RSI haemodynamics in the field

May 18, 2013 by  
Filed under All Updates, EMS, ICU, Kids, Resus, Trauma

intubated-prehosp-vol-iconThe 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.

Comments

4 Responses to “RSI haemodynamics in the field”

  1. Minh Le Cong on May 18th, 2013 14:26

    thanks Cliff. I have not really noticed much of a hypertensive response to RSI when using ketamine as induction. Certainly not as much as noted in this study where etomidate used. I must admit..since using ketamine as my main induction RSI agent for several years now..I rarely need or think I need to give fentanyl or morphine pre or peri RSI.

    what has been your observation in your own practice?

  2. Cliff on May 18th, 2013 14:34

    I just emailed Karel, Anthony and Brian about the same question!

    I said: “We should really look to see if this is replicated with our use of ketamine. I wouldn’t be surprised either way. The temptation is to assume it is, but we don’t know unless we look.”

    I haven’t noticed a similar response after ketamine, and we also use 3 minute obs cycles.

    But it could be confirmation bias, since I am a card-carrying member (and Chapter Leader) of the KetaMinh Kult.

    A bit like the propofol fans who don’t notice their patients keep arresting on induction.

  3. Minh Le Cong on May 18th, 2013 14:48

    LOL…I am glad the recent awake FOI did not harm your frontal lobe ;-)
    its not a bad idea for a retrospective study in fact in all seriousness!

    I just know doing our ketamine retrieval sedation registry audit..its very uncommon for a hypertensive red flag to be seen in our cases..and we do a lot of them! And sometimes our total doses ( over whole retrieval) far exceed RSI induction doses

    I have not done a prehosp RSI with propofol in about 2 years and even then I still wonder why I did it?!

  4. Yen Chow (@TBayEDguy) on May 18th, 2013 22:17

    Even in the very hypertensive patient, I wonder if ketamine would really add that much fuel to the fire or is it just a drop in the ocean? Do you run more risk with crashing the BP with a full dose of propofol? Do you risk having a bad airway attempt and inadequate induction with using midazolam and spike your ICP, BP / risk hypoxia hypoventilation even more? Etomidate is not available much and though we used to have it in our shop but it never seems to be around lately.

    A good study would be helpful at least in the routine intubations with full dose ketamine.

    Anecdotally, I don’t recall it being a concern with past intubation with full dose K whereas I do recall with procedural sedation analgesia with ketamine noting tachycardic responses. Are our emergency intubation patients just a different kettle of fish with ++sympathetic overload already that ketamine does not really do much in addition?

    Is the ketamine retrieval data published? It would be great to be able to review and reference data in the literature.