LIST OF ABBREVIATIONS
α – Alpha
ASA – American
Society of Anaesthesiologists bpm – Beats per minute
DBP – Diastolic
Blood Pressure HR – Heart rate
Inj – Injection
iv – Intravenous
kg – Kilogram
L/hr – litre/hour
MAC – Minimum
Alveolar Concentration MAP – Mean
Arterial Pressure
mcg – Microgram.
mg – Milligram
min – Minute
ml – Millilitre
pH – Negative logarithm of hydrogen ion concentration pka – Dissociation constant
PVC - Premature
Ventricular Contraction SBP – Systolic Blood Pressure
sec – Second
SpO 2 – Oxygen
saturation in blood.
Tab – Tablet
yrs – Years
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ABSTRACT
Laryngoscopy and tracheal intubation provoke cardiovascular, and
autonomic responses. This response is primarily because of sympatho-adrenal
stimulation that increases the myocardial oxygen demand, which may be
detrimental in comorbid patients. Attenuation of significant increase in blood
pressure and heart rate decreases the risk
of complications.
Many methods have been employed to blunt these responses and most
commonly used being intravenous lignocaine and topical anaesthesia of pharynx,
larynx and trachea.
In view of it, the present study was undertaken to evaluate and compare
the effects of 2% Lignocaine 2mg/kg nebulization given 10 minutes and 2%
Lignocaine 2mg/kg iv given 90 seconds before induction for the intubation response.
Materials & Methods:
90 ASA Grade I & II patients in the age group 18-45 years of either
sex scheduled for elective surgeries under general anaesthesia were recruited
for the study.
They were allocated into three groups, Group C, Group I, Group N with the
sample size of 30 in each. Group I received 2% lignocaine 2mg/kg intravenous
90sec and Group N received nebulization with 2% lignocaine 2mg/kg 10 minute
before induction.
In all patients general anaesthesia was administered. Heart rate,
systolic and diastolic blood pressure and mean arterial pressure, SpO2,
and ECG were recorded, basal values and subsequently at 1st, 2nd,
3rd, 5th, 7th, 9th, 11th
and 15th minute after intubation. Inj Glycopyrrolate and Fentanyl iv
for analgesia which was avoided earlier, so as to avoid their effects on
intubation response was given after the recordings.
Results:
It was noted that, in control group, the rise of heart
rate (HR), Systolic blood pressure (SBP), Diastolic blood pressure (DBP), Mean
arterial in pressure (MAP) were found to be
23.4 bpm, 42.6
mm Hg, 25.36 mm Hg, 29.44 mm Hg respectively. Group I, the rise of HR, SBP, DBP, MAP were found to be 18 bpm, 20.54
mm Hg, 13.84 mm Hg, 16.1 mm Hg respectively. In Group N, the rise of HR, SBP,
DBP, MAP were found to be 24.86 bpm, 32.26 mm Hg, 24.83 mm Hg, 27.3 mm Hg respectively.
Thus it was seen that use of lignocaine has suppressed heart rate and
blood pressure changes to laryngoscopy and endotracheal intubation. In fact
intravenous lignocaine has better suppressing property than nebulization of
lignocaine
KEYWORDS: Laryngoscopy,
endotracheal intubation; Cardiovascular response; Lignocaine, intravenous,
nebulization.
CONTENTS
|
Sl.No. |
|
Page no |
|
1 |
INTRODUCTION |
1 |
|
2 |
OBJECTIVES OF THE STUDY |
3 |
|
3 |
ANATOMICAL ASPECTS |
4 |
|
4 |
PHYSIOLOGY OF PRESSOR RESPONSE |
11 |
|
5 |
PHARMACOLOGY OF
LIGNOCAINE |
15 |
|
6 |
REVIEWOF LITERATURE |
22 |
|
7 |
METHODOLOGY |
35 |
|
8 |
OBSERVATIONS AND RESULTS |
40 |
|
9 |
DISCUSSION |
54 |
|
10 |
CONCLUSION |
65 |
|
11 |
SUMMARY |
66 |
|
12 |
BIBLIOGRAPHY |
68 |
|
13 |
ANNEXURES PROFORMA MATER CHART |
75 |
|
TABLE No. |
TITLE |
PAGE No. |
|
1 |
Table showing Age distribution |
41 |
|
2 |
Table showing Sex distribution |
42 |
|
3 |
Table showing Weight distribution |
43 |
|
4 |
Table showing Nature of Surgical
procedures |
44 |
|
5 |
Table showing changes in Mean Heart
Rate |
45 |
|
6 |
Table showing
changes in Mean Systolic Blood Pressure (SBP) |
47 |
|
7 |
Table showing changes in Mean Diastolic
Blood Pressure (DBP) |
49 |
|
8 |
Table showing changes in Mean Arterial
Pressure (MAP) |
51 |
|
9 |
Table showing changes in Mean
Saturation of Oxygen (SpO2) |
53 |
|
Figure No. |
Details |
Page No |
|
1 |
Entrance to larynx (posterior view) |
5 |
|
2 |
View of larynx during laryngoscopy |
7 |
|
3 |
Sympathetic supply to heart and lungs |
12 |
|
4 |
Photograph showing administration of
Nebulization |
39 |
|
5 |
Photograph showing CompAir Compressor
Nebulizer NE-C28 and Injection Lignocaine 2%. |
39 |
|
6 |
Graph showing Age
distribution |
41 |
|
7 |
Graph showing Sex distribution |
42 |
|
8 |
Graph showing Weight distribution |
43 |
|
9 |
Graph showing changes in Mean Heart
Rate (HR) |
45 |
|
10 |
Graph showing changes in Mean Systolic
Blood Pressure (SBP) |
47 |
|
11 |
Graph showing changes in Mean Diastolic
Blood Pressure (DBP) |
49 |
|
12 |
Graph showing changes in Mean Arterial Pressure
(MAP) |
51 |
|
13 |
Graph showing changes in Mean
Saturation of Oxygen (SpO2) |
53 |
INTRODUCTION
The major responsibility of an anaesthesiologist is
the management of airway to provide adequate ventilation to the patient by
securing airway during general anaesthesia. As such, no anaesthesia is safe
unless diligent efforts are devoted to maintain an intact functional airway.
Endotracheal intubation is the overall accepted, “Gold standard of securing the airway and
providing adequate ventilation.” However, endotracheal intubation requires
time, a skilled anaesthesiologist, appropriate instruments and adequate circumstances with respect to space and
illumination
Direct laryngoscopy and endotracheal intubation
following induction of anaesthesia is almost always associated with hemodynamic
changes due to reflex sympathetic discharge caused by epipharyngeal and
laryngopharyngeal stimulation.1 This increased sympatho-adrenal
activity may result in hypertension, tachycardia and arrhythmias.2,3,4
This increase in blood pressure and heart rate are usually transitory, variable
and unpredictable. Transitory hypertension and tachycardia are probably of no
consequence in healthy individuals5 but either or both may be
hazardous to patients with hypertension, myocardial insufficiency, penetrating
eye injuries, intracranial lesion, or cerebrovascular diseases. This
laryngoscopic reaction in such individuals may predispose to development of
pulmonary oedema6 myocardial insufficiency7 and
cerebrovascular accident.8 At least in such individuals there is a
necessity to blunt these harmful laryngoscopic reactions.
Attenuation of pressor responses to manipulation of
the airway has been practiced either by deepening the plane of anaesthesia,9,10
by the use of drugs known to obtund them or by using advanced airway devices.11,12
Many methods have been devised to reduce the extent
of hemodynamic events including high dose of opioids,5,13 alpha and
beta adrenergic blockers,14,15 calcium channel antagonist like
diltiazem, verapamil16 and vasodilatation drugs like nitroglycerine.17
α2 – agonist like Clonidine18 and Dexmedetomidine are used 19
Various studies have reviewed the effect of Lignocaine
in forms like viscous lignocaine20 aerosols,21
oropharyngeal sprays 22 and intravenous23,24 route to
blunt these responses.
Topical anaesthesia with lignocaine applied to the
larynx and trachea in a variety of ways remains a popular method used alone or
in combination with other techniques.
Intravenous lignocaine has been used to supress cough
during tracheal intubation,25 laryngospasm and cough during
extubation.26 It has also
been used to suppress airway hyperactivity and mitigate bronchoconstriction
after tracheal intubation.27 In a study using intravenous and inhaled
lignocaine, lignocaine in both the routes attenuated reflex bronchoconstriction
significantly. Lignocaine plasma concentrations were significantly lower in the
group where lignocaine was used via inhalational route.28
Intravenous lignocaine with its well established
centrally depressant and anti- arrhythmic effect was found to be a more
suitable alternate method to minimize this pressor response.23,24
The present study was undertaken to compare the
effect of Intravenous lignocaine and nebulization of lignocaine on blunting the
haemodynamic responses to endotracheal intubation.
OBJECTIVES OF THE STUDY
The main objectives of the
present study are:
1.
To study the effect of 2% lignocaine 2mg/kg iv, on
hemodynamic responses to laryngoscopy and endotracheal intubation.
2.
To study and compare effect of intravenous lignocaine
with nebulization of 2% lignocaine 2mg/kg on hemodynamic responses to
laryngoscopy and endotracheal intubation.
3. To evaluate any side effects
associated with the use of this drug in both
routes.
ANATOMICAL ASPECTS29, 30
The relevant anatomy of the posterior surface of the
tongue, the soft palate, epiglottis, larynx and trachea, with their nerve
supply is explained briefly to understand the physiological effects of
endotracheal intubation.
TONGUE:
It is a soft mobile organ which bulges upwards from
the floor of the mouth. The posterior part of the tongue forms the anterior
wall of the oropharynx. The dorsum of the tongue is long and extends from the
tip to the base of the epiglottis and with it forms the glosso-epiglottic fold.
It is separated into palatine and pharyngeal parts by a V shaped sulcus
terminalis. The thick mucous membrane covering the tongue is posteriorly
continuous with that on the anterior surface of epiglottis over the median and
lateral glosso-epiglottic folds and the valleculae of the epiglottis between
them.
EPIGLOTTIS:
It is likened to a leaf. It is attached at its lower
tapering end to the back of the thyroid cartilage by means of the
thyro-epiglottic ligament. Its superior extremity projects upwards and
backwards behind the hyoid and the base of the tongue, and overhangs the inlet
of the larynx. The posterior aspect of the epiglottis is free and bears a
bulge, termed the tubercle, in its lower part. The upper part of the anterior
aspect of the epiglottis is also free; it’s covering mucous membrane sweeps
forward centrally onto the tongue and, on either side, onto the side walls of
the oropharynx, to form, respectively, the median glosso-epiglottis and the
lateral glosso-epiglottic folds.
The valleys on either side of the median
glosso-epiglottic fold are termed the valleculae, The lower part of the
anterior surface of the epiglottis is attached to the back of the hyoid bone by
the hyoepiglottic ligament
SOFTPLATE:
Is a flexible muscular flap which extends
postero-inferiorly from the posterior edge of the hard palate into the
pharyngeal cavity. By varying its position, it can cut off the nasopharynx or
the mouth from the remainder of pharynx. It
is attached to the posterior edge of the hard palate and to the side
walls of pharynx and has the uvula hanging down from the middle of its free
posterior border. On each side, the posterior border is continuous with the
palatopharyngeal arch.
LARYNX:
Figure 1: Entrance to larynx (posterior view)
The competent anaesthesiologist should have a level
of knowledge of the anatomy of the larynx of which a laryngologist would not be
ashamed. Evolutionally, the larynx is essentially a protective valve at the
upper end of the respiratory passages; its development into an organ of speech
is a much later affair. Structurally, the larynx consists of a framework of
articulating cartilages, linked together by ligaments, which move in relation
to each other by the action of the laryngeal muscles. It lies opposite the 4th,
5th and 6th cervical vertebrae, separated from them by the laryngopharynx; its
greater part is easily palpable, since it is covered superficially merely by
the investing deep fascia in the midline and by the thin strap muscles
laterally.
The inlet of larynx is a large oblique shaped opening
bounded antero-posteriorly by the epiglottis. It
is bounded on each side by the aryepiglottic fold of mucous membrane and postero-inferiorly by the
inter-arytenoid fold of mucous membrane. Each aryepiglottic fold is a narrow
and deep fold that extends posterior-inferiorly from the margin of the
epiglottis to the arytenoid cartilage. It contains
the aryepiglottic muscle and near its inferior ends two small pieces of
cartilage which forms the cuneiform and corniculate tubercules in its free
edge. The interarytenoid fold of mucous membrane passing between them forms the
inferior boundary of inlet and encloses the muscle which pass between the
posterior surfaces of the arytenoid cartilages.
Vocal cords are two folds of mucous membrane
stretching antero-posteriorly from the vocal processes of the arytenoid
cartilage to the posterior surface of the thyroid cartilage and enclosed within
each of them is a band of fibroelastic tissue known as the vocal ligament. The
opening between the two folds forms the glottis which is the narrowest portion
of the airways in the adult.
LARYNGOSCOPIC ANATOMY
Figure 2: View
of the larynx at laryngoscopy.
To view the larynx at direct laryngoscopy and then to
pass a tracheal tube depends on getting the mouth, the oropharynx and the
larynx into one plane. Flexion of the neck brings the axes of the oropharynx
and the larynx in line but the axis of the mouth still remains at right angles
to the others; their alignment is achieved by full extension of the head at the
atlanto-occipital joint. This is the position, with the nose craning forwards
and upwards.
At laryngoscopy, the anaesthesiologist first views
the base of the tongue, the valleculae and the anterior surface of the
epiglottis. The laryngeal aditus then comes into view bounded in front by the
posterior aspect of the epiglottis, with its prominent epiglottic tubercle. The
aryepiglottic folds are seen on either side running postero - medially from the
lateral aspects of the epiglottis; they are thin in front but become thicker as they pass backwards where they contain the cuneiform
and corniculate
cartilages. The vocal cords appear as pale, glistening ribbons that
extend from the angle of the thyroid cartilage backwards to the vocal processes
of the arytenoids. Between the cords is the triangular (apex forward) opening
of the rima glottidis, through which can be seen the upper two or three rings
of the trachea.
TRACHEA:
It is a wide tube of 13-15 mm diameter and 11- 14 cm
in length. It commences at the larynx and terminates at the level of the fourth
thoracic vertebra, where it divides into the two main bronchi. In new born the
trachea is only 4 cm long. The tracheal architecture consists of a number of
horizontal C shaped cartilages which are joined posteriorly by the trachealis
muscle. Vertically these cartilages are joined to each other by fibroelastic
tissue. This gives the trachea an appearance similar to that of tyres pilled
one on top of the other, held together by elastic tissue and both covered by endothelium.
NERVE SUPPLY:
Glossopharyngeal nerve:
The ninth cranial nerve is a mixed nerve. Its motor
fibres supply the stylopharyngeus muscle. The parasympathetics supply to the
parotid glands is through glossopharyngeal nerve. It descends between the
internal and external carotid arteries and after passing between superior and
middle constrictors of pharynx, it branches into two terminal branches.
The pharyngeal
branch consists of :
1.
One or two branches which supply the mucous membrane
of the pharynx, posterior one third of the tongue, anterior surface of the
epiglottis, glosso-epiglottic folds, valleculae and pyriform fossa are also
supplied by this nerve.
2.
The larger branch accompanies the pharyngeal branches
of the vagus to the pharyngeal plexus. One of its branches joins a branch of
superior laryngeal nerve to form the carotid sinus nerve which supplies the
carotid sinus and the carotid body.
Vagus nerve:
This is also a mixed cranial nerve. In the neck it
descends vertically between the internal jugular vein and the internal carotid
artery above and the common carotid artery below. All three structures are
enclosed in the carotid sheath. It gives off numerous branches, three of which
supply those areas of the pharynx and larynx stimulated by the endotracheal
intubation.
1.
Pharyngeal branch: This branch forms the large part of
the pharyngeal plexus to which are contributed branches of the glossopharyngeal
nerve and fibres from the superior cervical sympathetic ganglion. This plexus
supplies the muscles and mucous membrane of the pharynx.
2.
Superior laryngeal nerve: This branch divides into
external and internal laryngeal nerves. The external branch descends on the
anterior aspect of the thyroid cartilage to the crocothyroid muscle to which it
supplies. The internal branch perforates the thyrohyoid membrane and lying in
the submucous plane of pyriform fossa.
Supplies sensory branches to the larynx above the level of the glottis.
3.
Recurrent laryngeal nerve: on the right side leaves
the vagus as the latter crosses the right subclavian artery; it then loops
under the artery and ascends to the larynx in the groove between the oesophagus
and trachea. On the left side, the nerve originates from the vagus as it crosses the aortic arch; the nerve then passes under
the arch to reach the groove between the oesophagus and the trachea. Once
it reaches the neck, the left nerve assumes the same relationships as on the
right. The recurrent laryngeal nerves provide the motor supply to the intrinsic
muscles of the larynx apart from cricothyroid, as well as the sensory supply to
the laryngeal mucosa inferior to the vocal cords.
PHYSIOLOGY OF PRESSOR RESPONSES30, 31
Direct laryngoscopy and endotracheal intubation
following induction of anaesthesia is almost always associated with hemodynamic
changes due to reflex sympathetic discharge caused by epipharyngeal and
laryngopharyngeal stimulation. Here in with have explained briefly the
physiology and effects of laryngoscopy and intubation to understand the
haemodynamic changes.
SYMPATHETIC NERVOUS SYSTEM.
The sympathetic efferent nerve fibres originate from
nerve cells in the lateral grey column of the spinal cord between the first
thoracic and second lumbar segments (the thoracic outflow). Preganglionic
fibres are myelinated. Ganglia are located either in the paravertebral
sympathetic trunk or in prevertebral ganglia, such as the celiac ganglion. The
sympathetic part of postganglionic fibres are long, non-myelinated sympathetic
part of the system has a wide spread action on the body as the resulting
preganglionic fibres synapsing on many postganglionic neurons and the
suprarenal medulla releasing the sympathetic transmitters epinephrine and nor
epinephrine. The sympathetic nervous system prepares the body for emergencies
and severe muscular activity. There is no sympathetic out flow from cervical
part of the cord nor from the lower lumbar and sacral parts. Those
preganglionic fibres which are destined to synapse with cell bodies whose
fibres are going to run with cervical nerves must ascend in the sympathetic
trunk and those of lower lumbar and sacral nerves must descend in the trunk to
lumbar and sacral ganglia.
Figure 3: Sympathetic supply to heart and lungs Afferent
sympathetic fibres
All the afferent fibres have their cell bodies in the
posterior root ganglia of spinal nerves. The afferent fibres reach the spinal
nerve in the white ramus communicants. Central processes enter the spinal cord
by posterior nerve root. From there they ascend through the cord to brain stem.
Afferent
sympathetic fibres
↓
Hypothalamus
↓
Transmits signals through preganglionic cell bodies located
in lateral horn cells of thoracic and upper two lumbar segments.
↓
Post ganglionic cell bodies in ganglia in peripheral nervous
system either in the sympathetic or
in autonomic plexuses.
↓
Causes
massive sympathetic discharge
THE CARDIOVASCULAR REFLEXES
The cardiovascular responses to noxious airway
manipulation are initiated by proprioceptors responding to tissue irritation in
the supraglottic region and trachea. Located in close proximity to the airway
mucosa, these proprioceptors consist of mechanoreceptors with small-diameter
myelinated fibers, slowly adapting stretch receptors with large-diameter
myelinated fibers, and polymodal endings of nonmyelinated nerve fibers. The
superficial location of the proprioceptors and their nerves is the reason that
topical local anaesthesia of the airway is such an effective means of blunting cardiovascular
responses to airway interventions. The glossopharyngeal and vagal afferent
nerves transmit these impulses to the brain stem, which, in turn, causes
widespread autonomic activation through both the sympathetic and
parasympathetic nervous systems.
In adults and adolescents, the more common response
to airway manipulation is hypertension and tachycardia, mediated by the
cardioaccelerator nerves and sympathetic chain ganglia. This response includes
widespread release of norepinephrine from adrenergic nerve terminals and
secretion of epinephrine from the adrenal medulla.
In addition to activation of the autonomic nervous
system, laryngoscopy and endotracheal intubation result in stimulation of the
central nervous system (CNS), as evidenced by increases in
electroencephalographic activity, cerebral metabolic rate, and cerebral blood
flow (CBF).
PHARMACOLOGY OF LIGNOCAINE31,
32, 33
Lignocaine was synthesised in 1943 in Sweden by Lofgren, it was introduced
into clinical practice by Gordh in the year 1948.
PHARMACOLOGY
Clinically lignocaine is an amino-amide of xylidine-de-ethyl amino 2:6
dimethyl acetanilidine.
STRUCTURAL FORMULA:
PHYSICAL PROPERTIES:
It is very stable, not decomposed by boiling, acids
or alkalies and withstands repeated autoclaving. The pKa of lignocaine is 7.72.
At the normal tissue pH of 7.4 approximately 65% of lignocaine exists in the
charged cationic form, whereas 35% exists in the uncharged base form.
Lipid solubility:
Determination of partition co-efficient by means of n-heptane/pH 7.4 buffer
system has given a value of 2.9.
Plasma protein binding: At a
concentration of 2mcg/ml approximately 65% is bound to plasma proteins.
Lignocaine is a local anaesthetic of moderate potency and duration, with good
penetrative powers and rapid onset of action. It is effective by all routes of
administration. Lignocaine sometimes causes vasodilation. Adrenaline as
adjuvant
prolongs the
duration of lignocaine as it reduces the rate of systemic absorption. With
repeated injections, tachyphylaxis often occurs.
The
hydrochloride salt in water has a pH of 6.5. Hepatic extraction ratio 65-70%.
Plasma half life 1.6 hrs.
Volume of distribution – 1.3 L/hr.
PREPARATIONS OF LIGNOCAINE
1.
Topical forms:
Topical spray 4% and 10%
solution
Gel: 2% or 2.5%
Solution: 2% or 4% or 5%
2.
Parenteral forms: 0.5%, 1% .2%, or 4% as
lignocaine hydrochloride.
Lignocaine is
stored at temperature < 25ºC protected from light. Lignocaine is also
available along with adrenaline in 1: 1 lakh or 1: 2 lakh concentrations.
PHARMACODYNAMICS
A. Local effects:
Lignocaine blocks the conduction of impulses in the nerve fibres at the
site of injection by closing sodium channels.
Sensory and motor fibres are
inherently equally sensitive to lignocaine.
Smaller fibres and nonmyelinated nerve fibres are blocked more easily
than longer and myelinated fibres.
Autonomic fibres are more susceptible than somatic fibres. Among somatic fibres
order of blockade are pain-temperature-touch-deep pressure sense.
Addition of vasoconstrictor
like Adrenaline (1:50,000 to 1:2 lakh) can
1. Prolong the
duration of action of lignocaine by decreasing the rate of removal from the
local site of injection in to the circulation
2. Reduces the
systemic toxicity; of lignocaine by decreasing the rate of absorption and
keeping the plasma concentration lower.
It is very effective surface analgesic causing rapid
absorption from mucosal surface. The peak blood concentration is achieved
within 4 to 15 minutes after
instillation. Given intravenously, peak blood levels are achieved immediately.
B. Systemic
effects
Cardiovascular system
Heart: Lignocaine is placed under
classification of class 1- B anti-arrhythmic drugs classification.
It suppresses the automaticity in ectopic foci by antagonizing phase IV
depolarization in Purkinje fibres and ventricular muscles by blocking sodium
channels.
It does not depress SA node automaticity.
The rate of phase-0 depolarization is not decreased except in presence of
hyperkalaemia.
Lignocaine markedly decreases the action potential duration and effective
refractory period in Purkinje fibres and ventricular muscles.
Conduction velocity is not
decreased.
It has practically no effect on action potential
duration and effective refractory period of atrial fibres. Atrial re-entry is
not affected.
It can suppress the re-entrant ventricular
arrhythmias either by abolishing one way block or by producing two way blocks.
At therapeutic plasma concentration of 3- 5mcg/ml, it causes little depression
of cardiac contractility. There are no significant autonomic actions. All
cardiac effects are direct actions.
Lignocaine is widely used in the management of
ventricular dysrhythmias in a dose of 1 to 2 mg/kg bolus intravenously and 2.4
mg/min as infusion. It acts by its
membrane stabilizing effect and depression of automaticity at atrio-ventricular
node. It has been used effectively in the management of ventricular arrhythmias
following myocardial infarction and cardiac surgery.
Vascular smooth muscle.
Lignocaine exists in two isomers, and the ability to
produce vasoconstriction appears vested in one of the isomers. Hence lignocaine
produces vasoconstriction with low doses and vasodilation at higher doses, very
large doses cause circulatory collapse as a result of medullary depression and
direct vasodilation.
At doses > 75mcg/kg/min with plasma concentration
of > 10-20mcg/ml lignocaine causes
asystole and cardiovascular collapse.
Central nervous system
It readily crosses blood brain barrier causing central
nervous system stimulation followed by depression with higher doses. The
severity of the central nervous system effect correlates with plasma
concentration. Central nervous system is more susceptible to toxic effects than
the cardiovascular system. Mild toxic effects may cause drowsiness and
sedation. Objective signs of central nervous system toxicity are usually excitatory
in nature and may cause shivering, muscular tithing and convulsions. It has
been shown to possess analgesic properties when given intravenously. Reduction
of MAC of inhalational anaesthetic agents is used as an index of its central
analgesic property. Higher serum levels produce a central stimulant effect and
this is due to initial blockade of inhibitory pathway at limbic or higher
centres in the cerebral cortex.
Neuromuscular junction
It can affect transmission at the neuromuscular junction and hence
potentiate the effect of the depolarizing and non-depolarizing muscle
relaxants.
Metabolism
It is metabolised by the liver microsomal enzymes,
oxidases and amidases. The main pathway in man appears to be due to oxidative
de-ethylation of lignocaine to monoethyl glycinexuylidide followed by
subsequent hydrolysis of monoethyl glycinexylidide to xylidine. Excretion
occurs through the kidneys.
Dosage
The safe dose limit for lignocaine has been much
disputed. The factors governing the dosage are the weight of the patients and
the different absorption rates from various sites and injections. The maximum
safe dose is to 4.5 mg/kg without epinephrine and 7 mg/kg with epinephrine.
A concentration of 0.25-5% of lignocaine
hydrochloride is used for infiltration. If extensive block is required then
0.5% with epinephrine is used. 0.5% lignocaine without adrenaline is used for
intravenous regional anaesthesia. 1% lignocaine is usually sufficient for most
nerve blocks. In dentistry, 2%
lignocaine with adrenaline 12.5 mcg/ml (1:80,000) is useful. A concentration of
1.5-2% solution of lignocaine is used for epidural analgesia and sometimes with
the addition of adrenaline 5 mcg/ml 1:200,000). For surface application,
lignocaine solution in a concentration of (4%) for spraying or for application
using wool pledgets.
It is used in a concentration of 2% as a lubricating
gel in urethral surgery and for lubricating endotracheal tubes. In the management of cardiac dysrhythmias
it is used in the dose of 1-2 mg/kg iv as a bolus dose followed
by 2-4 mg/min (20-60 mcg/kg/min) as
infusion and
then the dose is reduced. Caution must be exercised in the presence of low
cardiac output and after cardiac surgery and a slow infusion rate must be maintained.
Toxicity
The appearance of toxic symptoms is due to two factors. The toxicity of
the drug and its serum levels.
Toxic symptoms may occur at plasma levels of 5mcg/ml
in an awake patient, while levels of 10mcg/ml are toxic in the anaesthetised patient.
Plasma levels depend on the speed with which lignocaine enters the circulation,
which in turn depends on the dosage and rate of absorption of the drug from
various sites. Peak blood levels are attained in 1 minute after intravenous
administration and start decreasing by 3-4 minutes. Following laryngotracheal
administration, peak blood levels are attained in 9-15 minutes. Alveolar
absorption occurs at a faster rate than absorption from bronchial and
bronchiolar mucosa. It is thought
that, mucosal absorption simulate intravenous administration. However, systemic
absorption of lignocaine may be slowed through larynx and tracheal mucosa as it
is diluted with secretions lining the upper airway, impeding systemic
absorption. Hence laryngotracheal administration is associated with delayed
peak levels that are lower but more sustained. The peak blood levels after
epidural injection follow a similar pattern to those seen after intra-muscular
injection (average 18 minutes for plain lignocaine and after 23 minutes for
lignocaine with adrenaline)
Side effects
Commonest side effects are nausea, drowsiness, and
dizziness. At a higher levels shivering, muscular twitching, tremors and
convulsions, bradycardia, decreased respiration with hypoxia can occur. Circulatory
collapse may occur with very high dosage.
Hypersensitivity
This is due to an antigen-antibody reaction.
Hypersensitivity to local anaesthetics is more common with ester-linked drugs
than with amide group of drugs. This is more commonly seen in atopic
individuals and can manifest as local oedema, urticaria, or angioneurotic
oedema. Dermatitis may be encountered as a result of skin application.
Anaphylaxis occurs less commonly. Although amide agents appear to be
relatsively free from allergic type reactions, solution may contain
preservatives like paraben and methylparaben whose chemical structure is
similar to that of para-aminobenzoic acid.
REVIEW OF LITERATURE
HISTORICAL REVIEW
Endotracheal intubation has become an integral part
of the anaesthetic management and critical care. It has been practised
following its description by Rowbottam
and Magill in 1921.32 Laryngoscopy and endotracheal intubation
are attended by significant hypertension, tachycardia and arrhythmias. These
hemodynamic responses were first recognised as early as in 1940 by Reid and Brace et al.34 They postulated that the
disturbances in cardiovascular system were reflex in nature and mediated by the vagus nerve which originated in
the, trachea, larynx, bronchi, or lungs and effects by sudden increase in the
vagal tone. These reflexes were termed ‘vagovagal’ since both the efferent and
afferent paths of the reflex were assumed to be vagus nerve. But in 1950 Burstein and co-workers,2
had a different conclusion that attributed the effects of laryngoscopy and
tracheal intubation on ECG changes and suggested the pressor response as
consequences of an increase in sympathetic and sympathoadrenal activity and
also observed that deep anaesthesia minimizes ECG incident to tracheal
intubation. In 1951 King BD and
co-workers35 observed that during light general anaesthesia, direct
laryngoscopy or tracheal intubation, uncomplicated by cough, anoxia,
hypercarbia is capable of producing decided circulatory effects characterised
by rise in blood pressure and increase in heart rate.
These responses being transitory are well tolerated
by normal individuals but are more deleterious in patients with hypertension,
myocardial insufficiency and cerebrovascular diseases which result in
potentially dangerous effects like ventricular arrhythmias,4
myocardial ischemia,7 pulmonary oedema,6 left ventricular
failure,6 and
cerebrovascular accidents.8 This hemodynamic stimulus is
associated with increase in plasma nor-adrenaline concentrations parallel with
the increase in blood pressure.36
Many methods and strategies have been employed and advocated to minimize
and nullify the hemodynamic responses to laryngoscopy and intubation which work
on the reflex arc.33
1.
By blocking the peripheral sensory afferent inputs –
topical application and infiltration of superior laryngeal nerve.
2.
Block of central mechanism of integration of sensory inputs – morphine, fentanyl.
3.
Block of the efferent pathway effector sites – calcium
channel blockers, intravenous lignocaine, esmolol.
Increasing the depth of anaesthesia with the use of
inhalational agent like cyclopropane,9 trichloroethylene,37
chloroform and ethyl chloride38 for attenuation had been practised,
but with the drawback of stormy induction. Halothane and enflurane10
had an advantage of smooth and rapid induction, non-inflammable but was
associated with hypotension, bradycardia and myocardial ischemia which are
deleterious in patients with coronary insufficiency and hypertension.
Laryngoscopy and tracheal intubation causes a reflex
increase of sympathetic and sympathoadrenal system by irritation and
stimulation of the laryngeal and pharyngeal tissues, anaesthetising using local
anaesthetics like lignocaine at the site of stimulation was studied. And
various studies have reviewed the effects of lignocaine in the form of viscous,20
aerosol, 21 spraying,22 and intravenous 23, 24
routes for blunting the response.
As early as in 1960, alpha adrenergic blocker,
phentolamine14 was used to attenuate the laryngoscopic reactions.
However, these drugs had long duration of action and the authors observed
exaggerated fall in blood pressure during perioperative period,
because of their property of extensive vasodilation requiring rapid
transfusion it was not used.
Beta adrenergic blockers were extensively studied for
their negative chronotropic effects for blunting the hemodynamic responses to
laryngoscopy and intubation like proctolol15 and labetalol.39
but had a delayed onset and longer duration of action which caused
perioperative bradycardia and hypotension, hence a search for shorter acting
beta blockers like esmolol40 was started.
The investigators used low doses of opioids as
premedicants for blunting the laryngoscopic responses during 1970 and observed
significant reduction in the hemodynamic responses to laryngoscopy and
intubation. Use of morphine5 and fentanyl13 effectively
reduced the tachycardia and hypertension associated with laryngoscopy and
intubation but these agents were associated with respiratory depression, chest
wall rigidity and in addition they prolonged the recovery time.10
The availability of synthetic narcotics like alfentanyl41 and
sufentanyl42 with short duration and rapid onset of action helped
the investigators to overcome the problems associated with the use of above mentioned drugs.
Calcium channel blockers like nicardipine, verapamil
and diltiazem16 were studied widely to suppress the hemodynamic
responses to laryngoscopy and intubation. Calcium ions exert a major role in
the release of catecholamines from the adrenal gland and adrenergic nerve
endings, which affects plasma catecholamine concentrations, in response of sympathetic stimulation. The
investigators reported that calcium channel blockers interfere with
catecholamine release after tracheal intubation.
Directly acting vasodilators like sodium
nitroprusside43 and nitroglycerine17 were tried but set
back being that they caused reflex tachycardia being deleterious in patients
with co
morbidities and requirement of invasive arterial monitoring.
Laryngoscopy and tracheal intubation are also
employed for non-anaesthetic purposes. Diagnostic purposes for direct laryngoscopy
and flexible bronchoscopy.44 Endotracheal intubation may be required
for prevention of aspiration and protection of airway. Hence blunting the
response becomes important as these patients come as for emergency procedures
or critically ill.
CLINICAL REVIEW
Mounir N.
Abou-Madi et al
21
conducted a study on cardiovascular responses to
laryngoscopy and tracheal
intubation following nebulization of lignocaine.
20 patents scheduled for various procedures were selected for the study
and were divided into two groups.
Pre-treated group: received inhalation of 6-8ml of mixture of 1/3rd of 2%
viscous lignocaine + 2/3rd of 4% aqueous lignocaine
Control group: nebulized with saline instead of lignocaine in stage II,
10% lignocaine was nebulized instead of saline prior to intubation.
A standard premedication with Pentobarbitone 2mg/kg intramuscular was
given one and half an hour before the surgery.
In the pre-treated group
Stage I – Pre operative
observation period
ECG and BP was
recorded, arterial blood drawn for gases, serum potassium and lignocaine levels
was done
Stage II – Aerosol nebulization
was administered.
Stage III - Post
aerosol observation period. Blood samples drawn and parameters were recorded.
Stage IV -
Anaesthesia induced with Thiopentone sodium 4mg/kg, anaesthesia continued with
nitrous oxide, oxygen and halothane for 5 – 10 min.
Stage V – Steady state
For 2 minutes
tracing of readings was done Stage VI – Laryngoscopy
Intubation facilitated with Inj. Succinylcholine 1.0mg/kg Stage VII –
Intubation
Intubation performed, tracing done for 2min.
Stage VIII –
Final observation period Was continued till end of procedure
Three stages were taken for
statistical analysis
1.
Steady state
2.
Post laryngoscopy
3.
1minute after intubation
The authors
observed heart rate, systolic blood pressure, diastolic blood pressure and ECG
changes following laryngoscopy and intubation.
In control group
Heart rate increased by 38.8% (28 bpm), systolic
blood pressure increased by 56% (60 mm Hg) and diastolic blood pressure raised
by 66.0% (37 mm Hg) above the steady state values after 1minute post intubation
.
ECG changes: had serious new arrhythmias. The incidence was highest in
patients who had suffered the most acute rise in blood pressure.
Blood levels: after intubation the average blood level was 0.4 mcg/ml at
2min and at the end of study it was 0.3 mcg/ml
In Pre-treated group
Heart rate increased by 16.8% (17 bpm), systolic
blood pressure by 10.3% (12 mm Hg) and diastolic blood pressure by 16.4% (11 mm
Hg) above the steady state values after 1min post intubation.
ECG changes:
There were no new arrhythmias or ECG changes.
Blood levels: The average lignocaine levels following
nebulization was 1.4mcg/ml at 2min and 1.2mcg/ml at the end of the study.
The authors concluded,
1.
Topical anaesthesia applied immediately before intubation is ineffective.
2.
Systemic absorption of lignocaine probably accounts
for the absence of arrhythmia in pre-treated
group.
3.
Incidence of post intubation arrhythmias and
hypertension is marked in patients with arteriosclerotic heart diseases.
They believed that inhalation of lignocaine aerosol is a safe, simple,
effective, and generally acceptable method.
Mounir N. Abou-Madi et al23
conducted a study on cardiovascular responses to laryngoscopy and tracheal
intubation following small and large intravenous doses of lignocaine.
Thirty male patients scheduled for various surgical procedures were
selected for the study and were divided into three comparable groups A, B and C
Group A –
received normal saline iv and served as control Group B – received 1%
lignocaine 0.75 mg/kg iv
Group C – received 2%
lignocaine 1.5 mg/kg iv
All the patients were pre-medicated with Inj.
Meperidine 1 mg/kg and Inj. Atropine 0.4 mg/kg intramuscular one hour before
surgery. Anaesthesia was induced with Inj. Thiopentone 4 mg/kg and intubation
was facilitated with Inj. succinylcholine 1.0 mg/kg. Endotracheal intubation
was carried out within 2-3 min of injection of test drug.
Changes in heart rate, systolic blood pressure and
diastolic blood pressure in all the three groups were observed following
laryngoscopy and intubation.
In control group, heart rate increased by 15.3% (14 bpm), systolic blood
pressure increased by 30.3% (42 mm Hg) and diastolic blood pressure raised by
38.7% (31 mm Hg) above the pre- induction value .
In group B, (Lignocaine 0.75 mg/kg), heart rate
increased by 26% (21.1 bpm), systolic blood pressure by 11,9% (17.6 mm Hg) and
diastolic blood pressure by 25.2% (20 mm Hg) above the pre-induction value.
In group C, (Lignocaine 1.5 mg/kg) heart rate
increased by 8.5% (8.5 bpm), systolic blood pressure increased by 21.5% (30.4
mm Hg) and diastolic blood pressure by 22.3% (21.8 mm Hg) above the
pre-induction value.
The authors concluded that 1.5 mg/kg iv Lignocaine
given 3 min before laryngoscopy and intubation provides protection against both
tachycardia and hypertension. They also discussed the possible modes of action
•
Direct myocardial depressant action and indirect dose
stimulant effect but with predominance depressant effect during induction.
• Central stimulant effect
(indirect, dose dependent stimulant action)
• A peripheral vasodilating
effect and an effect on the synaptic transmission
• Suppress the cough reflex.
The authors also concluded that pre-induction aerosol
topical analgesia of the upper airways would still be their method of choice to
minimise post intubation cardiovascular reactions in patients with poor
myocardial reserve and severe hypertension.
Robert K Stoelting3
compared the clinical effects of intravenous lignocaine 1.5 mg/kg given 30 sec
before intubation and laryngotracheal viscous lignocaine 2 mg/kg given 10 min
before intubation in 24 patients scheduled for elective coronary artery bypass
graft operations.
Anaesthesia was induced with thiamylal 4 mg/kg and
intubation was facilitated with succinylcholine 1.5 mg/kg. The duration of
laryngoscopy was averaged less than 15 sec.
The authors observed no significant changes in heart rate following
laryngoscopy and intubation in both the groups. However, in control group, mean
arterial pressure raised by 17 mm Hg in viscous lignocaine group, by 14 mm Hg
and in intravenous lignocaine group, mean arterial pressure increased by 22 mm
Hg, above the pre-induction value.
The authors did not make any comment on changes in diastolic or systolic
pressures. Mean arterial pressure decreased spontaneously and reached
pre-induction levels by 2 min after intubation.
They concluded that a short duration direct
laryngoscopy combined with laryngotracheal lignocaine before tracheal
intubation minimises the pressor responses and ensures a spontaneous return of
mean arterial pressure and heart rate towards awake
levels following intubation. Viscous or intravenous lignocaine is not
helpful when laryngoscopy of short duration
Robert F. Bedford, et al45
compared the reduction in intracranial pressure following intravenous
administration of bolus lignocaine at 1.5mg/kg with Thiopentone. Lignocaine
significantly reduced the ICP with minimum changes in arterial pressure without
altering the cerebral perfusion. Rise in ICP due to intubation and surgical
stimulation is blunted by it.
James F. Hamill, et al46
they observed that in a light barbiturate–nitrous oxide anaesthesia, topical
laryngotracheal administration of 4ml of 4% lignocaine prior to laryngoscopy
and tracheal intubation causes a significant increase in ICP, heart rate, and
mean arterial pressure. 1.5mg/kg lignocaine intravenous administered 1minute
before intubation prevents both rise in ICP, and was useful in blunting the
hemodynamic response to laryngoscopy and endotracheal intubation. Cerebral
perfusion was well maintained and it decreased CMRO2 and cerebral blood flow.
Laryngotracheal topical application took 4-15 min for achieving plasma level of
1 - 2.7mcg/ml when compared with intravenous route.
Bahaman Venus,47 conducted
a study on cardiovascular responses to laryngoscopy and tracheal intubation
following nebulization of lignocaine
Study included 19 ASA class I and II adult patients
scheduled for general anaesthesia for wide excision and extremity amputation
procedures were divided into two groups.
Group I: 10 patients received of solution A (normal saline, 6ml) Group
II: 9 patients received of solution B (4% lignocaine, 6ml) both groups were
aerosolized with their
respective solutions 5 minute during pre-oxygenation before induction. A
contoured breathing mask with attached nebulizer was used to deliver the
aerosol.
All patients were pre-medicated with, atropine
0.05mg/10kg and morphine 1mg/10kg 1hour before the induction. Baseline measurements
of blood pressure, heart rate and ECG recordings were noted. A standard
technique for administration of general anaesthesia was followed and
laryngoscopy and endotracheal intubation was performed in both the groups. The
time and duration of each manoeuvre were recorded until 5 min after placement
of endotracheal tube. Blood gas analysis was
done.
They observed that the pressor response and
tachycardia following laryngoscopy and endotracheal intubation in the control
group I was clinically significant. The patients in aerosolized group
maintained significantly lower pressor response and heart rate. 4 patients
among the group I developed PVC and none in group II.
They concluded that
1.
The underlying mechanism is probably of reflex origin
to mechanical stimulation of the larynx and trachea, as the arterial blood gas
analysis was within the normal limits excluding the possible causes of
hypercarbia and hypoxia.
2.
Aerosolization
of lignocaine is a simple and effective technique for intubating patients with
borderline cardiovascular status.
Stanley Tam, et al24
studied the optimal time of lignocaine injection before tracheal intubation, to
prevent the pressor response. Seventy patients were divided into five groups
with 14 patients in each group. Group 1, Group II, Group III and Group IV,
received 1.5 mg/kg of lignocaine intravenously 1, 2, 3 and 5 minutes
respectively. Group V received normal saline and served as control. All the
patients received morphine 0.1 mg/kg and perphenazine, 0.05 mg/kg intramuscular
before induction of anaesthesia. Patients were
given d-tubocurarine 0.04 mg/kg 5 min before intubation followed by
thiopentone 4 mg/kg and suxamethonium 1.5 mg/kg before intubation. Heart rate,
mean arterial pressure, systolic and diastolic pressure were monitored
throughout the procedure.
The mean increase in heart rate in group I was 28 bpm, in group II it was
24 bpm, in group III it was 12 bpm and in group IV it was 22 bpm and in group V
it was 25 bpm.
The mean increase in systolic blood pressure in group
1 is 32 mm Hg, in group II 29 mm Hg, in group III 12 mm Hg, in group IV 31 mm Hg and in group V it was 38 mm
Hg.
The mean increase in diastolic blood pressure in
group I was 29 mm Hg, in group II 29 mm Hg, in group III 9 mm Hg, in group IV
22 mm Hg and in group V it was 26 mm Hg.
The mean increase in mean arterial pressure in group
I was 30 mm Hg. In group II 27 mm Hg, in group III 11 mm Hg, in group IV 27 mm
Hg and in group V 32 mm Hg.
The results of the study showed that the mean
increase in heart rate, systolic blood pressure, diastolic blood pressure and
mean arterial pressure in group III, where lignocaine was given in the dose of
1.5 mg/kg iv 3 min before laryngoscopy and intubation were comparatively less
than the other groups, when compared with the base line values.
The authors concluded that intravenous lignocaine at
1.5 mg/kg attenuated increase in heart rate and arterial blood pressure, only
when given 3 min before intubation. And it offers no protection against
post-intubation changes when given at 1, 2 and 5 min before intubation.
Splinter et al48
studied the haemodynamic response to laryngoscopy and tracheal intubation in
geriatric patients with thiopentone alone or in combination with 1.5mg/kg
lignocaine and with 1.5mg/kg or 3mcg/kg fentanyl were measured. They observed
that both the drugs decreased the rise in heart rate and blood pressure changes
with fewer
haemodynamic fluctuations in case of fentanyl. Lignocaine treated
patients had fewer cardiac dysrhythmias.
C D Miller and
S J Warren49 studied the effect of intravenous lignocaine on the
cardiovascular responses to laryngoscopy and tracheal intubation.
The study population consisted of 45 Chinese patients
of ASA Grade I and Grade II, posted for elective thoracic surgery. The patients
were divided into four groups.
Group I – Received normal saline 4 ml iv over 30 sec,
3 min before laryngoscopy and intubation and served as control
Group II – Received 1.5 mg/kg of lignocaine iv 3 min
before laryngoscopy and intubation.
Group III – Received 1.5 mg/kg of lignocaine iv 2 min
before laryngoscopy and intubation.
Group IV – Received 1.5 mg/kg of lignocaine iv 1 min
before laryngoscopy and intubation.
The patients were premedicated with morphine 0.2 mg/kg
and hyoscine 40mcg/kg intramuscular one hour before induction. Anaesthesia was
induced with thiopentone 5 mg/kg 2.5 minutes before laryngoscopy. Neuromuscular
block was produced with 1.5 mg/kg of suxamethonium iv given 1.5 min before
laryngoscopy and subsequent tracheal intubation were performed using standard
Macintosh laryngoscope and cuffed Portex endotracheal tube. Heart rate,
Systolic and Diastolic pressures were recorded and the Mean arterial pressure
and rate-pressure product were calculated.
The results of the study showed that, in control group the heart rate
increased by a maximum of 27 bpm, systolic blood pressure increased by 31 mm
Hg, diastolic blood pressure increased by 28 mm Hg. Group III and Group IV,
where lignocaine 1.5 mg/kg iv was given 2 and 1 minutes before laryngoscopy and
intubation, also showed that, statistically significant increase in heart rate,
systolic and diastolic blood pressure. The
authors concluded that, lignocaine 1.5 mg/kg given intravenously within 3
min of laryngoscopy and intubation failed to attenuate cardiovascular
responses.
Wilson IG, et al50
studied the effect of varying the time of prior doses of intravenous lignocaine
1.5mg/kg on the cardiovascular response and catecholamine responses to tracheal
intubation. Forty healthy patients were given intravenous lignocaine 2, 3, and
4 min prior to intubation. When compared with placebo there was significant
increase in heart rate in all groups, but no significant rise in mean arterial
pressure in all groups given lignocaine. Placebo group showed rise in mean
arterial pressure of 19% compared to basal values.
M.J.L.
Bucx, et al51 worked on
the relationship between forces applied during laryngoscopy and haemodynamic
changes. This helps in to differentiate between cardiovascular effect of
laryngoscopy and tracheal intubation. There was no significant relationship
between forces applied during laryngoscopy and cardiovascular changes. It is
the tracheal intubation more than laryngoscopy that caused changes in routine
uncomplicated and laryngoscopy and subsequent tracheal intubation.
Sklar BZ et al52
conducted a study to assess the effect of lignocaine inhalation at a dose of
40mg and 120mg and control group with intravenous lignocaine 1mg/kg and on
stress response to laryngoscopy and intubation. They observed that heart rate
response to intubation with inhalation was dose dependent and at a dose of
120mg rise in blood pressure was least compared to rest of the study groups.
Hence concluded that inhalation of lignocaine prior to induction of anaesthesia
is a safe and convenient method.
METHODOLOGY
A Study entitled Comparative study of lignocaine
nebulization with intravenous lignocaine on stress response to laryngoscopy and
tracheal intubation was undertaken in Victoria hospital and Bowring and Lady
Curzon hospitals, Bangalore during November 2008 to October 2010. Ethical
clearance was obtained for the study.
The study was conducted on 90 ASA grade I and II
patients in the age group of 18 to 45 years of either sex scheduled for
elective surgeries done under general anaesthesia.
Patients were
allocated into three groups with the sample size of 30 each. Group C (n=30)
received no drug, as control.
Group I (n=30)
received 2% Lignocaine 2mg/kg slow intravenous. Group N (n=30) received 2%
nebulization of Lignocaine 2mg/kg. Exclusion
criteria:
1.
Patients with chronic obstructive lung disease, cerebrovascular disease, cardiovascular
diseases, psychiatric illness and liver disorders.
2. Patients having known
allergy either to Lignocaine or its preservatives
3.
Patients coming for emergency surgical
procedure.
4. Patients with history of
laryngeal, tracheal surgery or any pathology.
A detailed pre-anaesthetic evaluation including
history of previous illness, previous surgeries, general physical examination,
and detailed examination of Cardiovascular system, Respiratory system and other
relevant systems were done. Baseline investigations were carried out and
recorded in the proforma.
The following investigations were
done in all patients
1. Haemoglobin estimation
2. Bleeding time and clotting time
3. Urine examination for
albumin, sugar and microscopy
4. Blood sugar, FBS/PPBS
5. Blood Urea and Serum Creatinine
6.
Standard 12- lead electrocardiogram
7. X-ray of Chest
An informed and written consent was taken after
explaining the anaesthetic procedure in detail. All the patient were
pre-medicated with Tab. Diazepam 10mg to allay anxiety and Tab. Ranitidine 150
mg on the night before surgery
Patient arrived to the preoperative room 30 minutes
before surgery and preoperative basal heart rate, non-invasive blood pressure
readings, SpO2, cardiac rate and rhythm were also monitored from a
continuous visual display of electrocardiogram from lead II were recorded.
The patient in group N were nebulized with 2%
lignocaine 2mg/kg body weight using a simple fitting face mask with CompAir
Compressor Nebulizer NE-C28 model of OMRON healthcare, 10min before induction.
On operating table intravenous line was secure with 18G cannula and ringer
lactate 500ml infusion started. Patients were connected to non-invasive
monitoring with 5 lead electrocardiograph (ECG), pulseoximeter, and
non-invasive sphygmomanometer. All patients were pre-medicated with Inj
Midazolam 1mg iv. All patients were pre-oxygenated with 100% oxygen for 3
minutes by a face mask.
Patients in Group C being the
control did not receive any drug.
Patients in Group I received 2% lignocaine 2mg/kg body weight 90 sec
before induction. Patient in group N were nebulized with 2% lignocaine 2mg/kg
body weight 10 min before induction.
INDUCTION OF ANAESTHESIA
Anaesthesia was induced with Inj. Thiopentone 5mg/kg
as 2.5 % solution, after loss of eye lash reflex and confirmation of adequacy
of mask ventilation endotracheal intubation was facilitated with
succinylcholine 1.5 mg/kg iv. Laryngoscopy was performed using Machintosh
laryngoscope, under visualization of vocal cords a lubricated (2% lignocaine jelly) cuffed
endotracheal tube of appropriate size was passed. After confirming bilateral
equal air entry, the endotracheal tube was secured.
Anaesthesia was maintained using 66% nitrous oxide
and 33% of oxygen and Halothane 1%. After the patients recovered from
succinylcholine further neuromuscular blockade was maintained with
non-depolarizing muscle relaxants vecuronium.
MONITORING
The following cardiovascular
parameters were recorded in all patients:
• Heart rate (HR) in beats per
minutes (bpm)
•
Systolic blood pressure (SBP) in mm Hg
•
Diastolic blood pressure (DBP) in mm
Hg
•
Mean arterial pressure (MAP) in mm Hg
The above cardiovascular
parameters were noted as below
1.
Basal before giving any study drugs and premedication
2.
One minute interval for 5 min after laryngoscopy and intubation
3.
Every two minutes interval for next 10
min.
After the recordings were obtained all patients
received 0.2mg Glycopyrrolate iv and 3mcg/kg of Fentanyl iv for analgesia which
was avoided earlier, so as to avoid their effects on intubation response. At
the end of the procedure patients were reversed with Neostigmine 0.05 mg/kg iv
and Glycopyrrolate 0.01 mg/kg iv and extubated after recovery of adequate
muscle power and consciousness.
Figure
4:Photograph showing administration of Nebulization
Figure
5:Photograph showing CompAir Compressor Nebulizer NE-C28 and Injection
Lignocaine 2%.
OBSERVATION AND RESULTS
STATISTICAL
METHODS.
Descriptive statistical analysis has been carried out
in the present study. Results on continuous measurements are presented on
Mean 
SD (Min-Max) and results on categorical measurements are presented
in Number (%). Significance is assessed at 5 % level of significance. Analysis
of variance (ANOVA) has been used to find the significance of study parameters
between three or more groups of patients, Chi-square/ Fisher Exact test has
been used to find the significance of study parameters on categorical scale between
two or more groups. Kruska Wallis test has been used to find the significance
of SPO2 between three groups
Significant figures
+ Suggestive significance (P
value: 0.05<P<0.10)
* Moderately significant (P value: 0.01<P 0.05)
** Strongly significant (P
value: P 0.01)
Statistical software: The Statistical
software namely SAS 9.2, SPSS 15.0, Stata 10.1, MedCalc 9.0.1, Systat 12.0 and
R environment ver.2.11.1 were used for the analysis of the data and Microsoft
word and Excel have been used to generate graphs, tables etc.
1.
AGE DISTRIBUTION
Table 1 : Table showing Age distribution
|
Age in years |
Group
C |
Group
I |
Group
N |
|||
|
No |
% |
No |
% |
No |
% |
|
|
18-20 |
4 |
13.3 |
2 |
6.7 |
6 |
20.0 |
|
21-30 |
6 |
20.0 |
10 |
33.3 |
8 |
26.7 |
|
31-40 |
8 |
26.7 |
10 |
33.3 |
6 |
20.0 |
|
41-50 |
12 |
40.0 |
8 |
26.7 |
10 |
33.3 |
|
Total |
30 |
100.0 |
30 |
100.0 |
30 |
100.0 |
|
Mean ± SD |
34.80±9.97 |
34.13±8.72 |
32.97±10.06 |
|||
50
45
40
35
30
25
20
15
10 Group C
Group I
5 Group N
0
18-20 21-30
31-40 41-50
Age in years
Figure 6: Graph showing Age
distribution.
Samples are age matched with
p=0.756
There was no significant
difference in age distribution in the three groups.
2.
SEX DISTRIBUTION
Table 2 : Table showing Sex distribution
|
Gender |
Group
C |
Group
I |
Group
N |
|||
|
No |
% |
No |
% |
No |
% |
|
|
Male |
11 |
36.7 |
12 |
40.0 |
8 |
26.7 |
|
Female |
19 |
63.3 |
18 |
60.0 |
22 |
73.3 |
|
Total |
30 |
100.0 |
30 |
100.0 |
30 |
100.0 |
100
90
80
70
60
50
40
30
20
10
0
Group
C
Group I
Group N
Gender
Male Female
Figure 7: Graph showing Sex
distribution.
Samples are gender matched with
p=0.527
There was no significant
difference in sex distribution in the three groups.
3.
WEIGHT DISTRIBUTION
Table 3 : Table showing Weight distribution
|
Weight (kg) |
Group
C |
Group
I |
Group
N |
|||
|
No |
% |
No |
% |
No |
% |
|
|
38-40 |
1 |
3.3 |
3 |
10.0 |
2 |
6.7 |
|
41-50 |
8 |
26.7 |
7 |
23.3 |
8 |
26.7 |
|
51-60 |
7 |
23.3 |
10 |
33.3 |
10 |
33.3 |
|
61-70 |
6 |
20.0 |
7 |
23.3 |
8 |
26.7 |
|
71-80 |
7 |
23.3 |
3 |
10.0 |
2 |
6.7 |
|
Total |
30 |
100.0 |
30 |
100.0 |
30 |
100.0 |
|
Mean ± SD |
60.63±12.93 |
57.00±11.70 |
56.00±10.10 |
|||
50
45
40
35
30
25
20
15 Group C
Group I
10 Group N
5
0
38-40 41-50 51-60 61-70 71-80
Weight (kg)
Figure 8: Graph showing Weight
distribution.
Samples are weight matched with
P=0.273
There was no significant
difference in body weight distribution in the three groups.
4.
NATURE OF SURGICAL PROCEDURES
Table 4: Table showing nature of
Surgical procedure
|
Surgery done |
Group
C |
Group
I |
Group
N |
|
HEAD AND NECK SURGERIES |
10 |
11 |
6 |
|
ABDOMINAL SURGERIES |
4 |
10 |
7 |
|
LAPROSCOPIC SURGERIES |
5 |
2 |
10 |
|
BREAST SURGERIES |
2 |
3 |
3 |
|
SPINE AND LIMB SURGERIES |
8 |
2 |
3 |
|
OTHERS |
1 |
2 |
1 |
|
TOTAL |
30 |
30 |
30 |
5.
CHANGES IN MEAN HEART RATE
Table 5
Table
showing changes in Mean Heart Rate
|
HR (bpm) |
Group C |
Group I |
Group N |
Significant
value |
||
|
Group
C- Group
I |
Group
C- Group
N |
Group I- Group N |
||||
|
Basal |
85.50±10.30 |
86.13±10.27 |
86.97±11.24 |
0.971 |
0.854 |
0.950 |
|
Post intubations |
|
|
|
|
|
|
|
1 min |
108.90±14.13 |
104.13±11.85 |
111.83±15.91 |
0.392 |
0.699 |
0.092+ |
|
2 min |
104.87±14.73 |
103.53±12.42 |
109.73±15.34 |
0.930 |
0.385 |
0.215 |
|
3 min |
100.10±13.93 |
101.03±15.07 |
105.87±16.47 |
0.969 |
0.310 |
0.438 |
|
4 min |
95.80±12.79 |
93.63±13.34 |
100.8±15.39 |
0.818 |
0.348 |
0.119 |
|
5 min |
95.07±10.85 |
93.60±11.79 |
95.93±14.81 |
0.894 |
0.962 |
0.754 |
|
7 min |
94.57±11.48 |
89.47±10.17 |
92.30±14.94 |
0.252 |
0.758 |
0.650 |
|
9 min |
91.33±12.12 |
87.00±7.72 |
91.60±14.71 |
0.338 |
0.996 |
0.296 |
|
11 min |
89.13±10.95 |
87.27±12.4 |
88.33±12.57 |
0.819 |
0.964 |
0.937 |
|
13 min |
87.57±8.53 |
86.00±9.87 |
85.53±12.50 |
0.830 |
0.732 |
0.984 |
|
15 min |
85.13±9.36 |
84.20±12.53 |
86.63±12.04 |
0.946 |
0.867 |
0.687 |
120
110
100
90
80
70
60
Basal 1 min 2 min 3 min 4
min 5 min 7
min 9
min 11 min 13 min 15 min
Post intubations
Figure 9:
Graph showing changes in Mean Heart Rate (HR)
In the control group, the basal HR was 85.50 bpm. One
minute after intubation, it was 108.90, representing a rise of 23.4bpm.
Subsequently, the elevated heart rate started settling down by 9 min By 3and 5
min it was 100 and 95.07 bpm respectively. The increase in HR at 1 minute after
intubation compared.
In group I, the basal HR was 86.13 bpm, 1 minute
after intubation, it was 104.13 representing a rise of 18 bpm. Subsequently,
the elevated heart rate started settling down 9minute. By 3 and by 5 minutes it
was 101.03 and 93.6 bpm respectively.
In group N, the basal HR was 86.97 bpm, 1 minute
after intubation, it was 111.83 representing a rise of 24.86 bpm. Subsequently,
the elevated heart rate started settling down by 11 minute. By 3 and by 5
minutes it was 105.87 and 95.93 bpm respectively.
When mean change in heart rate in first minute in
group I and group N were compared with control (group C) group independently,
there was no clinical or statistical significance.( group C v/s group I P =
0.392 , group C v/s group N p = 0.699 )
Intergroup comparison of change in heart rate in
first minute between the study groups (group N & group I) showed no
clinical or statistical significance (p = 0.092).
6. CHANGES IN THE MEAN SYSTOLIC BLOOD PRESSURE (SBP)
Table 6 : Table showing changes in Mean Systolic Blood Pressure (SBP)
|
SBP (mm Hg) |
Group C |
Group I |
Group N |
Significant
values |
||
|
Group
C- Group
I |
Group
C- Group
N |
Group I- Group N |
||||
|
Basal |
121.73±15.84 |
119.23±11.62 |
123.17±10.84 |
0.736 |
0.904 |
0.471 |
|
Post intubations |
|
|
|
|
|
|
|
1 min |
164.33±22.17 |
139.77±13.40 |
155.43±14.89 |
<0.001** |
0.119 |
0.002** |
|
2 min |
156.63±24.57 |
139.70±17.54 |
149.37±17.29 |
0.004** |
0.345 |
0.155 |
|
3 min |
148.00±18.20 |
130.13±19.53 |
138.40±18.67 |
0.001** |
0.124 |
0.210 |
|
4 min |
143.63±19.25 |
125.60±20.92 |
133.07±19.67 |
0.002** |
0.106 |
0.321 |
|
5 min |
139.63±17.58 |
125.73±18.84 |
129.67±15.63 |
0.007** |
0.074+ |
0.657 |
|
7 min |
134.73±15.30 |
126.53±15.25 |
127.47±13.65 |
0.085+ |
0.143 |
0.967 |
|
9 min |
130.53±14.57 |
122.57±12.67 |
127.97±12.44 |
0.057+ |
0.735 |
0.261 |
|
11 min |
128.63±12.95 |
124.67±11.24 |
125.37±10.53 |
0.387 |
0.524 |
0.970 |
|
13 min |
130.60±13.64 |
124.20±13.12 |
128.00±12.51 |
0.147 |
0.723 |
0.502 |
|
15 min |
127.50±13.37 |
125.60±13.41 |
128.60±11.25 |
0.832 |
0.940 |
0.633 |
200
190
Group C Group I Group
N
180
170
160
150
140
130
120
110
100
Basal 1 min 2 min 3 min 4
min 5 min 7
min 9
min 11 min 13 min 15 min
Post intubations
Figure 10: Graph showing changes in
Mean Systolic Blood Pressure (SBP)
In the control group the basal value of SBP was
121.73 mm Hg, 1 minute following intubation, the SBP increased by 164.33 mm Hg,
representing a rise of 42.6 mm Hg. This elevated pressure started coming down
by 3 minutes. By 3 minutes and by 5 minutes it was 148 mm Hg and 139.63mm Hg respectively.
In group I the basal value of SBP was 119.23 mm Hg, 1
minute following intubation, the SBP increased by 139.77 mm Hg, representing a
rise of 17.54 mm Hg. This elevated pressure started coming down by 3 minutes.
By 3 minutes and by 5 minutes it was 130.13 mm Hg and 125.73 mm Hg respectively.
In group N the basal value of SBP was 123.17 mm Hg, 1
minute following intubation, the SBP increased by 155.43 mm Hg, representing a
rise of 32.26 mm Hg. This elevated pressure started coming down by 3 minutes.
By 3 minutes and by 5 minutes it was 138.40 mm Hg and 129.67 mm Hg respectively.
Statistical evaluation between the groups showed that
the increase in SBP observed in control group was statistically highly
significant when compared to increase in SBP in group I and N.
The increase in SBP in group C and group I were
statistically highly significant compared to increase in SBP in group N(p <
0.001) and remained significant even up to 5minute post intubation.
Between group
C and group N was no statistical significance.
Between group I and group N, the increase in SBP in group N was
statistically significant compared to increase in SBP in group I (p <
0.002).
7. CHANGES IN THE MEAN DIASTOLIC BLOOD PRESSURE (DBP)
Table 7 : Table showing changes in Mean Diastolic Blood Pressure (DBP)
|
DBP (mm Hg) |
Group C |
Group I |
Group N |
Significant
values |
||
|
Group
C- Group
I |
Group
C- Group
N |
Group
I- Group
N |
||||
|
Basal |
78.27±8.75 |
77.93±9.72 |
78.87±7.89 |
0.988 |
0.962 |
0.912 |
|
Post intubations |
|
|
|
|
|
|
|
1 min |
103.63±11.71 |
91.77±11.12 |
103.70±11.21 |
<0.001** |
1.000 |
<0.001** |
|
2 min |
96.63±14.44 |
89.17±14.47 |
97.27±12.2 |
0.095+ |
0.983 |
0.064+ |
|
3 min |
90.83±12.09 |
85.03±13.04 |
89.57±10.65 |
0.152 |
0.912 |
0.312 |
|
4 min |
89.57±12.01 |
81.93±14.68 |
85.2±11.75 |
0.062+ |
0.392 |
0.590 |
|
5 min |
88.00±11.06 |
79.63±11.91 |
83.47±12.05 |
0.018* |
0.294 |
0.415 |
|
7 min |
84.80±11.13 |
82.40±12.59 |
83.30±10.21 |
0.692 |
0.866 |
0.949 |
|
9 min |
85.60±8.63 |
80.30±11.20 |
84.83±11.01 |
0.122 |
0.956 |
0.212 |
|
11 min |
83.97±9.13 |
81.70±8.38 |
82.73±7.62 |
0.551 |
0.837 |
0.883 |
|
13 min |
86.03±8.89 |
81.83±14.07 |
82.37±9.22 |
0.305 |
0.403 |
0.981 |
|
15 min |
84.03±8.05 |
81.57±12.18 |
83.83±7.41 |
0.572 |
0.996 |
0.624 |
110
100
90
80
70
60
50
Basal 1 min 2
min 3 min 4
min 5 min 7
min 9
min 11 min 13 min 15 min
Post intubations
Figure 11: Graph showing changes in
Mean Diastolic Blood Pressure (DBP)
In control group the basal value of DBP was 78.27 mm
Hg, at I minute following intubation, the DBP increased by 103.63 mm Hg,
representing a rise of 25.36 mm Hg. This elevated pressure started coming down
by 3 minutes. By 3 minutes and by 5 minutes it was 90.83 mm Hg and 88.00 mm Hg
respectively.
In group I the basal value of DBP was 77.93 mm Hg, at
1 minute following intubation, the DBP increased by 91.77 mm Hg, representing a
rise of 13.84 mm Hg. This elevated pressure started coming down by 3 minutes.
By 3 minutes and by 5 minutes it was 85.03 mm Hg and 79.63 mm Hg respectively.
In group N the basal value of DBP was 78.87 mm Hg, at
1 minute following intubation, the DBP increased by 103.70 mm Hg, representing
a rise of 24.83 mm Hg. This elevated pressure started coming down by 3 minutes.
By 3 minutes and by 5 minutes it was 89.57 mm Hg and 83.47 mm Hg respectively.
Statistical evaluation between the groups showed that
the increase in DBP observed in control group was statistically highly
significant when compared to increase in DBP in group I but not group N.
The increase in DBP in group C and group I were
statistically highly significant compared to increase in DBP in group N (p <
0.001).
Between group C and group N there
was no statistical significance.
Between group I
and group N, the increase in DBP in group N was statistically significant
compared to increase in DBP in group I (p < 0.001).
8. CHANGES IN THE MEAN ARTERIAL PRESSURE (MAP)
Table 8 : Table showing changes in Mean
Arterial Pressure (MAP)
|
MAP (mm Hg) |
Group C |
Group I |
Group N |
Significant
values |
||
|
Group
C- Group
I |
Group
C- Group
N |
Group I- Group
N |
||||
|
Basal |
92.73±9.85 |
91.70±9.40 |
93.63±8.07 |
0.900 |
0.923 |
0.692 |
|
Post intubations |
|
|
|
|
|
|
|
1 min |
122.17±15.39 |
107.80±10.59 |
120.93±11.64 |
<0.001** |
0.925 |
<0.001** |
|
2 min |
116.60±14.96 |
106.03±14.67 |
114.67±12.83 |
0.014* |
0.858 |
0.053+ |
|
3 min |
109.90±11.91 |
100.13±13.86 |
105.87±12.44 |
0.011* |
0.442 |
0.196 |
|
4 min |
107.67±12.64 |
96.60±16.09 |
101.13±13.71 |
0.009** |
0.182 |
0.436 |
|
5 min |
105.27±11.54 |
94.97±13.28 |
98.90±12.43 |
0.005** |
0.123 |
0.442 |
|
7 min |
101.43±11.65 |
97.07±12.46 |
98.03±10.4 |
0.312 |
0.491 |
0.944 |
|
9 min |
100.57±9.70 |
94.80±10.14 |
99.20±10.58 |
0.077+ |
0.861 |
0.219 |
|
11 min |
98.83±9.20 |
96.00±7.82 |
96.87±7.9 |
0.389 |
0.633 |
0.914 |
|
13 min |
100.93±8.79 |
95.93±12.57 |
97.60±9.07 |
0.150 |
0.425 |
0.806 |
|
15 min |
98.50±8.71 |
96.17±11.12 |
98.83±7.72 |
0.596 |
0.989 |
0.510 |
150
140
Group C Group I Group
N
130
120
110
100
90
80
70
60
50
Basal 1 min 2
min 3 min 4
min 5 min 7
min 9
min 11 min 13 min 15 min
Post intubations
Figure12: Graph showing changes in Mean
Arterial Pressure (MAP)
In the control group the basal value of MAP was 92.73
mm Hg, at 1 minute following intubation, the MAP increased by 122.17 mm Hg,
representing a rise of 29.44 mm Hg. This elevated pressure started coming down
by 3 minutes. By 3 minutes and by 5 minutes it was 109.90 mm Hg and 105.27mm Hg
respectively.
In group I the basal value of MAP was 91.70 mm Hg, at
1 minute following intubation, the MAP increased by 107.80 mm Hg, representing
a rise of 16.1 mm Hg. This elevated pressure started coming down by 3 minutes. By
3 minutes and by 5 minutes it was100.13 mm Hg and 94.97 mm Hg respectively.
In group N the basal value of MAP was 93.63 mm Hg, at
1 minute following intubation, the MAP increased by 120.93 mm Hg, representing
a rise of 27.3 mm Hg. This elevated pressure started coming down by 3 minutes.
By 3 minutes and by 5 minutes it was 105.87mm Hg and 98.90 mm Hg respectively.
Statistical evaluation between the groups showed that
the increase in MAP observed in control group was statistically highly
significant when compared to increase in MAP in group I but not group N.
The increase in MAP in group C and group I were
statistically highly significant compared to increase in MAP in group N (p <
0.001).
Between group C and group N there
was no statistical significance.
Between group I
and group N, the increase in MAP in group N was statistically significant
compared to increase in MAP in group I (p <
0.001).
9.
CHANGES IN
THE MEAN SATURATION OF OXYGEN (SpO2) Table 9 : Table
showing changes in Mean Saturation of Oxygen.
|
SpO2(%) |
Group C |
Group I |
Group N |
P value |
|
Basal |
98.13±0.51 |
98.57±0.57 |
98.43±0.5 |
NS |
|
Post intubations |
|
|
|
|
|
1 min |
100.00 |
100.00 |
100.00 |
NS |
|
2 min |
100.00 |
100.00 |
100.00 |
NS |
|
3 min |
100.00 |
100.00 |
100.00 |
NS |
|
4 min |
100.00 |
100.00 |
100.00 |
NS |
|
5 min |
100.00 |
100.00 |
100.00 |
NS |
|
7 min |
100.00 |
100.00 |
100.00 |
NS |
|
9 min |
100.00 |
100.00 |
100.00 |
NS |
|
11 min |
100.00 |
100.00 |
100.00 |
NS |
|
13 min |
100.00 |
100.00 |
100.00 |
NS |
|
15 min |
100.00 |
100.00 |
100.00 |
NS |