A key component in the planning of intubation is pre-oxygenation. Recently apnoeic oxygenation during laryngoscopy has been adopted too. These are just two components of an overall oxygenation strategy to consider when intubating the critically ill. Some patients will require proactive preparation of the components of successful post-intubation oxygenation, especially those with severe lung pathology like ARDS.
Here’s a handy list of things to consider when planning a peri-intubation oxygenation strategy. Some people like their airway stuff to begin with ‘P’, so I’ve obliged:
‘Traditional’ rapid sequence induction of anaesthesia is often described with inclusion of cricoid pressure and the strict omission of any artifical ventilation between paralytic drug administration and insertion of the tracheal tube. These measures are aimed at preventing pulmonary aspiration of gastric contents although there is no convincing evidence base to support that. However it is known that cricoid pressure can worsen laryngoscopic view and can occlude the paediatric airway. We also know that children desaturate quickly after the onset of apnoea, and although apnoeic diffusion oxygenation via nasal cannula can prevent or delay that, in some cases it may be preferable to bag-mask ventilate the patient while awaiting full muscle relaxation for laryngoscopy.
A Swiss study looked at 1001 children undergoing RSI for non-cardiac surgery. They used a ‘controlled rapid sequence induction and intubation (cRSII)’ approach for children assumed to have full stomachs. This procedure resembled RSI the way it is currently done in many modern critical care settings, including the retrieval service I work for:
- No cricoid pressure
- Ketamine for induction if haemodynamically unstable
- A non-depolarising neuromuscular blocker rather than succinylcholine
- No cricoid pressure
- Gentle facemask ventilation to maintain oxygenation until intubation conditions achieved
- Intubation with a cuffed tracheal tube
- Still no cricoid pressure
The authors comment:
The main finding was that cRSII demonstrated a considerably lower incidence of oxygen desaturation and consecutive hemodynamic adverse events during anesthesia induction than shown by a previous study on classic RSII in children. Furthermore, there was no incidence of pulmonary aspiration during induction, laryngoscopy, and further course of anesthesia.
Looks like more dogma has been lysed, and this study supports the current trajectory away from traditional teaching towards an approach more suitable for critically ill patients.
Controlled rapid sequence induction and intubation – an analysis of 1001 children
Paediatr Anaesth. 2013 Aug;23(8):734-40
BACKGROUND: Classic rapid sequence induction puts pediatric patients at risk of cardiorespiratory deterioration and traumatic intubation due to their reduced apnea tolerance and related shortened intubation time. A ‘controlled’ rapid sequence induction and intubation technique (cRSII) with gentle facemask ventilation prior to intubation may be a safer and more appropriate approach in pediatric patients. The aim of this study was to analyze the benefits and complications of cRSII in a large cohort.
METHODS: Retrospective cohort analysis of all patients undergoing cRSII according to a standardized institutional protocol between 2007 and 2011 in a tertiary pediatric hospital. By means of an electronic patient data management system, vital sign data were reviewed for cardiorespiratory parameters, intubation conditions, general adverse respiratory events, and general anesthesia parameters.
RESULTS: A total of 1001 patients with cRSII were analyzed. Moderate hypoxemia (SpO2 80-89%) during cRSII occurred in 0.5% (n = 5) and severe hypoxemia (SpO2 <80%) in 0.3% of patients (n = 3). None of these patients developed bradycardia or hypotension. Overall, one single gastric regurgitation was observed (0.1%), but no pulmonary aspiration could be detected. Intubation was documented as ‘difficult’ in two patients with expected (0.2%) and in three patients with unexpected difficult intubation (0.3%). The further course of anesthesia as well as respiratory conditions after extubation did not reveal evidence of ‘silent aspiration’ during cRSII.
CONCLUSION: Controlled RSII with gentle facemask ventilation prior to intubation supports stable cardiorespiratory conditions for securing the airway in children with an expected or suspected full stomach. Pulmonary aspiration does not seem to be significantly increased.
Comments Off on Atropine for Paediatric RSI?
In some areas it has been traditional to pre-medicate or co-medicate with atropine when intubating infants and children, despite a lack of any evidence showing benefit. It is apparently still in the American Pediatric Advanced Life Support (PALS) Provider Manual when age is less than 1 year or age is 1–5 years and receiving succinylcholine. However it is not recommended with rapid sequence intubation in the British and Australasian Advanced Paediatric Life Support manual and course.
A French non-randomised observational study compares intubations with and without atropine in the neonatal and paediatric critical care setting. Atropine use was associated with significant acceleration of heart rate, and no atropine use was associated with a higher incidence of new dysrhythmia, the most common being junctional rhythm, but with none appearing to be clinically significant.
The incidence of the most important peri-intubation cause of bradycardia – hypoxia – is not reported. It is also not clear how many intubation attempts were required. The authors admit:
“it is not possible using our methodology to deduce whether bradycardia was due to hypoxia, laryngoscopy, or sedation drugs.“
Actual rapid sequence was rarely employed – their use of muscle relaxants was low – making this difficult to extrapolate to modern emergency medicine / critical care practice.
My take home message here is that this study provides no argument whatsoever for the addition of atropine in routine RSI in the critically ill child. Why complicate a procedure with an unnecessary tachycardia-causing drug when the focus should be on no desat / no hypotension / first look laryngoscopy?
The Effect of Atropine on Rhythm and Conduction Disturbances During 322 Critical Care Intubations
Pediatr Crit Care Med. 2013 Jul;14(6):e289-97
OBJECTIVES: Our objectives were to describe the prevalence of arrhythmia and conduction abnormalities before critical care intubation and to test the hypothesis that atropine had no effect on their prevalence during intubation.
DESIGN: Prospective, observational study.
SETTING: PICU and pediatric/neonatal intensive care transport.
SUBJECTS: All children of age less than 8 years intubated September 2007-2009. Subgroups of intubations with and without atropine were analyzed.
MEASUREMENT AND MAIN RESULTS: A total of 414 intubations were performed in the study period of which 327 were available for analysis (79%). Five children (1.5%) had arrhythmias prior to intubation and were excluded from the atropine analysis. Atropine was used in 47% (152/322) of intubations and resulted in significant acceleration of heart rate without provoking ventricular arrhythmias. New arrhythmias during intubation were related to bradycardia and were less common with atropine use (odds ratio, 0.14 [95% CI, 0.06-0.35], p < 0.001). The most common new arrhythmia was junctional rhythm. Acute bundle branch block was observed during three intubations; one Mobitz type 2 rhythm and five ventricular escape rhythms occurred in the no-atropine group (n = 170). Only one ventricular escape rhythm occurred in the atropine group (n = 152) in a child with an abnormal heart. One child died during intubation who had not received atropine.
CONCLUSIONS: Atropine significantly reduced the prevalence of new arrhythmias during intubation particularly for children over 1 month of age, did not convert sinus tachycardia to ventricular tachycardia or fibrillation, and may contribute to the safety of intubation.
By Norwegian intensivist/anaesthetist/HEMS Physician Dr Per Bredmose.
[Warning – Rant level: Viking]
Etomidate has for a long time been known in some countries as the “drug of choice” for RSI in unstable/fragile patients. This is due to the fact that induction with etomidate is fairly cardiovascularly stable. However, there is a down side: a subsequent suppression of adrenal function. This was initially discovered after etomidate was used for sedation infusions on ICU.
It has for a long time been debated whether this is a side effect with clinical implications after a single dose induction… and yes it has.
A recent Japanese study demonstrates this(1). This is a large propensity based study. Now, propensity based statistics are pretty complex to explain. In short, it is an advanced method to strengthen the statistics when comparing groups in non-cross over studies.
In this study 2616 patients receiving etomidate for induction and a volatile agent for maintenance are included.
This showed an increased OR for 30-days mortality with a factor of 2.5 and 1.5 times greater chance for a major cardiovascular event in hospital. Interestingly enough, there were no significant differences in either perioperative vasopressor use or infections complications during hospital stay.
What does this mean?
In my mind and experience, it strengthens the fact that there is no wonder drug. And also that there seems to be a reason for why etomidate is de-registered in many countries.
Also, it tells me that for a safe prehospital RSI we need physicians capable of clinical judgment and “decision making” to tailor an (any) induction agent to the specific individual patient. In my mind, there is no room for an etomidate-only (dose / weight) induction protocol!
1. Komatsu R, You J, Mascha EJ, Sessler DI, Kasuya Y, Turan A.
Anesthetic induction with etomidate, rather than propofol, is associated with increased 30-day mortality and cardiovascular morbidity after noncardiac surgery.
Anesth Analg. 2013 Dec;117(6):1329-37
There was a jam-packed line up for the Pre-hospital and Air Ambulance Day which was Co-hosted by the Norwegian Air Ambulance Foundation.
My highlights were:
Dr Rasmus Hesselfeldt works in Denmark where they have a pretty good EMS system with ambulances, RRV’s and PHC doctors. Road conditions are good with the longest travel distance of 114 miles. So would the introduction of a HEMS service improve outcomes? He did an observational study looking at year of data post-trial and compared this with 5 months pre-trial. Trauma patients with ISS > 15 and medical emergencies greater than 30 min by road to the Trauma Centre (TC). Primary endpoint was time to TC, secondary outcomes were number of secondary transfers and 30 day mortality.
Results: Increase in on scene time 20 min vs 28 min, time to hospital increased but time to TC was less – 218 min vs 90 min, reduced mortality, increased direct transfer to TC and fewer secondary transfers.
Full article here: A helicopter emergency medical service may allow faster access to highly specialised care. Dan Med J. 2013 Jul;60(7):A4647
Prof Dan Davis ran through pre-hospital intubation. It seems that this man has spent his life trying to perfect airway management. Peter Rosen was his mentor and imprinted on him that RSI is the cornerstone of airway management.
So surely pre-hospital intubation saves lives. The evidence however begs to differ, or does it? As with all evidence we need to consider the validity of the results and luckily Prof Davis has spent a lot of time thinking through the reasons why there no evidence.
During his research he opened a huge can of worms:
1. Hyperventilation was common – any EtCO2 <30mmHg lead to a doubling in mortality.
2. First pass intubation is great, but not if you let your patient become hypoxic or hypotension or worse still both!
3. Hospital practice had similar issues.
So really the RSI processes he was looking at weren’t great.
The good news is that things have improved and he can now boast higher first pass rates and lower complication rates for his EMS system. His puts this success down to training.
The AIRPORT study was discussed at last years LTC. This year we have the results. 21 HEMS services in 6 countries were involved in the data collection including GSA HEMS. The headline findings are that intubation success rates are high (98%) with a complication rate of 10-12%. The more difficult airways were seen in the non-trauma group. 28.2% patients died (mainly cardiac arrest).
Matt Thomas reported on REVIVE – a pre-hospital feasibility study looking at airway management in OHCA (I-Gel vs LMA Supreme vs standard care). It was never powered to show a difference in these groups, the main aim was to see if research in this very challenging area was possible. And the answer is YES. The paramedics involved recruited more patients than expected and stuck to the protocol (prob better that docs would have!). A randomised controlled trial to look at the I-Gel vs ETT is planned.
Finally, Pre-hospital Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA) seems eminently possible – Dr Nils Petter Oveland showed us the training manikin they developed for training. Through training on this manikin they achieved an average skin to balloon time of 3.3mins. Animal data supports this procedure as a bridge to definitive care in non compressible haemorrhage.
London HEMS will be starting (P)REBOA in the New Year.
So now it’s stand up science, I’m off for my glass of wine…………….
Check out what they’re saying about the London Trauma Conference on Twitter
A 79 year old previously well female presents with loss of consciousness, having been found unresponsive by her daughter who saw her well one hour previously.
Examination reveals a GCS of E1V2M3 = 6 and reactive pupils with no lateralising signs. She is hypertensive. A VBG reveals a normal glucose and sodium and a pCO2 of 60 mmHg (7.9 kPa).
The emergency physician’s plan is to intubate and get a CT scan of her brain. This is explained to the daughter.
A no-brainer? You’d think so.
A consistent issue that recurs during discussions with UK emergency medicine colleagues is that of having to rely on anaesthesia and/or ICU colleagues for intubation of their patients in the ED. The pain comes not from disagreeing about who does the procedure or what drugs to use, but rather on the decision to intubate.
The refusal to intubate can stall or halt a resuscitation plan, delay care, result in risky transfers to the imaging suite, and even deny potential outcome-improving therapy (for example post-ROSC cooling). It can undermine team leadership and disrupt the team dynamic.
There are often different ways to ‘skin a cat’ and it is frequently helpful to invite the opinion of other critical care specialists. However, it is clear from multiple discussions with frustrated EM colleagues that the decision not to intubate is often influenced by non-clinical factors, most often ICU bed availability. Other times, it appears to be that the ‘gatekeeper’ to airway care (and to ICU beds) does not share the same appreciation of the clinical issues at stake. Examples here include the self-fulfilling pessimism post-ROSC based on inappropriate assignment of predictive value to neurological signs, and the assumption of non-treatable pathology in elderly patients presenting with coma.
The obvious solution to this is that the responsibility for managing the ‘A’ of ABC should not be delegated to non-emergency medicine personnel. Sadly, this is not achievable 24/7 in all UK departments right now for a number of awkward reasons.
So what’s a team leader to do when faced with a colleague’s refusal to intubate? The best approach would be to gently and politely persuade them to change their mind by stating some clinical facts that enable a shared mental model and agreed management plan, and to ensure the most senior available physicians are participating in the discussion.
Sometimes that fails. What next? Here’s a suggestion. This is slightly tongue-in-cheek but take away from it what you will.
It is imperative that the individual declining intubation appreciates the gravity of his or her decision. They must not be under the impression that they’ve done you (and the patient) a favour by giving their opinion after an ‘airway consult’. They have declined a resuscitative intervention requested by the emergency medicine team leader and should appreciate the consequences of this decision and the need to document it as such.
Perhaps say something along the lines of:
And here’s the form. It is provocative, cheeky, and in no way should really be used in its current form:
The noxious stimulus of laryngoscopy & tracheal intubation can precipitate hypertension, tachycardia, and intracranial pressure elevation, risking exacerbation of brain injury or haemorrhage. Physicians from an English Helicopter Emergency Medical Service examined the response of heart rate and blood pressure to prehospital rapid sequence intubation (RSI). While a retrospective study, the haemodynamic data were prospectively recorded and documented using standard monitor printouts, and time of intubation could be accurately determined by the onset of capnography recordings. Their standardised system documents blood pressure recordings every three minutes. Etomidate and suxamethonium were used for RSI.
They report their findings:
A hypertensive response occurred in 79% (70/89) of patients. MAP exceeded the upper limit of estimated intact cerebral autoregulation (150 mmHg) in 18% (16/89) of cases and 9% (8/89) of patients had a greater than 100% increase in MAP and/or SBP. A single hypotensive response occurred. A tachycardic response occurred in 58% (64/110) of patients and bradycardia was induced in one.
Of note, 97 of the 115 patients had injuries that included head trauma.
The authors note that opioids are often co-administered during in-hospital RSI and that this may offset the haemodynamic stimulation, while possible increasing the complexity of the procedure in the prehospital environment. They have modified their pre-hospital anaesthesia standard operating procedure to include the use of an opioid and will report the associated outcomes and complication rates ‘in due course’.
This is interesting and important stuff, and something we should all be looking at in our respective prehospital critical care services.
The haemodynamic response to pre-hospital RSI in injured patients
Injury. 2013 May;44(5):618-23
BACKGROUND: Laryngoscopy and tracheal intubation provoke a marked sympathetic response, potentially harmful in patients with cerebral or cardiovascular pathology or haemorrhage. Standard pre-hospital rapid sequence induction of anaesthesia (RSI) does not incorporate agents that attenuate this response. It is not known if a clinically significant response occurs following pre-hospital RSI or what proportion of injured patients requiring the intervention are potentially at risk in this setting.
METHODS: We performed a retrospective analysis of 115 consecutive pre-hospital RSI’s performed on trauma patients in a physician-led Helicopter Emergency Medical Service. Primary outcome was the acute haemodynamic response to the procedure. A clinically significant response was defined as a greater than 20% change from baseline recordings during laryngoscopy and intubation.
RESULTS: Laryngoscopy and intubation provoked a hypertensive response in 79% of cases. Almost one-in-ten patients experienced a greater than 100% increase in mean arterial pressure (MAP) and/or systolic blood pressure (SBP). The mean (95% CI) increase in SBP was 41(31-51) mmHg and MAP was 30(23-37) mmHg. Conditions leaving the patient vulnerable to secondary injury from a hypertensive response were common.
CONCLUSIONS: Laryngoscopy and tracheal intubation, following a standard pre-hospital RSI, commonly induced a clinically significant hypertensive response in the trauma patients studied. We believe that, although this technique is effective in securing the pre-hospital trauma airway, it is poor at attenuating adverse physiological effects that may be detrimental in this patient group.
A score to predict difficulty of intubation in ICU patients underwent derivation and validation in French ICUs. The main predictors included Mallampati score III or IV, obstructive sleep apnoea syndrome, reduced mobility of cervical spine, limited mouth opening, severe hypoxia, coma, and where the operator was a nonanesthesiologist.
The striking thing is the overall rate of difficult intubations, defined as three or more laryngoscopy attempts or taking over 10 minutes using conventional laryngoscopy(!) and the high rate of severe complications.
The incidence of difficult intubation was 11.3% (113 of 1,000 intubation procedures) in the original cohort and 8% (32 of 400 intubation procedures) in the validation cohort.
In the development cohort, overall complications occurred in 437 of 1,000 intubation procedures (43.7%), with 381 (38.1%) severe complications (26 cardiac arrests, 2.6%; five deaths, 0.5%; 274 severe collapses, 27.4%; 155 severe hypoxemia, 15.5%) and 112 (11.2%) moderate complications (15 agitations, 1.5%; 32 cardiac arrhythmias, 3.2%; 23 aspirations, 2.3%; 48 esophageal intubations, 4.8%; six dental injuries, 0.6%).
There is no comment on incidence of propofol use for induction; I was tempted to speculate whether it was implicated in any of the cardiac arrests – something we observe time and again in the critically ill – but the authors state: “The drugs used for intubation, in particular neuromuscular blockers, did not differ between groups… However, midazolam use was more frequent in case of difficult intubation.“
Capnography was used only in 46% of intubations, and there was no mention of checklist use. It is fascinating how some aspects of airway management that might be considered minimum and basic safety standards in some practice settings are not yet routine in other specialties or locations.
An interesting study, from which one of the take home messages for me has to be a resounding ‘Yikes!’.
Early Identiﬁcation of Patients at Risk for Difﬁcult Intubation in the Intensive Care Unit
Am J Respir Crit Care Med. 2013 Apr 15;187(8):832-9
Rationale: Difficult intubation in the intensive care unit (ICU) is a challenging issue.
Objectives: To develop and validate a simplified score for identifying patients with difficult intubation in the ICU and to report related complications.
Methods: Data collected in a prospective multicenter study from 1,000 consecutive intubations from 42 ICUs were used to develop a simplified score of difficult intubation, which was then validated externally in 400 consecutive intubation procedures from 18 other ICUs and internally by bootstrap on 1,000 iterations.
Measurements and Main Results: In multivariate analysis, the main predictors of difficult intubation (incidence = 11.3%) were related to patient (Mallampati score III or IV, obstructive sleep apnea syndrome, reduced mobility of cervical spine, limited mouth opening); pathology (severe hypoxia, coma); and operator (nonanesthesiologist). From the β parameter, a seven-item simplified score (MACOCHA score) was built, with an area under the curve (AUC) of 0.89 (95% confidence interval [CI], 0.85-0.94). In the validation cohort (prevalence of difficult intubation = 8%), the AUC was 0.86 (95% CI, 0.76-0.96), with a sensitivity of 73%, a specificity of 89%, a negative predictive value of 98%, and a positive predictive value of 36%. After internal validation by bootstrap, the AUC was 0.89 (95% CI, 0.86-0.93). Severe life-threatening events (severe hypoxia, collapse, cardiac arrest, or death) occurred in 38% of the 1,000 cases. Patients with difficult intubation (n = 113) had significantly higher severe life-threatening complications than those who had a nondifficult intubation (51% vs. 36%; P < 0.0001).
Conclusions: Difficult intubation in the ICU is strongly associated with severe life-threatening complications. A simple score including seven clinical items discriminates difficult and nondifficult intubation in the ICU.
A large single-centre study in an academic tertiary care center emergency department (where residents perform most of the intubations) examined 1,828 orotracheal intubations, of which 1,333 were intubated successfully on the ﬁrst attempt (72.9%).
Adverse events (AE) captured were oesophageal intubation, oxygen desaturation, witnessed aspiration, mainstem intubation, accidental extubation, cuff leak, dental trauma, laryngospasm, pneumothorax, hypotension, dysrhythmia, and cardiac arrest.
When the ﬁrst pass was successful, the incidence of AEs was 14.2%. More than one attempt was associated with signiﬁcantly more AEs. Patients requiring two attempts had 33% more AEs (47.2%) and as the number of attempts increased, so did the risk of AEs, with the largest increase in AEs occurring between an unsuccessful ﬁrst attempt and the second intubation attempt.
This is a powerful argument in favour of optimising first pass success. In the prehospital service I work for, We like to include this in a ‘first pass, no desat, no hypotension’ package that includes team simulation training, pre-intubation briefing, checklist use, optimisation of position, ketamine induction (and avoidance of propofol), apnoeic oxygenation, bougie use, bimanual laryngoscopy, and waveform capnography.
The Importance of First Pass Success When Performing Orotracheal Intubation in the Emergency Department
Academic Emergency Medicine 2013;20(1):71–78, Free Full Text
Objectives The goal of this study was to determine the association of first pass success with the incidence of adverse events (AEs) during emergency department (ED) intubations.
Methods This was a retrospective analysis of prospectively collected continuous quality improvement data based on orotracheal intubations performed in an academic ED over a 4-year period. Following each intubation, the operator completed a data form regarding multiple aspects of the intubation, including patient and operator characteristics, method of intubation, device used, the number of attempts required, and AEs. Numerous AEs were tracked and included events such as witnessed aspiration, oxygen desaturation, esophageal intubation, hypotension, dysrhythmia, and cardiac arrest. Multivariable logistic regression was used to assess the relationship between the primary predictor variable of interest, first pass success, and the outcome variable, the presence of one or more AEs, after controlling for various other potential risk factors and confounders.
Results Over the 4-year study period, there were 1,828 orotracheal intubations. If the intubation was successful on the first attempt, the incidence of one or more AEs was 14.2% (95% confidence interval [CI] = 12.4% to 16.2%). In cases requiring two attempts, the incidence of one or more AEs was 47.2% (95% CI = 41.8% to 52.7%); in cases requiring three attempts, the incidence of one or more AEs was 63.6% (95% CI = 53.7% to 72.6%); and in cases requiring four or more attempts, the incidence of one or more AEs was 70.6% (95% CI = 56.2.3% to 82.5%). Multivariable logistic regression showed that more than one attempt at tracheal intubation was a significant predictor of one or more AEs (adjusted odds ratio [aOR] = 7.52, 95% CI = 5.86 to 9.63).
Conclusions When performing orotracheal intubation in the ED, first pass success is associated with a relatively small incidence of AEs. As the number of attempts increases, the incidence of AEs increases substantially.
I ‘jumped ship’ from etomidate to ketamine for rapid sequence intubation (RSI) in sick patients about seven years ago. Good thing too, since I later moved to Australia where we don’t have etomidate. I’ve been one of the aggressive influences behind my prehospital service’s switch to ketamine as the standard induction agent for prehospital RSI. It’s no secret that I think propofol has no place in RSI in the critically ill.
I love ketamine for its haemodynamic stability compared with other induction agents. In fact, I very rarely see a drop in blood pressure when I use it for RSI even in significantly shocked patients. One should however try to remain open to evidence that disconfirms ones biases, lest we allow science to be replaced by religion. I therefore was interested to read a report of two cases of cardiac arrest following the administration of ketamine for rapid sequence intubation (RSI)(1).
The first case was a 25 year old with septic shock due to an intestinal perforation, with a respiratory rate of 30 ‘labored’ breaths per minute and hypoxaemia prior to intubation with 2mg/kg ketamine who became bradycardic and then had a 10-15 minute PEA arrest after ketamine administration (but prior to intubation). Pre-arrest oxygen saturation and pre-induction blood gases are not reported.
The second case was an 11 year old with septic shock and pneumonia, hypoxaemia, and a severe metabolic acidosis. She arrested with bradycardia then a brief period of asystole one minute after receiving 2.4 mg/kg ketamine with rocuronium for intubation.
Was the ketamine responsible for the arrests? Ketamine usually exhibits a stimulatory effect on the cardiovascular system, through effects which are incompletely understood but include a centrally mediated sympathetic response and probable inhibition of norepinephrine (noradrenaline) reuptake. However ketamine can have a direct depressant effect on cardiac output which is usually overridden by the sympathetic stimulation. In critically ill severely stressed patients the depressant effect may predominate. In a study on 12 critically ill surgical patients, haemodynamic indices were measured using pulmonary artery catheters within 5 minutes of ketamine administration (at a mean of 70 mg)(2). Six patients demonstrated decreases in ventricular contractility, and four had decreases in cardiac output. Mean arterial blood pressure decreased in four patients. The authors commented:
The patients..were septic, hypovolemic, or cirrhotic, and had severe stress preoperatively. It is possible that in these ill patients adrenocortical and catechol stores had been depleted prior to ketamine administration. Alternatively, in the setting of prolonged preoperative stress, there may be resistance to further sympathetic and/or adrenocotical stimulation by ketamine. In either case, preoperative stress may blunt the usual physiologic responses to ketamine, setting the stage for possible adverse effects.
The negative cardiovascular effects of ketamine may also be precipitated by larger doses or repeated doses of ketamine(3).
While this small case series of cardiac arrest following ketamine administration is interesting, we should bear in mind the other possible precipitants of arrest in these patients, which are not all discussed by the authors:
i) Both patients were hypoxaemic prior to induction and their peri-intubation oxygen saturations are not reported. Arrests following bradycardia at the time of induction in the critically ill are frequently related to hypoxaemia.
ii) The second patient had a severe metabolic acidosis and the first – an abdominal sepsis patient with a labored respiratory rate of 30 – very probably did too. A failure to match a patient’s compensatory respiratory alkalosis with hyperventilation after anaesthesia is known to precipitate arrest in acidaemic patients.
iii) Finally, if the ketamine was responsible for the arrests, one should consider that the doses given to these shocked and highly unstable patients were well in excess of what many of us would recommend, and doses in the range of 0.5-1 mg/kg might not have been associated with adverse effects.
The takehome points for me are that this report is a helpful reminder that the cardiovascular stimulation-inhibition balance of ketamine may be altered by severe critical illness, and that doses of any induction agent should be significantly reduced in the critically ill patient. In no way does this convince me that I should discard ketamine as my preferred choice for RSI in such patients.
1. Cardiac Arrest Following Ketamine Administration for Rapid Sequence Intubation
J Intensive Care Med. 2012 May 29. [Epub ahead of print]
Given their relative hemodynamic stability, ketamine and etomidate are commonly chosen anesthetic agents for sedation during the endotracheal intubation of critically ill patients. As the use of etomidate has come into question particularly in patients with sepsis, due to its effect of adrenal suppression, there has been a shift in practice with more reliance on ketamine. However, as ketamine relies on a secondary sympathomimetic effect for its cardiovascular stability, cardiovascular and hemodynamic compromise may occur in patients who are catecholamine depleted. We present 2 critically ill patients who experienced cardiac arrest following the administration of ketamine for rapid sequence intubation (RSI). The literature regarding the use of etomidate and ketamine for RSI in critically ill patients is reviewed and options for sedation during endotracheal intubation in this population are discussed.
2. Cardiovascular effects of anesthetic induction with ketamine
Anesth Analg. 1980 May;59(5):355-8
Anesthetic induction with ketamine has been reported to maintain or improve cardiovascular performance in severely ill patients. Using invasive cardiovascular monitoring, we studied physiologic responses to a single dose of ketamine in 12 critically ill patients. Six patient demonstrated decreases in ventricular contractility, and four had decreases in cardiac output. Mean arterial blood pressure decreased in four patients. Pulmonary venous admixture increased in four of six patients, while oxygen consumption decreased in eight of 11 patients. Thus, a single dose of ketamine produced decreases in cardiac and pulmonary performance and in peripheral oxygen transport in this group of patients. It is proposed that in severely ill patients, preoperative stress may alter the usual physiologic responses to ketamine administration, and adverse effects may predominate. Ketamine, therefore, should be used with caution for induction of anesthesia in critically ill and in acutely traumatized patients until additional studies and further information on cardiovascular responses to ketamine are available.
3. A comparison of some cardiorespiratory effects of althesin and ketamine when used for induction of anaesthesia in patients with cardiac disease
Br J Anaesth. 1976 Nov;48(11):1071-81
Cardiorespiratory effects of ketamine and Althesin were measured in two groups of premedicated patients with cardiac disease. The drugs were given in clinically equivalent doses with a second dose administered about 10 min after induction. The first dose of ketamine caused a marked increase in systemic and pulmonary arterial pressure, heart rate, and central venous and wedge pressures and cardiac index. The first dose of Althesin caused a decrease in systemic arterial pressure, central venous pressure, cardiac index and heart work, but little change in heart rate. The second dose of induction agent was administered before the cardiorespiratory effects of the initial dose had resolved. The second dose of Althesin caused changes similar to those following the first dose, but less marked. The changes following the second dose of ketamine were opposite to those following the first dose.