RSI haemodynamics in the field

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.

Awake intubation

I had some fun today getting intubated.

We used the Ambu aScope 2 and the Greater Sydney Area HEMS equipment and approach to airway management. I didn’t receive an antisialogogue or any analgesia or sedation.

The big learning point for me was how hard it was to anaesthetise the posterior part of my nasal cavity and nasopharynx. I thought the worst part would be any stimulation of my vocal cords or trachea with lidocaine or instrumentation, but this really was fine. Nebulised 2% lidocaine (the strongest concentration we have), atomised lidocaine (using a mucosal atomiser), and co-phenylcaine spray weren’t sufficient. I can see why people use pastes or gel to maintain mucosal contact while the lidocaine takes effect, but we don’t have those (yet). The best solution came from hooking up oxygen tubing to an iv cannula via a three way tap. Oxygen was run through at 2 l/min and lidocaine injected via the the three way tap. This enabled an atomised spray to be directed right onto the area concerned, and made the insertion of the nasotracheal tube more tolerable – although still unpleasant.

crazed-nutter-sm

The fact I could be intubated awake with reasonable topicalisation suggests most patients should tolerate it perhaps after even an analgesic dose of ketamine, eg. 30-40 mg in an adult. I suspect full dissocation would not be required, which is good for cooperation (“stick your tongue out sir”). I appreciate there are better agents, such as remifentanil or dexmedetomidine, but my area of interest is the retrieval setting – where I have neither the luxury of using these agents nor that of calling for anaesthetic back up.

Thanks to HEMS physicians Emily Stimson, Nirosha De Zoysa, Felicity Day, Chloe Tetlow, and Fergal McCourt for making it fun and safe.

Here’s the video:

Twitter has been helpful in gathering some advice, particularly from @DocJohnHinds:

Difficult intubation on ICU

icu-intub-iconA 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.

Intranasal ketamine for kids – 1mg / kg?

A small pilot study on a convenience sample of children presenting to the emergency department with acute limb injury pain evaluated the use of intranasal ketamine(1).

Initial dose averaged 0.84 mg/kg and a third of the patients required a top up dose at 15 minutes, resulting in a total dose of about 1.0 mg/kg to provide adequate analgesia by 30 min for most patients. The authors suggest that this could guide investigators on an appropriate dose of IN ketamine for use in clinical trials.

Adverse events were all transient and mild.

Prior to administration, the ketamine was diluted with saline to a total volume of 0.5 mL and was administered as 0.25 mL per nare using a Mucosal Atomiser Device (MAD, Wolfe Tory Medical, Salt Lake City, UT, USA). According to the protocols in my Service, this device requires 0.1 ml to prime its dead space(2). It is unclear whether this factor may have affected the total dose delivered to the patient in this study.

1. Sub-dissociative dose intranasal ketamine for limb injury pain in children in the emergency department: A pilot study
Emerg Med Australas. 2013 Apr;25(2):161-7


OBJECTIVE: The present study aims to conduct a pilot study examining the effectiveness of intranasal (IN) ketamine as an analgesic for children in the ED.

METHODS: The present study used an observational study on a convenience sample of paediatric ED patients aged 3-13 years, with moderate to severe (≥6/10) pain from isolated limb injury. IN ketamine was administered at enrolment, with a supplementary dose after 15 min, if required. Primary outcome was change in median pain rating at 30 min. Secondary outcomes included change in median pain rating at 60 min, patient/parent satisfaction, need for additional analgesia and adverse events being reported.

RESULTS: For the 28 children included in the primary analysis, median age was 9 years (interquartile range [IQR] 6-10). Twenty-three (82.1%) were male. Eighteen (64%) received only one dose of IN ketamine (mean dose 0.84 mg/kg), whereas 10 (36%) required a second dose at 15 min (mean for second dose 0.54 mg/kg). The total mean dose for all patients was 1.0 mg/kg (95% CI: 0.92-1.14). The median pain rating decreased from 74.5 mm (IQR 60-85) to 30 mm (IQR 12-51.5) at 30 min (P < 0.001, Mann-Whitney). For the 24 children who contributed data at 60 min, the median pain rating was 25 mm (IQR 4-44). Twenty (83%) subjects were satisfied with their analgesia. Eight (33%) were given additional opioid analgesia and the 28 reported adverse events were all transient and mild.


CONCLUSIONS: In this population, an average dose of 1.0 mg/kg IN ketamine provided adequate analgesia by 30 min for most patients

2. Case report: prehospital use of intranasal ketamine for paediatric burn injury
Emerg Med J. 2011 Apr;28(4):328-9


In this study, the administration of an intravenous ketamine formulation to the nasal mucosa of a paediatric burn victim is described in the prehospital environment. Effective analgesia was achieved without the need for vascular or osseous access. Intranasal ketamine has been previously described for chronic pain and anaesthetic premedication. This case highlights its potential as an option for prehospital analgesia.

Predicting volume responsiveness

IVCiconOne of the current Holy Grails of ED critical care is to find a reliable measure of fluid responsiveness in those patients with impaired organ perfusion, such as those with severe sepsis. This would enable us to identify those patients whose cardiac output would be improved by fluid therapy, and avoid subjecting ‘non-responders’ to the risks associated with fluid overload. Thanks to the uptake of early goal-directed therapy in sepsis, under-resuscitation is now much less common in the ED. However a growing evidence base reveals the dangers of over-resuscitation. We have a responsibility to optimise fluid therapy as best we can with the equipment we have, according to the latest evidence.

Inferior Vena Cava Ultrasound
Some tests of fluid responsiveness rely on the effect of respiration-induced changes in pleural pressure on the circulation. Inferior vena cava (IVC) size and degree of inspiratory collapse correlate with central venous pressure (CVP), but CVP is not a reliable predictor of volume status or responsiveness. Skinny, collapsing IVCs detected on ultrasound suggest volume responsiveness, but the lack of this finding does not exclude fluid responsiveness. IVC size and measurement can be affected by patient position, probe position, and a variety of health states from athleticism to increased abdominal pressure.

Pulse Pressure Variation
Respiratory pulse pressure variation derived from an arterial line trace in mechanically ventilated patients who are adequately sedated and receiving large tidal volumes can predict fluid responsiveness too. Variability in tidal volume, the presence of spontaneous breathing activity in a ventilated patient, and cardiac dysrhythmia can all confound the usefulness of this method.

End expiratory occlusion
Another test in mechanically ventilated patients is the end expiratory occlusion test. A positive pressure inspiratory breath cyclically decreases the left cardiac preload. Occluding the circuit at end-expiration prevents this cyclic impediment in left cardiac preload and acts like a fluid challenge. A 15 second expiratory occlusion is performed and an increase in pulse pressure or (if you can measure it) cardiac index predicts fluid responsiveness with a high degree of accuracy. The patient must be able to tolerate the 15 second interruption to ventilation without initiating a spontaneous breath.

Passive Leg Raise
Passive leg raising (PLR) involves measuring cardiac output (or its surrogate, velocity-time integral, or VTI) before and after tilting the semirecumbent patient supine and raising the legs to 45 degrees. This ‘autotransfuses’ blood from the lower limbs to the core and acts as a reversible fluid challenge. An increase in VTI identifies fluid responders. It would be nice if a PLR-induced increase in blood pressure revealed the answer, but BP does not reliably inform us of changes in cardiac output.

All these tests have limitations. Pulse pressure variation fails in patients with low respiratory system compliance, such as is found in ARDS(1). End-expiratory occlusion and PLR work in low respiratory system compliance, but the former still requires mechanical ventilation, and the latter requires a means of estimating cardiac output or a surrogate – oesophageal Doppler, the velocity-time integral measured by transthoracic echocardiography, and femoral artery flow (measured by arterial Doppler) have all been used. Non-invasive cardiac output monitors that are not operator dependent exist, such as the NICOM(TM) bioreactance device. Bioreactance cardiac output measurement is based on an analysis of relative phase shifts of an oscillating current that occurs when this current traverses the thoracic cavity. Its advantages are that it is noninvasive, it does not require endotracheal intubation or an arterial line, and it provides a good estimate of stroke volume in patients with atrial fibrillation.

A recent study evaluating the combination of PLR with NICOM(TM) bioreactance monitoring revealed that another tool could indicate volume responsiveness: an increase in carotid blood flow after PLR, as measured by carotid Doppler flow imaging(2). A threshold increase in carotid Doppler flow imaging of 20% for predicting volume responsiveness had a sensitivity and specificity of 94% and 86%, respectively. This was studied in a heterogenous group of hemodynamically unstable patients, suggesting applicability to the kind of patients who present to the ED, although numbers were small so more validation is required.

End-tidal carbon dioxide
End-tidal carbon dioxide (ETCO2) levels depend on cardiac output. Increasing cardiac output with a fluid challenge or PLR increases ETCO2,as long as ventilatory and metabolic conditions remain stable. In a recent small study, a PLR-induced increase in ETCO2 ≥ 5 % predicted a fluid-induced increase in cardiac index ≥ 15 % with sensitivity of 71 % (95 % confidence interval: 48-89 %) and specificity of 100 (82-100) %(3). The maximal effects of PLR on CI and ETCO2 were observed within 1 min.

So what can I use?
In summary, differentiating fluid responders from non-responders in the ED remains a challenge. The method used depends on available equipment and expertise, and whether the patient is spontaneously breathing or mechanically ventilated. The NICOM(TM) shows great promise but until your department can afford one, ultrasound is the way to go; small collapsing IVCs suggest fluid responders. Learning to measure a VTI on transthoracic echo or carotid Doppler flow will help you assess the response to a PLR in spontaneously ventilating patients. If they’re mechanically ventilated, then looking for an ETCO2 rise after PLR could be a simpler alternative.

Fluid responsiveness assessment – options in the Emergency Department

Inferior Vena Cava Ultrasound
Helpful if skinny / large degree of respirophasic collapse – suggests fluid responsive – ventilated or spontaneous breathing

Passive Leg Raise
Good in ventilated or spontaneous breathing patients; need to measure cardiac output or a surrogate, such as VTI (echo), NICOM(TM), carotid Doppler flow, or ETCO2 (if ventilation and metabolic status constant)

Pulse Pressure Variation
Requires full mechanical ventilation; no good if low respiratory compliance / disturbed heart-lung interaction

End expiratory occlusion
Requires mechanical ventilation and patient tolerance of 15 seconds of apnoea. Acts like a passive leg raise so need a measure of cardiac output or surrogate

 
I look forward to more studies on these modalities, and to trying some of them in the resus room at every available opportunity.

 

1. Passive leg-raising and end-expiratory occlusion tests perform better than pulse pressure variation in patients with low respiratory system compliance
Crit Care Med. 2012 Jan;40(1):152-7


OBJECTIVES: We tested whether the poor ability of pulse pressure variation to predict fluid responsiveness in cases of acute respiratory distress syndrome was related to low lung compliance. We also tested whether the changes in cardiac index induced by passive leg-raising and by an end-expiratory occlusion test were better than pulse pressure variation at predicting fluid responsiveness in acute respiratory distress syndrome patients.

DESIGN: Prospective study.

SETTING: Medical intensive care unit.

PATIENTS: We included 54 patients with circulatory shock (63 ± 13 yrs; Simplified Acute Physiology Score II, 63 ± 24). Twenty-seven patients had acute respiratory distress syndrome (compliance of the respiratory system, 22 ± 3 mL/cm H2O). In nonacute respiratory distress syndrome patients, the compliance of the respiratory system was 45 ± 9 mL/cm H2O.

MEASUREMENTS AND MAIN RESULTS: We measured the response of cardiac index (transpulmonary thermodilution) to fluid administration (500 mL saline). Before fluid administration, we recorded pulse pressure variation and the changes in pulse contour analysis-derived cardiac index induced by passive leg-raising and end-expiratory occlusion. Fluid increased cardiac index ≥ 15% (44% ± 39%) in 30 “responders.” Pulse pressure variation was significantly correlated with compliance of the respiratory system (r = .58), but not with tidal volume. The higher the compliance of the respiratory system, the better the prediction of fluid responsiveness by pulse pressure variation. A compliance of the respiratory system of 30 mL/cm H2O was the best cut-off for discriminating patients regarding the ability of pulse pressure variation to predict fluid responsiveness. If compliance of the respiratory system was >30 mL/cm H2O, then the area under the receiver-operating characteristics curve for predicting fluid responsiveness was not different for pulse pressure variation and the passive leg-raising and end-expiratory occlusion tests (0.98 ± 0.03, 0.91 ± 0.06, and 0.97 ± 0.03, respectively). By contrast, if compliance of the respiratory system was ≤ 30 mL/cm H2O, then the area under the receiver-operating characteristics curve was significantly lower for pulse pressure variation than for the passive leg-raising and end-expiratory occlusion tests (0.69 ± 0.10, 0.94 ± 0.05, and 0.93 ± 0.05, respectively).

CONCLUSIONS: The ability of pulse pressure variation to predict fluid responsiveness was inversely related to compliance of the respiratory system. If compliance of the respiratory system was ≤ 30 mL/cm H2O, then pulse pressure variation became less accurate for predicting fluid responsiveness. However, the passive leg-raising and end-expiratory occlusion tests remained valuable in such cases.

2. The use of bioreactance and carotid doppler to determine volume responsiveness and blood flow redistribution following passive leg raising in hemodynamically unstable patients
Chest. 2013 Feb 1;143(2):364-70


BACKGROUND: The clinical assessment of intravascular volume status and volume responsiveness is one of the most difficult tasks in critical care medicine. Furthermore, accumulating evidence suggests that both inadequate and overzealous fluid resuscitation are associated with poor outcomes. The objective of this study was to determine the predictive value of passive leg raising (PLR)- induced changes in stroke volume index (SVI) as assessed by bioreactance in predicting volume responsiveness in a heterogenous group of patients in the ICU. A secondary end point was to evaluate the change in carotid Doppler fl ow following the PLR maneuver.

METHODS: During an 8-month period, we collected clinical, hemodynamic, and carotid Doppler data on hemodynamically unstable patients in the ICU who underwent a PLR maneuver as part of our resuscitation protocol. A patient whose SVI increased by . 10% following a fluid challenge was considered a fluid responder.

RESULTS: A complete data set was available for 34 patients. Twenty-two patients (65%) had severe sepsis/septic shock, whereas 21 (62%) required vasopressor support and 19 (56%) required mechanical ventilation. Eighteen patients (53%) were volume responders. The PLR maneuver had a sensitivity of 94% and a specificity of 100% for predicting volume responsiveness (one false negative result). In the 19 patients undergoing mechanical ventilation, the stroke volume variation was 18.0% 5.1% in the responders and 14.8% 3.4% in the nonresponders ( P 5 .15). Carotid blood fl ow increased by 79% 32% after the PLR in the responders compared with 0.1% 14% in the nonresponders ( P , .0001). There was a strong correlation between the percent change in SVI by PLR and the concomitant percent change in carotid blood fl ow ( r 5 0.59, P 5 .0003). Using a threshold increase in carotid Doppler fl ow imaging of 20% for predicting volume responsiveness, there were two false positive results and one false negative result, giving a sensitivity and specificity of 94% and 86%, respectively. We noted a significant increase in the diameter of the common carotid artery in the fluid responders.

CONCLUSIONS: Monitoring the hemodynamic response to a PLR maneuver using bioreactance provides an accurate method of assessing volume responsiveness in critically ill patients. In addition, the study suggests that changes in carotid blood fl ow following a PLR maneuver may be a useful adjunctive method for determining fluid responsiveness in hemodynamically unstable patients.

3. End-tidal carbon dioxide is better than arterial pressure for predicting volume responsiveness by the passive leg raising test
Intensive Care Med. 2013 Jan;39(1):93-100


PURPOSE: In stable ventilatory and metabolic conditions, changes in end-tidal carbon dioxide (EtCO(2)) might reflect changes in cardiac index (CI). We tested whether EtCO(2) detects changes in CI induced by volume expansion and whether changes in EtCO(2) during passive leg raising (PLR) predict fluid responsiveness. We compared EtCO(2) and arterial pulse pressure for this purpose.

METHODS: We included 65 patients [Simplified Acute Physiology Score (SAPS) II = 57 ± 19, 37 males, under mechanical ventilation without spontaneous breathing, 15 % with chronic obstructive pulmonary disease, baseline CI = 2.9 ± 1.1 L/min/m(2)] in whom a fluid challenge was decided due to circulatory failure and who were monitored by an expiratory-CO(2) sensor and a PiCCO2 device. In all patients, we measured arterial pressure, EtCO(2), and CI before and after a fluid challenge. In 40 patients, PLR was performed before fluid administration. The PLR-induced changes in arterial pressure, EtCO(2), and CI were recorded.

RESULTS: Considering the whole population, the fluid-induced changes in EtCO(2) and CI were correlated (r (2) = 0.45, p = 0.0001). Considering the 40 patients in whom PLR was performed, volume expansion increased CI ≥ 15 % in 21 “volume responders.” A PLR-induced increase in EtCO(2) ≥ 5 % predicted a fluid-induced increase in CI ≥ 15 % with sensitivity of 71 % (95 % confidence interval: 48-89 %) and specificity of 100 (82-100) %. The prediction ability of the PLR-induced changes in CI was not different. The area under the receiver-operating characteristic (ROC) curve for the PLR-induced changes in pulse pressure was not significantly different from 0.5.

CONCLUSION: The changes in EtCO(2) induced by a PLR test predicted fluid responsiveness with reliability, while the changes in arterial pulse pressure did not.