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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 1^st, 2^nd, 3^rd, 5^th, 7^th, 9^th, 11^th and 15^th 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 intravenous^23,24 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 ASPECTS^{29, 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

 

 

100

 

 

98

 

 

96

 

 

94

 

 

92

 

 

90

Basal      1 min     2 min    3 min     4 min     5 min     7 min     9 min 11 min 13 min 15 min

Post intubations

 

Figure13: Graph showing changes in Mean Saturation of Oxygen (SpO₂) NS: Not significant

 

DISCUSSION

 

The frequent occurrence of cardiovascular reactions to laryngoscopy and endotracheal intubation has attracted the attention of anaesthesiologists for years. The reason being the reports of sudden death⁵³ immediately following intubation and its association with tachycardia, hypertension and arrhythmia.^2,3,4 This response is primarily because of sympatho-adrenal stimulation, associated with laryngoscopy and endotracheal intubation.¹ When Reid et al³⁴ found that stimulation of upper respiratory tract provoked an increase in vagal activity. A year later Burstein et al² totally contradicting Reid’s statement, found that the pressor response occurring at laryngoscopy and endotracheal intubation was due to augmented sympathetic response, provoked by stimulation of epipharynx and laryngopharynx. These factors were further confirmed by Prys-Roberts.⁴

The most important indications for attenuation of hemodynamic responses to laryngoscopy and endotracheal intubation becomes mandatory in patients with cardiovascular compromise like Ischemic heart disease (IHD) and Hypertension, patients with cerebrovascular diseases and in patients with intracranial aneurysms, even these transient changes can result in potentially deleterious effects like left ventricular failure,⁶ pulmonary oedema,⁶ myocardial ischemia⁷ and ventricular dysrhythmias⁴ and cerebral haemorrhage.⁸

Several techniques have been tried to modify the pressor response to laryngoscopy and tracheal intubation. None of these approaches entirely blocks the pressor response. Furthermore the methods themselves carry some additional risks, and agents used may be long-acting or have undesirable side effects.

 

Deep inhalational anaesthesia has been used to modify the response at the central nervous system level. However this technique cannot be used in the critically ill patients with diminished cardiovascular reserve.^{9, 10}

Opioids were found to be effective but they caused respiratory depression, chest wall rigidity and prolong the recovery time.^{5, 13}

Pharmacological blockade of the sympathetic system using nitruprusside⁴³ caused reflex tachycardia and required intra-arterial pressure monitoring and phentolamine¹⁴ causing intraoperative hypotension.

Beta blockers like esmolol, ⁴⁰ proctolol, ¹⁵ and labetolol ³⁹ are also used efficiently for blunting cardiovascular responses to laryngoscopy and intubation

Calcium channel antagonists like Nicardipine and Diltiazem¹⁶ are also effective in controlling the hemodynamic responses to laryngoscopy and intubation in normotensive as well as in hypertensive patients.

Local anaesthetic like lignocaine has been the most common agent used for blunting the haemodynamic responses to laryngoscopy and tracheal intubation.

Lignocaine has been used by the following routes to blunt the hemodynamic responses to intubation:

§  As lignocaine gargle for oropharyngeal analgesia.²⁰

 

21

§  As lignocaine aerosol for intratracheal analgesia.

 

§  As intravenous infusion for analgesia⁵⁴

 

§  As a topical spray.²²

 

Lignocaine has been successfully used to blunt the hemodynamic responses to intubation. The mechanisms explained for this action of lignocaine and desirable properties are as follows:

1.                      Suppression of airway reflexes elicited by irritation of epipharyngeal and larynggopharyngeal mucosa. ⁵⁵

2.                      Effectively prevents and treats laryngospasm²⁶

 

3.                      Excellent cough suppressant²⁵

 

4.                      Myocardial depression ²¹

 

5.                      Peripheral vasodilatation²¹

 

6.                      Antiarrythmic properties⁵⁶

 

7.                      Increasing depth of general anaesthesia, reduction in anaesthetic requirements of nitrous oxide and halothane⁵⁷

8.                      Depression of autonomic nervous system⁵⁸

 

9.                      Analgesic properties when given intravenously ⁵⁴

 

 

Gianelly et al⁵⁹ concluded that the concentration of lignocaine in the blood following intravenous administration was directly related to the dose given. They also concluded that an effective safe blood level of 2 to 5mcg/ml is obtained by intravenous bolus of 1 to 2mg/kg and major side effects may occur with blood levels 9mcg/ml.

Thomas et al⁶⁰ stated that blood concentrations were independent of dose in their investigation of absorption of lignocaine topically from vagina and episiotomy site, similarly Bromage states that from his results, the rate of absorption from trachea was not predictable.

Adriani⁶¹ asserts that the topical anaesthetic agents applied to the larynx and trachea are readily absorbed from the pulmonary alveoli.

 

The blood levels achieved after oropharyngeal anaesthesia with viscous lignocaine (25 ml of 2% as mouth wash and gargle 15 min before laryngoscopy) was found to be 0.5 mcg/ml at the time of laryngoscopy.²⁰ The average lignocaine level following aerosol anaesthesia of the upper airway (6-8 ml of a mixture of 1/3 of 2% viscous lignocaine and 2/3 of 4% aqueous lignocaine) was 1.2 mcg/ml at 1minute and 1.4mcg/ml at 2 minutes did prevent PVC²¹ in the treated patients even though minimum blood levels effective in suppression of premature ventricular contractions range from 0.6 – 2mcg/ml.⁶²

Inhalation of lignocaine aerosol is a safe, simple, effective and generally accepted method. Obvious limitations are small children, uncooperative patients, patients in whom there are danger due to regurgitation and vomiting and lack of time is another limitation.

With all the advantages and ease of administration of lignocaine and minimal side effects the present study was carried out to evaluate the efficacy of lignocaine in blunting the haemodynamic response to laryngoscopy and endotracheal intubation using two different routes of administration at similar dosage and look for any side effects.

We have studied 90 of ASA grade I and II patients of both sexes between 18-45 years of age posted for elective surgeries, which were allocated to three groups of 30 each.

The three groups were designated as,

 

 

Group C – received no drugs and served as control

 

Group I – received 2% lignocaine 2mg/kg slow intravenous 90sec before induction. Group N – received nebulization of 2% lignocaine 2mg/kg 10 min before induction.

 

Timing and Dosages of the drugs selected

 

Mounir Abou-Madi et al²³ compared two doses of 2% lignocaine when given intravenously for suppression of pressor response and suggested 1.5 mg/ kg provided better control of pressor response compared to 0.75 mg/ kg when given 2 to 3 min before laryngoscopy.

Stanlay Tam et al²⁴ observed that intravenous lignocaine at a dose of 1.5mg/kg attenuated the increase in Heart rate (HR) and Arterial Blood Pressure (ABP), only when given 3 min, before intubation and did not give any protection when given at 1 min, 2 min and 5 min before intubation.

We used 2 mg/ kg of 2% lignocaine for attenuation of pressor response and preferred to give 90 sec before induction.

Mounir Abou-Madi et al²¹ conducted a study on haemodynamic response to laryngoscopy and intubation following inhalation where pre-treated group of patients received inhalation of 6-8ml of mixture of 1/3rd of 2% viscous lignocaine + 2/3rd of 4% aqueous lignocaine using a bird nebulizer. Laryngoscopy and intubation was performed post 13 min with average plasma levels 1.4mcg/ml 2min of intubation. He observed that inhalation method used in the study protection was highly significant during  laryngoscopy but less convincing although significant, after intubation, probably because of incomplete anaesthesia of the trachea.

Bahaman Venus⁴⁷ studied the effects of nebulization of 6ml of 4% lignocaine on cardiovascular response to laryngoscopy and intubation 5 min before induction compared to control with saline nebulization. The pressor response and tachycardia was successfully prevented by the aerosol group than the control.

 

We wanted to find out whether the same dose of intravenous lignocaine when given by nebulization would have a similar pressor blunting effect. Hence the dose of 2 mg/ kg of 2% lignocaine was chosen.

ANALYSIS OF DATA WITHIN THE GROUP

 

Control group: The base line value of heart rate (HR) was 85.50 bpm. One min following laryngoscopy and intubation, the heart rate (HR) increased to 108.9 bpm, representing a rise of 23.4 bpm, above the baseline value. Thus the maximal rise of heart rate (HR) seen in the control group was by an average of 23.4bpm. It was seen that the elevated heart rate (HR) started settling down towards the base line value by 7 to11 min, but it was still above the base line value even at 7 min.

Mounir Abou-Madi et al²¹ noticed the increase in Heart rate (HR) in the control group following the laryngoscopy and intubation to be by 28bpm. Stanlay Tam et al²⁴ also noted that the maximal rise in Heart rate (HR) to be 25 bpm. Bahaman Venus⁴⁷ noticed a rise in the Heart rate (HR) of 32.6bpm. Miller CD et al⁴⁹noticed it to be around 27bpm.

Hence the results of the present study with regards to increase in the Heart rate (HR) observed in the control group following laryngoscopy and intubation concurs with the observation made by above mentioned authors.

In group I, where 2% Inj. Lignocaine 2mg/kg iv was administered to attenuate the hemodynamic response to laryngoscopy and intubation, the base line value of Heart rate (HR) was 86.13 bpm. One minute following laryngoscopy and intubation, the heart rate (HR) increased to 104.13 bpm, representing a rise of 18 bpm, above the base line value. Thus the maximal rise of Heart rate (HR) seen in the group I was by an average of 18 bpm. It was seen that the elevated Heart rate (HR) started settling down towards the baseline value by 7 min.

 

Mounir Abou-Madi²³ noticed the increase in the heart rate (HR) by 21.1 & 8.5 bpm using 1% lignocaine 0.75mg/kg iv and 2% lignocaine 1.5mg/kg iv respectively following laryngoscopy and intubation. Stanlay et al²⁴ noticed a rise in heart rate (HR) of 12 bpm. Miller CD⁴⁹ noticed a rise in the heart rate (HR) of 25 and Splinter et al⁴⁸  noticed it to be 19 bpm. The results obtained in our study were similar to those obtained by Splinter et al.

In group N, where nebulization of 2% Inj. Lignocaine 2mg/kg before laryngoscopy and intubation was used to blunt the pressor response, the base line value of Heart rate (HR) was 86.97 bpm. One minute following laryngoscopy and intubation, the heart rate (HR) increased to 111.83 bpm, representing a rise of 24.86 bpm above the base line value. Thus the maximal rise in heart rate (HR) seen was by an average of 24.86 bpm. It was seen that the elevated heart rate (HR) started settling down towards base line value by 11 min.

Mounir Abou-Madi et al²¹ observed in their study a rise of 13 bpm following 1min of laryngoscopy and intubation in the pre-treatment group with lignocaine nebulization. Bahaman Venus⁴⁷ noticed a rise of 6.2bpm. The rise of heart rate in our study compared to the above study is more, which can be attributed to the lesser percentage of the drug used for nebulization, and also the wastage of drug during exhalation in the processes of nebulization.

The maximum rise in heart rate was noted at 1 min following intubation in all the three groups which concurs well mentioned studies above. The mean rise in Heart rate at 1 min in control group was 23.4bpm compared to 18bpm and 24.86bpm in group I and group N respectively. The mean rise in the heart rate was comparatively lesser in the intravenous group but not statistically significant when compared to the group N and group C. There were no clinical or statistical significant difference between group C and

 

group I. In study conducted by Sklar BZ et al⁵² between intravenous lignocaine 1mg/kg and nebulized lignocaine at 40mg and 120mg control with saline, noticed that heart rate change was least with 120mg group when compared to other 3 groups. This does not concur with our study as the dose of intravenous lignocaine used above was only 1mg/kg.

There were no episodes of bradycardia in any of our study groups which was clinically significant.

BLOOD PRESSURE CHANGES

 

In the control group the basal value of Systolic blood pressure (SBP), Diastolic blood pressure (DBP), and Mean arterial pressure (MAP) was 121.73 mm Hg, 78.27 mm Hg, and 92.73 mm Hg respectively. Following laryngoscopy and intubation, the maximal rise in Systolic blood pressure (SBP) was found to be 42.6 mm Hg, that of Diastolic blood pressure (DBP) was 25.36 mm Hg and that of Mean arterial pressure (MAP) was 29.44 mm Hg. These elevated pressure readings started coming down by 5 minutes.

Mounir Abou-Madi et al²¹ noticed that, in control group SBP, DBP and MAP, increased by 60 mm Hg and 37 mm Hg respectively Stanley Tam et al²⁴ noticed that, in control group SBP, DBP and MAP, increased by 38 mm Hg, 26 mm Hg, and 32 mm Hg respectively. Miller CD⁴⁹ found that in control group, SBP and DBP increased by 31 mm Hg and 28 mm Hg respectively. Mounir Abou-Madi et al²³ found the rise in SBP and DBP to be 42 mm Hg and 30.7mm Hg respectively. Hence the results obtained in our study were similar to those obtained by the above mentioned authors.

In group I, where 2% Lignocaine 2mg/kg was employed 90sec before laryngoscopy and intubation to blunt the pressor responses, the maximal increase in the SBP, DBP and MAP was found to be 20.54 mm Hg, 13.84mm Hg and 16.1mm Hg respectively.

 

Mounir Abou- Madi et al²³ noticed the change in SBP by 17.6 and 30.4 mm Hg, change in the DBP was 20.1 and 21.8 mm Hg in lignocaine used in the doses of 0.75mg/kg and 1.5mg/kg IV respectively which does not concur as the dose used in the above study was lesser. Stanley Tam et al²⁴ employing Lignocaine 1.5 mg/kg IV observed maximal increase in SBP of 12 mm Hg, DBP of 9 mm Hg and MAP to be 11 mm Hg. Miller CD⁴⁹ noticed rise in SBP to be 33 mm Hg, DBP to be 37 mm Hg. Splinter et al⁴⁸ noticed a change in SBP to be 26 mm Hg, DBP to be 41 mm Hg and change in MAP to be 44 mm Hg.

In group N, where nebulization of 2% Inj. Lignocaine 2mg/kg before laryngoscopy and intubation to blunt the pressor response, the maximal increase in the SBP, DBP and MAP was found to be 32.26 mm Hg, 24.83mm Hg and 27.3mm Hg respectively.

Mounir Abou-Madi et al²¹ observed the changes in SBP, DBP following 1minute of laryngoscopy and intubation in the pre-treatment group with lignocaine nebulization to be 12mm Hg and 11mm Hg. Bahaman Venus ⁴⁷ noticed increase in the SBP, DBP and MAP to be 2.7mm Hg, 4mm Hg and 3.4mm Hg respectively. The rise of pressor response in our study compared to the above study is more, which can be attributed to the lesser percentage of only 2% being used when compared to above studies of the drug used for nebulization.

In our study the pressor response was highly significant in the intravenous group than the control which concurs well with Mounir Abou- Madi et al²³ as the dosage used by them was 1.5mg/kg when compared to 2mg/kg. In study conducted by Sklar BZ et al⁵² the maximum rise in mean arterial pressure of 21.2 mm Hg was noted with intravenous group and minimum with nebulized lignocaine of 120mg of 10.1 mm Hg which did not

 

concur with our study as the pressor response was much better statistically significant in group I when compared with the group N.

There were not much of significant changes in blood pressure in control and nebulization group in the current study as it can be attributed to the fact that a simple face mask was used for administration of nebulization, lesser concentration of drug used and the wastage of drug during exhalation.

ECG CHANGES

 

Prys-Roberts⁴ had commented that, sinus tachycardia is the most frequent ECG change observed during laryngoscopy and intubation. Burnsteil et al² reported that cardiac arrhythmias noticed in their study were most likely due to insufficient depth of anaesthesia, prolonged laryngoscopy, and numerous attempts at intubation. In our study we noticed, sinus tachycardia was the most common ECG abnormality. One of the patients in the control group, Case number (8) patient posted for Laproscopic cholecystectomy, had 4 to 5 premature ventricular contractions (PVC) per minute on continuous ECG monitoring immediately after intubation for a period of 5 minute, but the PVC’s were not associated with haemodynamic derangements. The patient was stable throughout the procedure, which was also noticed by Bahaman Venus and Venugopal Polassani ⁴⁷ in their study and as well by Mounir Abou-Madi et al²¹None of the patients, in any of the groups developed any ST-T changes.

There were no clinical or statistical changes that were seen with Oxygen saturation in any of the groups.

 

The majority of the patients who were nebulized with lignocaine complained of bitter taste post administration of the drug which we considered as a minor side effect but was not of much concern as it was for shorter period.

There were no other side effects or any hypersensitivity reactions to the drug documented in our study.

 

CONCLUSION

 

From the present study it can be concluded that

 

 

1.          Marked rise in the HR, SBP, DBP and MAP occur one minute following laryngoscopy and intubation, when no drug is employed to attenuate the pressor response to intubation.

2.          Intravenous lignocaine 2% in the dose of 2mg/kg before induction effectively controlled the haemodynamic response to laryngoscopy and endotracheal intubation. However, blood pressure changes seem to be better than heart rate changes.

3.          Nebulized lignocaine 2% in the dose of 2mg/kg was not effective in controlling the haemodynamic changes though there was marginal increase in blood pressure responses.

In our study though nebulization was not effective in blunting the haemodynamic responses to laryngoscopy and intubation, it is still a safe and a simple technique to be used.

In our opinion it could be beneficial if:

 

1.  Proper nebulization could be administered minimizing its wastage during exhalation even though we did not asses the percentage wasted in the present study.

2.  A higher concentration of the drug could have better beneficial aspects.

 

3.  A longer latent period of time for complete establishment of the effects of nebulization on the airway as we have used a lesser concentration of lignocaine in our study.

 

SUMMARY

 

The present study entitled “COMPARATIVE STUDY OF LIGNOCAINE NEBULIZATION WITH INTRAVENOUS LIGNOCAINE ON STRESS RESPONSE TO LARYNGOSCOPY AND TRACHEAL INTUBATION” was carried

out at Victoria Hospital and Bowring and Lady Curzon Hospitals, Bangalore from November 2008 to May 2010. The study population consisted of 90 patients divided in three groups.

 

 

1.  Control Group – Received no drugs and served as control (n=30).

 

2.  Group I – Received 2% Lignocaine 2mg/kg iv 90 seconds before induction (n = 30).

 

3.   Group N – Received nebulization with 2% Lignocaine 2mg/kg 10 minute before induction (n = 30).

The demographic changes such as Age, Sex, Weight, type of surgeries were comparable in all the groups.

The maximum rise in heart rate was noted at 1 min following intubation in all the three groups. The mean rise in Heart rate at 1 minute in control group was 23.4bpm compared to 18bpm and 24.86bpm in group I and group N respectively.

The maximum rise in Systolic blood pressure was noted at 1 min following intubation in all the three groups. The mean rise in Systolic blood pressure in control group was 42.6mm Hg compared to 17.54mm Hg and 32.26mm Hg in group I and group N respectively.

The maximum rise in Diastolic blood pressure was noted at 1 min following intubation in all the three groups. The mean rise in Diastolic blood pressure in control

 

group was 25.36 mm Hg compared to 13.84 mm Hg and 24.83 mm Hg in group I and group N respectively.

The maximum rise in Mean arterial blood pressure was noted at 1 min following intubation in all the three groups. The mean rise in Mean arterial blood pressure in control group was 29.44 mm Hg compared to 16.1 mm Hg and 27.3 mm Hg in group I and group N respectively.

In this study the maximum change in heart rate and blood pressure was noted in control group and minimum change in intravenous lignocaine group, though the rise in heart rate was similar in group C and group N. There was marginal and statistically insignificant decrease in blood pressure when compared to group C.

Intravenous lignocaine was effective in attenuating pressor response to laryngoscopy and endotracheal intubation. However, nebulization of 2% lignocaine did not sufficiently blunt the haemodynamic response to laryngoscopy and endotracheal intubation.

 

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ANNEXURES

BANGALORE MEDICAL COLLEGE AND RESEARCH INSTITUTE

Comparative Study of Lignocaine Nebulization with Intravenous Lignocaine on stress response to Laryngoscopy and Tracheal intubation.

 

NAME:                                       AGE/SEX:                                                   IP NO

 

 

ADDRESS:                                                                                           DOA:

 

DOS:

 

OCCUPATION:                                                                                          UNIT:

 

DIAGNOSIS:

 

PROCEDURE:

 

 

PRE ANAESTHETIC EVALUATION:

 

History:

 

 

GPE:

 

Pallor/icterus/clubbing/cyanosis/lymphnodes/Edema

 

Weight:  Height:

 

 

Vitals:                                                                              Airway assessment

 

Pulse rate:                                                                         MPT:

 

BP:                                                                                    Neck:

 

Spine:

 

Systemic Examination:

 

 

CVS:                                                                                 CNS:

 

RS:                                                                                    ABD:

 

Salient Investigation:

 

Hb:                                                                                    ECG:

 

BT/CT:                                                                             CXR:

 

RBS:                                                                                 ECHO:

 

FBS/PPBS:

 

BUN/SrCreat:

 

Urine routine:

 

 

Case accepted as ASA grade

 

CONSENT

 

 

 

I, /on behalf of my relative(specify),hereby give my consent for the study mentioned above and the benefits and risks of the procedure have been explained to me in my mother tongue.

 

 

Signature/LTI

 

 

Anaesthetic management:

 

IVL secured in                       with 18G VF and IVF started Monitors connected

 

Study groups:

 

Group C: will be control

 

Group N: will receive 2% Lignocaine nebulization 2mg/kg 10 min before induction

 

Group I: will receive 2% Lignocaine intravenously 2mg/kg 90 sec slowly before induction

 

Pre oxygenation: done with 100% of oxygen by mask for 3 minutes. Premedication: Inj Midazolam 1 mg iv.

Induction: Inj. Thiopentone 5 mg/kg iv + Inj. Succinyl choline 1.5mg/kg iv Intubation: Size of the endotracheal tube passed:

Maintenance of anaesthesia: O2 + N2O + Halothane + Vecuronium

Reversal of anaesthesia: Inj. Neostigmine 0.05 mg/kg + Inj. Glycopyrrolate 0.01 mg/kg.

 

Haemodynamic Monitoring

 

Time		Drugs	Pulse	SBP	DBP	MAP	SpO2	Remarks
Basal
Postintubatn	1st min
	2nd min
	3rd min
	4th min
	5th min
	7thmin
	9th min
	11th min
	15th min

 

 

 

 

 

Complications and side effects if any:

 

Post Op: general condition

 

Pulse:                                BP:             SpO_2:

GROUP I Inj LIGNOCAINE 2mg/Kg INTRAVENOUS

SL No

Name

Age(yrs)

Sex

Wt(Kg)

Diagnosis

Surgical procedure

Heart rate

Systolic Blood Pressure

Diastolic Blood Pressure

Mean arterial pressure

SPO2

Basal

Post intubation

Basal

Post Intubation

Basal

Post Intubation

Basal

Post intubation

Basal

Post intubation

								1min	2min	3min	4min	5min	7min	9min	11min	13min	15min		1min	2min	3min	4min	5min	7min	9min	11min	13min	15min		1min	2min	3min	4min	5min	7min	9min	11min	13min	15min		1min	2min	3min	4min	5min	7min	9min	11min	13min	15min		1min	2min	3min	4min	5min	7min	9min	11min	13min	15min
1	Yashaoda	38	F	68	Lump in Left Breast	MRM	86	94	98	78	78	79	76	79	77	67	70	122	131	135	123	120	125	116	111	107	107	107	80	89	86	80	80	84	75	74	70	67	69	94	103	102	94	93	98	89	86	82	80	82	98	100	100	100	100	100	100	100	100	100	100
2	Jayamma	40	F	60	Ca right breast	MRM	104	102	102	108	90	94	87	89	79	83	86	134	157	153	159	139	152	160	153	154	153	150	68	78	71	76	75	79	84	80	75	77	77	90	104	98	104	96	103	109	104	101	102	101	99	100	100	100	100	100	100	100	100	100	100
3	Lakshmi	28	F	57	Acute Cholecystitis	Cholecystectomy	92	106	100	95	96	120	103	84	113	111	116	106	122	127	119	125	139	130	124	125	119	119	74	65	80	91	93	99	87	88	85	90	87	85	84	96	100	104	112	101	100	98	100	98	98	100	100	100	100	100	100	100	100	100	100
4	Vijayalakshmi	50	F	65	Acute Cholecystitis	Cholecystectomy	89	90	88	93	67	78	79	85	81	84	87	115	127	127	147	84	102	128	127	137	144	142	76	90	85	106	57	65	77	90	80	105	81	89	102	99	120	66	77	94	102	99	118	101	99	100	100	100	100	100	100	100	100	100	100
5	Rathnamma	35	F	56	Sub acute intestinal obstruction	Ileo colic anastomosis	107	101	116	130	97	96	92	93	88	80	85	134	141	149	153	134	132	133	127	133	119	130	88	88	91	91	78	78	77	76	70	73	81	103	106	110	112	97	96	96	93	91	88	97	99	100	100	100	100	100	100	100	100	100	100
6	Lakshmi	45	F	60	Thyroid nodule	Hemi thyroidectomy	92	96	91	85	83	84	80	82	79	78	80	113	139	114	119	137	134	130	126	130	130	139	78	82	79	86	98	91	96	92	94	92	87	90	101	91	97	111	105	107	103	106	105	104	98	100	100	100	100	100	100	100	100	100	100
7	Ramanj	23	M	50	Appendicites	Appendectomy	88	97	90	108	95	86	83	86	120	98	88	112	128	113	111	111	106	107	111	118	115	119	67	91	67	74	74	67	67	66	84	84	88	82	103	82	86	86	80	80	81	95	94	98	99	100	100	100	100	100	100	100	100	100	100
8	Vanaja	30	F	54	MNG	Subtotal thyroidectomy	96	102	86	77	79	83	77	85	75	84	78	115	140	123	118	130	112	118	124	115	116	112	76	84	80	71	87	72	71	73	72	72	72	89	103	94	87	101	85	87	90	87	87	85	99	100	100	100	100	100	100	100	100	100	100
9	Sidappa	19	M	45	PBC Axilla	Release & SSG	82	107	106	102	98	98	91	87	90	90	80	109	144	142	140	132	143	134	130	124	111	123	69	91	92	86	94	86	98	85	84	71	81	82	109	109	104	107	105	110	100	97	84	95	98	100	100	100	100	100	100	100	100	100	100
10	lolakshi	26	F	40	Thyroid nodule	Hemi thyroidectomy	79	100	97	104	85	90	97	95	82	80	70	100	129	133	109	98	111	120	119	116	115	120	80	102	59	71	65	87	84	89	66	60	53	87	111	84	84	76	95	96	99	83	78	75	99	100	100	100	100	100	100	100	100	100	100
11	Kempaya	40	M	64	Mirizzi syndrome	Cholecystectomy	90	96	85	76	74	82	69	67	66	64	73	104	126	109	107	140	137	137	135	137	143	139	64	84	75	81	89	87	84	84	86	84	84	77	98	86	90	106	104	102	101	103	104	102	99	100	100	100	100	100	100	100	100	100	100
12	Manjula	45	F	50	Acute Cholecystitis	Cholecystectomy	76	106	100	102	106	103	103	106	103	95	100	104	136	136	109	103	133	132	133	120	124	130	86	103	103	103	86	100	100	86	86	95	86	92	114	114	105	92	111	111	102	97	105	101	98	100	100	100	100	100	100	100	100	100	100
13	Bhagyamma	42	F	42	Sub mandibular swelling	Excision	89	108	98	98	90	105	102	88	86	88	98	117	130	135	122	121	136	122	114	114	109	117	72	81	90	89	75	92	89	83	82	86	84	87	97	105	100	90	107	100	93	93	94	95	97	100	100	100	100	100	100	100	100	100	100
14	Yellanna	30	M	58	Acute Cholecystitis	Cholecystectomy	100	124	118	118	66	85	97	89	92	96	89	118	130	169	109	106	136	147	120	117	125	118	75	85	110	70	67	81	103	86	87	94	91	89	100	130	83	80	99	118	97	97	104	100	98	100	100	100	100	100	100	100	100	100	100
15	Rehmath sulthana	34	F	58	MNG	Subtotal thyroidectomy	96	109	101	98	99	93	87	88	96	95	90	114	157	153	133	122	120	123	120	125	115	128	72	100	95	79	74	81	74	90	84	80	86	86	119	114	97	90	94	90	100	98	92	100	98	100	100	100	100	100	100	100	100	100	100
16	Nagarathna	44	F	43	Appendicites	Appendectomy	78	84	91	91	90	91	88	87	93	90	96	144	159	171	189	194	182	168	135	120	143	149	91	103	117	124	134	105	113	99	95	113	105	109	122	135	146	154	131	131	111	103	123	120	98	100	100	100	100	100	100	100	100	100	100
17	Anjanayaswamy	28	M	66	MNG	Subtotal thyroidectomy	76	92	121	135	127	122	110	98	100	90	100	138	147	153	131	128	128	128	130	136	134	127	95	103	88	83	83	84	85	85	90	90	87	109	118	110	99	98	99	99	100	105	105	100	98	100	100	100	100	100	100	100	100	100	100
18	Ansar begum	34	F	54	Cholelithiasis	Cholecystectomy	90	97	108	93	86	92	89	83	94	98	98	126	147	162	133	118	118	122	129	133	147	146	89	104	115	92	82	81	85	91	92	100	100	101	118	131	106	94	93	97	104	106	116	115	98	100	100	100	100	100	100	100	100	100	100
19	Faisal ahmed	45	M	85	Colloid goitre	Subtotal thyroidectomy	90	105	103	107	114	106	98	96	98	99	103	130	139	138	140	118	108	120	122	118	128	126	84	104	96	95	83	76	93	80	78	70	84	99	116	110	110	95	87	102	94	91	89	98	99	100	100	100	100	100	100	100	100	100	100
20	Ramachandra	32	M	40	Papillary Ca Thyroid	Total thyroidectomy	93	100	100	102	97	83	73	76	65	76	71	120	115	140	143	135	105	108	109	116	132	141	82	79	84	86	88	71	72	73	76	82	97	95	91	103	105	104	82	84	85	89	99	112	99	100	100	100	100	100	100	100	100	100	100
21	Suresh	26	M	45	Colloid goitre	Hemi thyroidectomy	88	97	106	107	96	85	81	79	80	83	67	111	140	156	140	136	130	103	93	103	113	103	64	104	102	90	74	70	68	62	70	69	71	80	116	120	107	95	90	80	72	81	84	82	98	100	100	100	100	100	100	100	100	100	100
22	Hema	20	F	38	Sub mandibular swelling	Excision	74	133	133	116	96	75	77	76	79	76	74	122	161	135	113	115	99	104	105	113	110	106	78	114	91	75	77	66	69	72	81	76	76	93	130	106	88	90	77	81	83	92	87	86	99	100	100	100	100	100	100	100	100	100	100
23	Shivaraju	23	M	67	Csyt in the neck	Excision	98	136	129	120	102	100	98	90	86	90	92	102	129	118	117	98	116	110	102	119	122	103	51	79	72	67	57	70	61	51	80	61	54	68	96	87	84	71	85	77	68	93	81	70	99	100	100	100	100	100	100	100	100	100	100
24	Gangalakshmamma	21	F	50	Cholecystitis	Cholecystectomy	72	106	96	75	103	100	97	90	83	80	72	122	136	153	130	140	134	133	129	130	110	109	90	103	115	100	99	65	68	70	76	91	90	101	114	128	110	113	88	90	90	94	97	96	99	100	100	100	100	100	100	100	100	100	100
25	Dhanalakshmi	45	F	66	Phylloids Tumour	Simple mastectomy	71	88	91	89	86	80	86	83	86	81	67	114	130	132	126	126	115	128	123	120	119	120	74	84	84	75	76	67	70	70	70	70	67	87	99	100	92	93	83	89	88	87	86	85	99	100	100	100	100	100	100	100	100	100	100
26	DilshadBegum	30	F	58	Cholelithiasis	Laproscopic Cholecystectomy	80	110	116	106	98	98	95	92	84	89	86	115	138	131	103	100	102	128	130	129	134	120	82	80	82	76	71	72	94	97	96	98	92	93	99	98	85	81	82	105	108	107	110	101	99	100	100	100	100	100	100	100	100	100	100
27	Hemavathi	35	F	52	Axillary tail tumour	Excision	80	108	104	92	95	96	83	80	68	77	68	116	147	117	117	130	103	116	110	147	102	126	80	94	75	63	71	54	70	61	94	51	61	92	112	89	81	91	70	85	91	112	68	83	99	100	100	100	100	100	100	100	100	100	100
28	Riyaz	36	M	79	Recurrent appendicitis	Laproscopic appendicectomy	70	120	122	118	115	112	100	90	94	88	80	130	140	142	136	133	122	120	116	122	128	128	76	90	92	84	88	86	80	83	76	78	80	94	107	109	101	103	98	93	94	91	95	96	99	100	100	100	100	100	100	100	100	100	100
29	Nagesh	35	M	72	IVDP L4-L5	Fenestration discectomy	68	102	104	100	101	98	94	97	88	80	74	132	178	175	163	165	159	151	148	136	134	138	87	100	103	97	94	93	94	88	86	88	86	102	126	127	119	118	115	113	108	103	103	103	99	100	100	100	100	100	100	100	100	100	100
30	Munnishivanna gowda	45	M	68	# Left clavicle	ORIF with recon plate	90	108	106	108	100	94	92	90	93	90	88	138	150	150	145	130	133	120	122	126	125	133	90	99	96	90	89	80	84	85	86	88	90	106	116	114	108	103	98	96	97	99	100	104	99	100	100	100	100	100	100	100	100	100	100
GROUP N Inj LIGNOCAINE 2mg/Kg NEBULIZATION
SL No	Name	Age(yrs)	Sex	Wt(Kg)	Diagnosis	Surgical procedure	Heart rate											Systolic Blood Pressure											Diastolic Blood Pressure											Mean arterial pressure											SPO2
							basal	post intubation										Basal	Post Intubation										Basal	Post Intubation										Basal	Post intubation										Basal	Post intubation
								1min	2min	3min	4min	5min	7min	9min	11min	13min	15min		1min	2min	3min	4min	5min	7min	9min	11min	13min	15min		1min	2min	3min	4min	5min	7min	9min	11min	13min	15min		1min	2min	3min	4min	5min	7min	9min	11min	13min	15min		1min	2min	3min	4min	5min	7min	9min	11min	13min	15min
1	Byamma	45	F	62	MNG	Sub Total Thyroidectomy	112	104	109	104	113	99	101	103	99	84	82	124	155	153	131	145	147	142	142	151	147	151	68	105	80	89	90	96	93	96	97	98	95	87	122	104	103	108	113	109	111	115	114	114	99	100	100	100	100	100	100	100	100	100	100
2	Mariam Begum	34	F	62	Chronic Cholecystitis	Laproscopic Cholecystectomy	102	122	108	100	102	87	78	79	70	62	81	139	153	153	133	137	128	128	119	128	106	104	82	115	115	84	84	91	90	88	80	66	68	101	128	128	100	102	103	103	98	96	79	80	98	100	100	100	100	100	100	100	100	100	100
3	Muniyamma	44	F	70	CBDstone	CBD Exploration	90	95	89	82	94	87	84	93	77	77	82	130	177	166	156	177	153	157	158	146	151	146	77	113	96	80	97	77	86	88	88	86	80	95	134	119	105	124	102	110	111	107	108	102	98	100	100	100	100	100	100	100	100	100	100
4	rangaramaiah	45	F	68	cholilithiasis	Cholecystectomy	91	113	104	92	80	78	74	71	74	69	86	137	173	158	127	103	99	114	105	109	118	135	84	106	92	87	72	67	71	69	70	77	84	102	128	114	100	82	78	85	81	83	91	101	98	100	100	100	100	100	100	100	100	100	100
5	manchamma	45	M	64	GB Polyp with CBD Stone	Laprotomy and procedure	105	111	106	97	102	100	96	88	102	82	73	152	186	132	136	147	143	119	132	129	136	123	96	108	91	87	92	86	86	85	87	84	79	115	134	105	103	110	105	97	101	101	101	94	98	100	100	100	100	100	100	100	100	100	100
6	Jayamma	42	F	40	Papillary ca thyroid	Total thyroidectomy	76	93	99	109	107	98	94	91	83	85	83	114	134	167	122	115	113	119	123	117	121	123	75	91	125	90	84	82	87	90	85	80	90	88	105	139	101	94	92	98	101	96	94	101	98	100	100	100	100	100	100	100	100	100	100
7	Bibi Fathima	18	F	44	Colloid goitre	Sub Total Thyroidectomy	90	87	107	124	114	96	99	87	77	105	88	118	119	140	136	115	121	133	120	108	108	112	78	81	108	93	76	79	64	79	72	83	80	91	94	119	107	89	93	87	93	84	91	91	99	100	100	100	100	100	100	100	100	100	100
8	Lakshmi Shankar	37	F	56	Duplication of colon	Laprotomy and procedure	84	115	109	112	78	74	69	62	90	104	103	121	170	117	114	95	115	121	117	112	128	131	89	108	81	80	67	85	90	86	85	97	98	100	129	93	91	76	95	100	96	94	107	109	99	100	100	100	100	100	100	100	100	100	100
9	Heena	18	F	40	Appendecitis	LaproscopicAppendecectomy	108	143	134	137	134	130	127	126	118	111	110	110	170	133	109	106	101	98	96	108	121	116	71	125	79	68	57	44	57	40	62	59	83	84	140	97	82	73	63	71	59	77	80	94	99	100	100	100	100	100	100	100	100	100	100
10	Tabassum	29	F	42	Chronic Cholecystitis	Laproscopic Cholecystectomy	92	105	108	105	109	114	119	120	101	102	104	136	137	198	198	143	163	143	144	131	131	149	78	88	115	115	85	98	95	90	80	80	87	97	104	143	143	104	120	111	108	97	97	108	99	100	100	100	100	100	100	100	100	100	100
11	Meenakshi	23	F	46	Cholilithiasis	Laproscopic Cholecystectomy	76	102	98	94	97	92	82	78	72	79	65	116	159	140	110	117	127	113	129	128	126	125	83	106	84	75	83	80	72	99	92	86	82	94	124	103	87	94	96	86	109	104	99	96	98	100	100	100	100	100	100	100	100	100	100
12	Kamalamma	45	F	60	MNG	Sub Total Thyroidectomy	80	95	78	80	71	72	76	74	73	64	68	118	177	141	137	145	136	144	137	117	154	145	72	107	83	96	78	89	91	92	76	74	90	87	130	102	110	100	105	109	107	90	101	108	99	100	100	100	100	100	100	100	100	100	100
13	Ammeerunissa	45	F	45	Ca Pancrease head	Cholecystojejunostomy	84	134	133	114	115	114	116	114	109	102	106	132	144	178	150	147	134	122	119	115	115	129	82	90	104	89	79	86	75	74	79	78	82	99	108	129	109	102	102	91	89	91	90	98	98	100	100	100	100	100	100	100	100	100	100
14	Munirudhramma	35	F	59	MNG	Sub Total Thyroidectomy	100	132	139	139	118	106	100	106	98	96	91	132	177	175	162	145	132	110	130	134	133	128	80	122	120	96	92	80	81	96	97	90	92	97	140	138	118	110	97	91	107	109	104	104	99	100	100	100	100	100	100	100	100	100	100
15	Sumithra Bai	30	F	56	Hypertrophied scar chest	Excision and SSG	75	124	119	80	89	83	78	88	82	89	88	114	151	127	118	155	138	146	141	136	144	132	77	101	92	86	108	90	101	94	95	97	82	89	118	104	97	124	106	116	110	109	113	99	98	100	100	100	100	100	100	100	100	100	100
16	M.V.Bharathi	20	F	49	Acute Appendecitis	LaproscopicAppendecectomy	84	94	81	86	80	84	76	79	83	80	82	108	138	148	116	108	118	108	138	129	136	124	66	81	95	67	66	73	66	95	82	85	81	80	100	113	83	80	88	80	109	98	102	95	99	100	100	100	100	100	100	100	100	100	100
17	Mariyamma	45	F	50	Acalasia Cardia	Hellers procedure	79	94	105	111	100	102	97	87	86	85	79	134	151	145	140	127	133	119	120	112	126	145	96	111	106	110	98	92	89	88	84	94	106	109	124	119	120	108	106	99	99	93	105	119	98	100	100	100	100	100	100	100	100	100	100
18	Manjula	26	F	45	Secondary Ammenorrhoea	Diagnostic Laproscopy	80	97	98	93	86	93	79	75	70	68	69	118	140	129	140	126	128	114	111	132	105	129	78	87	84	84	84	86	75	75	86	69	80	91	105	99	103	98	100	88	87	101	81	96	98	100	100	100	100	100	100	100	100	100	100
19	Amar	24	M	44	Recurrent appendicites	LaproscopicAppendecectomy	98	141	127	102	93	86	89	102	87	85	112	123	160	127	113	114	112	115	142	136	141	143	74	122	88	84	75	70	78	93	79	82	84	90	135	101	94	88	84	90	109	98	102	104	98	100	100	100	100	100	100	100	100	100	100
20	Nage Nayak	41	M	78	Cholecystitis	Laproscopic Cholecystectomy	63	82	80	73	68	60	66	69	67	62	69	111	153	129	127	95	94	120	122	135	145	128	72	101	83	79	66	59	80	88	86	97	83	85	118	98	95	76	71	93	99	102	113	98	98	100	100	100	100	100	100	100	100	100	100
21	Kiran	30	M	66	Lipoma nape of neck	Excision	74	118	116	118	104	100	90	98	96	88	90	130	154	150	145	133	126	130	128	122	128	128	84	104	100	94	96	99	90	88	82	86	84	99	121	117	111	108	108	103	101	95	100	99	99	100	100	100	100	100	100	100	100	100	100
22	Rukmani	37	F	62	Fibroadenoma left breast	Excision	72	126	120	118	115	100	98	94	96	88	86	126	154	150	145	147	140	138	133	126	128	130	76	106	102	100	96	95	88	80	76	78	80	93	122	118	115	113	110	105	98	93	95	97	99	100	100	100	100	100	100	100	100	100	100
23	Devika	45	F	65	IVDP L4-L5,L5-S1	Fenestration discectomy	78	100	102	99	95	96	80	88	84	80	76	116	156	155	148	140	126	122	124	118	122	123	82	104	100	90	88	80	78	80	78	80	81	93	121	118	110	105	95	93	95	91	94	95	99	100	100	100	100	100	100	100	100	100	100
24	Chittamma	40	F	60	Cholilithiasis	Cholecystectomy	84	122	120	120	115	117	109	100	96	90	94	134	152	150	143	145	130	126	119	120	122	130	90	110	94	90	86	80	84	84	86	80	78	105	124	113	108	106	97	98	96	97	94	95	98	100	100	100	100	100	100	100	100	100	100
25	Santhosh	18	M	52	# Both bones right forearm	ORIF	86	118	120	116	106	90	94	92	88	89	86	118	158	156	148	140	138	139	135	128	119	122	88	100	99	96	90	84	88	86	79	79	82	98	119	118	113	107	102	105	102	95	92	95	98	100	100	100	100	100	100	100	100	100	100
26	Indramma	35	F	54	Fibroadenoma left breast	Excision	88	110	116	112	100	99	92	89	87	88	92	104	138	142	144	139	135	134	128	126	122	116	76	94	92	90	88	85	85	86	84	80	78	85	109	109	108	105	102	101	100	98	94	91	98	100	100	100	100	100	100	100	100	100	100
27	Mumtaz	30	F	56	Acute Appendecitis	Appendecectomy	88	120	118	119	112	100	96	98	99	84	88	122	160	158	155	150	147	142	136	128	128	126	84	110	98	96	94	95	87	88	88	89	88	97	127	118	116	113	112	105	104	101	102	101	98	100	100	100	100	100	100	100	100	100	100
28	Syed Sadiq	19	M	54	# Left clavicle	Open reduction with K wire	94	128	126	127	120	119	109	101	98	92	90	118	149	152	147	143	139	133	129	128	126	120	70	109	110	104	100	98	99	84	86	85	88	86	122	124	118	114	112	110	99	100	99	99	98	100	100	100	100	100	100	100	100	100	100
29	Perumal	25	M	73	Crush injury left hand	Debridement and SSG	86	115	116	109	107	100	99	95	89	83	84	128	165	164	158	155	140	142	132	130	134	130	70	108	106	100	98	90	91	88	84	80	76	89	127	125	119	117	107	108	103	99	98	94	99	100	100	100	100	100	100	100	100	100	100
30	Ganapathy	19	M	58	Left gynaecomastia	Subcutaneouse mastectomy	90	115	107	104	100	102	102	101	99	93	92	112	153	148	144	138	134	133	130	122	119	115	68	98	96	88	87	88	82	76	77	72	74	83	116	113	107	104	103	99	94	92	88	88	99	100	100	100	100	100	100	100	100	100	100
GROUP C  CONTROL
SL No	Name	Age(yrs)	Sex	Wt(Kg)	Diagnosis	Surgical procedure	HEART RATE											Systolic Blood Pressure											Diastolic Blood Pressure											Mean arterial pressure											SPO2
							Basal	Post intubation										Basal	Post Intubation										Basal	Post Intubation										Basal	Post intubation										Basal	Post intubation
								1min	2min	3min	4min	5min	7min	9min	11min	13min	15min		1min	2min	3min	4min	5min	7min	9min	11min	13min	15min		1min	2min	3min	4min	5min	7min	9min	11min	13min	15min		1min	2min	3min	4min	5min	7min	9min	11min	13min	15min		1min	2min	3min	4min	5min	7min	9min	11min	13min	15min
1	Pungodi	40	F	64	Right Ca Breast	MRM	98	125	111	104	100	100	96	89	82	89	87	138	175	213	121	127	138	145	135	147	143	134	77	101	92	83	86	85	84	80	98	102	92	97	126	132	96	100	105	104	98	114	116	106	99	100	100	100	100	100	100	100	100	100	100
2	Bharathamma	24	F	50	Lipoma Right shoulder	Excision	99	128	118	108	91	103	89	86	89	92	101	150	198	172	128	118	128	122	114	125	126	136	96	129	106	80	76	89	84	80	82	84	88	114	152	128	96	90	102	97	91	96	98	104	98	100	100	100	100	100	100	100	100	100	100
3	Honnappa	44	M	76	Lipoma back	Excision	90	100	75	76	68	81	76	68	100	96	80	128	174	116	143	134	124	127	123	128	130	135	88	123	86	116	102	84	86	84	86	83	87	101	140	96	125	113	97	100	97	100	99	103	98	100	100	100	100	100	100	100	100	100	100
4	Kamalamma	43	F	78	Solitary nodule thyroid	Left hemithyroidectomy	61	62	69	71	72	70	69	68	64	62	61	129	187	157	155	165	153	144	143	130	127	137	89	110	98	107	105	103	98	94	85	85	91	102	136	118	123	125	120	113	110	100	99	106	97	100	100	100	100	100	100	100	100	100	100
5	Chandrappa	45	M	80	Cholilithiasis with CBD Stone	Cholecystectomy ,CBDexpl	73	87	69	69	72	75	75	65	63	68	64	154	205	199	167	140	125	117	133	135	143	149	88	134	102	90	102	100	76	89	88	93	102	110	158	134	116	115	108	90	104	104	110	118	98	100	100	100	100	100	100	100	100	100	100
6	Mala	40	F	50	Hashimotos thyroiditis	Thyroidectomy	92	107	98	104	94	93	93	87	81	84	77	123	160	149	142	134	133	136	155	139	150	135	85	108	94	93	95	93	87	100	102	96	96	98	125	112	109	108	106	103	118	114	114	109	99	100	100	100	100	100	100	100	100	100	100
7	Govindaraju	26	M	54	Acut appendecites	Laproscopic appendecectomy	88	120	119	114	100	95	96	92	93	89	88	124	166	160	158	156	155	148	144	145	137	133	75	102	102	100	99	96	94	90	87	85	84	91	123	121	119	118	116	112	108	106	102	100	98	100	100	100	100	100	100	100	100	100	100
8	Hamsa	44	F	62	Cholecystitis	Laproscopic cholecystectomy	72	96	90	84	84	82	76	71	68	72	80	138	205	186	185	182	177	141	138	124	163	120	81	104	113	104	97	93	90	81	74	82	75	100	138	137	131	125	121	107	100	91	109	90	98	100	100	100	100	100	100	100	100	100	100
9	Marulaiah	45	M	50	Ca Rectum	APR	86	108	94	98	96	94	101	105	89	90	93	125	177	169	167	161	153	152	149	149	145	142	70	104	89	75	75	86	97	101	92	94	95	88	128	116	106	104	108	115	117	111	111	111	98	100	100	100	100	100	100	100	100	100	100
10	Maqbool	22	M	54	PBRA Anterior trunk	SSG	100	120	116	102	100	102	104	98	90	93	90	98	138	128	123	116	114	112	105	102	107	100	66	96	87	85	80	78	77	79	72	60	70	77	95	101	98	92	90	89	88	82	76	80	99	100	100	100	100	100	100	100	100	100	100
11	Shilpa	18	F	44	Burns both knees	SSG	86	125	120	116	100	101	96	94	93	90	87	109	148	147	145	142	138	135	129	128	124	120	72	104	103	100	101	95	90	92	87	81	74	84	119	118	115	115	109	105	104	101	95	89	98	100	100	100	100	100	100	100	100	100	100
12	Hema	18	F	40	PBC Left elbow	SSG	90	118	109	99	101	101	112	98	94	98	96	107	154	145	142	139	138	117	114	117	123	122	57	99	54	76	67	62	50	76	72	74	74	74	94	84	98	91	87	72	89	87	90	90	97	100	100	100	100	100	100	100	100	100	100
13	Faslunissa	44	F	56	Ca left breast	MRM	84	102	104	94	96	99	102	101	94	92	80	118	150	147	133	129	125	124	125	127	119	117	73	94	130	82	88	82	83	80	84	69	86	88	113	136	99	102	96	97	95	98	86	96	98	100	100	100	100	100	100	100	100	100	100
14	Baghyamma	18	F	42	Sub mandibular swelling	Excision	90	113	109	105	98	96	102	97	99	98	88	98	136	135	130	124	122	121	117	114	113	111	68	92	90	81	84	89	75	72	83	78	80	78	107	105	97	97	100	90	87	93	90	90	98	100	100	100	100	100	100	100	100	100	100
15	Rahimsulthana	34	M	66	MNG	Total Thyroidectomy	88	109	109	101	98	99	93	96	87	83	88	114	157	153	133	130	122	123	120	125	128	120	76	100	95	79	81	74	74	81	84	86	90	89	119	114	97	97	90	90	94	98	100	100	98	100	100	100	100	100	100	100	100	100	100
16	Ayesha	19	F	46	PBC Upper limb	SSG	110	130	132	135	130	122	123	117	111	103	105	91	121	119	117	115	112	109	107	112	104	100	75	85	86	88	83	70	70	83	70	83	71	80	97	97	98	94	84	83	91	84	90	81	98	100	100	100	100	100	100	100	100	100	100
17	Ashok	35	M	74	Swelling of left masseter	Excision biopsy	78	100	102	100	96	100	98	88	90	86	82	117	161	155	150	153	154	149	148	138	127	118	78	104	101	98	104	101	96	102	93	83	79	91	123	119	115	120	119	114	117	108	98	92	98	100	100	100	100	100	100	100	100	100	100
18	Ramu	31	M	68	Fracture shaft right humerus	ORIF	88	117	108	99	80	85	90	84	86	88	80	132	165	141	140	138	136	128	126	135	137	144	82	94	82	92	80	78	78	90	89	87	84	99	118	102	108	99	97	95	102	104	104	104	98	100	100	100	100	100	100	100	100	100	100
19	Valliyamma	45	F	66	Fracture shaft right humerus	ORIF	76	97	97	82	88	84	90	92	96	89	86	118	179	117	147	137	124	139	127	112	133	110	77	88	82	71	66	83	91	87	98	98	80	91	113	94	96	90	97	107	100	103	110	90	98	100	100	100	100	100	100	100	100	100	100
20	Karrimuniyappa	44	M	82	Ca right gingivobuccal sulcus	Excision	92	103	110	108	102	90	96	84	78	90	94	86	127	191	175	178	159	168	127	124	118	155	86	127	114	114	107	103	86	83	77	99	73	86	127	140	134	131	122	113	98	93	105	100	98	100	100	100	100	100	100	100	100	100	100
21	Manjunath	30	M	78	Fracture shaft right humerus	ORIF	90	115	112	102	98	88	95	102	98	90	88	117	161	158	151	151	149	139	127	110	112	133	75	102	109	95	95	99	91	87	80	98	98	89	122	125	114	114	116	107	100	90	103	110	98	100	100	100	100	100	100	100	100	100	100
22	Chikkahanumakka	43	F	60	Ca gallbladder	Whipples procedure	84	107	106	100	98	100	101	90	94	84	82	113	130	127	124	110	110	108	104	106	118	117	62	88	70	66	66	65	62	63	60	79	78	79	92	89	85	81	80	77	78	75	92	91	98	100	100	100	100	100	100	100	100	100	100
23	Lakshmidevamma	45	F	68	Hashimotos thyroiditis	Subtotal Thyroidectomy	88	116	104	94	88	86	90	89	100	96	83	135	191	189	170	168	164	142	125	145	142	135	84	101	92	89	92	76	89	77	78	89	84	101	131	124	116	117	105	107	93	100	107	101	98	100	100	100	100	100	100	100	100	100	100
24	Mumtaz	40	F	59	Nodular goitre	Subtotal Thyroidectomy	86	110	109	107	103	101	103	98	90	89	89	125	188	178	175	168	167	159	151	139	142	127	70	104	95	93	97	97	90	87	83	89	86	88	132	123	120	121	120	113	108	102	107	100	98	100	100	100	100	100	100	100	100	100	100
25	Vidhya	21	F	44	Swelling of right cheek	Excision biopsy	92	130	129	125	123	116	115	113	108	90	95	114	152	150	146	141	144	128	127	126	138	125	76	94	95	84	80	87	76	78	77	87	84	89	113	113	105	100	106	93	94	93	104	98	99	100	100	100	100	100	100	100	100	100	100
26	Sunanda	38	F	55	Diffuse goitre	Subtotal Thyroidectomy	84	111	108	107	107	106	94	102	92	90	91	130	179	176	171	161	146	144	150	138	141	126	84	102	112	87	89	90	96	91	87	89	78	99	128	133	115	113	109	112	111	104	106	94	99	100	100	100	100	100	100	100	100	100	100
27	Bhairaputtanayak	43	M	73	Cholecystitis	Laproscopic cholecystectomy	68	102	104	100	101	98	94	97	88	80	74	132	178	175	163	165	159	151	148	136	134	138	87	100	103	97	94	93	94	88	86	88	86	102	126	127	119	118	115	113	108	103	103	103	98	100	100	100	100	100	100	100	100	100	100
28	Ambika	25	F	42	Corrosive antral stricture	Bilroth procedure	84	112	114	100	99	98	92	93	89	85	86	120	150	137	130	127	122	121	119	118	115	114	80	103	100	101	99	99	95	92	93	90	86	93	119	112	111	108	107	104	101	101	98	95	99	100	100	100	100	100	100	100	100	100	100
29	Maqbool Jaan	41	F	78	Cholilithiasis	Laproscopic cholecystectomy	78	98	101	100	99	94	89	88	85	86	82	133	158	155	153	150	149	148	144	142	139	135	86	107	108	102	100	97	95	95	92	88	87	102	124	124	119	117	114	113	111	109	105	103	98	100	100	100	100	100	100	100	100	100	100
30	Parvathamma	39	F	60	Rectal prolapse	Laproscopic Rectopexy	70	99	100	99	92	93	87	88	83	85	77	136	160	155	156	150	149	145	142	143	140	137	85	110	109	97	97	93	90	86	80	82	83	102	127	124	117	115	112	108	105	101	101	101	98	100	100	100	100	100	100	100	100	100	100