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 Table of Contents  
Year : 2021  |  Volume : 4  |  Issue : 1  |  Page : 4-12

The physiologically difficult airway

1 Department of Anaesthesia, Bai Jerbai Wadia Hospital for Children, Mumbai, Maharashtra, India
2 Department of Anaesthesia, Critical Care and Pain, Tata Memorial Hospital, Homi Bhabha National Institute, Mumbai, Maharashtra, India

Date of Submission12-Mar-2021
Date of Acceptance21-Mar-2021
Date of Web Publication29-Apr-2021

Correspondence Address:
Prof. Sheila Nainan Myatra
Department of Anesthesiology, Critical Care and Pain, Tata Memorial Hospital, Dr. Ernest Borges Road, Parel, Mumbai, Maharashtra
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/arwy.arwy_10_21

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The physiologically difficult airway is defined as one in which severe physiologic derangements place patients at increased risk of cardiovascular collapse and death during tracheal intubation and transition to positive pressure ventilation. Patients with a physiologically difficult airway can be divided into those who are critically ill and those who are not. The critically ill patient with a physiologically difficult airway may present with hypoxaemia, hypotension, right ventricular failure, metabolic acidosis and neurologic injury. Noncritically ill patients with a physiologically difficult airway are patients who are obese, paediatric, pregnant or at risk of aspiration during tracheal intubation (after a meal, with gastroesophageal reflux disease, intestinal obstruction, etc). Recognition of this high-risk group of patients is essential to implement measures to avoid complications during tracheal intubation. Unlike the anatomically difficult airway, where placing the endotracheal tube safely within the trachea is the primary goal, in patients with a physiologically difficult airway, prevention of adverse events is equally important during airway management. Strategies to prevent complications associated with physiologically difficult airway include measures to improve the chance of first-pass success, effective peri-intubation oxygenation and measures to avoid hypotension and haemodynamic collapse.

Keywords: Airway in the obese, airway management in intensive care unit, airway management in the critically ill, difficult airway, obstetric airway, paediatric airway

How to cite this article:
Vakil B, Baliga N, Myatra SN. The physiologically difficult airway. Airway 2021;4:4-12

How to cite this URL:
Vakil B, Baliga N, Myatra SN. The physiologically difficult airway. Airway [serial online] 2021 [cited 2022 Aug 17];4:4-12. Available from: https://www.arwy.org/text.asp?2021/4/1/4/315157

  Introduction Top

The term ‘difficult airway’ has been defined by the American Society of Anesthesiologists taskforce as the clinical situation in which a conventionally trained anaesthetist experiences problems with mask ventilation or tracheal intubation or both.[1] Conventionally, the concept of difficult airway management has always focussed on anatomic factors which make mask ventilation, laryngoscopy or tracheal intubation difficult. Lot of attention has been paid to the anticipation of not being able to secure a definitive airway. Several scoring systems have been formulated for the prediction of a difficult airway. However, with the availability of devices such as videolaryngoscopes, flexible bronchoscopes, peri-intubation oxygenation devices such as high flow nasal oxygen (HFNO), tools for emergency invasive airway access, availability of guidelines and increased training, securing the anatomically difficult airway has become relatively less challenging than in earlier times.

Physiologic derangements or poor physiologic reserve, particularly seen in critically ill patients, tends to increase the risk of complications during tracheal intubation. Although other groups of patients may not be critically ill, their physiological alterations compared to a healthy adult patient places them at an increased risk of complications during tracheal intubation. These include obese, paediatric and pregnant patients. This type of difficulty faced by the physician while securing the airway is termed as a physiologically difficult airway. The physiologically difficult airway can be defined as one in which physiologic alterations place the patient at an increased risk for cardiovascular collapse and death during tracheal intubation and transition to positive pressure ventilation.[2]

Tracheal intubation in critically ill patients is associated with increased complications when compared to the operating room (OR) for anaesthesia. According to the Fourth National Audit Project Report, complications related to the airway leading to death or brain injury was seen in 61% of cases in the intensive care unit (ICU) compared to 14% during anaesthesia. One of the important factors leading to increased complications were the emergent need for securing the airway.[3] A cohort study done in the emergency department found that 1 in 25 patients who underwent emergency intubations suffered a cardiac arrest. Preintubation hypotension, hypoxaemia and obesity were factors associated with increased risk of cardiac arrest. This study suggests physiologic factors and derangements are associated with increased postintubation complications.[4] A multicentre study done to determine prevalence and risk factors for cardiac arrest in ICU found that the incidence of cardiac arrest was 2.7%, about 1 in 40 intubations, that increased both immediate and 28-day mortality. They attributed the risk factors for cardiac arrest to preintubation hypotension, preintubation hypoxaemia, obesity, nonperformance of preoxygenation, and age more than 75 years.[5] These studies suggest that physiologic derangements in critically ill patients make them susceptible to untoward complications during tracheal intubation.

Knowledge about these physiological factors and derangements is essential for all airway operators. This review will describe different physiologically difficult airways and provide guidance to prevent complications in this high-risk group during tracheal intubation.

  Critically Ill Patients Top


Patients with preexisting hypoxaemia are at increased risk of cardiopulmonary complications such as desaturation, hypoxic brain injury, cardiac dysrhythmias and cardiac arrest during intubation.[6] In patients with hypoxaemic respiratory failure, there is inability to maintain adequate arterial oxygenation. The common causes of acute hypoxaemic respiratory failure are pneumonia, pulmonary oedema, acute respiratory distress syndrome (ARDS), asthma, etc., The mechanism of hypoxia in these cases is due to a shunt and ventilation-perfusion (V/Q) mismatch. In a normal healthy mechanically ventilated patient under anaesthesia, there is the mismatch of V/Q; however, this mismatch can be easily overcome by recruiting the lungs and increasing the fractional inspired concentration of oxygen (FIO2). In critically ill patients, there is a significant shunt where alveoli in the affected area are unable to participate in gas exchange. In these cases, increasing the FIO2 would not help as the oxygen delivered is not able to reach the capillaries. Hence, these patients are at an increased risk of cardiopulmonary complications due to increased risk of rapid desaturation during attempts at tracheal intubation. In these patients, early identification of the potential physiologically difficult airway and use of measures to prolong the safe apnoea time (time until significant desaturation after inducing apnoea) become crucial irrespective of anatomical airway difficulty.

Methods to prolong safe apnoea time (time until significant desaturation following neuromuscular blockade) include adequate preoxygenation and apnoeic oxygenation. The aim of preoxygenation is to achieve maximal haemoglobin saturation and maximal partial pressure of arterial oxygen, thus creating a reserve and prolongation of safe apnoea time. Optimising preoxygenation leads to higher first-pass success rate and reduces the risk of desaturation and associated complications. Conventionally, preoxygenation was done with help of a non-rebreathing mask (NRM) over 3–5 min.[7] However, due to improper mask seal and entrainment of air, effective fraction of inspired oxygen is decreased, especially in critically ill patients who are tachypnoeic and have high minute ventilation. In the OR, patients are preoxygenated with a tight-fitting mask connected to the anaesthesia circuit with 100% oxygen and allowing the patient to breathe normal tidal volume breaths for 3–5 min. A study which evaluated different methods of preoxygenation found bag-mask ventilation and closed anaesthetic circuit to be more effective than NRM.[8] However, in critically ill patients with hypoxic respiratory failure, this may not improve apnoea time due to prominent shunt pathology. Baillard et al. compared non-invasive ventilation (NIV) for preoxygenation with conventional oxygen therapy using valve-bag face mask in ICU patients needing tracheal intubation and reported that preoxygenation with NIV was associated with better oxygen saturation and the incidence of desaturation during intubation was significantly reduced (46% to only 7%, P < 0.01). This was probably due to the recruitment of collapsed alveoli and increasing end-expiratory lung volume.[9] NIV as a method of preoxygenation in critically ill patients has been recommended and incorporated in the Montpellier ICU intubation bundle.[10]

Another method of preoxygenation is to use high-flow nasal oxygen (HFNO). Humidified oxygen is delivered at a very high flow rate of around 50–60 L/min. These high flow rates reduce the dead space, help in recruiting alveoli as well as maintain positive end-expiratory pressure (PEEP). HFNO can be used for preoxygenation as well as a method of providing apnoeic oxygenation during attempts at tracheal intubation. A study by Miguel-Montanes et al. compared HFNO with bag-mask reservoir facemask for desaturation during tracheal intubation and found that HFNO significantly improved preoxygenation and reduced the prevalence of severe hypoxaemia compared with nonrebreathing bag reservoir facemask.[11] In the PROTRACH study, preoxygenation with HFNO compared to standard bag-valve-mask oxygen in nonhypoxaemic patients found reduction in intubation-related adverse events in the HFNO group.[12] The FLORALI 2 study compared NIV and HFNO as methods of oxygenation during induction to laryngoscopy with NIV and during induction to tracheal intubation with HFNO. The incidence of severe hypoxaemia during tracheal intubation was 23.2% in the NIV group and 27.5% in the HFNO group (P = 0.39).[13] Current evidence suggests that NIV is a better method of preoxygenation compared to conventional bag-mask as well as HFNO in patients with moderate-to-severe hypoxaemia. In patients who are agitated or uncooperative for preoxygenation, a delayed sequence intubation using ketamine to induce a dissociative state and improve effective preoxygenation may be done before administration of neuromuscular blocking agent during rapid sequence intubation (RSI).[14]

Optimising position during preoxygenation and intubation can also lead to prolongation of safe apnoea time. Head-up position or the ramped position has been compared with the supine position for intubation. The first attempt success rate was higher with ramped compared to supine in an observational study, whereas another study found that the combination of ramped and sniffing positions significantly reduced complications.[15],[16] Head-up position improves preoxygenation, prevents reduction in the functional residual capacity (FRC) and may reduce the risk of pulmonary aspiration. The head-up position has been recommended by recent guidelines in patients at high risk of desaturation.[17],[18] Gentle mask ventilation during RSI after induction and before intubation was evaluated in the PREVENT study, which found that patients who received ventilation had a lower incidence of severe hypoxaemia without increasing the rate of pulmonary aspiration.[19]

Another method of maintaining saturation during the apnoea time is to provide apnoeic oxygenation with the help of standard nasal cannula (15 L/min oxygen flow) or HFNO. This works on the principle of mass flow of oxygen because of the pressure generated due to the differential diffusion capacity of oxygen and carbon dioxide (CO2). A systematic review and meta-analysis on respiratory support during intubation in ICU setup showed apnoeic oxygenation with either HFNO or standard nasal cannula was significantly associated with higher minimum SpO2 registered during the intubation procedure as compared to those who did not receive apnoeic oxygenation.[20] Jaber et al., in a proof of concept study (OPTINIV study), showed that the use of apnoeic oxygenation using HFNO combined with NIV for preoxygenation prevented desaturation during intubation in hypoxaemic patients compared to using NIV alone for preoxygenation.[21]

If feasible, preoxygenation for at least 3–5 min should be performed in these high-risk patients. Current guidelines recommend a minimum of 3 min of preoxygenation in critically ill patients with the help of NIV with an inspiratory pressure of 5–15 cm H2O, PEEP of 5 cm H2O and tidal volume of 6–8 mL/kg in a head-up position or with the help of HFNO.[22] Apnoeic oxygenation should be considered to prolong safe apnoea time during intubation. In combative agitated patients, use of ketamine to optimise preoxygenation in a technique termed “delayed sequence intubation” should be considered.[23] It should be borne in mind that even with preoxygenation and apnoeic oxygenation, the safe apnoea time may not be increased in this group of patients due to the widespread damage to the alveoli, highlighting the importance of first-pass intubation success. The operator with the maximum experience in tracheal intubation should preferably manage the airway using tools to improve intubation success such as videolaryngoscope and bougie.


Peri-intubation hypotension is associated with adverse events such as bradycardia, cardiovascular collapse and death. In an observational study, the incidence of cardiovascular collapse after intubation was 30% among critically ill patients.[24] Preexisting hypotension and shock index, i.e., heart rate/systolic blood pressure more than 0.8 has been found to have increased risk of postintubation hypotension and cardiac arrest.[25] Even though the presence of hypotension before tracheal intubation is associated with increased cardiovascular complications in the postintubation period, not all patients will be in shock due to reflex compensatory mechanisms. An elevated shock index is an early sign of shock despite otherwise normal vitals. Common causes of hypotension among critically ill patients are hypovolaemia, decreased peripheral vascular resistance, capillary leak and positive pressure ventilation following tracheal intubation. If hypovolaemia is present, adequate fluid resuscitation should be performed before intubation unless contraindicated. In patients who do not respond to fluids or are at risk of fluid overload following fluid therapy, a vasopressor infusion may be started to maintain the vascular tone and prevent hypotension and cardiac arrest.

In a spontaneously breathing person, negative intrathoracic pressure helps improve the venous return. Negative intrathoracic pressure helps the right atrium to siphon blood from the peripheral veins (vis a fronte). The gradient between the peripheral venous pressure and the right atrium also helps in the movement of blood.[26] When the pressure in the right atrium increases due to positive pressure ventilation, this increase in pressure decreases the venous return thereby decreasing the cardiac output. While normal healthy patients can easily compensate for this reduction in cardiac output by increasing the stroke volume, heart rate and systemic vascular resistance, critically ill patients who may already be hypotensive and have exhausted their compensatory mechanisms may worsen. Hence, it is imperative to prevent hypotension using fluids or vasopressors if possible and identify and treat the hypotension early if it occurs.

The decision about the type of drugs used for induction and intubation also plays a role for peri-intubation haemodynamic changes. Etomidate is a relatively cardiostable drug. However, etomidate does not suppress airway reflexes, thereby not preventing the response to laryngoscopy. This in turn causes haemodynamic fluctuations which indirectly negates the purpose of its use. Ketamine is an option, especially for critically ill patients with hypotension. Ketamine is a sympathomimetic drug that can increase blood pressure. However, reports have shown that ketamine can also cause cardiac arrest due to its direct cardiac depressant activity, particularly in catecholamine-depleted states. A study which compared etomidate with ketamine as induction agent among critically ill during RSI did not find any difference in intubating conditions or severe adverse events.[27] Propofol suppresses airway reflexes effectively but causes haemodynamic suppression due to its sympatholytic effect. Transient hypotension secondary to vasodilation due to anaesthetic drugs may be treated with vasopressors.

Right ventricular failure

The right ventricle (RV) is an often neglected chamber. The RV is a highly compliant, low-pressure chamber. Its unique structure allows it to accommodate greater volume, i.e., preload. However, it does not tolerate increases in afterload too well. The conditions that increase RV afterload are chronic pulmonary hypertension secondary to lung or left heart disease, pulmonary embolism and left ventricular failure. The RV responds to this increase in afterload by increasing contractility, preload and eventually undergoing hypertrophy. These patients need to be evaluated for the presence of RV dysfunction where some function of RV is preserved and for RV failure (RVF) where RV is unable to meet increased demands that can lead to dilatation, retrograde flow, decreased coronary perfusion, hypotension and cardiovascular collapse. In patients with RVF, mechanical ventilation has deleterious effects. Positive pressure ventilation can lead to increase in airway pressure which in turn gets transmitted to the pulmonary vasculature, resulting in an increase in afterload in addition to a reduction in preload. Thus, there is a high risk of cardiovascular collapse in patients with RVF.

Other conditions that increase pulmonary pressures and subsequently worsen RVF are hypoxia and hypercarbia. Therefore, patients with RVF should be carefully managed during airway management. A brief duration of apnoea can cause sufficient hypoxia and hypercarbia leading to raised pulmonary pressures.[28],[29] HFNO as a mode of apnoeic oxygenation is useful as it prevents hypoxia and flushes out CO2 by the flow-dependent ventilatory exchange.[30] Moreover, HFNO prevents atelectasis which can help to prevent hypoxic pulmonary vasoconstriction. Other methods to decrease pulmonary pressures include the use of pulmonary vasodilators such as epoprostenol and inhaled nitric oxide, use of NIV before intubation with a low CPAP, and upright position to prevent atelectasis.[31]

Bedside echocardiography can be used to look for RV function. An enlarged RV and a flattened septum during systole, suggest right ventricular dysfunction.[32] In patients with RV dysfunction, judicious fluid loading may be beneficial. However, in patients with RVF, this may be deleterious as it may worsen left ventricular filling and stroke volume. Vasopressors such as noradrenaline can be used before intubation with the goal of increasing the mean arterial pressure without increasing pulmonary artery pressures. If the patient requires tracheal intubation, the goals are to avoid hypoxia and hypercarbia during the peri-intubation period and maintenance of a low mean airway pressure.

Metabolic acidosis

Patients who are critically ill may have associated metabolic acidosis. Common causes are diabetic ketoacidosis, lactic acidosis and salicylate poisoning. In metabolic acidosis, the presence of organic acids increases in proportion to the nonorganic ions. This leads to a compensatory increase in alveolar ventilation to wash out CO2 to maintain acid-base balance. These patients with severe metabolic acidosis are at increased risk of complications during intubation as brief periods of apnoea can cause a sharp rise in CO2 that can derange acid-base balance. Following tracheal intubation, the increased ventilation requirements may not be met with the limitations due to lung-protective strategies used which can lead to a drop in arterial pH and precipitate cardiac arrest. Hence, these patients should be allowed to breathe spontaneously and tracheal intubation should be avoided if possible. A trial of NIV may be given to reduce work of breathing during which correction of underlying acidosis can take place. RSI is avoided and if deemed necessary, a short-acting muscle relaxant such as succinylcholine should be used. Following tracheal intubation, ventilator modes should be chosen that allows the patient to maintain their respiratory compensation. Modes such as pressure control mode and pressure support mode where the patient determines tidal volume and respiratory rate are preferred. However, these patients with high minute ventilation are at risk of developing relative hypoventilation, flow starvation, patient-ventilator asynchrony and worsened acidosis.[2]

Neurological injury

In patients with neurologic injury such as traumatic brain injury, it is important to maintain cerebral perfusion pressure and avoid secondary injuries such as hypoxia and hypercapnia. When these patients need tracheal intubation due to a low Glasgow Coma Score or are scheduled for surgery, induction of anaesthesia can lead to hypotension which may compromise cerebral perfusion pressure. Following induction, laryngoscopy and tracheal intubation can lead to sympathetic stimulation which may increase the intracranial pressure. Any hypoxia or hypercarbia during tracheal intubation can worsen the neurological injury.[21],[33]

When neurologically injured patients require tracheal intubation, the induction agent with least haemodynamic effects such as etomidate should be used. Ketamine may also be used safely as it has been disproven that its use leads to increase in intracranial pressure. Measures to reduce the tracheal intubation response such as prior administration of lignocaine, fentanyl and esmolol may be used.[34] The duration from laryngoscopy to tracheal intubation should be minimised. Hypoxia and hypercarbia should be avoided.[35]

  Paediatric Patients Top

The paediatric airway differs from the adult both anatomically and physiologically. The most dreaded complication anticipated during tracheal intubation in a child is hypoxaemia. The average oxygen consumption is around 6 mL/kg/min compared to only 3 mL/kg/min in adults. This, combined with a lower FRC and a higher closing capacity (CC), makes children very vulnerable to rapid desaturation and hypoxia. The younger the child, the faster is the rate of desaturation. These factors make children vulnerable to rapid desaturation during tracheal intubation.[36],[37]

  Obese Patients Top

The incidence of difficult tracheal intubation in nonobstetric obese patients (body mass index >30 kg/m2) has been estimated as 1.8%–7.5%.[38] These patients may have an anatomically difficult airway. In addition, these patients have a physiologically difficult airway due to the higher resting metabolic demand and higher oxygen consumption as well as a higher cardiac output by a margin of 100 mL/min for each kilogram increase in adipose tissue. It is also an independent risk factor for heart failure due to the structural and functional changes in the heart resulting from volume and pressure overload and vascular stiffness. The resulting progressive decrease in compliance of the left ventricle and its hypertrophy causes left ventricular failure.

Obese patients have a diminished total lung capacity and vital capacity. This, along with the decreased chest wall compliance and increased intra-abdominal pressure, significantly reduces the FRC and the CC to the extent that often the CC is higher than the FRC, thereby closing the smaller airways even during normal tidal volume breathing. These patients often have associated obstructive lung disease or other underlying lung pathology. Obese patients may have obstructive sleep apnoea causing intermittent and repeated upper airway collapse, leading to partial or total airway occlusion for short periods during sleep. This results in an irregular breathing pattern, episodic sleep-associated oxygen desaturation and hypercarbia, along with cardiovascular dysfunction and excessive daytime sleepiness. Such frequent episodes of hypoxia and hypercarbia may lead to an increase in pulmonary arterial pressures with subsequent right ventricular dysfunction in these patients. These factors result in an increased risk of hypoxaemia in these patients due to the short safe apnoea time, making tracheal intubation challenging.[39] [Figure 1] depicts differences in desaturation in a normal healthy adult, a critically ill adult, a child and an obese patient after administration of a neuromuscular blocking agent.
Figure 1: Graph showing differences in the time to critical oxygen desaturation in a normal healthy adult, a critically ill adult, a child and an obese patient after administration of neuromuscular blockade

Click here to view

  Pregnant Patients Top

The obstetric airway is handled only when a need arises to give general anaesthesia during an obstetric emergency related to the foetus or mother (emergency caesarean delivery) or critical illness of the mother. The obstetric airway is considered a difficult airway and the incidence of failed intubation in obstetrics was found to be 1 in 224 patients as per UK national study.[40] The reason is not restricted to anatomical changes, but also due to physiological alterations in the parturient. The FRC is low during pregnancy and further reduces during active labour. Oxygen demand is high and further increases during active labour. Anaemia related to pregnancy may contribute to decreased oxygen reserves. These factors reduce the safe apnoea time while securing the airway of the parturient, increasing the risk of hypoxaemia. In addition, the decrease in the tone of the lower oesophageal sphincter due to the action of progesterone and delayed gastric emptying makes them vulnerable for gastric reflux and pulmonary aspiration.[41]

  Patients at Risk for Aspiration Top

Pregnancy, obesity, gastroesophageal reflux disease, diabetes, intestinal obstruction and those with inadequate fasting status are considered to have a full stomach. These patients are at an increased risk for regurgitation and pulmonary aspiration during induction and tracheal intubation. Pulmonary aspiration can lead to hypoxia, pneumonitis, pneumonia, ARDS and even cardiovascular collapse and death. In these patients, RSI with predetermined doses of induction agent and muscle relaxant, avoidance of positive pressure ventilation and application of cricoid pressure until confirmation of tracheal intubation and inflation of the tracheal cuff should be routine practice.

  Strategies to Prevent Complications During Tracheal Intubation Top

Risk assessment

The traditional use of different scoring systems always aimed at the anatomical aspects of the difficult airway. However, recently a new system has been introduced which aims at looking not only at the anatomical but also the physiological aspects of the difficult airway along with the operator experience. De Jong et al. introduced a new scoring system called the MACOCHA system.[42] This score looks at the Mallampati score III or IV, obstructive sleep apnoea, decreased cervical mobility, mouth opening <3 cm, coma (Glasgow Coma Score <8), severe hypoxaemia and a nonanaesthesiologist. It, therefore, takes into account the anatomical, physiological and operator characteristics. The score has a maximum of 12 points, with 0 points predicting easy intubation and 12 points predicting a very difficult one. This test has a sensitivity of 73% for direct laryngoscopy; however, it has not been validated for videolaryngoscopy.

Planning, preparation and procedure

These include team preparation, appropriate patient positioning, peri-intubation oxygenation strategies, careful selection of induction agents, use of neuromuscular blocking agents, RSI in patients at risk of aspiration and use waveform capnography to confirm tracheal intubation. These strategies are summarised in [Table 1].
Table 1: Strategies to prevent complications during tracheal intubation in patients with a physiologically difficult airway

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  Conclusion Top

Critically ill patients, as well as paediatric, obstetric and obese patients, have a physiologically difficult airway. The physiologic alterations in these patients put them at an increased risk for hypoxaemia or cardiovascular collapse during tracheal intubation. Recognising the challenges involved during tracheal intubation in these patients, using appropriate strategies to improve first-pass success in tracheal intubation and avoiding complications is essential. Further research will help us better understand the optimal strategies to improve patient outcomes in these categories of patients.

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Conflicts of interest

There are no conflicts of interest.

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This article has been cited by
1 The physiologically difficult airway: an emerging concept
Sheila Nainan Myatra, Jigeeshu Vasishtha Divatia, David J. Brewster
Current Opinion in Anaesthesiology. 2022; 35(2): 115
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