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Review Articles: Narrative Review Article

Evaluation and Management of the Physiologically Difficult Airway: Consensus Recommendations From Society for Airway Management

Kornas, Rebecca L. MD*; Owyang, Clark G. MD; Sakles, John C. MD; Foley, Lorraine J. MD, MBA§; Mosier, Jarrod M. MD‡,‖; on behalf of the Society for Airway Management’s Special Projects Committee

Author Information
doi: 10.1213/ANE.0000000000005233


Many societies have published guidelines on airway crisis management or resource allocation; however, there are few recommendations on the physiologic considerations for airway management.1–4 The Society for Airway Management (SAM) was founded in 1995 as an interdisciplinary forum for physicians and nonphysicians from 28 different countries who specialize in airway management. A goal of SAM is to contribute to the scientific advancement of airway management through representation from multiple specialties; these recommendations aim to fill this void by creating physiologically directed recommendations sourced from a multidisciplinary group of providers.

Annually, there are over 141 million emergency department (ED) visits in the United States with nearly 2 million requiring intensive care unit (ICU) admission.5 Many of these patients require tracheal intubation, which is the third most commonly performed procedure in US hospitals,6 and carries high complication rates ranging from transient oxygen desaturation and hypotension to cardiovascular collapse and death.7,8

Physiologic derangements predominantly drive these risks with intubation in this population and often precipitate complications despite first attempt success. These pathophysiologic alterations limit the ability to preoxygenate, to maintain oxygenation during intubation, or to tolerate the transition to positive pressure ventilation. Collectively, these are commonly referred to as the “physiologically difficult airway.”9,10 Iatrogenic alterations to patient physiology through induction agents and resuscitation strategies contribute additional risk. The Special Projects Committee of the SAM developed the following list of recommendations to improve the safety of physiologically difficult airway management.


Over a 3-year time period (September 2016 to September 2019), 12 members of the Society for Airway Management’s Special Projects Committee representing Anesthesia, Critical Care Medicine, and Emergency Medicine developed recommendations for management of the physiologically difficult airway. Members of the Special Projects Committee performed study selection via a convenience sample after extensive literature review, and a representative working group searched relevant literature from various subspecialty backgrounds.

We used a modified Delphi method to develop a list of recommendations provided by each of the working group members. We then conducted an anonymous electronic survey via Qualtrics, where each of the members assigned their level of agreement with each recommendation on a visual analog scale ranging from 0% (complete disagreement) to 100% (complete agreement). The 12-member working group’s recommendations and level of agreement are provided below and in Supplemental Digital Content, Tables, Results are reported as mean and standard deviation. No formal risk of bias evaluation was performed.




In hypoxemic respiratory failure, there is a failure to maintain adequate arterial oxygenation, most commonly due to shunt and ventilation/perfusion (V/Q) mismatch. Critically ill patients are at high risk for rapid desaturation because of reduced functional residual capacity (FRC), V/Q mismatch, and shunt—all of which can be acutely worsened on induction.9 Subsequently, there is an increased risk for arrhythmia, hemodynamic instability, anoxic brain injury, and even cardiopulmonary arrest.11,12 While there was complete agreement among the Special Projects Committee that patients with hypoxemic respiratory failure are at high risk of desaturation during intubation (100% agreement [standard deviation {SD} 0%]), there was not complete agreement that desaturation is the biggest risk factor for cardiopulmonary arrest (87% agreement [SD 29%]) (Supplemental Digital Content, Table 1, All members agreed that reduced FRC, atelectasis, alveolar filling, shunt physiology, and increased dead space all contribute to difficulty with adequate preoxygenation (100% agreement [SD 0%]; Supplemental Digital Content, Table 1,

Optimizing preoxygenation to extend the time to desaturation improves the likelihood of first-pass success.13 Because desaturation occurs in 19%–70% of intubations and is the most common reason to abort first attempt at intubation, prioritization of preoxygenation, and apneic oxygenation are prudent in all patients.7,14–17 Historically, preoxygenation was achieved using a nonrebreather mask (NRM) without a leak delivering 100% oxygen over 3–5 minutes of tidal volume breathing or 8 vital capacity breaths (Table).18 The end points of maximal preoxygenation and denitrogenation are end-tidal oxygen (EtO2) concentration of approximately 90% and end-tidal nitrogen (EtN2) concentration of 5%.19,20 When a NRM lacking a tight seal is used, there is a leak around the edges of the mask and patients mix the supplied oxygen with entrained ambient air, decreasing the effective fraction of inspired oxygen. This is particularly relevant to critically ill patients with high minute ventilation who are likely to entrain large volumes of room air.

Table 1. - Top 10 Society for Airway Management Key Recommendations for Evaluation and Management of the Physiologically Difficult Airway
Physiology Recommendations
Hypoxemia 1. Preoxygenation should be performed using high-flow oxygen for at least 3 min, or 8 vital capacity breaths. 99% agreement (SD 4.5%)
2. Desaturation is the biggest risk factor for cardiopulmonary arrest. 87% agreement (SD 29%)
3. If the patient has significant shunt physiology or reduced functional residual capacity (eg, pregnancy, obesity, ARDS), preoxygenation should be performed with PEEP using NIPPV. 98% agreement (SD 7.5%)
4. Patients should be preoxygenated in the upright position when possible. 98% agreement (SD 6.3%)
5. Delayed sequence intubation is an option for patients who cannot tolerate preoxygenation with NIPPV or HFNO. 100% agreement (SD 0%)
Hypotension 6. Risk factors for decompensation include vascular and cardiac effects of induction agents and effects of positive pressure ventilation. 99% agreement (SD 3%)
7. Peri-intubation hypotension is independently associated with poor outcomes, including mortality, length of stay, and end-organ injury. 96% agreement (SD 12%)
8. Patients should be screened for high risk of hemodynamic collapse with intubation. Those with a shock index >0.7 are at increased risk. 99% agreement (SD 1.5%)
9. Fluid-responsive and fluid-tolerant patients should be fluid resuscitated before intubation, or at least during the intubation attempt. 99.5% agreement (SD 1.5%)
10. When possible, vasopressor infusions should be started before intubation in patients that are not volume responsive or fluid tolerant. 99.5% agreement (SD 1.5%)
Abbreviations: ARDS, acute respiratory distress syndrome; HFNO, high-flow nasal oxygenation; NIPPV, noninvasive positive pressure ventilation; PEEP, positive end-expiratory pressure; SD, standard deviation.

Recent studies have evaluated the efficacy of different methods of preoxygenation. Groombridge et al21 found NRM mask at 15 liters per minute (LPM) less effective than bag-valve-mask (BVM) or a closed anesthetic circuit. Driver et al22,23 showed that increasing the oxygen flow by using flush rate (oxygen flowmeter turned maximally up ~ 50–70 LPM) through a standard NRM was not inferior to BVM preoxygenation at 15 LPM or flush rate. Of note, if a mask leak is present, the addition of a nasal cannula (NC) at 10 LPM is helpful in improving EtO2.24 Patients should be preoxygenated using a NRM at flush rate as well as a NC at 15 LPM allowing for continued apneic oxygenation,21,24 and physiologic end points (eg, EtO2) should be implemented to improve practice.

Preoxygenation is closely linked with the concept of apneic oxygenation, which serves to continuously replenish the oxygen consumed from the FRC during apnea.25,26 Apneic oxygenation has proven effective in prolonging safe apnea time in operating room (OR), prehospital, and ED studies.27–31 Standard or wide-bore nasal prongs at 10–15 LPM are well tolerated, low-cost, and low-risk apneic oxygenation methods.32 Use of capnography cannulas is discouraged because they will not achieve adequate apneic oxygenation given that they only allow for administration of effective oxygen flow rates of 0–6 LPM, often via cloud delivery while the nasal prongs sample exhaled gas.32 High-flow nasal oxygen (HFNO) systems deliver humidified oxygen via proprietary NCs at 40–70 LPM, which increases apnea time and reduces the rate of carbon dioxide increase by gaseous mixing and flushing of dead space.33

While the individual studies vary, the benefits of apneic oxygenation will not rescue inadequate preoxygenation.34 An ICU-based randomized controlled trial comparing 15 LPM apneic oxygenation via low-flow nasal oxygenation to usual care found no difference in median lowest arterial saturation or incidence of desaturation to <90% (45% vs 47%).35 Notably, one-third of the patients in apneic oxygenation group were preoxygenated with NRM at 15 LPM, which is a poor method of preoxygenation.21,22,24 Another randomized controlled trial of ED patients found no difference in the mean lowest saturation in the control (93%) and apneic oxygenation (92%) groups. These patients all had short periods of apnea, 64 seconds in the control group versus 58 seconds in the apneic oxygenation group. Importantly, these cases were rapid intubations with 90% patients successfully intubated in <100 seconds.36 In this group of patients, it is likely that preoxygenation alone provided adequate oxygen reservoir to prevent desaturation (Supplemental Digital Content, Table 2,

Shunt physiology reduces the efficacy of preoxygenation with or without apneic oxygenation. In patients with shunt physiology (ie, a high alveolar-arterial [A-a] gradient), the FRC is less available to resaturate hemoglobin.9,28,37 In this case, the partial pressure of arterial oxygen reflects the availability of the alveolar-capillary interface. Hemoglobin is typically saturated early in the transit across the alveolar-capillary interface, and excess oxygen is then dissolved in the blood down a concentration gradient. In a patient with acute respiratory distress syndrome, for example, a small volume FRC that is fully denitrogenated (EtO2 >90%) and a Pao2 of 100 reflects a patient at risk of rapid desaturation even if the oxygen saturation is >93% or the addition of apneic oxygenation because the oxygen reserve is not available to the pulmonary circulation. Reducing shunt physiology and improving V/Q mismatch becomes the priority, which is best accomplished with alveolar recruitment using a positive pressure strategy.

Noninvasive positive pressure ventilation (NIPPV) delivers a high oxygen concentration, unloads respiratory muscles, and recruits atelectatic alveoli.37 Extraglottic devices are also useful for preoxygenation, especially if the patient requires higher airway pressures or cannot tolerate NIPPV mask.38 Some of these devices have particularly high oropharyngeal seal pressures such as second-generation supraglottic airway devices (iGel >20 cm H2O) and should be considered for preoxygenation in patients that have high positive end-expiratory pressure (PEEP) requirements (Supplemental Digital Content, Table 2, Derecruitment is possible when continuous positive pressure is removed, which should be considered in the intubation strategy.

HFNO may be an effective alternative to NIPPV for patients with shunt physiology who cannot achieve peripheral arterial oxygen saturation (SpO2) > 93% on NRM at flush rate; who cannot tolerate a mask; or in whom an awake intubation is planned. These systems deliver continuous high-flow oxygen which increases end-expiratory volume and improves inspiratory flow dynamics, thus decreasing respiratory rate, reducing work of breathing, and improving thoracoabdominal synchrony. The constant concentration of oxygen delivered via HFNO is heated and humidified more closely approximating physiologic conditions than NIPPV. HFNO produces varying amounts of continuous positive pharyngeal pressure depending on flow rate, which provides a PEEP-like effect.40,41

Patients who do not achieve SpO2 > 93% with a NRM at flush rate likely have significant shunt physiology. These patients should be transitioned to a positive pressure preoxygenation strategy using either NIPPV or assisted breathing through a BVM and a PEEP valve at 5–10 cm H2O (Table),42,43 or potentially HFNO (Table). When hypoxemia is refractory to high-flow oxygen and PEEP, inhaled pulmonary vasodilators may be useful adjuncts to improve V/Q mismatch and improve oxygenation. Inhaled pulmonary vasodilators improve hypoxemia by inducing local vasodilation of alveolar capillaries adjacent to well-ventilated areas of the lung and thereby improving V/Q mismatch. Finally, an awake intubation while maintaining spontaneous respiration may provide the safest approach for patients with refractory hypoxemia. These patients recruit dependent portions of the lung and have exaggerated pendelluft flow mediated through stress risers that is immediately lost on cessation of spontaneous breathing leading to worsening V/Q mismatch and often precipitous desaturation.9

Coronavirus disease 2019 (COVID-19), which has ravaged the globe in 2020, has presented a unique problem related to airway management. Patients present with often profound hypoxemia, most likely through alterations in V/Q mismatch induced by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) action on the renin-angiotensin-aldosterone system (RAAS) pathway. Given the high rate of health care worker transmission during the SARS epidemic, aerosol-generating procedures when necessary are to be performed thoughtfully in the context of emerging evidence.44–46 Recommendations regarding aerosol-generating procedures and therapies limit NIPPV use (which vents directly into the room), acknowledge limited data on aerosols produced with HFNO, and discourage awake intubations.47,48 Patients are generally preoxygenated with 15 LPM by NRM and intubated using rapid sequence induction, without apneic oxygenation, despite profound hypoxemia. As data begin to emerge on the risks of COVID-19 transmission with the use of NIPPV, HFNO, apneic, and awake intubation, more research is needed to optimize safe airway management while avoiding health care worker transmission.46,49

Critically ill patients should be preoxygenated in the 20°–30° upright position, when feasible (Table). OR studies show that preoxygenating patients in a head-up position increases the FRC, which improves preoxygenation and prolongs the safe apnea time.50 A recent ICU-based randomized controlled trial by Semler et al51 of ICU patients showed no improvement in oxygenation between groups preoxygenated in the head-up position versus supine position. However, most patients in this study had shunt physiology and the method of preoxygenation was not standardized, which may have limited the benefits of upright preoxygenation.

In combative or delirious patients, who are resistant to standard preoxygenation, ketamine, or a similar dissociative or nonrespiratory depressant sedative (eg, dexmedetomidine) can be considered to facilitate preoxygenation (Table). Once the patient is pharmacologically compliant, optimal preoxygenation can be performed before administration of the neuromuscular blocking agent (NMBA). In 1 small observational study, most patients had improved postsedation oxygen saturations52; however, intubation-related and patient-centered outcomes data are lacking. When performing this technique, a NMBA should be prepared and intubation equipment ready for immediate intubation before ketamine administration (Supplemental Digital Content, Table 2, Ketamine, while it generally preserves airway reflexes and spontaneous respirations, can induce apnea, laryngospasm, increased airway secretions, hypotension, and cardiac arrest.54


  1. All patients should be maximally preoxygenated before intubation. 96% agreement (SD 12%)
  2. Preoxygenation should be performed using high-flow oxygen for at least 3 minutes, or 8 vital capacity breaths. 99% agreement (SD 4.5%)
  3. Maintenance of oxygenation during apneic period should be performed to prolong the duration of safe apnea. 100% agreement (SD 0%)
  4. Apneic oxygenation can be performed with a standard NC at 15 LPM or HFNO systems at 40–70 LPM. 99% agreement (SD 3%)
  5. If a tight-fitting NRM or NIPPV facemask is not available for preoxygenation, assisted spontaneous respirations with a BVM with a PEEP valve and 1-way exhalation valve should be used. 100% agreement (SD 0%)
  6. If the patient cannot tolerate a tight-fitting NRM or NIPPV mask, heated HFNO systems with 40–70 LPM of flow should be used. 99% agreement (SD 4.5%)
  7. If the patient has significant shunt physiology or reduced FRC (eg, pregnancy, obesity, acute respiratory distress syndrome [ARDS]), preoxygenation should be performed with PEEP using NIPPV versus BVM with a PEEP valve. 98% agreement (SD 7.5%)
  8. Inhaled pulmonary vasodilators can be considered to improve ventilation-perfusion mismatch before intubation in patients with severe hypoxemia. 90% agreement (SD 18%)
  9. When higher levels of PEEP are required, an extraglottic device should be considered for preoxygenation. 76% agreement (SD 40%)
  10. Awake intubation to maintain spontaneous respiration should be strongly considered for patients with refractory hypoxemia. 95% agreement (SD 9%)
  11. Patients should be preoxygenated in the upright position when possible. 98% agreement (SD 6.3%)
  12. Ramped positioning should be performed when possible to improve grade of view, improve maintenance of oxygenation, and reduce aspiration risk. 99% agreement (SD 3.1%)
  13. When delayed sequence intubation (DSI) is used, the operator should be ready for emergent intubation because the dissociative ketamine dose can be unreliable. 99.5% agreement (SD 1.5%)
  14. Regarding DSI, we recommend using small doses of ketamine (10–20 mg aliquots) or dexmedetomidine to avoid apnea from a dissociative dose. 97% agreement (SD 7.5%)


Peri-intubation shock is independently associated with severe complications and death after emergency airway management.55,56 As few as 10 minutes of hypotension can lead to poor outcomes in high-risk patients.57 While awareness of peri-intubation hemodynamics has increased, there is no consensus definition of peri-intubation hypotension (PIH). Because there is no standard definition, the incidence of PIH varies widely from 0% to 44%.58 Most definitions include any of the following in the 60-minute postintubation period: systolic blood pressure ≤90 mm Hg; mean arterial pressure ≤65 mm Hg; reduction in median systolic blood pressure of ≤20%; or any vasopressor administration.59,60

Risk factors for PIH include low mean arterial pressure (MAP) 60 minutes before intubation, preintubation shock index (SI, heart rate/systolic blood pressure) elevation, intubation for acute respiratory failure, advanced age, and chronic renal failure cormorbidities.58,59 Associated with PIH, elevated SI (>0.8, normal SI 0.5–0.7) is associated with deteriorating cardiac performance, and can be an early sign of shock, indicating limited cardiovascular reserve during emergency airway management (Table).61 Adverse events like organ dysfunction or death are associated with PIH in a dose-response manner, and quality improvement initiatives like intubation bundle checklists may improve the associated hypotension and hypoxemia.16

From the NEAR II data registry on 8937 ED intubations, cardiac arrest complications comprised 0.4% of all encounters.62 A number of recent analyses have reinforced the importance of physiologic reserve and hemodynamic resuscitation in the peri-intubation time period. Multiple retrospective studies have shown the importance of preintubation SI and hypotension for significant association with peri-intubation hemodynamic collapse.8,63–65 Similar to fluid responsiveness in the context of right ventricular (RV) failure, assessing volume status, increasing mean systemic filling pressure, and determining fluid responsiveness in peri-intubation patients with high shock indices may decrease the risk of peri-intubation cardiac arrest (Table). In patients deemed fluid intolerant or vasoplegic, early vasopressors should be administered to maintain perfusion pressure and vascular tone.

Traditionally, vasopressor infusions required immediate central venous access; however, recent studies show that peripherally infused vasopressors are low risk and reasonable alternatives to central infusions when given for short durations.66,67 Norepinephrine is the preferred vasopressor in critically ill patients and should be started as a continuous infusion in patients with preintubation hypotension or shock.68 Phenylephrine is a pure vasoconstrictor and increases vascular resistance and thereby blood pressure, but without associated inotropy, the increased blood pressure is at the cost of a lower cardiac output.69 Dilute phenylephrine boluses (eg, 100 µg/mL) may be helpful to address hypotension induced by anesthetic agents to maintain systemic vascular resistance and diastolic perfusion of the coronary arteries until transient hypotension resolves or fluid resuscitation can be optimized; however, patients with a high SI or hypotension should be started on a continuous infusion of vasopressors with inotropic properties (eg, norepinephrine; Table).70 Bolus doses of epinephrine can be effective, as well, when short-term vasoconstriction and inotropy are desired.

Laryngoscopy and tracheal intubation cause a sympathetic response, which may induce myocardial or cerebral malperfusion in ICU patients with little physiologic reserve. Most induction agents are sedative hypnotics without analgesia.71 Propofol and benzodiazepines have sympatholytic effects that lead to myocardial depression and decreased vascular tone.72 Etomidate is hemodynamically neutral with little effect on myocardial contractility.73,74 There are concerns about development of adrenal insufficiency in patients with sepsis; however, there is little evidence of harm when etomidate is used solely for induction.75,76 Induction agent dose reductions to as low as 10% of standard dosing is reasonable in patients with shock or a high SI,77,78 but should not replace adequate preintubation resuscitation.

Ketamine is an attractive induction agent in hypotension because of its sympathomimetic properties,79 and has an overall complication rate similar to etomidate.80 Jabre et al79 compared etomidate and ketamine in 2009 and found no difference in serious complications for emergency intubation in septic patients. However, ketamine is also associated with laryngospasm, increased airway secretions, myocardial depression, increased cardiac output leading to myocardial ischemia and even cardiac arrest.54


  1. Patients should have intravenous access sufficient for rapid fluid administration before intubation. 100% agreement (SD 0%)
  2. Patients should be screened for high risk of hemodynamic collapse with intubation. Those with a SI >0.7 are at increased risk. 99% agreement (SD 1.5%)
  3. Hypotensive patients due to obstructive shock secondary to acute or acute-on-chronic RV failure should be managed per the RV failure guidelines. 99% agreement (SD 3%)
  4. Fluid-responsive and fluid-tolerant patients should be fluid resuscitated before intubation, or at least during the intubation attempt. 99.5% agreement (SD 1.5%)
  5. When possible, vasopressor infusions should be started before intubation in patients that are not volume responsive or fluid tolerant. 99.5% agreement (SD 1.5%)
  6. When vasopressor infusions are not possible, bolus-dosed vasopressors should be available and used to maintain systemic pressure during and after the intubation, until an infusion can be started. 100% agreement (SD 0%)
  7. When bolus-dosed vasopressors are used, diluted epinephrine should be considered as the vasopressor of choice in patients with depressed myocardial function. 97% agreement (SD 5.6%)
  8. Hemodynamically neutral induction agents should be used. 100% agreement (SD 0%)

Special Circumstances

RV Dysfunction.

Emergency airway management in the critically ill patient requires consideration of the heart-lung interactions that characterize RV physiology interacting with venous return, pulmonary vascular resistance, and the cardiac output of the left ventricle (LV). In patients with chronic pulmonary arterial hypertension, pulmonary embolism, or acute RV failure, the exacerbation of RV performance with intubation can be the precipitating event for cardiac arrest. Thus, one must be able to diagnose and manage RV failure during airway management to mitigate risk of precipitating unfavorable hemodynamics or cardiac arrest with intubation.

RV dysfunction is characterized by the reduced ability of the right heart to provide adequate blood flow through the pulmonary circulation at a normal central venous pressure.81 It is caused by any pathophysiologic process that reduces myocardial contractility or increases pulmonary vascular resistance and RV afterload.82 The reduced downstream cardiac output is characterized by decreased LV end-diastolic volume. In a simplified manner, these downstream hemodynamic effects of RV pressure overload can be acutely worsened with the addition of positive intrathoracic pressure from mechanical ventilation, or volume overload from aggressive fluid resuscitation.

RV dysfunction often is characterized by RV dilation and reduced RV systolic longitudinal displacement. The RV is particularly sensitive to changes in afterload.83 RV stroke volume decreases sharply (roughly 30%) with a 20 mm Hg pressure afterload increase; in contrast, a 20 mm Hg increase in LV afterload only drops LV stroke volume by roughly 10%.82,83 Increased afterload eventually reaches a critical point in RV wall tension that leads to RV dilation, incompetence of the tricuspid valve with tricuspid regurgitation, and precipitates a downward spiral of ischemia—potentiating right and left ventricular failure via ventricular interdependence.81

Once RV dysfunction has been identified, any potential for improvement in RV function with increased preload should be closely scrutinized (Supplemental Digital Content, Table 1, Traditional dynamic methods of evaluating volume responsiveness by evaluating LV stroke volume swings with changes in intrathoracic pressure can be misleading because the RV is always preload responsive in the setting of RV dysfunction. Thus, volume responsiveness of the RV, not the LV, needs to be evaluated. When the RV is preload responsive, fluid boluses should be small (250 mL) to avoid rapid volume overload. If the RV is volume overloaded, aggressive diuresis may be beneficial before induction for improvement in RV hemodynamics. Norepinephrine may improve ventricular systolic function without increasing pulmonary vascular resistance.83

For clinical situations when the RV is not preload responsive or volume overloaded, afterload reduction becomes the only remaining therapeutic option. This can be accomplished by treating any hypoxemia, atelectasis, and hypercapnia that all independently increase pulmonary vascular resistance. Inhaled pulmonary vasodilators are available to reduce the RV afterload and can be given without significant logistical difficulty (Supplemental Digital Content, Table 1, The major side effects of these include systemic hypotension and worsening of V/Q mismatch.84


  1. Patients should be screened for significant RV dysfunction before intubation given the risk of decompensation with the transition to positive pressure ventilation. 94% agreement (SD 11%)
  2. When RV dysfunction is present, patients should be evaluated for RV systolic function, and fluid and vasopressor tolerance. Empiric fluid resuscitation without this evaluation can further reduce RV function. 98% agreement (SD 4%)
  3. Fluid and vasopressor tolerant patients should be resuscitated accordingly. 99.9% agreement (SD 0.3%)
  4. Fluid-intolerant patients should have RV afterload reduced with inhaled or intravenous pulmonary vasodilators. 96% agreement (SD 8%)
  5. Preintubation extracorporeal membrane oxygenation (ECMO) cannulation should be considered if available in patients with RV failure–induced shock. 98% agreement (SD 6%)
  6. Preintubation diuresis should be considered in patients with RV volume overload. 100% agreement (SD 0%)
  7. Hypercapnia should be avoided. 97% agreement (SD 8%)
  8. Mean arterial pressure should be augmented to maintain coronary perfusion pressure. In patients with chronic pulmonary arterial hypertension, a higher mean arterial pressure should be targeted to keep mean arterial pressure > mean pulmonary artery pressure. 100% agreement (SD 0%)
  9. Ventilation strategy after intubation should include a low mean airway pressure and a higher PEEP to avoid atelectasis. 94% agreement (SD 15.7%)

Severe Metabolic Acidosis

Carbon dioxide dissolved in the blood is cleared through alveolar ventilation. Therefore, reduction in ventilatory drive, neuromuscular inefficiency (increased ventilator load or reduced effort), or increased dead space will lead to an increase in CO2 and a reduced pH. This respiratory acidosis can be corrected with an improvement in alveolar ventilation, generally in a 1:1 relationship where doubling the alveolar ventilation will reduce the CO2 by half. BVM, NIPPV, or mechanical ventilation rapidly reduces inspiratory work of breathing and overcomes neuromuscular weakness to correct respiratory acidosis.10

In ventilatory failure due to metabolic acidosis, however, the bicarbonate buffering system is overwhelmed and compensatory removal of CO2 through increased alveolar ventilation reaches a plateau. Severe metabolic acidosis such as diabetic ketoacidosis, salicylate or metformin toxicity, and severe lactic acidosis outpace the respiratory compensation attempts to keep blood pH in a normal range. Any reduced ventilatory compensation leads to a rapidly downward spiral of worsening acidosis and cardiopulmonary arrest.85 Thus, intubating these patients with severe acidemia from an uncompensated metabolic acidosis can be particularly troublesome. It is challenging to match the ventilatory requirement of the patient with the capacity of the mechanical ventilator especially in the context of the apneic period during induction.

Before intubation, preoxygenation with NIPPV will allow for a reduction in work of breathing and will provide an estimate of the minute ventilation requirement to maintain the profoundly acidemic state. If the minute ventilation requirement is higher than can be safely achieved in a passively breathing patient, then one should consider avoiding rapid sequence intubation and especially long-acting paralytics. An awake approach with a spontaneously breathing patient and the use of a spontaneous breathing (ie, pressure supported) mode of mechanical ventilation may be the option of choice for safely managing these airways. The use of a high-flow NC system that washes out dead space and improves ventilation may be incredibly beneficial to prevent a respiratory acidosis component during the procedure (Supplemental Digital Content, Table 1, Preintubation bicarbonate boluses in patients with very high minute ventilation are controversial, lack data, and had a low rate of agreement among the workgroup 77% agreement (SD 37%).


  1. Patients with severe metabolic acidosis are at high risk of decompensation due to volume depletion and inadequate alveolar ventilation after intubation. 100% agreement (SD 0%)
  2. Patients with high minute ventilation requirements should be considered for awake intubation to maintain spontaneous respiration. 99% agreement (SD 3%)
  3. Consider a spontaneous breathing mode after intubation in patients with very high minute ventilation requirements. 99% agreement (SD 3%)

Neurologically Injured Patients

It is imperative to maintain eucapnia and normoxia during intubation in the neurologically compromised patient, because cerebral blood flow is very sensitive to changes in CO2 and oxygen saturations.86 During induction, extremes of mean arterial pressure, intracranial pressure (ICP), and subsequent variability in cerebral perfusion pressure should be prevented. Maintenance of stable hemodynamics in the severe traumatic brain injury patient is critical for adequate cerebral perfusion (cerebral perfusion pressure = mean arterial pressure [MAP] – ICP). The brain is able to autoregulate perfusion over a range of cerebral perfusion pressure from 50 to 100 mm Hg. However, severe traumatic brain injury affects the ability to autoregulate.

Severe traumatic brain injury is a common process complicating airway patency in the prehospital environment often necessitating endotracheal intubation. Unfortunately, laryngoscopy and endotracheal intubation are noxious stimuli precipitating sympathetic discharge and a significant cardiovascular response. Pretreatment with lidocaine and opiates, such as fentanyl, have limited evidence to strongly support out-of-OR use in acute severe traumatic brain injury.87 Much of the data is either in small OR patient cohorts or is in elective surgery or brain tumor populations.88,89 Topical application of 4% lidocaine may be of use; however, the data are limited without randomized, blinded trials.

Esmolol has also been investigated as a potential quick-acting pharmacologic intervention in the management of the out-of-OR airway. Prospective study by Ugur et al90 in 2007 found that esmolol pretreatment could control tachycardia and rate-pressure product markers of hemodynamics when compared to lidocaine. Chung et al91 in 1992 noted a potential synergistic effect of esmolol and fentanyl to attenuate hemodynamic response greater than either agent alone (fentanyl 2 µg/kg or esmolol 2 mg/kg).91

In addition to pharmacologic pretreatment approaches, the choice and dose of a hemodynamically neutral induction agent are particularly important in the physiologic management of the neurocritical care patient. While ketamine was previously thought to have negative impacts on ICP, this dogma has since been overturned (Supplemental Digital Content, Table 1,


  1. Eucapnia should be maintained before, during, and after intubation. 99.9% agreement (SD 0.3%)
  2. Hemodynamically neutral induction agents should be used. 100% agreement (SD 0%)
  3. Patients should be positioned 30° upright, when possible. 100% agreement (SD 0%)
  4. Postintubation management should include limiting PEEP to promote cerebral venous drainage. 92.5% agreement (SD 23.7%)


As more data rapidly emerge on the physiology of endotracheal intubation, there exists a need for focused guidelines on the heart-lung interactions and the pharmacologic interventions that underpin airway management. The above guidelines serve to show the general level of agreement for various physiologic tenets of airway management among a diverse group of specialists specific to the out-of-OR environment. Although randomized trials may not necessarily show statistically significant outcomes with particular well-regarded interventions (eg, Semler et al35 with apneic oxygenation), these SAM guidelines reflect the sentiment and practice patterns of practicing airway specialists. The diverse backgrounds within the working group provide a variety of perspectives on the utility of various interventions within the resource limitations of the out-of-OR environment.

Limitations of the guidelines are the lack of a risk of bias assessment. Furthermore, no librarian formalized the literature search process. However, because most of the recommendations have limited to no data in published literature, we decided against a traditional Delphi process and instead sent out the list to the SAM Committee to generate their level of agreement with each recommendation.

The multidisciplinary approach of SAM provides an avenue for discourse that transcends subspecialty and cultural barriers. Because the various recommendations from the Committee are diverse and expansive in breadth, the top 10 recommendations from the multidisciplinary group are summarized in the Table. By highlighting themes in the context of a physiologic approach, these SAM guidelines for the physiologically difficult airway define principles that extend beyond a single practice environment and highlight areas where research is needed.


Name: Rebecca L. Kornas, MD.

Contribution: This author helped with the study design/concept, acquisition of data, analysis of data, drafting the manuscript, and critical manuscript revision.

Conflicts of Interest: None.

Name: Clark G. Owyang, MD.

Contribution: This author helped with the study design/concept, acquisition of data, analysis of data, drafting the manuscript, and critical manuscript revision.

Conflicts of Interest: None.

Name: John C. Sakles, MD.

Contribution: This author helped with the study design/concept, analysis of data, and critical manuscript revision.

Conflicts of Interest: J. C. Sakles has previously served as a consultant for Verathon Inc (Bothwell, WA).

Name: Lorraine J. Foley, MD.

Contribution: This author helped with the study design/concept, analysis of data, and critical manuscript revision.

Conflicts of Interest: L. J. Foley is a paid consultant for Vyaire Medical.

Name: Jarrod M. Mosier, MD.

Contribution: This author helped with the study design/concept, acquisition of data, analysis of data, drafting the manuscript, and critical manuscript revision.

Conflicts of Interest: J. M. Mosier previously served as a consultant Vyaire, and is a consultant for Verathon, Inc.

This manuscript was handled by: Narasimhan Jagannathan, MD, MBA.


Thomas Terndrup, MD; Art French, MD; Richard Galgon, MD; Thomas Friedland, MD; Jessica Feinleib, MD, PhD; David J. Olvera; Chivas Guillote, RN; Drew Fuller, MD; Carin Hagberg, MD; Monique Steffani; Lynette Mark, MD; Clark G. Owyang, MD.


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