Sunday 20 December 2020

how to write medical thesis protocol 2021




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


medical thesis sample pdf,

medical thesis topics,

medical thesis online full text india,

thesis for medical students,

how to write medical thesis,

proforma for medical thesis,

medical thesis guide,

how to write medical thesis protocol,

medical thesis india,

medical thesis sample pdf,

medical thesis online full text india,

medical dissertation pdf,

thesis topics in medicine free download,

aiims general medicine thesis topics,

md thesis,

medical dissertation examples,

how to write medical thesis 2021,


ABSTRACT

 

Laryngoscopy and tracheal intubation provoke cardiovascular, and autonomic responses. This response is primarily because of sympatho-adrenal stimulation that increases the myocardial oxygen demand, which may be detrimental in comorbid patients. Attenuation of significant increase in blood pressure and heart rate decreases the risk  of complications.

Many methods have been employed to blunt these responses and most commonly used being intravenous lignocaine and topical anaesthesia of pharynx, larynx and trachea.

In view of it, the present study was undertaken to evaluate and compare the effects of 2% Lignocaine 2mg/kg nebulization given 10 minutes and 2% Lignocaine 2mg/kg iv given 90 seconds before induction for the intubation response.

Materials & Methods:

 

90 ASA Grade I & II patients in the age group 18-45 years of either sex scheduled for elective surgeries under general anaesthesia were recruited for the study.

They were allocated into three groups, Group C, Group I, Group N with the sample size of 30 in each. Group I received 2% lignocaine 2mg/kg intravenous 90sec and Group N received nebulization with 2% lignocaine 2mg/kg 10 minute before induction.

In all patients general anaesthesia was administered. Heart rate, systolic and diastolic blood pressure and mean arterial pressure, SpO2, and ECG were recorded, basal values and subsequently at 1st, 2nd, 3rd, 5th, 7th, 9th, 11th and 15th minute after intubation. Inj Glycopyrrolate and Fentanyl iv for analgesia which was avoided earlier, so as to avoid their effects on intubation response was given after the recordings.


Results:

 

It was noted that, in control group, the rise of heart rate (HR), Systolic blood pressure (SBP), Diastolic blood pressure (DBP), Mean arterial in pressure (MAP) were found to be

23.4   bpm, 42.6 mm Hg, 25.36 mm Hg, 29.44 mm Hg respectively. Group I, the rise of HR, SBP, DBP, MAP were found to be 18 bpm, 20.54 mm Hg, 13.84 mm Hg, 16.1 mm Hg respectively. In Group N, the rise of HR, SBP, DBP, MAP were found to be 24.86 bpm, 32.26 mm Hg, 24.83 mm Hg, 27.3 mm Hg respectively.

Thus it was seen that use of lignocaine has suppressed heart rate and blood pressure changes to laryngoscopy and endotracheal intubation. In fact intravenous lignocaine has better suppressing property than nebulization of lignocaine

KEYWORDS: Laryngoscopy, endotracheal intubation; Cardiovascular response; Lignocaine, intravenous, nebulization.


CONTENTS

 

Sl.No.

 

Page no

1

INTRODUCTION

1

2

OBJECTIVES OF THE STUDY

3

3

ANATOMICAL ASPECTS

4

4

PHYSIOLOGY OF PRESSOR RESPONSE

11

5

PHARMACOLOGY OF LIGNOCAINE

15

6

REVIEWOF LITERATURE

22

7

METHODOLOGY

35

8

OBSERVATIONS AND RESULTS

40

9

DISCUSSION

54

10

CONCLUSION

65

11

SUMMARY

66

12

BIBLIOGRAPHY

68

13

ANNEXURES

 

PROFORMA MATER CHART

75


 

TABLE

No.

TITLE

PAGE

No.

1

Table showing Age distribution

41

2

Table showing Sex distribution

42

3

Table showing Weight distribution

43

4

Table showing Nature of Surgical procedures

44

5

Table showing changes in Mean Heart Rate

45

6

Table showing changes in Mean Systolic Blood Pressure (SBP)

47

7

Table showing changes in Mean Diastolic Blood Pressure (DBP)

49

8

Table showing changes in Mean Arterial Pressure (MAP)

51

9

Table showing changes in Mean Saturation of Oxygen (SpO2)

53


 

 

Figure No.

Details

Page No

1

Entrance to larynx (posterior view)

5

2

View of larynx during laryngoscopy

7

3

Sympathetic supply to heart and lungs

12

4

Photograph showing administration of Nebulization

39

5

Photograph showing CompAir Compressor Nebulizer NE-C28

 

and Injection Lignocaine 2%.

39

6

Graph showing Age distribution

41

7

Graph showing Sex distribution

42

8

Graph showing Weight distribution

43

9

Graph showing changes in Mean Heart Rate (HR)

45

10

Graph showing changes in Mean Systolic Blood Pressure (SBP)

47

11

Graph showing changes in Mean Diastolic Blood Pressure (DBP)

49

12

Graph showing changes in Mean Arterial Pressure (MAP)

51

13

Graph showing changes in Mean Saturation of Oxygen (SpO2)

53


 

INTRODUCTION

 

The major responsibility of an anaesthesiologist is the management of airway to provide adequate ventilation to the patient by securing airway during general anaesthesia. As such, no anaesthesia is safe unless diligent efforts are devoted to maintain an intact functional airway.

Endotracheal intubation is the overall accepted, “Gold standard of securing the airway and providing adequate ventilation.” However, endotracheal intubation requires time, a skilled anaesthesiologist, appropriate instruments and adequate  circumstances with respect to space and illumination

Direct laryngoscopy and endotracheal intubation following induction of anaesthesia is almost always associated with hemodynamic changes due to reflex sympathetic discharge caused by epipharyngeal and laryngopharyngeal stimulation.1 This increased sympatho-adrenal activity may result in hypertension, tachycardia and arrhythmias.2,3,4 This increase in blood pressure and heart rate are usually transitory, variable and unpredictable. Transitory hypertension and tachycardia are probably of no consequence in healthy individuals5 but either or both may be hazardous to patients with hypertension, myocardial insufficiency, penetrating eye injuries, intracranial lesion, or cerebrovascular diseases. This laryngoscopic reaction in such individuals may predispose to development of pulmonary oedema6 myocardial insufficiency7 and cerebrovascular accident.8 At least in such individuals there is a necessity to blunt these harmful laryngoscopic reactions.

Attenuation of pressor responses to manipulation of the airway has been practiced either by deepening the plane of anaesthesia,9,10 by the use of drugs known to obtund them or by using advanced airway devices.11,12


 

Many methods have been devised to reduce the extent of hemodynamic events including high dose of opioids,5,13 alpha and beta adrenergic blockers,14,15 calcium channel antagonist like diltiazem, verapamil16 and vasodilatation drugs like nitroglycerine.17 α2 agonist like Clonidine18 and Dexmedetomidine are used 19

Various studies have reviewed the effect of Lignocaine in forms like viscous lignocaine20 aerosols,21 oropharyngeal sprays 22 and intravenous23,24 route to blunt these responses.

Topical anaesthesia with lignocaine applied to the larynx and trachea in a variety of ways remains a popular method used alone or in combination with other techniques.

Intravenous lignocaine has been used to supress cough during tracheal intubation,25 laryngospasm and cough during extubation.26 It has also been used to suppress airway hyperactivity and mitigate bronchoconstriction after tracheal  intubation.27 In a study using intravenous and inhaled lignocaine, lignocaine in both the routes attenuated reflex bronchoconstriction significantly. Lignocaine plasma concentrations were significantly lower in the group where lignocaine was used via inhalational route.28

Intravenous lignocaine with its well established centrally depressant and anti- arrhythmic effect was found to be a more suitable alternate method to minimize this pressor response.23,24

The present study was undertaken to compare the effect of Intravenous lignocaine and nebulization of lignocaine on blunting the haemodynamic responses to endotracheal intubation.


 

 

OBJECTIVES OF THE STUDY

 

The main objectives of the present study are:

 

 

 

 

1.  To study the effect of 2% lignocaine 2mg/kg iv, on hemodynamic responses to laryngoscopy and endotracheal intubation.

2.  To study and compare effect of intravenous lignocaine with nebulization of 2% lignocaine 2mg/kg on hemodynamic responses to laryngoscopy and endotracheal intubation.

3.  To evaluate any side effects associated with the use of this drug in both routes.


 

ANATOMICAL ASPECTS29, 30

 

The relevant anatomy of the posterior surface of the tongue, the soft palate, epiglottis, larynx and trachea, with their nerve supply is explained briefly to understand the physiological effects of endotracheal intubation.

TONGUE:

 

It is a soft mobile organ which bulges upwards from the floor of the mouth. The posterior part of the tongue forms the anterior wall of the oropharynx. The dorsum of the tongue is long and extends from the tip to the base of the epiglottis and with it forms the glosso-epiglottic fold. It is separated into palatine and pharyngeal parts by a V shaped sulcus terminalis. The thick mucous membrane covering the tongue is posteriorly continuous with that on the anterior surface of epiglottis over the median and lateral glosso-epiglottic folds and the valleculae of the epiglottis between them.

EPIGLOTTIS:

 

It is likened to a leaf. It is attached at its lower tapering end to the back of the thyroid cartilage by means of the thyro-epiglottic ligament. Its superior extremity projects upwards and backwards behind the hyoid and the base of the tongue, and overhangs the inlet of the larynx. The posterior aspect of the epiglottis is free and bears a bulge, termed the tubercle, in its lower part. The upper part of the anterior aspect of the epiglottis is also free; it’s covering mucous membrane sweeps forward centrally onto the tongue and, on either side, onto the side walls of the oropharynx, to form, respectively, the median glosso-epiglottis and the lateral glosso-epiglottic folds.


 

The valleys on either side of the median glosso-epiglottic fold are termed the valleculae, The lower part of the anterior surface of the epiglottis is attached to the back of the hyoid bone by the hyoepiglottic ligament

SOFTPLATE:

 

Is a flexible muscular flap which extends postero-inferiorly from the posterior edge of the hard palate into the pharyngeal cavity. By varying its position, it can cut off the nasopharynx or the mouth from the remainder of pharynx. It is attached to the posterior edge of the hard palate and to the side walls of pharynx and has the uvula hanging down from the middle of its free posterior border. On each side, the posterior border is continuous with the palatopharyngeal arch.

LARYNX:

 


 

 

Figure 1: Entrance to larynx (posterior view)


 

The competent anaesthesiologist should have a level of knowledge of the anatomy of the larynx of which a laryngologist would not be ashamed. Evolutionally, the larynx is essentially a protective valve at the upper end of the respiratory passages; its development into an organ of speech is a much later affair. Structurally, the larynx consists of a framework of articulating cartilages, linked together by ligaments, which move in relation to each other by the action of the laryngeal muscles. It lies opposite the 4th, 5th and 6th cervical vertebrae, separated from them by the laryngopharynx; its greater part is easily palpable, since it is covered superficially merely by the investing deep fascia in the midline and by the thin strap muscles laterally.

The inlet of larynx is a large oblique shaped opening bounded antero-posteriorly by the epiglottis. It is bounded on each side by the aryepiglottic fold of mucous  membrane and postero-inferiorly by the inter-arytenoid fold of mucous membrane. Each aryepiglottic fold is a narrow and deep fold that extends posterior-inferiorly from the margin of the epiglottis to the arytenoid cartilage. It contains the aryepiglottic muscle and near its inferior ends two small pieces of cartilage which forms the cuneiform and corniculate tubercules in its free edge. The interarytenoid fold of mucous membrane passing between them forms the inferior boundary of inlet and encloses the muscle which pass between the posterior surfaces of the arytenoid cartilages.

Vocal cords are two folds of mucous membrane stretching antero-posteriorly from the vocal processes of the arytenoid cartilage to the posterior surface of the thyroid cartilage and enclosed within each of them is a band of fibroelastic tissue known as the vocal ligament. The opening between the two folds forms the glottis which is the narrowest portion of the airways in the adult.


 

LARYNGOSCOPIC ANATOMY

 


 

Figure 2: View of the larynx at laryngoscopy.

 

 

To view the larynx at direct laryngoscopy and then to pass a tracheal tube depends on getting the mouth, the oropharynx and the larynx into one plane. Flexion of the neck brings the axes of the oropharynx and the larynx in line but the axis of the mouth still remains at right angles to the others; their alignment is achieved by full extension of the head at the atlanto-occipital joint. This is the position, with the nose craning forwards and upwards.

At laryngoscopy, the anaesthesiologist first views the base of the tongue, the valleculae and the anterior surface of the epiglottis. The laryngeal aditus then comes into view bounded in front by the posterior aspect of the epiglottis, with its prominent epiglottic tubercle. The aryepiglottic folds are seen on either side running postero - medially from the lateral aspects of the epiglottis; they are thin in front but become thicker as they pass backwards where they contain the cuneiform and corniculate


 

cartilages. The vocal cords appear as pale, glistening ribbons that extend from the angle of the thyroid cartilage backwards to the vocal processes of the arytenoids. Between the cords is the triangular (apex forward) opening of the rima glottidis, through which can be seen the upper two or three rings of the trachea.

TRACHEA:

 

It is a wide tube of 13-15 mm diameter and 11- 14 cm in length. It commences at the larynx and terminates at the level of the fourth thoracic vertebra, where it divides into the two main bronchi. In new born the trachea is only 4 cm long. The tracheal architecture consists of a number of horizontal C shaped cartilages which are joined posteriorly by the trachealis muscle. Vertically these cartilages are joined to each other by fibroelastic tissue. This gives the trachea an appearance similar to that of tyres pilled one on top of the other, held together by elastic tissue and both covered by endothelium.

NERVE SUPPLY:

 

Glossopharyngeal nerve:

 

The ninth cranial nerve is a mixed nerve. Its motor fibres supply the stylopharyngeus muscle. The parasympathetics supply to the parotid glands is through glossopharyngeal nerve. It descends between the internal and external carotid arteries and after passing between superior and middle constrictors of pharynx, it branches into two terminal branches.

The pharyngeal branch consists of :

 

1.          One or two branches which supply the mucous membrane of the pharynx, posterior one third of the tongue, anterior surface of the epiglottis, glosso-epiglottic folds, valleculae and pyriform fossa are also supplied by this nerve.


 

2.           The larger branch accompanies the pharyngeal branches of the vagus to the pharyngeal plexus. One of its branches joins a branch of superior laryngeal nerve to form the carotid sinus nerve which supplies the carotid sinus and the carotid body.

Vagus nerve:

 

This is also a mixed cranial nerve. In the neck it descends vertically between the internal jugular vein and the internal carotid artery above and the common carotid artery below. All three structures are enclosed in the carotid sheath. It gives off numerous branches, three of which supply those areas of the pharynx and larynx stimulated by the endotracheal intubation.

1.          Pharyngeal branch: This branch forms the large part of the pharyngeal plexus to which are contributed branches of the glossopharyngeal nerve and fibres from the superior cervical sympathetic ganglion. This plexus supplies the muscles and mucous membrane of the pharynx.

2.          Superior laryngeal nerve: This branch divides into external and internal laryngeal nerves. The external branch descends on the anterior aspect of the thyroid cartilage to the crocothyroid muscle to which it supplies. The internal branch perforates the thyrohyoid membrane and lying in the submucous plane of  pyriform fossa. Supplies sensory branches to the larynx above the level of the glottis.

3.          Recurrent laryngeal nerve: on the right side leaves the vagus as the latter crosses the right subclavian artery; it then loops under the artery and ascends to the larynx in the groove between the oesophagus and trachea. On the left side, the nerve originates from the vagus as it crosses the aortic arch; the nerve then passes under


 

the arch to reach the groove between the oesophagus and the trachea. Once it reaches the neck, the left nerve assumes the same relationships as on the right. The recurrent laryngeal nerves provide the motor supply to the intrinsic muscles of the larynx apart from cricothyroid, as well as the sensory supply to the laryngeal mucosa inferior to the vocal cords.


 

PHYSIOLOGY OF PRESSOR RESPONSES30, 31

 

Direct laryngoscopy and endotracheal intubation following induction of anaesthesia is almost always associated with hemodynamic changes due to reflex sympathetic discharge caused by epipharyngeal and laryngopharyngeal stimulation. Here in with have explained briefly the physiology and effects of laryngoscopy and intubation to understand the haemodynamic changes.

SYMPATHETIC NERVOUS SYSTEM.

 

The sympathetic efferent nerve fibres originate from nerve cells in the lateral grey column of the spinal cord between the first thoracic and second lumbar segments (the thoracic outflow). Preganglionic fibres are myelinated. Ganglia are located either in the paravertebral sympathetic trunk or in prevertebral ganglia, such as the celiac ganglion. The sympathetic part of postganglionic fibres are long, non-myelinated sympathetic part of the system has a wide spread action on the body as the resulting preganglionic fibres synapsing on many postganglionic neurons and the suprarenal medulla releasing the sympathetic transmitters epinephrine and nor epinephrine. The sympathetic nervous system prepares the body for emergencies and severe muscular activity. There is no sympathetic out flow from cervical part of the cord nor from the lower lumbar and sacral parts. Those preganglionic fibres which are destined to synapse with cell bodies whose fibres are going to run with cervical nerves must ascend in the sympathetic trunk and those of lower lumbar and sacral nerves must descend in the trunk to lumbar and sacral ganglia.


 

 

 

 

Figure 3: Sympathetic supply to heart and lungs Afferent sympathetic fibres

All the afferent fibres have their cell bodies in the posterior root ganglia of spinal nerves. The afferent fibres reach the spinal nerve in the white ramus communicants. Central processes enter the spinal cord by posterior nerve root. From there they ascend through the cord to brain stem.


 

Afferent sympathetic fibres

 

         Hypothalamus

 

Transmits signals through preganglionic cell bodies located in lateral horn cells of thoracic and upper two lumbar segments.

 

Post ganglionic cell bodies in ganglia in peripheral nervous system either in the sympathetic or in autonomic plexuses.

 

Causes massive sympathetic discharge

 

THE CARDIOVASCULAR REFLEXES

 

The cardiovascular responses to noxious airway manipulation are initiated by proprioceptors responding to tissue irritation in the supraglottic region and trachea. Located in close proximity to the airway mucosa, these proprioceptors consist of mechanoreceptors with small-diameter myelinated fibers, slowly adapting stretch receptors with large-diameter myelinated fibers, and polymodal endings of nonmyelinated nerve fibers. The superficial location of the proprioceptors and their nerves is the reason that topical local anaesthesia of the airway is such an effective means of blunting cardiovascular responses to airway interventions. The glossopharyngeal and vagal afferent nerves transmit these impulses to the brain stem, which, in turn, causes widespread autonomic activation through both the sympathetic and parasympathetic nervous systems.


 

In adults and adolescents, the more common response to airway manipulation is hypertension and tachycardia, mediated by the cardioaccelerator nerves and sympathetic chain ganglia. This response includes widespread release of norepinephrine from adrenergic nerve terminals and secretion of epinephrine from the adrenal medulla.

In addition to activation of the autonomic nervous system, laryngoscopy and endotracheal intubation result in stimulation of the central nervous system (CNS), as evidenced by increases in electroencephalographic activity, cerebral metabolic rate, and cerebral blood flow (CBF).


 

PHARMACOLOGY OF LIGNOCAINE31, 32, 33

 

 

Lignocaine was synthesised in 1943 in Sweden by Lofgren, it was introduced into clinical practice by Gordh in the year 1948.

PHARMACOLOGY

 

Clinically lignocaine is an amino-amide of xylidine-de-ethyl amino 2:6 dimethyl acetanilidine.

STRUCTURAL FORMULA:

 

 

 


 

PHYSICAL PROPERTIES:

 

It is very stable, not decomposed by boiling, acids or alkalies and withstands repeated autoclaving. The pKa of lignocaine is 7.72. At the normal tissue pH of 7.4 approximately 65% of lignocaine exists in the charged cationic form, whereas 35% exists in the uncharged base form.

Lipid solubility: Determination of partition co-efficient by means of n-heptane/pH 7.4 buffer system has given a value of 2.9.

Plasma protein binding: At a concentration of 2mcg/ml approximately 65% is bound to plasma proteins. Lignocaine is a local anaesthetic of moderate potency and duration, with good penetrative powers and rapid onset of action. It is effective by all routes of administration. Lignocaine sometimes causes vasodilation. Adrenaline as adjuvant


 

prolongs the duration of lignocaine as it reduces the rate of systemic absorption. With repeated injections, tachyphylaxis often occurs.

The hydrochloride salt in water has a pH of 6.5. Hepatic extraction ratio 65-70%.

Plasma half life 1.6 hrs.

 

Volume of distribution – 1.3 L/hr.

 

PREPARATIONS OF LIGNOCAINE

 

1.   Topical forms:

 

Topical spray 4% and 10% solution

 

Gel: 2% or 2.5%

 

Solution: 2% or 4% or 5%

 

2.   Parenteral forms: 0.5%, 1% .2%, or 4% as lignocaine hydrochloride.

 

Lignocaine is stored at temperature < 25ºC protected from light. Lignocaine is also available along with adrenaline in 1: 1 lakh or 1: 2 lakh concentrations.

PHARMACODYNAMICS

 

A.  Local effects:

 

Lignocaine blocks the conduction of impulses in the nerve fibres at the site of injection by closing sodium channels.

Sensory and motor fibres are inherently equally sensitive to lignocaine.

 

Smaller fibres and nonmyelinated nerve fibres are blocked more easily than longer and myelinated fibres.

Autonomic fibres are more susceptible than somatic fibres. Among somatic fibres order of blockade are pain-temperature-touch-deep pressure sense.

Addition of vasoconstrictor like Adrenaline (1:50,000 to 1:2 lakh) can


 

1.  Prolong the duration of action of lignocaine by decreasing the rate of removal from the local site of injection in to the circulation

2.  Reduces the systemic toxicity; of lignocaine by decreasing the rate of absorption and keeping the plasma concentration lower.

It is very effective surface analgesic causing rapid absorption from mucosal surface. The peak blood concentration is achieved within 4 to 15 minutes after  instillation. Given intravenously, peak blood levels are achieved immediately.

B.  Systemic effects

 

Cardiovascular system

 

Heart: Lignocaine is placed under classification of class 1- B anti-arrhythmic drugs classification.

It suppresses the automaticity in ectopic foci by antagonizing phase IV depolarization in Purkinje fibres and ventricular muscles by blocking sodium channels.

It does not depress SA node automaticity.

 

The rate of phase-0 depolarization is not decreased except in presence of hyperkalaemia.

Lignocaine markedly decreases the action potential duration and effective refractory period in Purkinje fibres and ventricular muscles.

Conduction velocity is not decreased.

 

It has practically no effect on action potential duration and effective refractory period of atrial fibres. Atrial re-entry is not affected.

It can suppress the re-entrant ventricular arrhythmias either by abolishing one way block or by producing two way blocks. At therapeutic plasma concentration of 3- 5mcg/ml, it causes little depression of cardiac contractility. There are no significant autonomic actions. All cardiac effects are direct actions.


 

Lignocaine is widely used in the management of ventricular dysrhythmias in a dose of 1 to 2 mg/kg bolus intravenously and 2.4 mg/min as infusion. It acts by its membrane stabilizing effect and depression of automaticity at atrio-ventricular node. It has been used effectively in the management of ventricular arrhythmias following myocardial infarction and cardiac surgery.

Vascular smooth muscle.

 

Lignocaine exists in two isomers, and the ability to produce vasoconstriction appears vested in one of the isomers. Hence lignocaine produces vasoconstriction with low doses and vasodilation at higher doses, very large doses cause circulatory collapse as a result of medullary depression and direct vasodilation.

At doses > 75mcg/kg/min with plasma concentration of > 10-20mcg/ml  lignocaine causes asystole and cardiovascular collapse.

Central nervous system

 

It readily crosses blood brain barrier causing central nervous system stimulation followed by depression with higher doses. The severity of the central nervous system effect correlates with plasma concentration. Central nervous system is more susceptible to toxic effects than the cardiovascular system. Mild toxic effects may cause drowsiness and sedation. Objective signs of central nervous system toxicity are usually excitatory in nature and may cause shivering, muscular tithing and convulsions. It has been shown to possess analgesic properties when given intravenously. Reduction of MAC of inhalational anaesthetic agents is used as an index of its central analgesic property. Higher serum levels produce a central stimulant effect and this is due to initial blockade of inhibitory pathway at limbic or higher centres in the cerebral cortex.


 

Neuromuscular junction

 

It can affect transmission at the neuromuscular junction and hence potentiate the effect of the depolarizing and non-depolarizing muscle relaxants.

Metabolism

 

It is metabolised by the liver microsomal enzymes, oxidases and amidases. The main pathway in man appears to be due to oxidative de-ethylation of lignocaine to monoethyl glycinexuylidide followed by subsequent hydrolysis of monoethyl glycinexylidide to xylidine. Excretion occurs through the kidneys.

Dosage

 

The safe dose limit for lignocaine has been much disputed. The factors governing the dosage are the weight of the patients and the different absorption rates from various sites and injections. The maximum safe dose is to 4.5 mg/kg without epinephrine and 7 mg/kg with epinephrine.

A concentration of 0.25-5% of lignocaine hydrochloride is used for infiltration. If extensive block is required then 0.5% with epinephrine is used. 0.5% lignocaine without adrenaline is used for intravenous regional anaesthesia. 1% lignocaine is usually sufficient for most nerve blocks. In dentistry, 2% lignocaine with adrenaline 12.5 mcg/ml (1:80,000) is useful. A concentration of 1.5-2% solution of lignocaine is used for epidural analgesia and sometimes with the addition of adrenaline 5 mcg/ml 1:200,000). For surface application, lignocaine solution in a concentration of (4%) for spraying or for application using wool pledgets.

It is used in a concentration of 2% as a lubricating gel in urethral surgery and for lubricating endotracheal tubes. In the management of cardiac dysrhythmias it is used in the dose of 1-2 mg/kg iv as a bolus dose followed by 2-4 mg/min (20-60 mcg/kg/min) as


 

infusion and then the dose is reduced. Caution must be exercised in the presence of low cardiac output and after cardiac surgery and a slow infusion rate must be maintained.

Toxicity

 

The appearance of toxic symptoms is due to two factors. The toxicity of the drug and its serum levels.

Toxic symptoms may occur at plasma levels of 5mcg/ml in an awake patient, while levels of 10mcg/ml are toxic in the anaesthetised patient. Plasma levels depend on the speed with which lignocaine enters the circulation, which in turn depends on the dosage and rate of absorption of the drug from various sites. Peak blood levels are attained in 1 minute after intravenous administration and start decreasing by 3-4 minutes. Following laryngotracheal administration, peak blood levels are attained in 9-15 minutes. Alveolar absorption occurs at a faster rate than absorption from bronchial and bronchiolar mucosa. It is thought that, mucosal absorption simulate intravenous administration. However, systemic absorption of lignocaine may be slowed through larynx and tracheal mucosa as it is diluted with secretions lining the upper airway, impeding systemic absorption. Hence laryngotracheal administration is associated with delayed peak levels that are lower but more sustained. The peak blood levels after epidural injection follow a similar pattern to those seen after intra-muscular injection (average 18 minutes for plain lignocaine and after 23 minutes for lignocaine with adrenaline)

Side effects

 

Commonest side effects are nausea, drowsiness, and dizziness. At a higher levels shivering, muscular twitching, tremors and convulsions, bradycardia, decreased respiration with hypoxia can occur. Circulatory collapse may occur with very high dosage.


 

Hypersensitivity

 

This is due to an antigen-antibody reaction. Hypersensitivity to local anaesthetics is more common with ester-linked drugs than with amide group of drugs. This is more commonly seen in atopic individuals and can manifest as local oedema, urticaria, or angioneurotic oedema. Dermatitis may be encountered as a result of skin application. Anaphylaxis occurs less commonly. Although amide agents appear to be relatsively free from allergic type reactions, solution may contain preservatives like paraben and methylparaben whose chemical structure is similar to that of para-aminobenzoic acid.


 

REVIEW OF LITERATURE

 

HISTORICAL REVIEW

 

Endotracheal intubation has become an integral part of the anaesthetic management and critical care. It has been practised following its description by Rowbottam and Magill in 1921.32 Laryngoscopy and endotracheal intubation are attended by significant hypertension, tachycardia and arrhythmias. These hemodynamic responses were first recognised as early as in 1940 by Reid and Brace et al.34 They postulated that the disturbances in cardiovascular system were reflex in nature and mediated by the vagus nerve which originated in the, trachea, larynx, bronchi, or lungs and effects by sudden increase in the vagal tone. These reflexes were termed ‘vagovagal’ since both the efferent and afferent paths of the reflex were assumed to be vagus nerve. But in 1950 Burstein and co-workers,2 had a different conclusion that attributed the effects of laryngoscopy and tracheal intubation on ECG changes and suggested the pressor response as consequences of an increase in sympathetic and sympathoadrenal activity and also observed that deep anaesthesia minimizes ECG incident to tracheal intubation. In 1951 King BD and co-workers35 observed that during light general anaesthesia, direct laryngoscopy or tracheal intubation, uncomplicated by cough, anoxia, hypercarbia is capable of producing decided circulatory effects characterised by rise in blood pressure and increase in heart rate.

These responses being transitory are well tolerated by normal individuals but are more deleterious in patients with hypertension, myocardial insufficiency and cerebrovascular diseases which result in potentially dangerous effects like ventricular arrhythmias,4 myocardial ischemia,7 pulmonary oedema,6 left ventricular failure,6 and


 

cerebrovascular accidents.8 This hemodynamic stimulus is associated with increase in plasma nor-adrenaline concentrations parallel with the increase in blood pressure.36

Many methods and strategies have been employed and advocated to minimize and nullify the hemodynamic responses to laryngoscopy and intubation which work on the reflex arc.33

1.          By blocking the peripheral sensory afferent inputs – topical application and infiltration of superior laryngeal nerve.

2.          Block of central mechanism of integration of sensory inputs – morphine, fentanyl.

 

3.          Block of the efferent pathway effector sites – calcium channel blockers, intravenous lignocaine, esmolol.

Increasing the depth of anaesthesia with the use of inhalational agent like cyclopropane,9 trichloroethylene,37 chloroform and ethyl chloride38 for attenuation had been practised, but with the drawback of stormy induction. Halothane and enflurane10 had an advantage of smooth and rapid induction, non-inflammable but was associated with hypotension, bradycardia and myocardial ischemia which are deleterious in patients with coronary insufficiency and hypertension.

Laryngoscopy and tracheal intubation causes a reflex increase of sympathetic and sympathoadrenal system by irritation and stimulation of the laryngeal and pharyngeal tissues, anaesthetising using local anaesthetics like lignocaine at the site of stimulation was studied. And various studies have reviewed the effects of lignocaine in the form of viscous,20 aerosol, 21 spraying,22 and intravenous 23, 24 routes for blunting the response.

As early as in 1960, alpha adrenergic blocker, phentolamine14 was used to attenuate the laryngoscopic reactions. However, these drugs had long duration of action and the authors observed exaggerated fall in blood pressure during perioperative period,


 

because of their property of extensive vasodilation requiring rapid transfusion it was not used.

Beta adrenergic blockers were extensively studied for their negative chronotropic effects for blunting the hemodynamic responses to laryngoscopy and intubation like proctolol15 and labetalol.39 but had a delayed onset and longer duration of action which caused perioperative bradycardia and hypotension, hence a search for shorter acting beta blockers like esmolol40 was started.

The investigators used low doses of opioids as premedicants for blunting the laryngoscopic responses during 1970 and observed significant reduction in the hemodynamic responses to laryngoscopy and intubation. Use of morphine5 and fentanyl13 effectively reduced the tachycardia and hypertension associated with laryngoscopy and intubation but these agents were associated with respiratory depression, chest wall rigidity and in addition they prolonged the recovery time.10 The availability of synthetic narcotics like alfentanyl41 and sufentanyl42 with short duration and rapid onset of action helped the investigators to overcome the problems associated with the use of above mentioned drugs.

Calcium channel blockers like nicardipine, verapamil and diltiazem16 were studied widely to suppress the hemodynamic responses to laryngoscopy and intubation. Calcium ions exert a major role in the release of catecholamines from the adrenal gland and adrenergic nerve endings, which affects plasma catecholamine concentrations, in  response of sympathetic stimulation. The investigators reported that calcium channel blockers interfere with catecholamine release after tracheal intubation.

Directly acting vasodilators like sodium nitroprusside43 and nitroglycerine17 were tried but set back being that they caused reflex tachycardia being deleterious in patients

with co morbidities and requirement of invasive arterial monitoring.


 

Laryngoscopy and tracheal intubation are also employed for non-anaesthetic purposes. Diagnostic purposes for direct laryngoscopy and flexible bronchoscopy.44 Endotracheal intubation may be required for prevention of aspiration and protection of airway. Hence blunting the response becomes important as these patients come as for emergency procedures or critically ill.

CLINICAL REVIEW

 


Mounir N. Abou-Madi et al


21

conducted a study on cardiovascular responses to


 

laryngoscopy and tracheal intubation following nebulization of lignocaine.

 

20 patents scheduled for various procedures were selected for the study and were divided into two groups.

Pre-treated group: received inhalation of 6-8ml of mixture of 1/3rd of 2% viscous lignocaine + 2/3rd of 4% aqueous lignocaine

Control group: nebulized with saline instead of lignocaine in stage II, 10% lignocaine was nebulized instead of saline prior to intubation.

A standard premedication with Pentobarbitone 2mg/kg intramuscular was given one and half an hour before the surgery.

In the pre-treated group

 

Stage I – Pre operative observation period

 

ECG and BP was recorded, arterial blood drawn for gases, serum potassium and lignocaine levels was done

Stage II – Aerosol nebulization was administered.

 

Stage III - Post aerosol observation period. Blood samples drawn and parameters were recorded.


 

Stage IV - Anaesthesia induced with Thiopentone sodium 4mg/kg, anaesthesia continued with nitrous oxide, oxygen and halothane for 5 – 10 min.

Stage V – Steady state

 

For 2 minutes tracing of readings was done Stage VI – Laryngoscopy

Intubation facilitated with Inj. Succinylcholine 1.0mg/kg Stage VII – Intubation

Intubation performed, tracing done for 2min.

 

Stage VIII – Final observation period Was continued till end of procedure

Three stages were taken for statistical analysis

 

1.          Steady state

 

2.          Post laryngoscopy

 

3.          1minute after intubation

 

The authors observed heart rate, systolic blood pressure, diastolic blood pressure and ECG changes following laryngoscopy and intubation.

In control group

 

Heart rate increased by 38.8% (28 bpm), systolic blood pressure increased by 56% (60 mm Hg) and diastolic blood pressure raised by 66.0% (37 mm Hg) above the steady state values after 1minute post intubation .


 

ECG changes: had serious new arrhythmias. The incidence was highest in patients who had suffered the most acute rise in blood pressure.

Blood levels: after intubation the average blood level was 0.4 mcg/ml at 2min and at the end of study it was 0.3 mcg/ml

In Pre-treated group

 

Heart rate increased by 16.8% (17 bpm), systolic blood pressure by 10.3% (12 mm Hg) and diastolic blood pressure by 16.4% (11 mm Hg) above the steady state values after 1min post intubation.

ECG changes: There were no new arrhythmias or ECG changes.

 

Blood levels: The average lignocaine levels following nebulization was 1.4mcg/ml at 2min and 1.2mcg/ml at the end of the study.

The authors concluded,

 

1.          Topical anaesthesia applied immediately before intubation is ineffective.

 

2.          Systemic absorption of lignocaine probably accounts for the absence of arrhythmia in pre-treated group.

3.          Incidence of post intubation arrhythmias and hypertension is marked in patients with arteriosclerotic heart diseases.

They believed that inhalation of lignocaine aerosol is a safe, simple, effective, and generally acceptable method.

Mounir N. Abou-Madi et al23 conducted a study on cardiovascular responses to laryngoscopy and tracheal intubation following small and large intravenous doses of lignocaine.


 

Thirty male patients scheduled for various surgical procedures were selected for the study and were divided into three comparable groups A, B and C

Group A – received normal saline iv and served as control Group B – received 1% lignocaine 0.75 mg/kg iv

Group C – received 2% lignocaine 1.5 mg/kg iv

 

All the patients were pre-medicated with Inj. Meperidine 1 mg/kg and Inj. Atropine 0.4 mg/kg intramuscular one hour before surgery. Anaesthesia was induced with Inj. Thiopentone 4 mg/kg and intubation was facilitated with Inj. succinylcholine 1.0 mg/kg. Endotracheal intubation was carried out within 2-3 min of injection of test drug.

Changes in heart rate, systolic blood pressure and diastolic blood pressure in all the three groups were observed following laryngoscopy and intubation.

In control group, heart rate increased by 15.3% (14 bpm), systolic blood pressure increased by 30.3% (42 mm Hg) and diastolic blood pressure raised by 38.7% (31 mm Hg) above the pre- induction value .

In group B, (Lignocaine 0.75 mg/kg), heart rate increased by 26% (21.1 bpm), systolic blood pressure by 11,9% (17.6 mm Hg) and diastolic blood pressure by 25.2% (20 mm Hg) above the pre-induction value.

In group C, (Lignocaine 1.5 mg/kg) heart rate increased by 8.5% (8.5 bpm), systolic blood pressure increased by 21.5% (30.4 mm Hg) and diastolic blood pressure by 22.3% (21.8 mm Hg) above the pre-induction value.

The authors concluded that 1.5 mg/kg iv Lignocaine given 3 min before laryngoscopy and intubation provides protection against both tachycardia and hypertension. They also discussed the possible modes of action

Direct myocardial depressant action and indirect dose stimulant effect but with predominance depressant effect during induction.


 

Central stimulant effect (indirect, dose dependent stimulant action)

 

A peripheral vasodilating effect and an effect on the synaptic transmission

 

Suppress the cough reflex.

 

The authors also concluded that pre-induction aerosol topical analgesia of the upper airways would still be their method of choice to minimise post intubation cardiovascular reactions in patients with poor myocardial reserve and severe hypertension.

 

 

Robert K Stoelting3 compared the clinical effects of intravenous lignocaine 1.5 mg/kg given 30 sec before intubation and laryngotracheal viscous lignocaine 2 mg/kg given 10 min before intubation in 24 patients scheduled for elective coronary artery bypass graft operations.

Anaesthesia was induced with thiamylal 4 mg/kg and intubation was facilitated with succinylcholine 1.5 mg/kg. The duration of laryngoscopy was averaged less than 15 sec.

The authors observed no significant changes in heart rate following laryngoscopy and intubation in both the groups. However, in control group, mean arterial pressure raised by 17 mm Hg in viscous lignocaine group, by 14 mm Hg and in intravenous lignocaine group, mean arterial pressure increased by 22 mm Hg, above the pre-induction value.

The authors did not make any comment on changes in diastolic or systolic pressures. Mean arterial pressure decreased spontaneously and reached pre-induction levels by 2 min after intubation.

They concluded that a short duration direct laryngoscopy combined with laryngotracheal lignocaine before tracheal intubation minimises the pressor responses and ensures a spontaneous return of mean arterial pressure and heart rate towards awake


 

levels following intubation. Viscous or intravenous lignocaine is not helpful when laryngoscopy of short duration

Robert F. Bedford, et al45 compared the reduction in intracranial pressure following intravenous administration of bolus lignocaine at 1.5mg/kg with Thiopentone. Lignocaine significantly reduced the ICP with minimum changes in arterial pressure without altering the cerebral perfusion. Rise in ICP due to intubation and surgical stimulation is blunted  by it.

James F. Hamill, et al46 they observed that in a light barbiturate–nitrous oxide anaesthesia, topical laryngotracheal administration of 4ml of 4% lignocaine prior to laryngoscopy and tracheal intubation causes a significant increase in ICP, heart rate, and mean arterial pressure. 1.5mg/kg lignocaine intravenous administered 1minute before intubation prevents both rise in ICP, and was useful in blunting the hemodynamic response to laryngoscopy and endotracheal intubation. Cerebral perfusion was well maintained and it decreased CMRO2 and cerebral blood flow. Laryngotracheal topical application took 4-15 min for achieving plasma level of 1 - 2.7mcg/ml when compared with intravenous route.

Bahaman Venus,47 conducted a study on cardiovascular responses to laryngoscopy and tracheal intubation following nebulization of lignocaine

Study included 19 ASA class I and II adult patients scheduled for general anaesthesia for wide excision and extremity amputation procedures were divided into two groups.

Group I: 10 patients received of solution A (normal saline, 6ml) Group II: 9 patients received of solution B (4% lignocaine, 6ml) both groups were aerosolized with their


 

respective solutions 5 minute during pre-oxygenation before induction. A contoured breathing mask with attached nebulizer was used to deliver the aerosol.

All patients were pre-medicated with, atropine 0.05mg/10kg and morphine 1mg/10kg 1hour before the induction. Baseline measurements of blood pressure, heart rate and ECG recordings were noted. A standard technique for administration of general anaesthesia was followed and laryngoscopy and endotracheal intubation was performed in both the groups. The time and duration of each manoeuvre were recorded until 5 min after placement of endotracheal tube. Blood gas analysis was done.

They observed that the pressor response and tachycardia following laryngoscopy and endotracheal intubation in the control group I was clinically significant. The patients in aerosolized group maintained significantly lower pressor response and heart rate. 4 patients among the group I developed PVC and none in group II.

They concluded that

 

1.          The underlying mechanism is probably of reflex origin to mechanical stimulation of the larynx and trachea, as the arterial blood gas analysis was within the normal limits excluding the possible causes of hypercarbia and hypoxia.

2.          Aerosolization of lignocaine is a simple and effective technique for intubating patients with borderline cardiovascular status.

Stanley Tam, et al24 studied the optimal time of lignocaine injection before tracheal intubation, to prevent the pressor response. Seventy patients were divided into five groups with 14 patients in each group. Group 1, Group II, Group III and Group IV, received 1.5 mg/kg of lignocaine intravenously 1, 2, 3 and 5 minutes respectively. Group V received normal saline and served as control. All the patients received morphine 0.1 mg/kg and perphenazine, 0.05 mg/kg intramuscular before induction of anaesthesia. Patients were


 

given d-tubocurarine 0.04 mg/kg 5 min before intubation followed by thiopentone 4 mg/kg and suxamethonium 1.5 mg/kg before intubation. Heart rate, mean arterial pressure, systolic and diastolic pressure were monitored throughout the procedure.

The mean increase in heart rate in group I was 28 bpm, in group II it was 24 bpm, in group III it was 12 bpm and in group IV it was 22 bpm and in group V it was 25 bpm.

The mean increase in systolic blood pressure in group 1 is 32 mm Hg, in group II 29 mm Hg, in group III 12 mm Hg, in group IV 31 mm Hg and in group V it was 38 mm Hg.

The mean increase in diastolic blood pressure in group I was 29 mm Hg, in group II 29 mm Hg, in group III 9 mm Hg, in group IV 22 mm Hg and in group V it was 26 mm Hg.

The mean increase in mean arterial pressure in group I was 30 mm Hg. In group II 27 mm Hg, in group III 11 mm Hg, in group IV 27 mm Hg and in group V 32 mm Hg.

The results of the study showed that the mean increase in heart rate, systolic blood pressure, diastolic blood pressure and mean arterial pressure in group III, where lignocaine was given in the dose of 1.5 mg/kg iv 3 min before laryngoscopy and intubation were comparatively less than the other groups, when compared with the base line values.

The authors concluded that intravenous lignocaine at 1.5 mg/kg attenuated increase in heart rate and arterial blood pressure, only when given 3 min before intubation. And it offers no protection against post-intubation changes when given at 1, 2 and 5 min before intubation.

Splinter et al48 studied the haemodynamic response to laryngoscopy and tracheal intubation in geriatric patients with thiopentone alone or in combination with 1.5mg/kg lignocaine and with 1.5mg/kg or 3mcg/kg fentanyl were measured. They observed that both the drugs decreased the rise in heart rate and blood pressure changes with fewer


 

haemodynamic fluctuations in case of fentanyl. Lignocaine treated patients had fewer cardiac dysrhythmias.

C D Miller and S J Warren49 studied the effect of intravenous lignocaine on the cardiovascular responses to laryngoscopy and tracheal intubation.

The study population consisted of 45 Chinese patients of ASA Grade I and Grade II, posted for elective thoracic surgery. The patients were divided into four groups.

Group I – Received normal saline 4 ml iv over 30 sec, 3 min before laryngoscopy and intubation and served as control

Group II – Received 1.5 mg/kg of lignocaine iv 3 min before laryngoscopy and intubation.

Group III – Received 1.5 mg/kg of lignocaine iv 2 min before laryngoscopy and intubation.

Group IV – Received 1.5 mg/kg of lignocaine iv 1 min before laryngoscopy and intubation.

The patients were premedicated with morphine 0.2 mg/kg and hyoscine 40mcg/kg intramuscular one hour before induction. Anaesthesia was induced with thiopentone 5 mg/kg 2.5 minutes before laryngoscopy. Neuromuscular block was produced with 1.5 mg/kg of suxamethonium iv given 1.5 min before laryngoscopy and subsequent tracheal intubation were performed using standard Macintosh laryngoscope and cuffed Portex endotracheal tube. Heart rate, Systolic and Diastolic pressures were recorded and the Mean arterial pressure and rate-pressure product were calculated.

The results of the study showed that, in control group the heart rate increased by a maximum of 27 bpm, systolic blood pressure increased by 31 mm Hg, diastolic blood pressure increased by 28 mm Hg. Group III and Group IV, where lignocaine 1.5 mg/kg iv was given 2 and 1 minutes before laryngoscopy and intubation, also showed that, statistically significant increase in heart rate, systolic and diastolic blood pressure. The


 

authors concluded that, lignocaine 1.5 mg/kg given intravenously within 3 min of laryngoscopy and intubation failed to attenuate cardiovascular responses.

Wilson IG, et al50 studied the effect of varying the time of prior doses of intravenous lignocaine 1.5mg/kg on the cardiovascular response and catecholamine responses to tracheal intubation. Forty healthy patients were given intravenous lignocaine 2, 3, and 4 min prior to intubation. When compared with placebo there was significant increase in heart rate in all groups, but no significant rise in mean arterial pressure in all groups given lignocaine. Placebo group showed rise in mean arterial pressure of 19% compared to basal values.

M.J.L.   Bucx, et al51 worked on the relationship between forces applied during laryngoscopy and haemodynamic changes. This helps in to differentiate between cardiovascular effect of laryngoscopy and tracheal intubation. There was no significant relationship between forces applied during laryngoscopy and cardiovascular changes. It is the tracheal intubation more than laryngoscopy that caused changes in routine uncomplicated and laryngoscopy and subsequent tracheal intubation.

Sklar BZ et al52 conducted a study to assess the effect of lignocaine inhalation at a dose of 40mg and 120mg and control group with intravenous lignocaine 1mg/kg and on stress response to laryngoscopy and intubation. They observed that heart rate response to intubation with inhalation was dose dependent and at a dose of 120mg rise in blood pressure was least compared to rest of the study groups. Hence concluded that inhalation of lignocaine prior to induction of anaesthesia is a safe and convenient method.


 

METHODOLOGY

 

A Study entitled Comparative study of lignocaine nebulization with intravenous lignocaine on stress response to laryngoscopy and tracheal intubation was undertaken in Victoria hospital and Bowring and Lady Curzon hospitals, Bangalore during November 2008 to October 2010. Ethical clearance was obtained for the study.

The study was conducted on 90 ASA grade I and II patients in the age group of 18 to 45 years of either sex scheduled for elective surgeries done under general anaesthesia.

Patients were allocated into three groups with the sample size of 30 each. Group C (n=30) received no drug, as control.

Group I (n=30) received 2% Lignocaine 2mg/kg slow intravenous. Group N (n=30) received 2% nebulization of Lignocaine 2mg/kg. Exclusion criteria:

1.      Patients    with    chronic   obstructive   lung disease,    cerebrovascular disease, cardiovascular diseases, psychiatric illness and liver disorders.

2.      Patients having known allergy either to Lignocaine or its preservatives

 

3.      Patients coming for emergency surgical procedure.

 

4.      Patients with history of laryngeal, tracheal surgery or any pathology.

 

A detailed pre-anaesthetic evaluation including history of previous illness, previous surgeries, general physical examination, and detailed examination of Cardiovascular system, Respiratory system and other relevant systems were done. Baseline investigations were carried out and recorded in the proforma.


 

The following investigations were done in all patients

 

1.       Haemoglobin estimation

 

2.       Bleeding time and clotting time

 

3.       Urine examination for albumin, sugar and microscopy

 

4.       Blood sugar, FBS/PPBS

 

5.       Blood Urea and Serum Creatinine

 

6.       Standard 12- lead electrocardiogram

 

7.       X-ray of Chest

 

An informed and written consent was taken after explaining the anaesthetic procedure in detail. All the patient were pre-medicated with Tab. Diazepam 10mg to allay anxiety and Tab. Ranitidine 150 mg on the night before surgery

Patient arrived to the preoperative room 30 minutes before surgery and preoperative basal heart rate, non-invasive blood pressure readings, SpO2, cardiac rate and rhythm were also monitored from a continuous visual display of electrocardiogram from lead II were recorded.

The patient in group N were nebulized with 2% lignocaine 2mg/kg body weight using a simple fitting face mask with CompAir Compressor Nebulizer NE-C28 model of OMRON healthcare, 10min before induction. On operating table intravenous line was secure with 18G cannula and ringer lactate 500ml infusion started. Patients were connected to non-invasive monitoring with 5 lead electrocardiograph (ECG), pulseoximeter, and non-invasive sphygmomanometer. All patients were pre-medicated with Inj Midazolam 1mg iv. All patients were pre-oxygenated with 100% oxygen for 3 minutes by a face mask.


 

Patients in Group C being the control did not receive any drug.

 

Patients in Group I received 2% lignocaine 2mg/kg body weight 90 sec before induction. Patient in group N were nebulized with 2% lignocaine 2mg/kg body weight 10 min before induction.

INDUCTION OF ANAESTHESIA

 

Anaesthesia was induced with Inj. Thiopentone 5mg/kg as 2.5 % solution, after loss of eye lash reflex and confirmation of adequacy of mask ventilation endotracheal intubation was facilitated with succinylcholine 1.5 mg/kg iv. Laryngoscopy was performed using Machintosh laryngoscope, under visualization of vocal cords a  lubricated (2% lignocaine jelly) cuffed endotracheal tube of appropriate size was passed. After confirming bilateral equal air entry, the endotracheal tube was secured.

Anaesthesia was maintained using 66% nitrous oxide and 33% of oxygen and Halothane 1%. After the patients recovered from succinylcholine further neuromuscular blockade was maintained with non-depolarizing muscle relaxants vecuronium.

MONITORING

 

The following cardiovascular parameters were recorded in all patients:

 

  Heart rate (HR) in beats per minutes (bpm)

 

  Systolic blood pressure (SBP) in mm Hg

 

  Diastolic blood pressure (DBP) in mm Hg

 

  Mean arterial pressure (MAP) in mm Hg

 

The above cardiovascular parameters were noted as below

 

1.          Basal before giving any study drugs and premedication

 

2.          One minute interval for 5 min after laryngoscopy and intubation

 

3.          Every two minutes interval for next 10 min.


 

After the recordings were obtained all patients received 0.2mg Glycopyrrolate iv and 3mcg/kg of Fentanyl iv for analgesia which was avoided earlier, so as to avoid their effects on intubation response. At the end of the procedure patients were reversed with Neostigmine 0.05 mg/kg iv and Glycopyrrolate 0.01 mg/kg iv and extubated after recovery of adequate muscle power and consciousness.


 

 

 

Figure 4:Photograph showing administration of Nebulization


Figure 5:Photograph showing CompAir Compressor Nebulizer NE-C28 and Injection Lignocaine 2%.


 

OBSERVATION AND RESULTS

 

STATISTICAL METHODS.

 

Descriptive statistical analysis has been carried out in the present study. Results on continuous measurements are presented on Mean  SD (Min-Max) and results on categorical measurements are presented in Number (%). Significance is assessed at 5 % level of significance. Analysis of variance (ANOVA) has been used to find the significance of study parameters between three or more groups of patients, Chi-square/ Fisher Exact test has been used to find the significance of study parameters on categorical scale between two or more groups. Kruska Wallis test has been used to find the significance of SPO2 between three groups

Significant figures

 

+ Suggestive significance (P value: 0.05<P<0.10)

 

* Moderately significant (P value: 0.01<P    0.05)

 

** Strongly significant (P value: P 0.01)

 

Statistical software: The Statistical software namely SAS 9.2, SPSS 15.0, Stata 10.1, MedCalc 9.0.1, Systat 12.0 and R environment ver.2.11.1 were used for the analysis of the data and Microsoft word and Excel have been used to generate graphs, tables etc.


 

1.   AGE DISTRIBUTION

 

Table 1 : Table showing Age distribution

 

 

 

Age in years

Group C

Group I

Group N

No

%

No

%

No

%

18-20

4

13.3

2

6.7

6

20.0

21-30

6

20.0

10

33.3

8

26.7

31-40

8

26.7

10

33.3

6

20.0

41-50

12

40.0

8

26.7

10

33.3

Total

30

100.0

30

100.0

30

100.0

Mean ± SD

34.80±9.97

34.13±8.72

32.97±10.06

 

 

 

50

 

45

 

40

 

35

 

Text Box: Percentages30

 

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


 

Text Box: Percentages60

 

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

 

Text Box: Percentages30

 

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

 

Text Box: HR (bpm)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

 

Text Box: SBP (mm Hg)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

 

Text Box: DBP (mm Hg)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

 

Text Box: MAP (mm Hg)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

 

 

Text Box: SPO2(%)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.


 

BIBLIOGRAPHY

 

 

1.          Shribman AJ, Smith G, Achola KJ: Cardiovascular and chatecholamine responses to laryngoscopy with or without tracheal intubation. British Journal of Anaesthesia 1987; 59:295

2.          Burstein CL, Lo Pinto FJ and Newman W. Electrocardiographic studies during endotracheal intubation 1, effects during usual routine techniques. Anesthesiology. 1950; 11:224.

3.          Robert K. Stoelting. Blood pressure and heart rate changes during short-duration laryngoscopy for tracheal intubation. Influence of viscous or intravenous lidocaine. Anesthesia Analgesia. 1978; 57: 197-199.

4.          Prys-Roberts, Greene LT, Meloche R and Foex P. Studies of anaesthesia in relation to hypertension-II. Haemodynamic consequences of induction and endotracheal intubation. British Journal of Anaesthesia. 1971; 43: 541-547.

5.          Forbes AM and Dally FG. Acute hypertension during induction of anaesthesia and endotracheal intubation in normotensive man. British Journal of Anaesthesia. 1970; 42: 618-622.

6.          Fox EJ, Sklar GS, Hill CH, Villanueva R, King BD: Complications related to the pressor response to endotracheal intubation. Anesthesiology 1977; 47:524-525.

7.          Dalton B and Guiney T et al. Myocardial ischaemia from tachycardia and hypertension in coronary heart disease – Patient’s undergoing anaesthesia. Ann. Mtg. American Society of Anaesthesiologists, Boston. 1972; pp. 201-202.

8.          Donegan MF and Bedford RF. Intravenously administered lignocaine prevents intracranial hypertension during endotracheal suctioning. Anesthesiology, 1980; 52:516-518.


 

9.          Nair GC, Hariwar Singh and Preetam Singh. Vital signs and electrocardiography during intubation. Indian Journal of Anaesthesia. 1965 Feb; 40-57.

10.    Bedford RF and Lt Marshal K. Cardiovascular responses to endotracheal intubation during four anaesthetic techniques. Acta Anaesthesiologica Scandinavia. 1984; 28: 563-566.

11.    Braude N, Clements EA, Hodges UM, and Andrews BP. The pressor response and laryngeal mask insertion. A comparison with tracheal intubation.

Anaesthesia 1989; 44:551.

 

12.    Wood ML, Forrest ET: The haemodynamic response to the insertion of the laryngeal mask airway: A comparison with laryngoscopy and tracheal intubation. Acta Anaesthesiol Scand 1994; 38: 510.

13.    Chen C: Fentanyl dosage for suppression of circulatory response to laryngoscopy and endotracheal intubation. Anesthesiol Rev 1986; 13:37.

14.    Devault M, Greifenstein FE and Harris JR. LC. Circulatory responses to endotracheal intubation in light general anaesthesia; the effect of atropine and phentolamine. Anesthesiology. 1960; 21: 360-362.

15.    Prys-Roberts C, Foex P, Biro GP and Roberts JG. Studies of anaesthesia in relation to hypertension – V: Adrenergic beta-receptor blockade. British Journal of Anaesthesia. 1973; 45: 671-680.

16.    Mikawa K, Nishina K, Maekawa N, Obara H: Comparison of nicardipine, diltiazem and verapamil for controlling the cardiovascular responses to tracheal intubation. British Journal of Anaesthesia 1996; 76:221.

17.    Gallagher JD, Moore RA, Jose AB, et al: Prophylactic nitroglycerin infusions during coronary artery bypass surgery. Anesthesiology 1986; 64:785.


 

18.    Mikawa K, Nishina K, Maekawa N, et al: Attenuation of the catecholamine response to tracheal intubation with oral clonidine in children. Canadian Society Anaesthesia Journal. 1995; 42:869.

19.    Aho M, Lehtinen AM, Erkola O, et al: The effects of intravenously administered dexmedetomidine on perioperative hemodynamiccs and isoflurane requirements in patients undergoing abdominal hysterectomy. Anesthesiology 1991; 74:997 – 1002.

20.    Stoelting RK: Circulatory response to laryngoscopy and tracheal intubation with or without prior oropharyngeal viscous lidocaine. Anesth Analg 1977; 56: 618

21.    Abou-Madi M, Keszler H, and Yacoub O. A method for prevention of cardiovascular reactions to laryngoscopy and intubation. Canadian Society Anaesthesia Journal. May 1975; 22: 316.

22.    Williams KA, Barker GL, Harwood RJ, Woodall NM. Combined nebulization and spray–as–you-go topical local anaesthesia of the airway. British Journal of Anaesthesia. 2005; 95:549-553.

23.    Abou-Madi M, Keszler H, and Yacoub JM. Cardiovascular reactions to laryngoscopy and tracheal intubation following small and large intravenous dose of lidocaine. Canadian Society Anaesthesia Journal. 1977; 24(1):12-18.

24.    Tam S, Chung F, and Michael Campbell M. Intravenous lignocaine: Optimal time for injection before tracheal intubation. Anesth Analg.1987; 66: 1036-1038.

25.    Yakioka H, Hayashi M, Yoshimoto N, et al. IV Lidocaine as a suppressant of coughing during tracheal intubation. Anesth Analg 1985; 64: 1189-1192.

26.    Baraka A. Intravenous lidocaine controls extubation laryngospasm in children.

 

Anesth Analg 1978; 57:506-507.


 

27.    Adamizik M, Groeben H, Farahan R, Lehmann N, Peters J. Intravenous lidocaine after tracheal intubation mitigates bronchoconstriction in patients with asthma. Anesth Analg.1993; 77: 309 – 312.

28.    Groeben H, Silvanus MT, Beste M, Peters J. Both intravenous and inhaled lidocaine attenuate reflex bronchoconstriction but at different plasma concentrations. Am. J. Respir. Crit Care Med. 1999; 159:530-535.

29.    Williams, Warnick. Gray’s Anatomy. 36th ed. Edinburg: Churchill Livingstone; 1984.

30.    Carin A. Hagberg. Basic clinical science considerations. In: Benumof’s Airway Management – Principles and Practice. 2nd ed. Philadelphia; Mosby Elsevier; 1996.

31.    Robert K. Stoelting, Simon C. Hillier. Pharmacology and Physiology in Anesthetic Practice. 4th ed. Philadelphia: Lippincott Williams & Wikkings; 2006.

32.    Charles B. Berde, Gary R. Strichartz. Local anaesthetics. In: Ronald D Miller, editors. Miller’s Anesthesia. 7th ed. Philadelphia: Churchill Livingstone Elsevier; 2005. P.913 - 940

33.    Collins VJ. Local Anesthetics. In: Principles of Anesthesiology – General and Regional Anesthesia. 3rd ed. Philadelphia: Lea and Febiger; 1993.

34.    Reid LC and Brace DE. Initiation of respiratory tract reflexes and its effects on heart. Surgy. Gynae. Obstretrics. 1940; 70: 157.

35.    King BD, Harris IC Jr., Freifenstein FE, Elder JD and Dripps RD. Reflex circulating responses to direct laryngoscopy and tracheal intubation performed during general anaesthesia. Anesthesiology. 1951; 12: 556-566.


 

36.    Hassan HG, el-Sharkawy TY, Renck H, et al: Hemodynamic and catecholamine responses to laryngoscopy with vs. without endotracheal intubation. Acta Anaesthesiol Scand 1991; 35:442.

37.    Sharma VC and Srivasthava SL et al. Variations in the various components of ECG during laryngoscopy and intubation and extubation. Indian Journal of Anaesthesia. 1984; 32(3): 234-242.

38.    Harnath Babu K and Dhanraj VJ. Electrocardiographic variations during induction of anaesthesia with six different agents. Indian Journal of Anaesthesia. 1974; 48: 53-58.

39.    Van Aken H, Puchstein C, Hidding J: The prevention of hypertension at intubation. Anaesthesia 1982; 37:82.

40.    Gold MI, Brown M, Coverman S, Herrington C: Heart rate and blood pressure effects of esmolol after ketamine induction and intubation.

Anesthesiology 1986; 64:718.

 

41.    Ausems ME, Hug Jr CC, Stanski DR, Burm AG: Plasma concentrations of alfentanil required to supplement nitrous oxide anesthesia for general surgery. Anesthesiology 1986; 65:362.

42.    Kay B, Nolan D, Mayall R, Healy TEJ. The effects of sufentanil on the cardiovascular response to tracheal intubation. Anaesthesia. 1987; 42: 382-386.

43.    Stoelting RK: Attenuation of blood pressure response to laryngoscopy and tracheal intubation with sodium nitroprusside. Anesth Analg 1979; 58:116.

44.    Gjonag ST, Lowenthal DB, and Dozor AJ. Nebulized lidocaine administered to infants and children undergoing flexible bronchoscopy. Chest 1997; 112:1665 – 1669.


 

45.    Bedford RF, John A, Persing, Pobereskin L, Buttler A. Lidocaine or thiopentone for rapid control of intracranial hypertension. Anesth Analg 1989; 59: 435 - 447

46.    Hamil JF, Bedford RF, Weaver DC, Colohan AR. Lidocaine before endotracheal intubation: Intravenous or Laryngotracheal ? Anesthesiology 1981;55:578 - 581

47.    Venus B, Polassani V, and Pham CG. Effects of aerosolized lidocaine on circulatory responses to laryngoscopy and tracheal intubation. Crit Care Med April 1984; 12(4): 391-394.

48.    Splinter WM, Cervenko. Haemodynamic responses to laryngoscopy and tracheal intubation in geriatric patients: effects of fentanyl, lidocaine and thiopentone. Canadian Journal of Anaesthesia. 1989; 36(4): 370-376.

49.    Miller CD and Warren SJ. IV lignocaine fails to attenuate the cardiovascular response to laryngoscopy and tracheal intubation. British Journal of Anaesthesia. 1990; 65: 216-219.

50.    Wilson IJ, Meiklejohn BH, Smith G. Intravenous lignocaine and sympathoadrenal responses to laryngoscopy and intubation. The effects of varying time of injection. Anaesthesia 1991, March; 46(3):177-180.

51.    Bucx MJL, Vangeel RTM, Scheck PAE, Stijnen T. Cardiovascular effects of forces applied during laryngoscopy. Anaesthesia 1992; 47:1029 – 1033

52.    Sklar BZ, Luri S, Ezri T, Krichelli D, Savir I, Soroker D. Lidocaine inhalation attenuates the circulatory response to laryngoscopy and endotracheal intubation. Journal of Clinical Anaesthesia September-October 1992; 4(5):382-385.

53.    Gibbs JM. The effects of endotracheal intubation on cardiac rate and rhythm. N.Z, Med. J. 1967; 66:465


 

54.    Koppert W, Weigand M, Neumann F, Sittl R, Schuettler J, Schmelz M, and Hering W. Perioperative intravenous lidocaine has preventive effects on postoperative pain and morphine consumption after major abdominal surgery. Anesth Analg 2004; 98: 1050 – 1055.

55.    Nishino T, Hiraga K and Sugimori K. Effects of i.v. lignocaine on airway reflexes elicited by irritation of the tracheal mucosa in humans anaesthetized with enflurane. British Journal of Anaesthesia. 1990; 64: 682-687.

56.    Churchill-Davidson HC. A practice of anaesthesia, 5th ed. New Delhi: P.G. Publishing Limited; 1984.

57.    Himes R, Difazio C, Burney R. Effects of lidocaine on the anaesthetic requirement for nitrous oxide and halothane. Anesthesiology. 1977; 47: 437-440.

58.    Crawford DC, Fell D, Achola KJ. Effects of Alfentanil on the pressure and catecholamine response to tracheal intubation. British Journal of Anaesthesia. 1987; 59: 707-712.

59.    Gianelly R, Von Der Groeben JO, Spiracki A and Harrison DC. Effect of lidocaine on ventricular arrhythmias in patients with coronary heart disease. New England J. Med. 1967; 277: 1215

60.    Thomas J, Long G and Mather LE. Plasma lignocaine concentration following topical aerosol application. British Journal of Anaesthesia 1969;41:5

61.    Adriani J and Campbell D. Fatalities following topical application of local anaesthetics to mucous membranes. J.A.M.A. 1956; 162:1527

62.    Polek NV, Baughman VL, Lauritio et al. Adequate serum lidocaine levels fail to control the haemodynamic responses to intubation. Anesthesia Analgesia. 1989; Abstracts; 68: S225.


 

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:             SpO2:


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

 

No comments:

Post a Comment