The physiologically difficult airway

The "physiologically difficult airway" is a concept which most senior critical care people will instantly recognise the meaning of, without having to dig especially deep into their cognitive resources, making it harder to understand why it was not developed sooner. We have had this terminology only since the twentyteens, as the earliest mention dredged up by Google Scholar seems to be a footnote from the Proceedings of the 22nd Postgraduate Course in Critical Care Medicine, where Sorbello et al (2007) refers to it in the context of extubation. The concept developed into its modern form with Mosier et al (2015), who gave it a new meaning with a modern definition; though the same Arizona group were already trying to separate anatomical and physiological difficulty in their analysis of videolaryngoscopy from 2013.  In the ensuing ten years this concept has very appropriately infiltrated all levels of airway-related thinking and now hopefully occupies a warm spot close to the amygdala of anybody who regularly handles a laryngoscope.

In summary:

Definition of a physiologically difficult airway:

• A physiologically difficult airway is where the patient has physiological characteristics that create a high chance of adverse events from the induction agents, ventilation or response to laryngoscopy, even though the laryngoscopy itself may be technically uncomplicated.

Contributing factors to the increased risk:

• Risk of post-intubation hypoxia:
  • Reduced capacity for denitrogenation/preoxygenation (delirium, respiratory arrest)
  • Small FRC (obesity, pregnancy)
  • Increased demand (sepsis, thyrotoxicosis)
• Risk of cardiovascular collapse
  • Any shock states, eg. hypovolemia, poor cardiac contractility, obstructive shock states
  • Reduced cardiovascular reserve, eg. unrevascularised coronary artery disease
  • Metabolic acidosis
  • Pro-arrhythmic state, eg. severe electrolyte derangement
  • Fragile aortic or cerebrovascular aneurysmal pathology
• Risk of neurological injury
  • Raised ICP, hypertensive crisis

Optimisation strategies

• Correct hypovolemia and acidosis
• Pre-empt vasodilation and reduced cardiac output on induction with pre-intubation introduction of vasopressors and inotropes
• Specifically look for, and target, RV failure (eg. with pulmonary vasodilators and inodilators)
• Preoxygenate with NIV/HFNP
• Use lower doses of cardiostable induction agents like ketamine

 This concept has appeared in the CICM exams only once, as Question 5 from the second paper of 2025; whereas all the other historical questions have focused on anatomical difficulty instead. This Question was labelled as belonging to Syllabus Section 2.1.19, Intensive Care Procedures, where "Intubation" is listed. But one might argue that intubation is merely the vulgar act of adding tube to face, whereas airway management from Section 2.1.5 describes the refined art of not killing the patient with your induction, and so extends beyond the purely procedural aspects. As such, the author will insist that it belongs among tracheostomy complications, airway injuries, extubation assessment, and other clever ICU topics, rather than with the central lines and NG tubes of Section 2.1.19. And it would be tedious to pretend that the author's aversion to recategorising six chapters and forty SAQs played no part in this decision.

The best resources for this would have to be official society statments such as the 2021 Society of Airway Management guideline, or Delphi consensus distillations like Karamchandani et al (2024). Interestingly, the 2025 DAS guidelines casually brush past this concept on their way to "Obesity" and "Human Factors". The reader whose cannot be satisfied by these sources is redirected to the comprehensive Manual of Airway Management in Critical Care by Mosier et al (2024), which elaborates the subject over four hundred pages.

Definition of the physiologically difficult airway

A physiologically difficult airway is loosely defined in the literature as:

"...one in which physiologic derangements place the patient at higher risk of cardiovascular collapse with intubation and conversion to positive pressure ventilation."

- Mosier et al (2015)

"..one in which the patient’s physiological and pathophysiological alterations increase the risk for complications during tracheal intubation and transition to positive pressure ventilation"

- Karamchandani et al (2024)

"Physiologic derangements (which) ... precipitate complications despite first attempt success... (because they) limit the ability to preoxygenate, to maintain oxygenation during intubation, or to tolerate the transition to positive pressure ventilation ... (together with) ...iatrogenic alterations to patient physiology through induction agents and resuscitation strategies"

- 2021 SAM guideline

The reader is invited to add their own definition to the list, in case it is more coherent or descriptive, and for exam purposes it woudl have exactly the same value as the above, because we cannot agree on where to draw the boundaries. At the most fundamental level, a physiologically difficult airway is any physiological problem sufficiently serious that it will destabilise the patient during intubation, even if laryngoscopy is completely straightforward from a technical perspective. That could obviously be just about anything, but the data on post-intubation instability seems to coalesce into common patterns.

Phenotypes of the physiologically difficult airway

Mosier et al (2015) list "hypoxemia, hypotension, severe metabolic acidosis, and right ventricular failure" as four classical tropes of peri-intubation drama. SAM also add raised intracranial pressure, obesity and pregnancy, but removed acidosis, as they felt it was more of a ventilation problem. The college examiners clearly disagree with this, as they included acidosis in the list of things that would characterise an "above standard" answer to Question 5 from the second paper of 2025. That question specifically asked for the "physiological factors that could increase the risk of adverse events during intubation",  for four marks. The answer would have needed some structure, and the examiners remarked that a typical ABCDE format contains "A" which is explicitly not the issue. "A system based or problem-based approach" was clearly better; but in all honesty, the candidate who can summon a system-based or problem-based structure for a question like this is already beyond the need for structural aides. For the rest of us who struggle to stay coherent, to discard BCDE just because A is unsuitable does not make much sense, and one of the suggested structures makes the most of this familiar schema. 

Physiological factors that could increase the risk of adverse events during intubation, in some kind of stupid alphabetical system:

• B - Respiratory
  • Hypoxia 
    • Due to shunt, VQ mismatch, and reduced FRC (shortens the timeframe for a successful attempt)
    • Due to diffusion problems, eg. pulmonary fibrosis (makes the patient intolerant of a brisk increase in cardiac output, which will precipitate hypoxia)
  • High airway resistance (eg. asthma; requires a long expiratory time during BVM)
  • Dynamic hyperinflation (increases risk of cardiovascular collapse)
  • Increased risk from BVM (pneumothorax, abdominal distension)
  • Increased oxygen demand (shortens the available timeframe; obesity, pregnancy, sepsis and thyrotoxicosis fall into this category)
• C- Cardiovascular (this is a big one and could stand to be more subdivided):
  • Rate
    • Dependence on tachycardia for cardiac output (eg. haemorrhagic shock)
    • Dependence on a slow rate for cardiac output (eg. severe aortic stenosis, 
  • Rhythm
    • Dependence on a sinus rhythm (eg. acute severe mitral regurgitation)
    • Propensity to arrhythmias (eg. overdose with an arrhythmogenic agent such as a QT-prolonging or cardiomyopathy-inducing antipsychotic)
  • Contractility
    • Poor ventricular function (increased sensitivity to the cardiodepressant effects of induction agents)
    • Dependence on a hyperdynamic circulation (eg. young septic shock or haemorrhagic shock)
    • Intolerance of increased coronary demand (eg. critical left main stenosis)
  • Preload
    • Dependence on a high sympathetic tone for venous return (eg. haemorrhagic shock)
    • Dependence on positive pressure ventilation  (eg. CPAP) because of pulmonary oedema
  • Afterload
    • Dependence on high afterload for LVOT patency (eg. HOCM, SAM)
    • Intolerance of high afterload due to poor coronary perfusion or valvular incompetence (eg. severe aortic regurgitation, severe mitral regurgitation)
    • Intolerance of an abrupt change in vascular resistance (hypertensive crisis, where the blood pressure should not be allowed to fall precipitously)
  • Right ventricle problems
    • Pulmonary afterload sensitivity (intolerance of hypoxia, hypercapnia, acidosis, low systemic diastolic blood pressure or high positive intrathoracic pressure during intubation)
  • Supply/demand mismatch
    • Increased oxygen consumption (eg. 
• Neurological
  • Raised intracranial pressure (rises further with laryngoscopy)
  • Delirium or aggressive behaviour (reduces the level of cooperation with preoxygenation, and introduces an element of chaos into the team dynamics)
  • Seizures (increases oxygen demand and produces a sympathetic storm state, which abates rapidly with sedation and precipitously depresses the blood pressure)
• Electrolyte and Acid - Base
  • Metabolic or respiratory acidosis (cardiac contractility and sympathetic tone are significantly dependent on the pH-sensitive relationship between catecholamines and their receptors) 
  • Severe electrolyte derangement that promotes arrhythmias
  • Poor choice of muscle relaxant (eg. suxamethonium where the patient is already hyperkalemic)

Another way of looking at this answer would be to adopt a structure that focuses on the Things that Could Go Wrong. The Delphi paper by Karamchandani et al (2024) does exactly this, except they clearly believed that their drab colourless paragraphs could be enlivened by some insultingly posterised art from BioRender.com (because everyone knows that clinicians understand risk better when it is represented by a colourcoded gauge with a needle in the red). Though the paper itself does not ever compile into an easily parsed classification of factors, they unitentionally list them this way when they discuss their mitigating strategies, and that was used to create the structure below. This reads better than ABCDE but it is, admittedly, difficult to summon in an exam.

• Factors that prevent recognition of risk before induction:
  • The intubation is usually an emergency situation (but that's not really a physiological factor? Language or consent barriers, incomplete history, time pressure - these conspire against you, but they are not really "physiological" per se).
• Factors that promote peri-intubation cardiovascular collapse: 
  • Peri-intubation shock state, of whatever cause; but if you had to list them,
    • Hypovolemia
    • Decreased cardiac contractility
    • Sympathetic hypoactivity (eg. spinal injury or epidural)
    • Distributive shock like sepsis, that compensates for vasodilation with a hyperdynamic circulation
    • Obstructive shock, in particular those variants that increase RV afterload
  • Right ventricular dysfunction:
    • Poor RV tolerance for afterload, eg. existing RV failure
    • Already excessive RV afterload, eg. PE or a background of pulmonary hypertension
  • Left ventricular dysfunction:
    • Limitation of supply, eg. severe unrevascularised coronary disease or aortic stenosis
    • Increased demand, eg. hyperdynamic circulatory states like thyrotoxicosis or sympathomimetic overdose
• Factors that interfere with preoxygenation: 
  • Lung disease, eg.  ARDS, pneumonia, pulmonary oedema, atelectasis, pleural effusion, pneumothorax, bronchospasm,  etc etc.
  • Increased work of breathing
  • NIV intolerance
  • Vomiting
  • Delirium (intolerance of everything in general)
  • Decreased level of consciousness sufficiently deep to produce apnoea or ineffective shallow gasping
• Factors that decrease the amount of time available for intubation: 
  • Factors that decrease FRC:
    • Obesity
    • Pregnancy
    • Need to be in a supine position (eg. literally just came off the angiography table)
  • Causes of increased oxygen consumption
    • Fever, sepsis, thyrotoxicosis, malignant hyperthermia (obesity and burns could probably also be listed here)
  • Decreased oxygen delivery capacity
    • Critical anaemia
    • Carbon monoxide poisoning or some other dyshaemoglobinaemia
• Factors that increase the risk of aspiration: 
  • Respiratory muscle fatigue or neuromuscular disease (which will also encourage you to manually bag the patient during RSI, which you ordinarily would not)
  • Bowel obstruction, ileus, pregnancy, etc
  • There are arguments that this is an anatomical difficulty, but one could also argue that aspiration is both due to,  and the cause of, a serious physiological problem (in other words, in both easy and anatomically difficult airways, aspiration could happen equally easily if the physiological conditions are right)
• Factors that interfere with proper positioning:
  • Obesity, pregnancy, kyphoscoliosis (though some might call that an anatomical factor rather than a physiological one, in which case you could argue that it belongs in the "things that prevent preoxygenation" section, as a restrictive lung disease)
  • Profound shock states dependent on a precarious venous return
  • Severe asthma with dynamic hyperinflation (performs best when supine, paradoxically, because the flat position decreases the size of Zone 1; but the patient's instinct is to sit upright to tripod)
• Factors that increase the risk from poor NMJ  blocker choices:
  • hyperkalaemia, denervation or skeletal muscle myopathy, significant burn injury, malignant hyperthermia history, etc. Basically, all the reasons suxamethonium might not be appropriate. 
  • myasthenia gravis

Assessment of the physiologically difficult airway

Similarly to the anatomically difficult airway, some exterior features can be detected even on a casual inspection of the patient (eg. "is that a balloon pump?"), whereas others require a veteran frontliner (someone who's chaired a few Critical Incident Review Meetings) to look at a situation and say, "I see what you're planning here, and it's not going to go well". The latter version is clearly more concerning because the physiological difficulty is therefore a surprise to all involved. Unfortunately, other than going through the checklist of risk factors noted above, nothing more sophisticated exists. A CICM exam candidate may wish to become aware of scoring systems so that they may quote them in vivas:

• HEAVEN: 
  • Hypoxemia (SpO2 ≤ 93% at initial laryngoscopy),
  • Extremes of size,
  • Anatomical challenge,
  • Vomit, blood, or fluid in the airway,
  • Exsanguination
  • Anemia,
  • Neck mobility issues.
  • Basically LEMON with extra steps. 

• MACOCHA: 
  • MAllampati score III or IV (5 points),
  • obstructive sleep Apnoea (2 points),
  • reduced Cervical spine mobility (1 point),
  • Limited mouth Opening <3 cm (1 point),
  • Coma (GCS ≤8) (1 point),
  • severe Hypoxemia (SpO2 <85% on room air) (1 point),
  • non-Anaesthesiologist performing intubation (1 point).
  • Feel free to feed "MORLCHN" into any anagram generator and you will see why they settled on this mnemonic non-initialism.
• CRASH:
  • Consumption (increased oxygen consumption),
  • Right Ventricular Failure,
  • Acidosis (severe metabolic acidosis),
  • Saturation (severe hypoxemia),
  • Hypotension.
• DAPS:
  • An exhausting 12-parameter inventory, almost guaranteed to be applied to situations retrospectively as a forensic tool
  • Respiratory distress,
  • Vomiting,
  • Level of consciousness decreased (GCS < 15)
  • Temperature (fever)
  • Shock with hypotension,
  • Acidosis (pH < 7.3),
  • Delirium, agitation
  • Gender (female)
  • Acidosis
  • Shock index ≥ 0.9,
  • Middle age (age ≥ 45 years),
  • Everybody could see it coming ("anticipated decline due to unstable patient clinical condition")
  • Night shift 
  • so, REVOLT SAD GASMEN could have theoretically been the acronym/mnemonic, but we can all see why they didn't.

Optimisation of the physiologically difficult airway

One could make a strong argument for the avoidance of such an intubation scenario through careful management of a deteriorating patient, such that they arrive at a point where intubation is necessary in a better condition, but many of us do not have that option, whether because we receive the patient from the street in a completely unsorted state, or because we aren't very good at ICU. In either case, rescue strategies can mitigate the risks of intubation, and these are obviously phenotype-specific. The UpToDate article on this is actually an excellent reference for a well-structured approach to handling both assessment and management in one answer, as they give problems and their solutions concurrently as they move through what seems like an A-B-C-E pathway. Mosier, in his haemodynamics chapter from the Manual of Airway Management in Critical Care, also suggests a stepwise approach, which can be summarised as:

1. Fluids
2. Vasopressors
3. Inotropes
4. Non-lethal induction agent choices
5. What if vasopressors and inotropes, but for the RV

 The author will adjust this slightly, integrating and  rearranging the recommendations in order of their expected duration of implementation, starting with the ones that take the longest, and which would therefore need to be addressed first (if time permits). 

Thus:

• Identify and address acidosis with an ABG. pH was independently the most important independent predictor of cardiovascular collapse for the DASH authors, and the interruption of respiratory compensation by apnoea is said to raise your CO₂ by about 10-13 mmHg over the timeframe that it takes for the rocuronium to fully kick in (although everyone who ever writes this is usually referencing a 1961 paper by Eger & Severinghaus). This could produce the kind of drop of pH that could completely uncouple the catecholamine receptors from their ligands, and do many other bad things besides. Though the specific thresholds are probably incredibly individual, one can suggest a pH of 7.20 as the boundary of a danger zone, as patients below this threshold were rather more likely to arrest for Kim et al (2019).
  • Metabolic acidosis should be pre-medicated with IV sodium bicarbonate, with the goal of raising the pH to at least above 7.20, and ideally above 7.30 (because we know it will drop to around 7.20). Because this takes time to arrange and infuse, it should start well beforehand.
  • Respiratory acidosis, if present alongside metabolic, or on its own, will probably frustrate the effectiveness of bicarbonate, as every 100 mmol of bicarbonate can potentially dissociate into 100 mmol of CO₂ gas, which is about 2.5L (equating to ~150 breaths, or ~13 min of normal minute volumes). In this scenario, ventilation is the thing that needs to improve. Scala et al (2005) were said to have found that patients who were trialed on NIV prior to intubation had a better post-intubation pH, though on inspection, their paper does not mention this (and it hardly seems applicable as the mean duration of ventilation was 4 days). In any case, NIV takes time to work, so this should be an early priority.
• Identify and address shock.
  • The same ABG, and the unpleasant act of hunting for the thready pulse to get the ABG, will have informed the clinician about the shock state, whether by clinical acumen or by lactate. In either case the situation should be dealt with, but if time permits, a POCUS assessment of the heart should be performed so that the three main phenotypes can be distinguished, those being:
  • LV failure
  • RV failure
  • Hypovolemia
  • One cannot overestimate the value of a bedside TTE to rapidly conclude on these, as without it one would be entirely blind to whole classes of shock differentials. Unless the crashing patient is already in the ICU and fully instrumented with advanced haemodynamic monitoring, there's probably no better option for a rapid assessment of cardiac function and volume status.  
• Intuitively, the management of these states follows:
  • Fluid resuscitation is almost always the solution for hypovolemia, where by "fluid" we loosely mean anything ranging from blood and clotting factors to crystalloid. In the ED one must also consider the possibility that the LV/RV failure patient is also presenting with some relative hypovolemia. Wrinkling of the usually oedematous skin of the legs will be a clue that they have lost some of their usually expanded volume. 
  • Noradrenaline preemptively is a good idea even if the shock state is not really vasoplegic. The role this plays is mostly in defending coronary perfusion during intubation. As the diastolic pressure drops in response to the induction agents, the loss of coronary perfusion will decrease the cardiac output, and with it the venous return will also become sluggish. Therefore, any vasoactive agents given peripherally into this sort of circulation will not reach the heart before it stops. On this basis, one may argue that starting them well before induction is the key. There is no shame in having a higher MAP than 65 during this critical period, and most reasonable people would agree that a primed and running infusion of a low-dose vasopressor at this exact moment can really hold the room together.
  • Inotropes preemptively and/or reactively should be prepared, because noradrenaline alone may not be sufficient if the cause of shock is truly an extremely poor cardiac function;  in which case one should prepare both an infusion to run concurrently, and generous boluses to accompany the induction agents. "Generous" for adrenaline is obviously going to be determined by where the patient is on the spectrum between alive (1mcg boluses) and deceased (1mg boluses). The specific choice of agent will be
  • RV management  could consist of pulmonary vasodilators (UpToDate authors mention "nitric oxide bled into the circuit") or diuresis if the POCUS shows septal flattening, but realistically, one often does not have the time for these to be arranged, or to take effect. The maintenance of good coronary flow and the prevention of hypoxia and control of acidosis are therefore the most important elements of reducing RV afterload and maintaining RV contractility. Which brings us to:
• Preoxygenation is something that requires careful attention, and the most recent data from Gibbs et al (2024) and Pitre et al (2025) suggests that NIV is superior to HFNP, and HFNP are superior to standard techniques (including, potentially, the heroic end-of-bed mastery of holding the manual bag-valve-mask to the struggling patient's face). 
• Choice of induction agents will be dictated by the situation, but under most circumstances, a small amount of ketamine is the agent of choice in countries where etomidate is not available. Even the dose of an agent usually described as "cardiostable" still needs to be reduced, particularly as none of them are genuinely "stable" (eg. ketamine has a direct cardiodepressant effect which is revealed under the exact circumstances when the sympathetic nervous system is silenced with acidosis and sedatives).

The last point calls for some deliberation.

The induction agents for a patient who cannot afford to lose sympathetic activation

That describes a large number of patients who would fall into the "physiologically difficult" category because most of the ways in which one might become "physiologically difficult" involve severe systemic insults that tend to horrify the autonomic nervous system. Consider the abovelisted phenotypes: haemorrhagic shock, cardiogenic shock, obstructive shock, severe acidosis (because shocked) - these are all different variations on the theme of circulatory incompetence, a state that should naturally produce a forceful sympathetic response. The sympathetic nervous system, in this situation, is an ally; and the induction agent choice should seek to preserve, or at least replace, its life-sustaining cardiovascular effects. This is unfortunate, because most of the agents we use to sedate patients will decrease the activity of the sympathetic nervous system along with the higher functions of consciousness. The best one can do is pick an agent which has the least sympatholytic effect, or at least no intrinsic cardiodepressant effects.

Etomidate  is thought to be the most cardiostable agent, but one must take into account the fact that the usual induction dose will turn off steroid synthesis for 24-48 hrs, and that it is not completely free of haemodynamic effects. In the RSI trial (2025), etomidate caused haemodynamic collapse in merely 17% of patients (defined as systolic BP <65 mmHg). So, not in 100%, but also not 0%. A much more important caveat is that it is simply not available in Australia, except as a component of illegal vapes. 

Ketamine is the next best thing locally, but again is not completely free from haemodynamic side effects (in the same RSI trial, the rate of haemodynamic collapse was 22% with ketamine). 

Anything but with sympathomimetics is a valid alternative, where the user excuses their sedation choices by co-administering something like adrenaline pre-emptively with the expectation that the patient is preparing a profound haemodynamic flop. Abdullah & Leena (2021) presented a case series of such inductions (10-20 mcg of adrenaline was given; most of the patients were induced with etomidate). The authors did not report any adverse events, but one must contemplate the possibility that this was purely a happy accident, considering that the dose of pre-emptive agent is a complete guess on the part of the clinician and could just as easily be a factor-of-ten underdose as it could be a factor-of-ten overdose, depending on how well or how poorly one has read the haemodynamic scenario. Readers preparing to use their own judgment should be encouraged by the thought that this idea is sufficiently mainstream that serious people are writing systematic reviews about it. Practices listed in that review vary along the lines of:

• push dose adrenaline (10-20 mcg)
• push dose phenylephrine (~200 mcg)
• pre-intubation noradrenaline infusion if the diastolic pressure is <35 mmHg

On the other hand, Ho & Mizubuti (2019) had nothing good to say about this practice, although the discussion revolved more around the routine use of this technique with frail and elderly patients, rather than anyone genuinely "physiologically difficult". 

Nothing, or very little, is surprisingly considered as an option in a large number of situations. One may remark, looking over the peri-arrest patient about to be intubated, that the patient is already mostly comatose, and that there is no point in making them even more comatose (because how much more comatose do you want?) Following from this, one may take the stance that, if survival is the objective goal and there are no convenient/immediate methods to offer the patient the usual perilaryngoscopy comforts, then one should focus on preserving life, and offer them postlaryngoscopy apologies instead. Colloquially referred to as the "sux and sorry" induction, this method has a surprising number of proponents, a league largely held together by the belief that the preservation of life is a goal that justifies waiving all other moral imperatives, or that post-procedural amnestic agents like midazolam will help the patient forget the faces of their rescuers and make it harder to describe them to the police after the incident.

That belief is probably not wrong, but the practice itself probably is, on some fundamental level; as most people would agree that giving muscle relaxant to patients who have a reasonable chance of being aware is monstrously evil. Tshering et al (2024) recorded a 24% incidence of such intubations in their Emergency department, but the practice was limited to patients being intubated during a cardiac arrest, and the authors hastened to add that ketamine or benzodiazepine infusions followed, though they do not report following up to understand whether the practice ablated all recall of the experience. Similarly, Graham et al (2003) and Jarvis et al (2025) report the drugless airway instrumentation was considered justified only in severely brain injured or unconscious cardiac arrest patients as an expedient means of handling their airway protection, rather than as some sort of oversight or a deliberate haemodynamic strategy.

On the other hand,  Weingart et al (2013) report the genuinely nightmarish finding that over 50% (and possibly as few as 25%) of all intubations in US emergency departments between 2006 and 2009 had no documented anaesthetic agents. "Our study is consistent with prior studies", the authors deplored. Mayberry et al (2021) points out that consciousness during CPR is common enough that even patients in cardiac arrest should not be spared sedation; "it takes minimal time to draw up an anaesthetic to complement paralysis", they admonish, pointing to the finding that ~2% of cardiac arrest survivors can recall details from their own resuscitation. Moreover, it appears that the amnestic effects of midazolam are mostly anterograde, and one cannot reliably expect a uniquely traumatic event to be wiped from the memory of a survivor with a post-hoc dose of sedation.

The induction agents for a patient who cannot afford to gain sympathetic activation

The other potential physiologically difficult phenotype is the patient whose sympathetic nervous system is not an ally, and where it is in fact desirable to suppress it. The variants of this include:

• The patient with raised intracranial pressure
• The patient with an unstable acute aortic syndrome, fragile intracerebra anaurysm, or some other kind of pressure-sensitive vascular surgical catastrophe.
• The patient with critical proximal coronary artery stenosis

And surely many others, because the number of situations when one does not want an excess of blood pressure peri-intubation is certainly larger than the auther's patience with his own imagination. The key features that unite these phenotypes are:

• A lower blood pressure would be acceptable (as the current blood pressure is already too high)
• A higher blood pressure would be unacceptable
• Tachycardia is undesirable

Fortunately, this is a much more familar pathway, as hypertension and tachycardia are the usual responses to laryngoscopy, which are entirely reflexive, and which can be modified with a range of agents, of which the best practiced would probably be opioids like fentanyl. An extremel;y fentanyl-heavy induction is therefore favoured. This is a technique older than most of the readers, described in the 1980s, eg Dahlgren & Messeter (1981) and Payne et al (1988). The doses described by these early pioneers ranged from 5mcg/kg to 50mcg/kg (that's right, a 5000 mcg bolus for a 100-kg ASA-III patient);  the reason such excesses were left in the 1980s was because they genuinely tended to depress LV function. These days a more modest dose ceiling of ~10 mcg/kg (i.e 600-1000 mcg) seems to be the more common practice.