Management of acute respiratory distress isn’t an exact science. Good patient outcomes rely on your ability to assess ventilation, oxygenation, work of breathing (WOB), lung function, airway resistance and air flow. The number of treatment choices is increasing, and they’re becoming more complex. Does your patient need medication, suctioning, airway management, ventilation, intubation, non-invasive ventilation or just close observation?
Some practices of the past served only to disguise deterioration. With everything available to today’s EMS provider, you need some pearls of wisdom for effectively assessing and successfully treating patients having difficulty breathing.
Shortness of breath, or dyspnea, is a subjective complaint.(1) As with any subjective complaint, an EMS provider risks undervaluing the significance of the problem if they allow personal bias to interfere with a good search for objective signs of respiratory distress. Studies have repeatedly demonstrated that EMS providers under-treat pain, largely because of under-assessment.(2) Patients rarely die of pain, but they often die from acute respiratory distress. Thus, a rapid and thorough assessment is crucial.
Complaints of dyspnea account for a significant number of EMS responses. Attempts to stratify the significance of respiratory distress by emergency medical dispatch (EMD) protocols have been largely unsuccessful, leaving most EMD protocols to triage patients with breathing problems into a high-priority response. Besides ineffective breathing or respiratory arrest, which are suggested though information volunteered by 9-1-1 callers, some objective assessment clues can often be obtained by 9-1-1 operators. These include difficulty speaking between breaths and the presence of cyanosis and diaphoresis, each of which are objective and significant assessment findings.(3) Although any dispatch for difficulty breathing could be serious, the presence of these objective findings certainly raises the index of suspicion.
Imminent Respiratory Arrest
Immediate assessment priorities for any difficulty breathing call include quickly determining if the patient has a febrile illness, most efficiently done by asking the patient if they feel feverish. Fever in any patient with respiratory distress compels you to provide the patient with a simple surgical mask. After assuring that the scene is safe and conducting an immediate assessment for adequate circulation, airway and breathing (CAB), you can begin to focus on dyspnea. The mask allows you to work safely in the three-foot “respiratory hot zone” around the patient. Crews can also don a mask for additional protection.
Three signs that suggest imminent respiratory arrest in a patient with acute respiratory distress are:
1. Decreased level of consciousness;
2. Inability to maintain respiratory effort; and
Presence of one or more of these warrants immediate intervention, because untreated respiratory arrest will lead to cardiac arrest in very short order.
Immediate life-threatening conditions associated with complaints of dyspnea include foreign body airway obstruction, acute coronary syndrome, acute heart failure, major arrhythmias, tamponade, massive pulmonary embolism, pneumonia, exacerbation of chronic obstructive pulmonary disorder, asthma, anaphylaxis, poisoning and trauma—all of which would be treated during the initial assessment.
Assessing Work of Breathing (WOB)
For dyspneic patients without immediate life threats, your next assessment focus should be to determine the patient’s WOB. Assessing WOB is a challenging process that improves with practice and experience. EMS requires multitasking; depending on the personnel and resources available, simultaneously having other crew members measure pulse oximetry and capnography (if available) while others obtain a history and demographics from family or friends will accelerate your assessment process and allow you to more quickly formulate a treatment plan.
Five key signs you want to look for that suggest severe respiratory distress include:(4)
1. Retractions and the use of accessory muscles to breathe;
2. Inability to speak full sentences (or difficulty speaking be-tween breaths);
3. Inability to lie flat;
4. Extreme diaphoresis; and
5. Restlessness, agitation or declining level of consciousness.
Each of these signs is closely tied to WOB and suggests the patient is working too hard to breathe. When WOB is significantly elevated for prolonged periods of time, patients tire and become unable to sustain an adequate respiratory effort.
The only way to discover retractions is to visualize the chest. The presence or absence of retractions can tell more about the degree of respiratory distress than lung sounds. Surprisingly, in the rush to examine patients, there’s a tendency not to take a quick peek under their clothing at the anterior and posterior chest walls. Learn to recognize retractions and accessory muscle use. If you’re unfamiliar with what these look like in an actual patient, a quick Internet video search will teach you to rapidly recognize both.
The ability to speak is also directly related the degree of distress. This often necessitates obtaining history from family or friends because patients with severe respiratory distress will often only be able to provide one- or two-word answers to questions.
Orthopnea, or the inability to lie flat, is not a test, but rather, a question to ask the patient. Sweating, and particularly profuse diaphoresis in an environment where others are not sweating, suggests significant distress. Although we’re quick to correlate declining level of consciousness with imminent respiratory arrest, we can be fooled by patients who are extremely restless and perhaps progress to combativeness. These behaviors, in the presence of acute dyspnea, are highly suggestive of severe respiratory distress.
Valuable Vital Signs
Two BLS vital sign measurements that are helpful in assessing and monitoring the degree of respiratory distress are respiratory rate and oxygen saturation. Tachypnea in adults is generally defined as a respiratory rate greater than 25 breaths per minute.5 The higher the respiratory rate, the greater the WOB and the more likely the patient will eventually tire. Trending respiratory rates over time can let you know the effects of treatments by suggesting improvement or deterioration.
For those responsible for patient care: Be wary of respiratory rates measured by others. Studies of healthcare providers at all levels suggest that reported respiratory rates may not be accurate.(6,7) Just as physicians are instructed when making treatment decisions to count respirations themselves, use a capnography device or have a trusted partner make the assessment for you. Many healthcare providers are quick to attribute rapid respiratory rates to anxiety (i.e., acute onset anxiety or hyperventilation syndrome). This is a slippery slope and can quickly land a clinician in trouble.
First, anxiety is common in patients with significant medical problems, just as it is in trauma patients. COPD patients, for example, experience anxiety attacks three times more often than the general population.(8) The safest practice is to assume that tachypnea is related to the underlying disease process rather than anxiety.
Second, even healthy young patients may have a medical cause for hyperventilation. Skipping a thorough assessment could miss important clues to a medical or traumatic condition.
Likewise, oxygen saturation is a vital sign with great value in not only assessing but also following the progress of a patient with acute respiratory distress. Since pulse oximetry is now included in the EMS educational standards at the EMT level, there’s no reason why any EMS response unit shouldn’t carry and use a pulse oximeter. From the introduction of pulse oximetry into EMS some 30 years ago, it has saved many lives and provided early detection of hypoxemia in countless patients.(9)
Prior to the availability of pulse oximetry, EMS providers (like their hospital colleagues) often relied on cyanosis as a clinical indicator for hypoxemia. Unfortunately, obvious cyanosis isn’t typically seen in a healthy person until their oxygen saturation drops below 67%, and even this value is highly variable in patients with low hemoglobin concentrations, poor circulation or darker skin pigmentations.(10) Today, cyanosis is considered not only a highly unreliable sign of hypoxemia, but a very late one as well.
Like overreliance on respiratory rate, pulse oximetry has its pitfalls. There are two significant limitations of pulse oximetry. The first is the tendency to confuse oxygenation with ventilation. The second is an inability (with conventional pulse oximeters) to account for abnormal hemoglobins, such as carboxyhemoglobin as seen in carbon monoxide poisoning, methemoglobin and sulfhemoglobin—all of which may be mistaken for oxyhemoglobin or otherwise interfere with accurate pulse oximetry readings.(11) Newer generation pulse oximeters using multiple wavelengths of light can accurately identify carboxyhemoglobin and methemoglobin in the blood, eliminating erroneous assessments in carbon monoxide- or methemoglobin-poisoned patients.(12)
Pulse oximetry has been invaluable to the anesthesia profession as a patient assessment and monitoring tool, transitioning anesthesia from a medical specialty with the largest number of lawsuits for adverse respiratory events to one of the least likely to be sued.(13) There can be no argument against the assertion that hypoxia is bad for patients. Failure to detect hypoxia when it occurs will cause providers to invariably miss the window of opportunity to intervene appropriately, often with catastrophic consequences for patients. That said, EMS is becoming more informed that the drug providers use most often, oxygen, isn’t as safe as previously believed. (See “The Perils of Oxygen,” below, for more.)
Pulse oximetry is an incredibly valuable monitoring tool for patients with acute respiratory distress. It allows a provider to administer oxygen only when needed, carefully titrating to avoid patient harm from too much oxygen.
Lastly, when pulse oximetry is used to monitor a patient in respiratory distress and saturations are normal (94–98%), desaturation is a warning of decompensation. The past practice of routinely giving oxygen to every patient in respiratory distress did little to alleviate their difficulty breathing and, in patients who were not hypoxic, effectively masked deterioration that would have been seen in a falling oxygen saturation.
Capnography is also a valuable assessment and monitoring tool in acute respiratory distress. Although it’s included in EMT training, capnography has traditionally been an ALS tool. Capnography provides excellent confirmation and continuous monitoring of respiratory rate. Waveform analysis can suggest bronchospasm and airway obstruction, and it can also quantify the effectiveness of treatments.
The measured end-tidal carbon dioxide (EtCO2) value provides helpful insight into the need for ventilation assistance and is an excellent feedback tool for titrating continuous positive airway pressure (CPAP) or positive-pressure ventilation. One caution regarding capnography is the influence of cardiac output.(14) Decreasing cardiac output is reflected as a falling end tidal CO2. Failure to account for changes in cardiac output can lead to misinterpretation of the EtCO2 values.
The following three assessment questions direct patient treatment:
1. Is the airway patent?
2. How adequate is breathing?
3. Is oxygenation sufficient?
Airway patency: This is reflected by unobstructed flow. Abnormal breath sounds often point to the obstruction—listening over the neck focuses on the upper airway. Snoring indicates obstruction of the airway, usually by the tongue. Inspiratory stridor suggests obstruction above the vocal cords such as a foreign body or epiglottitis; expiratory stridor often comes from below the cords as in croup or a deeper foreign body.
Coarse lung sounds, formerly called rhonchi, generally result from secretions in the airway. Wheezing suggests flow restriction below the level of the trachea, whereas crackles (or rales) indicate presence of fluid or atelectasis at the alveolar level. Simple interventions can lead to marked improvement. For example, a nasopharyngeal airway (NPA) often eliminates snoring; nasotracheal suctioning of accumulated secretions using a soft flexible catheter clears coarse-sounding lungs; administration of an inhaled bronchodilator significantly reduces wheezing.(15)
Adequacy of breathing: This is perhaps the most difficult assessment in patients with acute respiratory distress, and unfortunately, failure to recognize inadequate breathing will likely lead to cardiopulmonary arrest. The three signs of impending respiratory arrest mentioned earlier are late signs—as is bradycardia. Decreasing heart rate in any patient should be a red flag for you to assess their breathing.
WOB assessment ties directly in with the adequacy of breathing. If breathing is inadequate, ventilation must be provided without delay. Ventilation can be non-invasive or invasive. Non-invasive, also called called non-invasive positive-pressure ventilation (NIPPV), refers to ventilatory support provided through the patient’s upper airway, usually using a mask,such as a bag-valve mask (BVM) or CPAP unit. Invasive ventilation involves bypassing the upper airway with an endotracheal tube, supraglottic airway (e.g., laryngeal mask airway or laryngeal tube) or tracheostomy. When a patient has problems with both their airway and breathing, invasive ventilation is reasonable and appropriate. In cases where the airway is patent yet breathing
is becoming inadequate, a trial of non-invasive ventilation is warranted and may offer a multitude of benefits for both patient
CPAP is the most often-used prehospital non-invasive ventilation device aside from a BVM. CPAP is appropriate for nearly all patients who have a patent airway with inadequate breathing, with the exception of those who are apneic or have low respiratory rates (typically less than eight breaths per minute for adults). It’s also an excellent tool for patients who appear to be tiring from excessive WOB.
Some patients are known to respond favorably to non-invasive ventilation. This includes those who are younger, are able to cooperate, have minimal air leak from the mask, have EtCO2 between 45 and 92 mmHg, and show early improvement in respiratory rate, heart rate and oxygenation with CPAP.(16)
Use of CPAP requires familiarity with the equipment, obtaining a good mask seal, coaching and reassuring the patient, and titrating the pressure for effectiveness.
All patients on CPAP should be sitting at least 30 degrees upright. CPAP is associated with significantly less complications compared to invasive ventilation. This includes fewer intensive care unit admissions, shorter hospital lengths of stay, fewer cases of pneumonia, better oxygenation and lower mortality rates.(17)
There’s no standardized approach to initiating non-invasive ventilation. Experts recommend starting CPAP at 8–12 cm of water pressure and gradually increasing the pressure up to 20 cm as required based on respiratory rate, patient comfort and oxygen saturation.(16) Capnography is also helpful for monitoring the effects of CPAP and should demonstrate a decrease in EtCO2 when optimal pressures are achieved. EtCO2 can also be used to wean CPAP. The most common complication associated with CPAP is facial trauma from the tightly fitted mask.(16)
BVM ventilation is another means of non-invasive ventilation. The ability to provide bag-valve mask ventilation to a conscious patient requires practice and skill. The best way to learn how to “track” and assist the ventilations of a spontaneously breathing patient is to practice on another EMS provider. A benefit of BVM ventilation is the ability to quickly discover if a patient will tolerate non-invasive ventilation and if so, whether there’s improvement in their respiratory distress, heart rate, saturation and WOB.
Deciding to use invasive ventilation is risky but completely warranted in some patients. Candidates for invasive ventilation include patients whose airway patency can’t be restored using conventional methods. This is especially true in those with trauma and/or unmanageable secretions and patients who are apneic. Additionally, patients who fail a trial of non-invasive ventilation are also candidates for invasive ventilation.
Regardless of which type of advanced airway device is used, it’s important to have continuous waveform capnography attached to any invasive airway inserted in a patient.(18) In the uncontrolled and often chaotic EMS environment, the only way to assure that an invasive airway is patent and the patient is being properly ventilated is with continuous waveform capnography.
Sufficient oxygen: Hypoxia, the lack of sufficient oxygen in the body, may result from an airway problem or poor ventilation, or a patient may have an intact airway with good breathing but poor oxygenation. In situations requiring airway management and/or ventilation, oxygen saturations often increase when the airway is cleared and ventilation improves. In some cases, hypoxia may be an isolated problem. Given what we now know about the dangers of hyperoxia, the approach to correcting hypoxia mandates careful titration of oxygen, ideally to maintain saturations at 94–98%.
With only a nasal cannula and a non-rebreather mask, an EMS provider may find themselves lacking in ability to deliver moderate levels of oxygen. Hence, the newest EMS educational standards have reintroduced a variety of oxygen delivery devices, including the simple face mask, partial rebreather masks, Venturi masks, tracheostomy masks and humidifiers. These tools are necessary to deliver the right percentage of oxygen to maintain the saturation in the 94–98% range.
Although high-flow nasal cannula devices aren’t yet ready for field use, hospitals have employed them since the mid-1990s to deliver heated and humidified oxygen at flows of up to 60 Liters per minute to patients with significant hypoxia.(19)
At these high flow rates, high-flow nasal cannula devices deliver low level pressure to the airways, slightly resembling the pressures delivered with CPAP. In fact, high-flow nasal cannula devices have all but replaced the nasal CPAP device previously used on premature babies and neonates with respiratory distress syndrome. Despite the high flows, heating and humidification of the oxygen make high-flow nasal cannula therapy tolerable, if not comfortable, for patients.
Acute respiratory distress is a common and often serious emergency. Good patient outcomes require rapid and skilled assessment of the airway, breathing and oxygenation. The ability to assess work of breathing and knowing when and how to intervene before a patient with acute respiratory distress tires will enhance your ability to care for this challenging complaint.
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The Perils of Oxygen
Oxygen has been a mainstay of medicine since the late 1700s, when it was first used to treat a variety of diseases.
It has seemed theoretically logical that oxygen administered to a patient with acute dyspnea would alleviate their breathlessness. Yet the truth, in study after study, is that oxygen does not alleviate breathlessness.(1,2)
Today, we understand that oxygen administered to patients who aren’t hypoxic can be quite harmful. As reflected in the 2010 American Heart Association Guidelines for CPR and Emergency Cardiac Care, we know oxygen constricts coronary vessels, lowers myocardial oxygen delivery and likely increases infarct size in the setting of an acute myocardial infarction.(3) In addition to increasing mortality in trauma patients, stroke victims and neonates, prehospital high-flow oxygen increases mortality in patients with acute respiratory distress. A large Australian EMS study comparing high-flow oxygen to nasal oxygen titrated to maintain a saturation of 88–92% reduced the risk of death by 78% in chronic obstructive pulmonary disorder patients and 58% in all other patients.(4) Obviously, blind administration of oxygen by protocol to every patient has gone by the wayside.
1. Moore RP, Berlowitz DJ, Denehy L, et al. A randomised trial of domiciliary, ambulatory oxygen in patients with COPD and dyspnoea but without resting hypoxaemia. Thorax. 2011;66(1):32–37.
2. Cabello JB, Burls A, Emparanza JI, et al. Oxygen therapy for acute myocardial infarction. Cochrane Database Syst Rev. 2010;16(6): CD007160.
3. Kones R. Oxygen therapy for acute myocardial infarction—then and now. A century of uncertainty. Am J Med. 2011;124(11):1000–1005.
4. Austin MA, Wills KE, Bilzzard L, et al. Effect of high flow oxygen on mortality in chronic obstructive pulmonary disease patients in prehospital setting: Randomised controlled trial. BMJ. 2010;34:c5462.
Editor’s note: A version of this article originally appeared in JEMS in July 2013.