blunt the haemodynamic respon from laryngoscopy and endotracheal intubation

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17 January 2014 No. 02BLUNTING THE INTUBATION RESPONSE: FACT OR FICTION

K PurchaseModerator: C Evans

Discipline of AnaestheticsCONTENTS4MECHANISM OF THE INTUBATION RESPONSE

7BLUNTING THE HAEMODYNAMIC RESPONSE

7LIGNOCAINE

8OPIOIDS

10 2 AGONISTS

11 BLOCKERS

12MAGNESIUM SULPHATE (MGSO4)

13NOVEL IDEAS

15SUMMARY OF EVIDENCE

17BENEFITS OF ATTENUATING THE RESPONSE

20CONCLUSION

21REFERENCES

OBJECTIVES Discuss the mechanism of the intubation response Explore the various pharmacological methods to attenuate the intubation the response Attempt to determine the benefits of blunting the intubation responseBLUNTING THE INTUBATION RESPONSE: FACT OR FICTION

INTRODUCTIONLaryngoscopy and tracheal intubation are noxious stimuli associated with a transient increase in autonomic response. King et al described this response more than 60 years ago.(1)It is most often associated with an increase in heart rate and blood pressure and is thought to be of little consequence in the healthy individual but could be deleterious in the vulnerable patient.(2) This response varies with depth of anaesthesia, duration and difficulties during laryngoscopy and intubation, and certain patient factors including history of diabetes(3) and cardiovascular disease(4)(5)

MECHANISM OF THE INTUBATION RESPONSE

Basic anatomy:

Figure 1: the sensory innervation of the airways(6)

The pharynx: sensory innervation Glossopharyngeal nerve supplies the posterior third of the tongue, the fauces and tonsillae, anterior epiglottis and all parts of the pharynx with visceral sensory bers.Motor innervation- the pharynx receives efferent supply from the vagus nerve through its pharyngeal branch.(6)The larynx: sensory innervation the internal laryngeal nerve, branch of the superior laryngeal nerve, provides sensory supply from the posterior epiglottis to the vocal cords. The recurrent laryngeal nerve supplies the larynx below the vocal cords and the trachea.

Motor innervation: the recurrent laryngeal nerve supplies all intrinsic muscles of the larynx except the cricothyroid muscles. (6)

Figure 2: innervation of the larynx (7)

Simply put, with regards to sensory innervation, the oropharynx, posterior third of the tongue and anterior part of the epiglottis are supplied by glossopharyngeal. The posterior epiglottis and distal airway structures are supplied by branches of the vagus nerve.

Mechanism of the intubation response

The precise mechanism of the intubation response (IR) is elusive but it has been established that it has both a sympathetic and parasympathetic element. The effect is transient occurring 30 seconds after intubation and lasting for less than 10 minutes thereafter.(8) The sympathetic response is a polysynaptic pathway with the glossopharyngeal and vagus nerve forming the afferent arc to the sympathetic nervous system via the brain stem and spinal cord. This ensures a diffuse autonomic response at the efferent side including increased firing of the cardio-accelerator fibres and release of adrenergic mediators including norepinephrine, epinephrine and vasopressin. The net effect of this autonomic surge is an increased Blood pressure (BP), heart rate (HR), pulmonary artery wedge pressure and decreased ejection fraction.The parasympathetic reflex is monosynaptic and more common in children but can occur in some adults. The reflex is mediated by increased vagal tone at the SA node. (2)The haemodynamic response to laryngeal and endo- tracheal intubation (LETI) is transient and in most patients thought to be of little consequence. In patients with coronary artery disease (CAD), hypertension, raised intra cranial or intra ocular pressure it may be associated with myocardial ischaemia, infarction, arrhythmias, cardiac failure, pulmonary oedema and cerebral haemorrhage. (5)The process of intubation comprises of different phases and these affect the haemodynamic response differently. Orotracheal intubation consists of 2 phases: direct laryngoscopy and passing of endotracheal tube through the vocal cords and trachea. (9)Four studies looked at this differential effect. Sing(9), Shinji(10) and Hassan(11) concur that tracheal intubation and cuff inflation produce a substantial haemodynamic effect, significantly greater than laryngoscopy alone. Shribman(12) however found that orotracheal intubation did not significantly contribute to the haemodynamic effect. These studies give the impression that greatest increase in HR occurs during LETI and greatest increase in BP occurs during laryngoscopy.

With no active attempt at blunting this haemodynamic response, increases in SBP of 41-53 mmHg, HR 20-23 and MAP of up to 100% above baseline have been documented.(1)(13)BLUNTING THE HAEMODYNAMIC RESPONSE

The possibilities to offset or blunt the intubation response are numerous. Options include pharmacological, peripheral blocks and variations in techniques including various blades and conduits for intubations.

This booklet will only focus on pharmacological techniques.

Pharmacological options:

Local anaesthetics

Opioids

2 agonists

2 blockers

MgSO4 Gabapentin, pregabalin

LIGNOCAINE:

The effectiveness of lignocaine to blunt the intubation response (IR) is contentious. Numerous studies dating from 1960 have looked at different doses, timing and routes of administering Lignocaine. From the discussion above on the nerve supply of the larynx and the effect that tracheal intubation has on the IR it is apparent why laryngeal tracheal routes will not entirely blunt the response.(14)(15)

Hamill et al and Laurito et al both looked at the IV route of Lignocaine to blunt the response to LETI.

Hamill (14) used a dose of 1.5mg/kg, ivi 1minute prior to LETI and compared this to 4ml of a 4% solution sprayed laryngealtracheally. The group that received topical lignocaine sustained significant increase in HR and BP after LETI that lasted for more than 2 minutes. The authors note that the IV route did not completely attenuate the response as there was still significant increase in BP and HR although only sustained for 1 minute or less. Laurito et al(16) compared IV Lignocaine (2mg/kg) 1 minute pre LETI to nebulized lignocaine 4mg/kg 15 minutes prior to LETI. Within each group all haemodynamic variables increased significantly. With mean arterial pressures of 140mmHg recorded.

Miller et al(17) also failed to demonstrate that Lignocaine attenuates the haemodynamic response to LETI. They studied Lignocaine 1.5mg ivi given 1,2 and 3 minutes prior to LETI. Sklar et al (18)found that aerosol application of lignocaine 120mg was effective in attenuating the both the BP and HR response in adults. This was applied for 5 minutes duration and 8.5 min prior to induction.

Various other studies support the use of Lignocaine 1,5mg/kg ivi given between 2-4 minutes to attenuate the response. Tam et al(19) and Splinter et al(20) could only demonstrate benefit with regards to the BP response, however Helfman(21) found a dose of 1,5 mg/kg, given 2 minutes prior to LETI, to blunt both the BP and HR response.

The principal limitation when comparing studies is heterogeneity of the studies. Various doses, timings, pre medications and induction agents are used.

At best, intra venous Lignocaine will occasionally blunt the BP response and almost never the HR response. If administered it should be at a dose of 1,5mg/kg, 3 minutes prior to intubation.(2)

Topical routes are not effective in blunting the intubation response and few studies have shown convincing benefit of the aerosol route.(22)OPIOIDS

The addition of opioids deepens the level of anaesthesia and therefor decreases the sympathetic outflow.

Alfentanil: numerous studies show that a dose of 30g/kg given between 1.5 and 2 minutes prior to intubation provides complete attenuation of the haemodynamic response.(23)(24)(25)(26)Lower dosages, 15g/kg, seem to attenuate the BP response but not the HR response.(26)In the elderly 10g/kg given 3-4 minutes pre induction has also been shown to completely blunt the haemodynamic response.(27)Higher dosages have been associated with bradycardia and hypotension.(23)Few studies distinguish between hypertensive and non-hypertensive patients. Only Miller(25) et al used patients from ASA 1-3 stages but did not specify the reason for the staging.

A dose of Alfentanil 10g/kg given over 30 seconds has been suggested to be effective in blunting the cardiovascular effect in hypertensive patients on long term treatment. In this study 3/20 patients developed hypotension requiring Ephedrine.(28)Remifentanil:

The rapid onset and short duration of Remifentanil makes it an attractive drug for attenuating the IR.

Thompson et al(29) initially found that a dose of 1g/kg followed by and infusion of 0.5g/kg/min attenuated the haemodynamic response in healthy adults. This dose was associated with profound bradycardia and hypotension in half the patients.

A subsequent study(30) indicated that 0.5g/kg followed by an infusion of 0.25g/kg/min was as effective in blunting the response with no incidence of bradycardia or hypotension requiring treatment. They also indicate that at the higher doses, pre-treatment with glycopyrrolate 200g, decreases the incidence of side effects.

Maguire et al (28)demonstrated that a bolus dose of 0.5g/kg followed by infusion at 0.1g/kg/min effectively reduces the response to LETI in hypertensive patients on treatment. Of note is that all patients were pre-treated with glycopyrrolate 200 g. None of the patients developed a bradycardia but 7/20 patients required rescue medication for hypotension. (SBP 80-100 mmHG).