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Nasal cannula or high-flow oxygen for patients with COPD in acute respiratory distress?

Tasota, Frederick J. MSN, RN; Kress, Terri L. MSN, RN, CEN; Conlin, Tiffany L. MSN, RN, CMSRN; Scarmack, Natalie M. MSN, RN, CCRN

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doi: 10.1097/01.NURSE.0000743096.13461.b6
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CHRONIC obstructive pulmonary disease (COPD) is the third leading cause of death in the US. Currently, it affects more than 15 million Americans and 64 million people worldwide.1 In 2015, COPD contributed to an estimated 3.17 million deaths globally.2 Patients with COPD are at an increased risk for respiratory compromise during hospitalization, and the effective use of oxygen administration is crucial. This article addresses nursing misconceptions regarding the use of high-flow oxygen via non-rebreather mask instead of low-flow oxygen via nasal cannula in patients with COPD who are experiencing acute respiratory distress. This article also details the results of a simulation exercise and survey of the nursing staff about this issue at the authors' facility.

Background

One of the initial nursing actions with patients experiencing respiratory distress involves administering oxygen to relieve hypoxemia. Typically, patients are placed on high-flow oxygen with a non-rebreather mask, but nurses often question this type of oxygen administration for those with COPD.

In school and in practice, nurses have been taught that patients with COPD retain carbon dioxide (CO2) and that too much oxygen may inhibit their respiratory drive, leading to rising CO2 levels and apnea. However, uncorrected hypoxemia is more dangerous than the potential for hypercapnia from oxygen administration. In fact, as the authors established in the educational exercise discussed below, this oversimplification of complex physiologic processes may lead nurses to avoid the judicious use of oxygen delivery devices to provide higher levels of oxygen to these patients, resulting in suboptimal care.

The authors' facility, the University of Pittsburgh Medical Center Presbyterian Hospital, admitted 275 patients with a primary COPD diagnosis in 2019. This figure did not include a significant number of patients whose COPD was not the reason for their visit, as patients with COPD are more likely to have comorbid conditions such as cardiovascular disease, diabetes, kidney disease, and mental health issues.3 The 758-bed tertiary care hospital has a well-established medical emergency team (MET), which responds to seven or more crises a day on average. The MET includes designated rapid response nurses, ICU nurses, respiratory therapists, and critical care providers.

Given the number of emergencies handled by the MET, the authors' facility has prioritized educating clinical nurses on initial patient management during crises. During a required RN Orientation Skills Day, all nurses who are new to the facility participate in a 45-minute educational session on emergency interventions to prepare them to carry out important tasks before the arrival of the MET (see Staff expectations before the arrival of the MET). This education incorporates a simulated case study in which participants respond to a patient with COPD who is experiencing acute respiratory distress using a high-fidelity human simulator, a lifelike mannequin that mimics patient physiologies in simulated clinical environments.4

Participant surveys

During multiple sessions, the authors noted a pattern in which orientation participants consistently responded incorrectly to a question related to oxygen therapy for patients with COPD who were experiencing respiratory distress. Specifically, they believed these patients should receive only low-flow oxygen using a nasal cannula rather than high-flow oxygen via a non-rebreather mask. This anecdotal finding led to formal surveying in which participants responded to a five-question multiple-choice emergency response questionnaire, including one question related to supplemental oxygen administration during respiratory crises. Additional questions were added to the survey as distractors to avoid focusing on the choice of oxygen administration device.

The authors' inquiry centered on the response to the following question: “The patient with respiratory distress has a history of COPD. While waiting for the MET to arrive, is it appropriate to apply high-flow oxygen via a non-rebreather mask for this patient?”

Over 5 months, 105 nurses completed the survey and participated in the simulation. Besides survey responses, the participants' choice of oxygen administration device and flow during the simulation were documented. After the participants completed the simulation, a debriefing session focused on important takeaway points.

During the simulation scenario, one of the participants acted as the clinical nurse and received the patient report from an instructor acting as the charge nurse. The simulation also included a volunteer fellow nurse and a nursing assistant. Below is the case study used in the simulation:

PS, 72, is admitted to the medical-surgical unit with fatigue and malaise. Her history includes COPD, heart failure, diabetes, and atrial fibrillation. After a safe handoff, no acute issues were noted from her baseline during the bedside shift report. Two hours later, the nurse observes PS to be in acute respiratory distress and rapid atrial fibrillation. She is using accessory muscles to breathe and has audible inspiratory crackles. PS is anxious and states to the nurse, “please help me breathe easier.” Her vital signs are: heart rate (HR), 135; respiratory rate, 30; BP, 140/90 mm Hg; and SpO2, 85% on room air, which is significantly lower than her baseline of 90% to 92% on room air.

In most simulation cases, the clinical nurse (participant) called for help, the others (volunteers) responded to assist, and the MET was summoned. As PS's head was elevated and lung sounds auscultated, the crash cart was brought into the room, monitor/defibrillator pads were applied, and the portable monitor/defibrillator was used to monitor HR and rhythm. Due to the patient's history of COPD, however, the participants consistently hesitated regarding oxygen administration.

After approximately 3 minutes to allow participants to manage the situation, PS remained in acute respiratory distress with respiratory improvement based on method of oxygen administration. The charge nurse (instructor) arrived and delegated tasks not yet completed after receiving a situation, background, assessment, and recommendation (SBAR) report. If it was not already in place, the charge nurse would ask to replace the cannula and administer oxygen via non-rebreather mask—to which the clinical nurse would often reply, “but she has COPD”

Replacing myths with facts

The debate about providing too much supplemental oxygen to patients with COPD and the myth regarding suppression of the respiratory drive started decades ago and continues today. In reality, several complex mechanisms are responsible for differences in the response to supplemental oxygen among patients both with and without COPD. These include anatomical changes in the lungs, the degree of variation in the stimulus to breathe, decreased alveolar ventilation due to increased anatomic and alveolar dead space, ventilation/perfusion mismatch, and the Haldane effect. (See Key terms and definitions.) As discussed below, the interplay of these factors can justify the judicious use of high-flow supplemental oxygen for patients with COPD experiencing respiratory distress.

  • Anatomical changes in the lungs. Patients with COPD develop multiple anatomic changes that can lead to chronic inflammatory processes, including enlargement of the mucous glands in those with chronic bronchitis and tissue deterioration such as airway narrowing and the collapse and destruction of the alveolar walls in those with emphysema. In addition, smooth muscle thickening in the smaller pulmonary arteries is associated with vasoconstriction from long-term hypoxemia.5

Although anatomic changes may lead to hypoxemia in patients with mild COPD, not all patients with COPD are CO2 retainers with chronically high CO2 levels; in fact, these patients are in the minority.5 As the disease progresses and lung damage worsens, however, patients are more likely to exhibit hypoxemia and develop hypercapnia, which may lead to respiratory acidosis. To maintain normal pH levels in the bloodstream, functioning kidneys will compensate for increased CO2 levels by retaining serum bicarbonate. When stable patients with COPD experience an acute exacerbation, however, their CO2 levels rise quickly. Unfortunately, there is inadequate time for the kidneys to respond, which can lead to acute or uncompensated respiratory acidosis.6,7

  • Variation in breathing stimulus. Respiratory homeostasis is maintained by the central and peripheral chemoreceptors in the medulla and the carotid bodies. Typically, these receptors increase the respiratory rate to remove excess CO2 in response to low pH levels in the bloodstream. However, patients with chronically high CO2 levels no longer experience the same response and either do not or cannot increase their respiratory rate.5

Peripheral receptors also respond to oxygen, CO2, and pH levels in the bloodstream. This response to lower oxygen levels is called the hypoxic drive, which some clinicians incorrectly believe to be the only mechanism to stimulate breathing for patients with COPD.8 Although CO2 levels can rise with the administration of supplemental oxygen in these patients, this rise is not proportional to the comparably minor changes in their drive to breathe.9

Patients with chronically high levels of CO2 in their bloodstream may experience a decreased drive to breathe, and many believe they rely solely on the hypoxic drive to do so due to stimulation of the peripheral receptors.5 In reality, hypoxic stimulus accounts for only 10% to 15% of the total drive to breathe.

Pathophysiologic factors

The following factors are related to the pathophysiology of COPD and responsible for the need to cautiously use oxygen:8

  • Decreased alveolar ventilation. In patients with normal lung function, the alveoli are typically about 0.2 mm in diameter and surrounded by an extensive network of pulmonary capillaries to provide a large surface area for gas exchange.10 However, patients with emphysema can have areas of distended alveoli from 20 to 100 times the normal size, with diameters greater than 1 cm.11 These patients may also lose the walls that separate small discrete alveoli, creating a subsequent loss of the surrounding capillaries and surface area for gas exchange. These changes lead to decreased alveolar ventilation and further inhibit CO2 removal, enhance hypercapnia, and lower pH levels.12

Additionally, alveolar ventilation may decrease with rapid shallow breathing, or tachypnea, which increases the amount of anatomic dead space in the upper airways, where there is ventilation but no perfusion to remove CO2. Any patient experiencing respiratory distress may become tachypneic. Unfortunately, this increased respiratory rate may be accompanied by a decreased tidal volume with fatigue. Rapid shallow breathing patterns result in increased anatomical dead space, further decreasing alveolar ventilation and increasing CO2 retention.13

  • Ventilation/perfusion mismatch. This is related to increased perfusion in the pulmonary capillaries relative to ventilation of the alveoli. Patients with COPD who have decreased oxygen levels typically experience hypoxic vasoconstriction, a response that occurs naturally when less oxygen is available from the pulmonary capillaries due to the distended and underventilated alveoli associated with emphysema. As such, the pulmonary capillaries constrict to allow more blood to flow to better-ventilated alveoli.12

When high levels of supplemental oxygen are provided, however, oxygen levels in the patient's bloodstream increase and localized vasoconstriction no longer occurs. This leads to increased capillary blood flow to poorly ventilated alveoli, an inability to remove CO2, reduced blood flow to better ventilated alveoli, increased alveolar dead space, and CO2 retention.8,12 (See Loss of hypoxemic vasoconstriction.)

  • The Haldane effect. This physiologic process involves the oxygen and CO2 molecules that bind to and release from hemoglobin. Oxygen binds with hemoglobin in the lungs and is released in the tissue, but the ability of hemoglobin to bind with CO2 increases as it moves into the tissues and the hemoglobin becomes deoxygenated. As these carbaminohemoglobin molecules return to the lungs, CO2 is released and removed via exhalation.8,12

When more oxygen is provided and more hemoglobin is saturated, it leaves less deoxygenated hemoglobin free to bind with CO2, increasing CO2 retention and subsequently elevating CO2 levels in the bloodstream. Unless alveolar ventilation is increased to remove it, the pH will fall. As such, patients with COPD who are unable to increase alveolar ventilation and remove the CO2 may experience increased CO2 retention and develop respiratory acidosis. However, this phenomenon is more likely to occur only in patients with COPD who chronically retain CO2 when receiving supplemental oxygen for significant hypoxemia.8,12

Supplemental oxygen

Nurses should be cautious with oxygen administration based on the varying pathophysiologic mechanisms in patients with COPD, but the assumption that these patients lose “the drive to breathe” from oxygen administration is false. Each patient is different, as is each situation.

The dangers of long-term use of high concentrations of supplemental oxygen in patients with COPD are well documented.14 Today's literature reinforces these dangers in patients experiencing COPD exacerbations. Careful monitoring and titration of oxygen to SaO2 levels between 88% and 92% and arterial oxygen tension levels between 55 mm Hg and 65 mm Hg is crucial, as is the assessment of serial arterial blood gases to avoid dangerous hypercapnia and potentially life-threatening respiratory acidosis.15

Returning to the dilemma of a decompensating patient with COPD in a hospital setting, which was encountered during the simulation at the authors' facility: If a patient with COPD is experiencing respiratory distress with severe tachypnea and an SaO2 level below 88%, the MET should be called to facilitate resuscitation. The nursing staff should place the patient on high-flow oxygen via a non-rebreather mask before the arrival of the MET to combat hypoxemia and attempt to raise the patient's SpO2 levels. When using high-flow oxygen via a non-rebreather mask, nurses must also remember to keep the bag attached to the mask inflated to prevent rebreathing CO2.

Despite the potential for CO2 retention, patients will not stop breathing due to hyperoxygenation. The MET will be able to monitor the partial pressure of CO2 and pH levels via arterial blood gases and assess for hypercapnia and respiratory acidosis. After the MET arrives, high-flow oxygen via a non-rebreather mask may be replaced with a low-flow nasal cannula if the hypoxemia has been corrected. Patients who do not improve or further deteriorate can be intubated and sent to the critical care unit for further treatment.

Some healthcare organizations may use a protocolized approach, initially providing low-flow oxygen via a nasal cannula followed by an air-entrainment or Venturi mask to deliver higher flows and provide between 24% and 50% of supplemental oxygen in increments if the hypoxemia has not resolved. If these measures are unsuccessful, advancing to a non-rebreather mask is then recommended. If patients become exhausted or cannot maintain adequate ventilation for CO2 removal, the ICU staff may initiate either noninvasive bilevel positive pressure ventilation or endotracheal intubation and mechanical ventilation.

Survey results

The authors surveyed 105 nurses, of which 49 (47%) were newly graduated nurses. Of the total nurse participants, 66 nurses (63%) believed high-flow oxygen was inappropriate for patients with COPD who were experiencing respiratory distress and chose low-flow oxygen for patients in this simulated clinical situation. (See COPD response survey question.) Specifically, although the simulation participants responded quickly and administered oxygen, 78 nurses (75%) chose to use low-flow oxygen via a nasal cannula. In response to this simulation option, the patient's SpO2 levels would not increase.

If the participants failed to address their patient's hypoxemia effectively, the charge nurse (instructor) requested high-flow oxygen via non-rebreather mask and emphasized this technique for all patients in respiratory distress during the debriefing. The instructor also discussed the difference between routine oxygen administration for patients with COPD and for those experiencing an acute event.

The results of the authors' survey demonstrated that both experienced and inexperienced nurses chose low-flow over high-flow oxygen administration for patients with COPD who were experiencing acute respiratory distress with hypoxemia due to concerns about administering too much oxygen. Nurses need to be aware of the various physiologic processes that initiate CO2 retention when patients with COPD receive supplemental oxygen. They should also follow best practices and be unafraid of the potential complications of oxygen administration if the patient is likely to experience harm such as hypoxic damage to the brain and heart without it. If hypercapnia develops during a crisis, it can be adequately managed by monitoring for acidosis and treatment with invasive or non-invasive ventilation.

By sharing best practices, these misconceptions will become less prevalent and nurses can use individualized, situation-based, and appropriate interventions in the care of patients with COPD experiencing acute respiratory distress.

Staff expectations before the arrival of the MET

  • Assess responsiveness.
  • Call for unit assistance and activate the MET.
  • Pull bed away from wall, allowing for 360° of patient access.
  • Place patient in the appropriate position.
  • Support the airway.
  • Retrieve the emergency cart.
  • Insert and maintain functional I.V. access.
  • Monitor oxygenation status via pulse oximetry.
  • Apply supplemental oxygen based on patient SpO2 levels.
  • Apply monitor/defibrillator pads and monitor HR and rhythm.
  • Obtain vital signs.
  • Ensure suction readiness.
  • Check glucose and verbalize the results.
  • Begin documentation.
  • Remove obstacles, such as furniture, and facilitate crowd control.
  • Direct the MET to the area and use an SBAR report to provide information.
  • Continue to support the patient and family.

Key terms and definitions8,12

These terms were defined and explained based on the authors' experience and knowledge.

  • Alveolar dead space: Areas in the alveoli where there is ventilation but no contact with pulmonary capillaries, which can lead to lack of oxygen and CO2 movement across the alveolar capillary membrane.
  • Anatomic dead space: An area where no gas exchange occurs, including the space from the nose and mouth to the terminal bronchioles and alveoli.
  • Ventilation/perfusion mismatch: Deviations from the normal ventilation-to-perfusion ratio of 8 to 10 (air to blood) in the lungs, leading to problems in gas exchange in the affected areas of the lungs.
  • Hypoxic vasoconstriction: A normal pulmonary capillary response in areas of the lung where there is increased alveolar dead space and decreased oxygen availability. This action diverts blood flow to better ventilated areas to improve oxygenation and occurs in various respiratory disorders such as atelectasis, pneumonia, pulmonary edema, and COPD.
  • Haldane effect: A physiologic process that occurs as oxygen is released from hemoglobin in the blood and moves into tissues, where deoxygenated hemoglobin binds with CO2, moves into the bloodstream, and is eliminated via the lungs.

Loss of hypoxemic vasoconstriction8,12

This figure demonstrates the movement of blood through two pulmonary capillaries. One capillary passes a normal alveolus, while the other passes an overdistended alveolus in a patient with COPD. Deoxygenated blood (in blue) moves past both alveoli, with each receiving 100% oxygen. Under normal circumstances, the capillary near a poorly oxygenated, overdistended alveolus would constrict to allow greater blood flow to normal alveoli, where more oxygen can be diffused across the alveolar-capillary membrane and more CO2 can be removed. However, many patients with COPD have lost the ability to appropriately vasoconstrict. When these patients are administered high levels of supplemental oxygen, the capillary remains dilated, allowing more blood to flow past the overdistended, poorly ventilated alveolus. The capillary in contact with the overdistended alveolus picks up less oxygen and retains more CO2 due to the loss of alveolar/capillary interface.

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COPD response survey question

In the authors' survey, 105 total nurse participants were asked the following before the simulation activity: A patient with respiratory distress has a history of COPD. While waiting for the rapid response team to arrive, is it appropriate to apply high-flow oxygen for this patient?

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11. Martínez-Jiménez S, Rosado-de-Christenson ML, Carter B. Specialty Imaging: HRCT of the Lung. 2nd ed. Amsterdam, Netherlands: Elsevier; 2017.
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Keywords:

chronic bronchitis; chronic obstructive pulmonary disease; COPD; emphysema; high-flow oxygen; low-flow oxygen; nasal cannula; non-rebreather mask

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