or arm. Morphine sulfate is a great medication because it will not only treat any existing chest pain, thus making the patient more comfortable, but also act as a mild vasodilator, lessening the preload on the heart. Finally, furosemide is a potassium-wasting loop diuretic that is used to help the patient eliminate any excess fluid. Furosemide use is rapidly decreasing in paramedic treatments and is being eliminated in many systems. Higher doses of nitrates are far more helpful than furosemide in treating the patient with CHF.

Pneumothorax
Pneumothorax in the nontrauma patient is caused when a weakened area of the lung, called a bleb, ruptures. The bleb can be pathological (i.e., congenital) or caused by COPD. The rupture could be caused by any event that increases pressure inside the chest, including a sneeze or a cough or positive pressure ventilation. Air then leaks out of the lung from this ruptured bleb into the intrapleural space and collects there. After a certain amount of time, the lung will be crushed by the building pressure in that space, and difficulty in breathing will begin as the surface area for gas exchange is reduced.
These patients will have shortness of breath and decreased or absent lung sounds over 1 or more lung fields on the same side of the chest or back. As intrathoracic pressure builds, the mediastinum will shift toward the unaffected side. This shift will minimize the pumping ability of the heart, which is seen as JVD, and it will cause the trachea to deviate from the midline toward the unaffected side late in the process. These patients also may have a ventilation-perfusion mismatch; despite giving high-flow O2, their pulse oximetry readings do not increase above a certain number, which is expected. The affected side also becomes hyperresonant to percussion, that is, it will sound hollow.
Treatment beyond O2 includes a procedure called needle thoracostomy. During this procedure, an over-the-needle catheter is inserted into the chest through the 2nd intercostal space—the midclavicular line—just above the 3rd rib on the affected side. There will be a rush of air when the needle is removed as the pressure is released, which will allow the lung to slowly reinflate. If this is the cause of the difficulty breathing, the patient will improve rapidly after the needle insertion.

Pleural Effusion
Fluid collecting in the intrapleural space is a pleural effusion that often is caused by trauma, cancer, or infection. As with a pneumothorax, as pressure builds up, the lung begins to collapse, and respiratory distress begins. The position of the patient will affect the location and distribution of the fluid. Lung sounds may be difficult to hear over the effused area. Definitive treatment for this effusion is a thoracentesis, which can be done only at a hospital. The paramedic should provide supportive care, including O2 if needed, and transport the patient in the position of maximal comfort, which is usually sitting up.

Pulmonary Embolism
PE is most commonly caused when a piece of a clot that formed in the deep veins of the leg (DVT) travels through the right side of the heart and lodges in the lung somewhere. Large clots will block off a larger percentage of the lung, resulting in a large area of the lung that is ultimately well ventilated but completely lacking in circulation. DVT can form in people who are bedridden for long periods of time, people on birth control pills for any reason, or people who have a clotting disorder. Other sources of an embolism include fat embolism from a broken bone, air embolism from a laceration to a large vein or an incompletely flushed intravenous line where a large amount of air is injected, or amniotic fluid during pregnancy.
A patient with a PE often will complain of a sudden onset of chest pain with a sudden onset of shortness of breath. The patient will be tachypnic, trying to compensate for the area of lung that is no longer exchanging gases. There often is a marked ventilation perfusion mismatch because it will appear that the patient is moving air appropriately, and lung sounds over all lung fields will be clear; however, the pulse oximetry readings will be low, and the patient will have extensive cyanosis. A large enough embolus could result in almost immediate cardiac arrest, which is typically not survivable. Patients in cardiac arrest from such a large embolus will present with cape cyanosis, which is deep, irreversible cyanosis of the head, neck, chest, and back despite otherwise effective CPR and rescue breathing with 100% O2.

Clinical Correlate

Geriatric Corner

When it comes to pneumonia, geriatric patients are at an increased risk of not only getting pneumonia but being hospitalized with it. Aside from simply age, the elderly are at increased risk for pneumonia because people with underlying health problems also are at greater risk. People who have vascular disease, have COPD, or are receiving cancer therapy have a greater risk of any infectious disease, including pneumonia. In addition, bed confinement or any condition that limits the ability to take deep breaths further increases the risk. The elderly often have 1 or more of these associated risks, which cause the illness to last longer and be more severe than what a younger adult might get. Furthermore, the elderly do not usually have a fever, chills, and a productive cough; they frequently lack a fever and expected cough and are simply suddenly confused.