“EFFECTS OF INTRAVENOUS LIGNOCAINE 2% AND LIGNOCAINE SPRAY 10% FOR INTUBATION RESPONSE IN PATIENTS WITH EJECTION FRACTION <50% - COMPARATIVE STUDY"
INTRODUCTION
Laryngoscopy
and tracheal intubation is one of the commonest procedures done by all
anesthesiologists on daily basis. Direct laryngoscopy and intubation leads to
reflex release of catecholamines resulting in hemodynamic response meaning
transient increase in heart rate, systolic blood pressure, diastolic blood
pressure[1,2] and occasionally cardiac arrhythmias[3] .
Laryngoscopy
and endotracheal intubation is an essential part of general anaesthesia in
cardiac surgery. Direct laryngoscopy and intubation through the larynx is a
noxious stimulus, which can provoke unwanted response in the cardiovascular,
respiratory and other physiological systems[4] .
Lignocaine is the most frequently used local
anesthetic, available in multiple concentrations. It is also routinely used by
various techniques for local, peripheral and epidural anesthesia. One of the
uses of lignocaine is to anaesthetize airway. Intravenous lignocaine acts by
inhibiting sympathetic response associated with intubation by increasing
threshold for stimulation of airway and central inhibition of sympathetic
transmission, dose which used for this action is 1.5mg/kg IV bolus which has 30%
depressive effect on CVS [5,6,7].
Lignocaine has been evaluated in numerous
trials as a spray or gel to suppress response associated with laryngoscopy[8,9,10].
It has also been used to reduce the incidence of postoperative sore throat,
cough, and hoarseness of voic1[11,12,13,14]. This anesthetic has
also been given via nebulizer for awake intubation in difficult airway patients[15,16].
More commonly, lignocaine inhalation has been utilized to reduce the frequency
of chronic cough in patients with asthma and chronic obstructive lung disease
(COPD)[17,18]. This route of administration appears to produce low
serum levels and a reduced frequency of adverse effects compared to gel or
spray formulations.
We plan to compare lignocaine spray
(10%) and intravenous lignocaine(2%, 1.5mg/kg) to attenuate the sympathoadrenal
response along with standard drugs used for premedication and induction. This
study has been designed to assess the effects on hemodynamic parameters due to
laryngoscopy and endotracheal intubation in patient undergoing CABG with
ejection fraction less than or equal to 50%.
AIMS & OBJECTIVES
Aim
of this comparative study is to assess effects of lignocaine spray and
Intravenous Lignocaine
on
the following:
1)
Hemodynamic response to laryngoscopy on:
1.
Heart rate
2.
Systolic and Diastolic blood pressure
3.
Mean Arterial Pressure
4.
Central Venous Pressure
5.
ECG for Arrhythmias
2)
Post-operative sore throat.
MATERIALS AND METHOD
This Prospective Randomized study was conducted in
Department of Anaesthesiology, D Y
Patil University School of Medicine & Hospital, Nerul, Navi Mumbai.
STUDY DESIGN:
Prospective
Comparative study
STUDY DURATION:
October
2017 to June 2019
Eligibility Criteria:
INCLUSION
CRITERIA
1. Patient
with Ejection Fraction(EF) <50% undergoing Coronary Artery Bypass Graft
(CABG) under general anaesthesia
2. Adult
patients in the age group of 30 to 75 yrs.
3. American
Society of Anesthesia (ASA) status II or III for patients undergoing elective surgeries
4.
Patients with all laboratory
investigations within normal limits and
hemodynamically stable patient.
EXCLUSION
CRITERIA
1.
Those unwilling to participate.
2. Patients
with difficult airway (MPC III / IV)
3.
Patients with ASA status IV.
4. Patients
undergoing emergency surgery.
5.
Patients known or suspected to have an
allergy to lignocaine.
SAMPLE SIZE AND SUBJECT:
Approval of
Institutional Ethics Committee was obtained before start of the study in October
2017. A valid informed written consent was obtained prior to enrolling the
subject in the study.
A prospective, randomized, comparative study was
conducted in 60 patients of ASA grade II or III between the age group 30-75
years posted for CABG with ejection fraction less than or equal to 50%
requiring general anesthesia to compare the effect of intravenous lignocaine
and lignocaine spray on hemodynamic response to laryngoscopy and endotracheal
intubation.
MATERIAL USED:
Following materials were available for our study:
a)
Lignocaine
(preservative free) – 2%
b)
Lignocaine
(topical) - 10% spray
c)
10 ml
syringe
d)
Normal
saline for dilution
PREPARATION OF DRUGS:
1)
1.5mg/kg of
study drug 2% lignocaine was diluted till 10ml with normal saline for
intravenous injection.
2)
Lignocaine 10%
spray attached with spraying
nozzle.
STUDY
PROCEDURE/ DATA COLLECTION METHOD:
Pre
anaesthesia assessment:
Prior to surgery, preoperative visit were made
and a detailed history of the patient was taken. Informed consent was taken
from all the patients included in the study.
Following
informed consent along with proper preoperative evaluation and relevant
investigations as per the case record form the patient was randomly allocated
to either of the two groups.
Randomization was done using random number
table generated from computer software.
The
patients were randomly divided into 2 groups:
├Ш
Group
1 (n=30):
Intravenous 2% lignocaine (preservative free)
1.5mg/kg
├Ш
Group
2 (n=30):
lignocaine spray 10%
├Ш
After
obtaining written consent, initial pre-operative counseling was done to gain
confidence of patient, thereby minimizing the emotional component of stress.
All
the patients were given intradermal test dose of 0.2ml 2 % lignocaine on
ventral aspect of left forearm.
The
nature of the procedure was explained to the patients. Baseline reading which
included heart rate (beats/min), systolic blood pressure (mmHg), diastolic
blood pressure (mmHg) and mean arterial pressure (mmHg), central venous
pressure (CVP) and electrocardiogram (ECG) for all cases were noted pre
operatively.
Procedures
for study drug administration and for anesthetic induction were rigorously
standardized.
· GROUP 1: After
standard induction, this group of patients received intravenous 2% Lignocaine
(preservative free) 3 minutes prior to laryngoscopy .
· GROUP 2:
Patients vocal cords were sprayed with 10% lignocaine spray as soon as the
vocal cords are visualized by direct laryngoscopy.
Patient
taken to the operation theatre, where automated recordings (Data scope) of
heart rate (HR) and systolic (SBP), diastolic (DBP), and mean (MBP) blood
pressures were recorded at 0 min, 1 min, 3min and repeated at 5-minute interval
till 20 mins from induction. After 3 minutes of pre-oxygenation, premedication
with Inj. Glycopyrrolate (4ug/kg), Inj. Midazolam (0.03mg/kg), Inj. buprenorphine
(1mcg/kg) was given. This was followed by induction of General Anaesthesia with
Inj. Thiopentone (5 mg/kg) followed by Inj. Vecuronium (0.1mg/kg) and the
patient was intubated.
Group
1 received intravenous 2% lignocaine (preservative free) 1.5 mg/kg 180 sec just
before laryngoscopy.
Laryngoscopy
was done at 3 minutes after dose of Vecuronium for passage of the endotracheal tube followed
by mechanical ventilation with 1.2% Isoflurane
in 60% Air/ 40%
O2 at
2 L/min and adequate tidal volume. The patient was left undisturbed for an additional 20 minutes
of hemodynamic recordings, at which point the study was terminated.
The
standard monitors were used on all patients to eliminate variability in
determining blood pressure or heart rate and recording data. Our induction
technique was parallel the drug dosages and sequence frequently used in the
anesthesia department.
Method
for Statistical Analysis:
The
quantitative data was represented as their Mean ± SD. Categorical
and nominal data were expressed in percentage. The t-test was used for
analyzing quantitative data, or else non parametric data, was analysed by
Mann-Whitney test. Categorical data was analysed by using chi-square test. The
significance threshold of p value was set at < 0.05. All analysis was
carried out by using SPSS software version 21.
AIRWAY ANATOMY [19, 20]
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 is present in 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:
Epiglottis
is a leaf like structure. Its lower tapering end is attach to the back of the
thyroid cartilage with the help of thyro-epiglottic ligament
LARYNX:
The anaesthesiologist should be thorough with knowledge of the anatomy of the
larynx. The larynx is located within the anterior aspect of the neck, anterior
to the inferior portion of the pharynx and superior to the trachea. Its primary
function is to protect the lower airway by closing abruptly upon mechanical
stimulation, thereby halting respiration and preventing the entry of foreign
matter in to the airway. Other function of larynx includes phonation, coughing,
the Valsalva maneuver and control of ventilation, and acting as sensory organ. Structurally,
the larynx composed of 3 large unpaired cartilages (cricoid, thyroid,
epiglottis); 3 paired cartilages which are small (arytenoids, corniculate,
cuneiform); and a number of intrinsic muscles. The hyoid bone, while
technically not a part of larynx, provides muscular attachments from above that
aid in laryngeal motion. Larynx extends from C4-C6 cervical vertebra.
Figure
1. Entrance to larynx (posterior view)
The
laryngeal inlet has large oblique shaped opening bounded by epiglottis antero-posteriorly.
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 postero-inferiorly
from the margin of the epiglottis to the arytenoid cartilage. It contains the aryepiglottic muscle and
near its inferior end two small pieces of cartilage which form the cuneiform
and corniculate tubercules in its free edge. The interarytenoid fold of mucous
membrane passes between them forms the inferior boundary of inlet and encloses
the muscle which passes 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.
Figure 2. Laryngoscopic view of vocal cord
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.
On
laryngoscopy, 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:
Trachea
is a wide tube with 13-15 mm diameter and 11- 14 cm in length. It begins at the
larynx and terminates at the level of the fourth thoracic vertebra, where it bifurcates
into the two main bronchi. The tracheal architecture consists of C shaped
cartilages which are joined posteriorly by the trachealis muscle. Vertically
these cartilages are joined to each other by fibroelastic tissue.
NERVE SUPPLY:
Glossopharyngeal
nerve:
This cranial nerve is a mixed type of nerve. Motor fibers of this
nerve supply the stylopharyngeus
muscle. Parasympathetic fibers supplies the parotid gland.
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.
Figure 3. Nerve Supply of the Airway
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:
Vagus
is a mixed type of cranial nerve. In the neck it is found with 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 multiple branches, among all
three of which supply those areas of the pharynx and larynx stimulated by the
endotracheal intubation.
1. Pharyngeal branch
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 cricothyroid
muscle to which it supplies. The internal branch, Supplies sensory branches to
the larynx above the level of the glottis.
3.
Laryngeal
nerve: 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 RESPONSES[21,22]
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 4.
Sympathetic supply to heart
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.
THE CARDIOVASCULAR REFLEXES
The
cardiovascular responses to noxious airway manipulation are initiated by
proprioceptors responding to tissue irritation in the supraglottic region and
trachea. It is located in close proximity to the airway mucosa. 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 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 cardio accelerator 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 LIGNOCAINE23,24,25
Lignocaine
was synthesised in 1943 in Sweden by Lofgren, it was introduced into clinical
practice by Gordh in the year 1948. It is most commonly used local anesthetic
agent.
PHARMACOLOGY
Clinically lignocaine is an amino-amide of xylidine-de-ethyl amino 2:6
dimethyl acetanilidine.
STRUCTURAL FORMULA:
PHYSICAL
PROPERTIES:
It
consists of lipophilic aromatic group, hydrophilic tertiary amine and
intermediate amide bond. It is a stable, colorless crystalline solid whose
hydrochloride salt is readily soluble in water, not decomposed by boiling,
acids or alkalies and withstands repeated autoclaving. It should be stored at
room temperature.
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 has rapid onset
of action. It is effective by all routes of administration. Lignocaine
sometimes causes vasodilation, Adrenaline may be used 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 of 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 < 25┬║C protected from light.
Lignocaine is also available along with adrenaline in 1: 1 lakh or 1: 2 lakh concentrations.
Figurer 5. Lignocaine 2%
Each ml contains:
Lignocaine Hydrochloride I.P. 21.3 mg
Sodium Chloride I.P. 6.0 mg
Water for injection 1.P. q.s.
Figure 6. lignocaine spray 10%
Each
ml contains:
Lidocaine USP 100mg
Ethanol
I.P. 30.4% v/v
Flavoured Base q.s.
PHARMACODYNAMICS
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) cap
Prolong
the duration of action of lignocaine by decreasing the rate of removal from the
local site of injection in to the circulation
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.
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:
Lignocaine
gets metabolized 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. Lignocaine is excreted by kidneys.
Dosage:
The
factors on which the dosage of lignocaine depends are the weight of the
patients and the different absorption rates from various sites and injections.
The maximum safe dose of lignocaine is 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 level
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
Ul
Islam M, Ahmad
I, Shah
AA, Islam
A;Attenuation of haemodynamic response to
laryngoscopy and oral endotracheal intubation in coronary artery bypass surgery
patients: intravenous morphine and lidocaine versus intravenous morphine and
lidocaine spray. J
Ayub Med Coll Abbottabad. 2014
Jul-Sep;26(3):275-8[26].
In 2014, there was
randomized control trial conducted with 60 patients who were schedules for
elective CABG. There were two groups i.e group A (IV morphine 0.1mg/kg & IV
lignocaine 1.5mg/kg) and group B (IV morphine 0.1mg/kg & lignocaine spray
1.5mg/kg). Demographic data was comparable in both groups.
With this study they
concluded that lignocaine spray in addition to IV morphine had no better effect
on attenuation of hemodynamic changes to laryngoscopy and intubation compared
to intravenous lignocaine and morphine in CABG surgery patients.
Abou-Madi
MN, Keszler
H, Yacoub
JM;Cardiovascular
reactions to laryngoscopy and tracheal intubation following small and large
intravenous doses of lidocaine. Can Anaesth Soc J. 1977 Jan;24(1):12-9[27].
In
1977, Abou-Mandi MN et al, studied hemodynamics changes to laryngoscopy and
endotracheal intubation after giving small and large intravenous doses of
lignocaine (0.75mg/kg & 1.5mg/kg).
With
this study they came to a conclusion that 1.5mg/kg dose of lignocaine had
complete protection against cardiac arrythmias of all types. Small dose of
lignocaine (0.75mg/kg) was ineffective in this respect. While the larger dose
also had borderline protection against hypertention and tachycardia, the small
dose prevented only the rise in systolic blood pressure. Possible mechanisms
for theses observations are direct myocardial depressant effect, a central
stimulant effect, a peripheral vasodilation effect and finally an effect on
synaptic transmission.
This study was carried out at the tertiary
level hospital in India. After Approval
from the Institutional Ethics Committee, written informed consent
was obtained from close relatives
of the patients. A total f 60 patients with LVEF>
35%, between30 and 75 years
of age, undergoing elective cardiac
surgery requiring laryngoscopy and intubation were enrolled
for this prospective randomized double blind
study. There were two groups;
Group
A received Lignocaine 1.5mg/kg
i.v and group
B received an
additional dose of
injection Fentanyl 3
mcg/kg i.v. 3
min prior to laryngoscopy. During induction various
hemodynamic parameters was recorded during induction and 10 min intervals after
tracheal intubation.
In
conclusion, given 3 minutes prior to intubation, lignocaine (1.5
mg/kg) and fentanyl
(3╬╝g/kg) both attenuated the
rise in HR, .
We
conclude that both
lignocaine and fentanyl
can be safely used for attenuation of stress
response during laryngoscopy and TI in
patients with cardiac
disease undergoing elective cardiac surgery.
This study was carried out in the department
of Anaesthesiology at the M.R. Medical College’s Basaveshwar Hospital, Govt
General Hospital Gulbarga during the period of two years. Seventy five Patients
of either sex, aged between 20 and 60 Years.
Group-I Received Fentanyl 4┬╡g /kg body weight.
Group-II Received Lignocaine(xylocaine) 1.5 mg
/kg body weight
Group-III Received normal saline.
After intubation, incidence of tachycardia
(HR>100/min) was significantly greater in placebo and lignocaine group than
in fentanyl group (p<0.05). Rise in systolic blood pressure (SBP) and
diastolic blood pressure (DBP) were also statistically significant in placebo
and lignocaine group than in fentanyl group (p<0.05) as compared with
baseline value.
In the present study, Attenuation of pressor
response was seen both with lignocaine and fentanyl. Of the 2 drugs fentanyl
4┬╡g/kg bolus provides a consistent, reliable and effective attenuation of
haemodynamic response to laryngoscopy and endotracheal intubation as compared
to lignocaine 1.5mg/kg iv. bolus.
Fifty
controlled hypertensive ASA grade II patients of either sex aged between 35 and
65 years undergoing routine elective surgical procedures under general
anaesthesia participated in this prospective randomized study. Ethical
committee approval was received and informed consent was obtained from all
patients.
Patients
were randomly assigned one of 2 groups each comprising 25 patients. Group I
received lignocaine 10% (LOX Topical spray, Neon Labs) spray 2 minutes before
induction of anaesthesia. Group II received normal saline spray prior to
induction of anaesthesia and served as control.
There
was a statistically significant (p< 0.05) increase in heart rate, systolic
,diastolic and mean arterial pressure in group II when compared to group I and
also when compared to baseline values. It was concluded that topical lignocaine
10% when sprayed prior to induction of anaesthesia attenuated the pressor
response to laryngoscopy and intubation, but did not abolish it completely.
Mostafa SM1, Murthy
BV, Barrett PJ, McHugh P;Comparison of the effects of topical lignocaine spray
applied before or after induction of anaesthesia on the pressor response to
direct laryngoscopy and intubation. Eur J Anaesthesiol. 1999 Jan;16(1):7-10[9].
In an attempt to attenuate the cardiovascular
pressor response to laryngoscopy and intubation, 30 patients presenting for
routine ophthalmic surgery were studied and were randomly allocated into two
groups: group A (n = 15) received direct laryngeal/tracheal lignocaine spray
immediately before intubation; and group B (n = 15) received orolaryngeal
lignocaine spray before the induction of anaesthesia.
Laryngoscopy and endotracheal intubation
caused a significant increase in heart rate, by 28% in group A and 23% in group
B (P < 0.05 in both), and in diastolic blood pressure, by 28% in group A and
24% in group B (P < 0.05 in both). In group A, the systolic blood pressure
also increased significantly (by 18%) after intubation, but there was no
significant change in group B.
It was concluded that topical lignocaine
administration as an orolaryngeal spray before the induction of anaesthesia is
effective in reducing but not abolishing the pressor response to laryngoscopy
and endotracheal intubation.
Patients were randomly divided into two
groups, 30 in each group.
Group I
received 50 mg of esmolol
group
II received lignocaine 2 mg/kg.
Haemodynamic parameters like pulse, systolic
blood pressure, diastolic blood pressure and mean arterial pressure were
measured before induction of anaesthesia, immediately after intubation then at
intervals of one minute, three minutes, five minutes, seven minutes and 10 1minutes.
There was no significant difference in
demographic or base line vital signs between two groups (Table 1). The mean
systolic blood pressure (SBP) increased on laryngoscopy and tracheal intubation
by 15 mmHg in the group I whereas in group II it was 17.4 mmHg.
There was a significant rise in diastolic
blood pressure (DBP) in both the groups, but the rise was lesser in group II
than in group I.
Both esmolol and lignocaine were not effective
in attenuating hemodynamic stress response to laryngoscopy and tracheal
intubation; however esmolol was superior to lignocaine in blunting the stress
response.
Dr. V. Madhuri
Gopal;Comparative Study of Pressor Response to Laryngoscopy and Intubation with
Oral Spray of Nitroglycerine and Oropharyngeal Spray of Lignocaine;
Sch. J. App. Med.
Sci., 2017; 5(4D):1463-1469[32].
A
clinical prospective comparative randomized study of attenuation of sympathetic
response to laryngoscopy and intubation was done in 60 patients posted for
elective surgeries. The study was conducted after an approval from the hospital
ethics committee.
Group
L - Lignocaine group (n=30) - received oropharyngeal Lignocaine 10% spray 100
mg 3 minutes before induction.
Group
N - Nitroglycerin group (n=30) - received oral nitroglycerin spray 0.8mg 30
seconds before induction.
Heart
rate, systolic and diastolic blood pressure were recorded at baseline, at
induction, 1, 3, 5 and 10 minute intervals after laryngoscopy
From
the present study it can be concluded that
· In Lignocaine
spray group patients who received 10 puffs ( 100 mg) oropharyngeally , 3
minutes before induction , there was a significant rise in the mean heart rate
(HR), systolic blood pressure (SBP), diastolic blood pressure (DBP) , mean
arterial pressure (MAP) occurred one minute following laryngoscopy and
intubation .
·
In Nitroglycerine spray group, who received 2 puffs (0.8 mg) orally 30 seconds
before induction, effectively attenuated arterial pressure response to
laryngoscopy and intubation. Hence, it is concluded that Nitroglycerine oral
spray in the dose of 0.8 mg, given 30 seconds before induction can be a better
alternative in attenuating the haemodynamic responses to laryngoscopy and
intubation without adverse side effects.
Stoelting,
Robert K; Blood pressure and heart rate changes during short-duration
laryngoscopy for tracheal intubation: influence of viscous or intravenous
lidocaine. Anesth Analg 1978; 7:19734[33].
In
1978, Stoelting, Robert K studied blood pressure and heart rate changes during short-duration
laryngoscopy for tracheal intubation. Influence of viscous or intravenous
lignocaine and concluded that the best way to prevent laryngoscopic response
was to minimize the duration of laryngoscopy and intubation to 15 seconds.
He
also suggested that, intravenous lignocaine given in the doses of 1.5 mg/kg 3
mins before laryngoscopy and intubation, sufficiently attenuates the
laryngoscopic reactions. The advantage of intravenous lignocaine claimed by
this author was, it depresses the autonomic nervous system and in addition has
anti arrhythmic properties.
HAMILL
J. F.; BEDFORD, R. F.; WEAVER, D. C.; COLOHAN, A. R. (1981); Lidocaine before
endotracheal intubation: Intravenous or laryngotracheal? Anesthesiology 55,
578-581[34].
Hamill,
bedfore, Weva and Colohan (1981)
compared the effects of intravenous lignocaine verses laryngotracheal topical
lignocaine in attenuation of intubation response. They were interested in
identifying preferred route for the administration of lignocaine prior to
endotracheal intubation. In addition to measuring heart rate and blood
pressure, these authors measured intracranial pressure (ICP) to see if either
route was preferable in preventing a rise in ICP. The patients were randomly
assigned to each group. Each subject received the same induction protocols,
thiopentone 3 mg/kg and succinylcholine 1.5 mg/kg. 1 min after laryngoscopy and
endotracheal intubation 50% nitrous oxide and 50% oxygen was administered.
Using a Mackintosh laryngoscope blade 3, 11 patient received laryngotracheal 4%
lignocaine, via “laryngotracheal anaesthesia” (LTA) set. The other eleven
patients received lignocaine 1.5 mg/kg IV. 2 mins after induction, laryngoscopy
was performed with a Mackintosh blade. Endotracheal intubation was accomplished
in 20 sacs. There was no difference between groups with regards to age, heart
rate, base line blood pressure prior intubation. The group which received
laryngotracheal lignocaine showed significant rise in heart rate, blood
pressure and ICP which remained elevated for 2 mins. The group which received
IV lignocaine showed significant rise in heart rate and blood pressure. However
this rise was limited to 1 min, after which cardiovascular values returned to
base line. ICP in the group which received IV lignocaine did not significantly
increase after endotracheal intubation.
This
data suggested that IV administration of lignocaine is the preferred technique
for administering lignocaine prior to endotracheal intubation.
BENJAMIN
DRENGER AND JACOB Peter; Attenuation of ocular and systemic responses to
tracheal intubation by intravenous lignocaine; British Journal of
Ophthalmology, 1987, 71, 546-54838[35].
This
study was undertaken to determine whether intravenous lignocaine could mitigate
or prevent the ocular reactions and especially the acute increase in
intraocular pressure associated with laryngoscopy and tracheal intubation. Two
groups of children undergoing minor eye surgery under nitrous
oxide-oxygen-halothane anaesthesia were examined. The experimental group (n=
17) received 2 mg/kg lignocaine and the controls (n=18) an equivalent volume of
saline. The incidence of local laryngeal and ocular reflexes was much lower in
the lignocaine group. Pulse acceleration was significantly lower in the lignocaine
group (p<0.025), and the maximal mean intraocular pressure was significantly
less than in the control group (p<0.025). Other ocular reactions were
recorded, and all were attenuated after lignocaine administration. The
beneficial effects of lignocaine, a suppressant of autonomic reflexes, suggest
that intraocular pressure, like the heart rate, rises after intubation as a
result of autonomic stimulation. The use of intravenous lignocaine is thus
recommended for children at risk, such as those needing an urgent operation
because of lacerated eye injury under rapid sequence induction of anaesthesia.
Laurito
CE1, Baughman
VL, Becker
GL, Polek
WV, Riegler
FX, VadeBoncouer
TR;
Effects of aerosolized and/or intravenous lidocaine on hemodynamic responses to
laryngoscopy and intubation in outpatients; Anesth Analg. 1988 Apr;67(4):389-92[36].
A
randomized, double-blind study was carried out on 40 unpremedicated, ASA I-II
adult surgical outpatients to assess the effects of aerosolized lidocaine,
intravenous lidocaine, both, or neither, on circulatory responses to
laryngoscopy and intubation. Lidocaine (4 mg/kg) or saline was given by
nebulizer in the holding area beginning at −15 minutes. The patient underwent a
standarized induction of anesthesia that included IV curare (3 mg)
and O2 by facemask at minute 2, followed by IV thiopental (5 mg/kg) and
succinylcholine (1.5 mg/kg) at minute 5. Lidocaine (2 mg/kg) or saline was
given by IV push at minute 4. Laryngoscopy was begun at 5 minutes and continued
for 45 seconds before intubation. Heart rate and systolic, diastolic, and mean
blood pressures were automatically recorded at 1-minute intervals from 0 to 11
minutes. The four treatment groups included: group 1, aerosolized and IV
saline; group 2, aerosolized saline, IV lidocaine; group 3, aerosolized
lidocaine, IV saline; and group 4, aerosolized and IV lidocaine. There were no
differences among the four treatment groups (n = ten per group) in any of the
four hemodynamic variables before laryngoscopy and intubation. Within each
group, after intubation all four hemodynamic variables increased significantly
over the corresponding baseline values for that group. However, the maximum
values attained after intubation did not differ significantly among the four
treatment groups for any of the four hemodynamic variables, whether those
maxima were expressed as absolute values or as a percentage of baseline. Having
found no difference in the effects of aerosolized and/or intravenous lidocaine
and saline placebo on hemodynamic response to laryngoscopy and intubation in
adult surgical outpatients using a rigidly standardized protocol, it is
recommended that such usage of lidocaine be abandoned.
The
results obtained was that, there was significant rise in all four parameters in
all 4 groups. But the absolute values from each group after laryngoscopy and
intubation had no significant difference with use of aerosolized and
intravenous lignocaine and both or none.
The
pressor response is known to be exaggerated in patients with pregnancy-induced
hypertension, which can result in increased morbidity and mortality in both
mother and newborn. Various pharmacological agents have been used before
induction in an attempt to attenuate the adrenergic response but with varying
degree of success. Esmolol, an ultra short-acting cardioselective ╬▓-blocker
with rapid onset and short elimination half-life, is an attractive choice for
attenuating the adrenergic response in pregnant patients. In a prospective,
randomised double blind study we evaluated the efficacy of two bolus doses of
esmolol with or without lidocaine, in patients with pregnancy-induced
hypertension. Eighty such patients undergoing lower segmental caesarean section
were randomly divided into four groups and received the following study drugs
before intubation: group I, esmolol 1 mg·kg−1; group II, esmolol 2 mg·kg−1;
group III, esmolol 1 mg·kg−1 and lidocaine 1.5 mg·kg−1; and group IV, esmolol 2
mg·kg−1 and lidocaine 1.5 mg·kg−1. In groups II, III and IV, the changes in
maternal heart rate, systolic blood pressure and mean arterial pressure in
response to laryngoscopy and intubation were attenuated to a comparable degree
(P>0.05). No adverse effects were noticed in mother or baby. We conclude
that esmolol 1 mg·kg−1 with lidocaine 1.5 mg·kg−1 is effective in attenuating
the adrenergic responses to laryngoscopy and intubation in patients with pregnancy-induced
hypertension.
The
conclude that Esmolol 1 mg/kg with lignocaine 1.5 mg/kg was effective in
attenuating the adrenergic responses to laryngoscopy and intubation in cases of
PIH for LSCS.
The
aim of this study was to investigate the efficacy of lidocaine solution in the
cuff of the endotracheal tube in reducing mucosal damage following tracheal
intubation.
This
was a randomized controlled trial study undertaken in the intensive care unit
patients. Participants, who met all eligibility criteria, were randomly
assigned to one of two groups of patients, according to whether lidocaine or
air was used to fill the tracheal tube cuff. The tracheal mucosa at the site of
cuff inflation was inspected by fiberoptic bronchoscopy and scored at the 24 h
and 48 h after intubation.
In
all, 51 patients (26 patients in the lidocaine group and 25 patients in the
control group) completed the study. After 24 h, erythema and/or edema of
tracheal mucosa were seen in 2 patients (7.7%) of lidocaine group and 6
patients (24%) of air group (P = 0.109). Binary logistic regression analysis
showed that lidocaine has a significant protective effect against mucosal
damage (odds ratio = 0.72, confidence interval = 0.60-0.87).
The
inflation of the tracheal tube cuff with lidocaine was superior to air in
decreasing the incidence of mucosal damage in the 24 h and 48 h post
intubation.
40
patients of ASA grade I and II aged 20-50 years were selected for elective
surgery requiring general anaesthesia for endotracheal intubation.
They
were divided into 2 groups
Group-1:
Lignocaine hydrochloride group. Here patients received inj. Lignocaine
hydrochloride 1.5 mg/ kg i.v. bolus 3 min prior to induction.
Group-2:
Fentanyl citrate group. Here patients received injection Fentanyl citrate 2
mcg/kg i.v. bolus 3 min prior to induction.
All
patients were pre-oxygenated with 100% O2 for 3 min before induction. Induction
was achieved with injection Thiopentone sodium 5 mg/kg i.v. and injection
succinylcholine 2 mg/kg was given i.v. IPPV given with 100% O2 and after
adequate relaxation laryngoscopy and intubation was done. Anaesthesia was
maintained with O2(33%), N2O(67%), Isoflurane(0.5-1.0%) and injection
Vecuronium omide. Peri-operative vitals and complications were recorded.
Reversal was achieved with injection Neostigmine 0.05 mg/kg i.v. and injection
glycopyrollate 0.004 mg/kg i.v.
This
study concluded that Changes in mean pulse rate and MAP was significant after
intubation and intraoperatively with mean pulse rate, MAP being higher in
group-1 than group-2. Thus Fentanyl citrate provides better haemodynamic
stability by increasing sedation, analgesia and depth of anaesthesia. Fentanyl
citrate is safer and more effective in attenuation of haemodynamic response to
laryngoscopy and intubation.
In
Kidwai Memorial Institute Oncology, Banglore, they studied effects of
lignocaine (15 mg/kg) on pressor response during laryngoscopy and intubation in
50 patient of age 20-60 years. They monitored heart rate systolic blood
pressure and rate pressure product
immediately after intubation followed by 2 minutes and 5 minutes.
The
result shows that heart changed from pre induction 81.80 ± 6.74 bpm to 102.20 ±
7.11 bpm immediately after intubation i.e 25% rise. While SBP and MAP changed
from 121.20 ± 8.72 to 153.92 ± 10.25 and 90.59 ± 5.74 to 107.47 ±6.36
immediately after intubation respectively. RPP changed from 9921.60 ± 1148.51
to 9921.60 ± 1148.51 after intubation.
Thus
concluded that intravenous lignocaine is less effective to attenuate the
pressor response and a better alternative should be used after further
comparative studies.
A prospective randomized cross over study was
conducted in Lokmanya Tilak Municipal Medical College and Government Hospital,
Sion, Mumbai, India during the period of January 2012 to September 2013. Sixty
patients requiring tracheal suction through an endotracheal tube received 1.5
mg/kg of lignocaine in the nebulized form or as an intravenous injection on two
different occasions. Heart rate (HR), mean arterial pressure (MAP), systolic
and diastolic blood pressure (SBP and DBP) and peripheral capillary oxygen
saturation (SPO2) were recorded at baseline, after the administration of
lignocaine, after two successive suctions and once in two minutes for the next
16 minutes
In the present study, SPO2 decreased in response to
ETT suctioning in both the study groups as compared to the pre-suctioning
value. However the changes in the SPO2 were not significant when compared
between the groups. Changes in HR, SBP, DBP and MAP were not significantly
different between the two routes of lignocaine administration.
From the present study, we can conclude that the
abolition of haemodynamic response to tracheal suction is similar with both
intravenous and nebulized lignocaine. But the return of MAP towards baseline
value was observed to be earlier with nebulized lignocaine than with
intravenous lignocaine which favours use of nebulized lignocaine over
intravenous lignocaine.
Laryngoscopy and tracheal intubation causes
sympathoadrenal stimulation and cause transient rise in pulse rate and blood
pressure. We evaluated the efficacy of Esmolol and Lignocaine in attenuating
the pressor response during laryngoscopy and inutbation as compared to placebo.
60 patients of ASA I & II between the age group of 20-60 were
randomized to receive either Esmolol 1.5 mg/Kg, Lignocaine 1.5mg/Kg or 5ml normal
saline just prior to induction of anaesthesia. Heart rate (HR), systolic blood
pressure (SBP) and diastolic blood pressure (DBP) were recorded before
induction (baseline) and at regular intervals of 1, 3, 5, 7 and 10 minutes
after induction. Statistical analysis was done using Student’s t test and
chi-square test and p values obtained.
There is an increase in HR, SBP and DBP in the control
group which is maximum at 3 mins after induction (i.e. during laryngoscopy and
tracheal intubation). Whereas in the study groups there was no significant
variation in these parameters from baseline which is found to be more effective
with Esmolol (p-value < 0.001) than Lignocaine.
Esmolol 1.5mg/Kg was found to be more effective in
attenuating pressor response to laryngoscopy and intubation when compared to
Lignocaine.
The
study aimed to evaluate the effects of lignocaine spray on hemodynamic response
of endotracheal intubation patients.
This
study is a randomized clinical trial on a study population comprising patients
admitted to the ICU.
The
patients were divided into three groups using a permuted block randomization.
Group
1, inhaled nebulized lignocaine 4% (75.0 mg/kg). In
Group
2, intravenous (IV) lignocaine 2% (75.0/mg/kg) was injected.
No lignocaine was prescribed for or
administered to the control group. One and four minutes after intubation, the
patients' hemodynamic and vital signs were measured.
Although
the mean arterial blood pressure (MAP) of Group 1 (inhaled nebulized
lignocaine) was smaller than that of Group 2 (IV lignocaine), there was no
significant difference between the two groups. Both groups' MAPs were
significantly different from that of the control group. As for the average
number of pulses, a significant difference was observed between the inhaled and
IV lignocaine groups; hence, the average number of pulses in Group 1
(inhalation) was lower than that of Group 2 (IV injection). This concluded
that:
As
blood pressure is considered to be normal under 140/90 and may not entail any
hemodynamic complications, it can be concluded that inhaled nebulized
lignocaine can control the hemodynamic changes of intubation more effectively
than IV lignocaine.
The aim of this
study was to compare of intravenous and
oropharyngeal spray of lidocaine and high dose of fentanyl on systolic and
diastolic blood pressures and heart rate of patients over
65 years during tracheal intubation.
In this clinical trial, 160 patients over
65 yrs who were randomly divided into five groups of 32 patients. For group one lidocaine spray 10%, group two intravenous lidocaine 1.5 mg/kg, group three lidocaine spray along
with intravenous lidocaine 0.75
mg/kg, and for group four fentanyl 5╬╝g/kg were administered and group
five patients were controls which were
given 1 mg of midazolam along with 2 ╬╝g/kg fentanyl. Systolic and diastolic
blood pressures and heart rate were measured before and after anesthesia
and intubation. ANOVA, Scheffe's and Repeated
measure tests were used for data comparison and P<0.05 was considered
significant.
This study concluded that all methods were effective for
efficient blood pressor control during laryngoscopy and tracheal intubation.
Sixty patients with a
cerebral aneurysm were randomly divided into three groups by lidocaine
administration methods before endotracheal intubation: Group 1 (Control, 2%
lidocaine 1.5 mg/kg, intravenous injection); Group 2 (10% lidocaine 1 mg/kg,
intralaryngotracheal spray); Group 3 (10% lidocaine 1.5 mg/kg,
intralaryngotracheal spray). Anesthesia was induced intravenously with
midazolam (0.02 mg/kg) and thiopental sodium (2 - 3 mg/kg), and then maintained
with 50% nitrous oxide in oxygen and 1.0 vol% isoflurane. Blood pressure and
heart rate were measured preinduction, before laryngoscopy, immediately after
epiglottis elevation, immediately after intubation and 3 minutes after
intubation. Data were compared and analyzed within and between groups.
Immediately after
intubation, the increase in blood pressure and heart rate were blunted
significantly in the groups 2 and 3 compared to the intravenous lidocaine
injection group (P < 0.01). However, there were no significant hemodynamic
changes between groups 2 and 3.this study concluded that;
The elevation of blood
pressure and heart rate after endotracheal intubation can be prevented by
intralaryngotracheal spray of 1 mg/kg of 10% lidocaine 3 minutes before
endotracheal intubation.
OBSERVATION
AND RESULT
Table 1. Age of the
participants in the two study groups
|
Age
in years |
Group 1 (2% intravenous lignocaine) |
Group 2 (10% lignocaine spray) |
P-value |
|
Mean (SD) |
64.4 (8.2) |
61.3 (8.8) |
0.12 |
Group
1 (2% intravenous lignocaine); Group 2 (10% lignocaine spray)
The
mean (SD) age of the participants was 64.4 (8.2) years in the group receiving
2% intravenous lignocaine (group 1). In the group receiving 10% lignocaine
spray, the mean (SD) age was 61.3 (8.8) years. The differences in mean age
across the two groups was not statistically significant (P=0.12). Figure 1
presents the diagrammatic representation of the distribution of mean age of the
study subjects according to the two groups.
Figure 1. Age of the participants
in the two study groups
Table 2. Sex distribution
of the participants in the two study groups
|
Sex of the participants |
Group 1 |
Group 2 |
P-value |
|
N (%) |
N (%) |
||
|
Male |
24 (80.0) |
23 (76.7) |
0.75 |
|
Female |
6 (20.0) |
7 (23.3) |
Group
1 (2% intravenous lignocaine); Group 2 (10% lignocaine spray)
In
the group receiving 2% intravenous lignocaine (group 1), the proportion of
subjects who were males was 80% whereas in the group receiving 10% lignocaine
spray, 76.7% were males. The proportion of study subjects according to their
sex among the two groups was not statistically significant (P=0.75). Figure 2
presents the sex distribution of the participants in the two groups.
Figure 2. Sex
distribution of the participants in the two study groups
Table 3. Weight
distribution of the participants in the two study groups
|
|
Group 1 |
Group 2 |
P-value |
|
Mean
weight (Kg) |
62.7 (9.0) |
59.6 (10.5) |
0.23 |
Group
1 (2% intravenous lignocaine); Group 2 (10% lignocaine spray)
The
mean (SD) weight participants was 62.7 (9.0) Kg in the group receiving 2%
intravenous lignocaine (group 1). In the group receiving 10% lignocaine spray,
the mean (SD) weight was 59.6 (10.5) Kg. The differences in mean weight across
the two groups was not statistically significant (P=0.23). Figure 3 presents
the diagrammatic representation of the distribution of mean weight of the study
subjects according to the two groups.
Figure 3. Mean weight of
the participants in the two study groups
Table 4. Diabetics or
Non-diabetics in the participants in the two study groups
|
Group 1 |
Group 2 |
|
|
N (%) |
N (%) |
|
|
Diabetics |
12 (40.0) |
14 (46.6) |
|
Non-diabetics |
18 (60.0) |
16 (53.3) |
Group
1 (2% intravenous lignocaine); Group 2 (10% lignocaine spray)
In
the group receiving 2% intravenous lignocaine (group 1), the proportion of
subjects who were diabetics were 40% whereas in the group receiving 10%
lignocaine spray (group 2), 46.6% were diabetics. Figure 4 presents the
distribution of the diabetics and non-diabetics in the participants in the two
groups.
Figure 4. Diabetics or
Non-diabetics in the participants in the two study groups
Table 5. Mean Left
ventricular ejection fraction (LVEF) of the participants in the two study
groups
|
|
Group 1 |
Group 2 |
P-value |
|
Mean (SD) LVEF (%) |
46.5 (4.7) |
47.3 (3.6) |
0.45 |
Group
1 (2% intravenous lignocaine); Group 2 (10% lignocaine spray)
The
mean (SD) left ventricular ejection fraction (%) of the participants was 46.5
(4.7) in the group receiving 2% intravenous lignocaine (group 1). In the group
receiving 10% lignocaine spray, the mean (SD) LVEF (%) was 47.3 (3.6). The
differences in mean LVEF across the two groups was not statistically
significant (P=0.45). Figure 5 presents the diagrammatic representation of the
distribution of mean LVEF of the study subjects according to the two groups.
Figure 5. Mean Left
ventricular ejection fraction (LVEF) of the participants in the two study
groups
Table 6. Distribution of
the participants in the two study groups by presence of arrythmia
|
Arrythmia |
Group 1 |
Group 2 |
P-value |
|
N (%) |
N (%) |
||
|
Present |
0 (0.0) |
4 (13.3) |
0.04* |
|
Absent |
30 (100.0) |
26 (86.7) |
Group
1 (2% intravenous lignocaine); Group 2 (10% lignocaine spray); *statistically
significant
In
the group receiving 2% intravenous lignocaine (group 1), none of the subjects
developed arrythmia whereas in the group receiving 10% lignocaine spray, 13.3%
developed arrythmia. The proportion of study subjects developing arrythmia
among the two groups was statistically significant (P=0.04). Figure 6 presents
the distribution of the participants in the two groups by presence and absence
of arrythmia.
Figure 6. Distribution of
the participants in the two study groups by presence of arrythmia
Table 7. Distribution of
the participants in the two study groups by presence of sore throat
|
Sore
throat |
Group 1 |
Group 2 |
P-value |
|
N (%) |
N (%) |
||
|
Present |
14 (46.7) |
7 (23.3) |
0.02* |
|
Absent |
16 (53.3) |
23 (76.7) |
Group
1 (2% intravenous lignocaine); Group 2 (10% lignocaine spray); * Statistically
significant
In
the group receiving 2% intravenous lignocaine (group 1), 46.7% of the subjects
developed sore throat whereas in the group receiving 10% lignocaine spray,
23.3% of the subject developed sore throat which is lower than that of group 1.
The proportion of study subjects developing sore throat among the two groups
was statistically significant (P=0.02). Figure 7 presents the distribution of
the participants in the two groups by presence and absence of sore throat.
Figure 7. Distribution of
the participants in the two study groups by presence of sore throat
Table 8. Pre-intubation
hemodynamic parameters in the study subjects in the two study groups
|
|
|
HR |
SBP |
DBP |
MAP |
CVP (mm Hg) |
|
|
|
Beats/minute |
MmHg |
MmHg |
mmHg |
|
|
Pre-intubation |
Group
1 |
85.3 (9.8) |
120.8 (14.1) |
78.1 (9.8) |
92.2 (9.9) |
5.9 (1.7) |
|
|
Group
2 |
86.9 (11.2) |
123.2 (10.8) |
78.8 (7.8) |
93.6 (8.1) |
6.3 (2.1) |
Group
1 (2% intravenous lignocaine); Group 2 (10% lignocaine spray)
Table
8. shows the pre-intubation hemodynamic parameters among the study participants
in the two groups. The parameters assessed were heart rate, systolic and
diastolic blood pressure, mean arterial pressure and central venous pressure.
The findings show that there were no statistically significant differences in
these hemodynamic parameters. Figure 8 shows the diagrammatic representation of
the pre-intubation hemodynamic parameters in the study subjects across the two
groups.
Figure 8. Pre-intubation
hemodynamic parameters in the study subjects in the two study groups
Table 9. Hemodynamic
parameters, immediately post intubation, in the study subjects in the two study
groups
Group
1 (2% intravenous lignocaine); Group 2 (10% lignocaine spray); * Statistically
significant
Table
9. shows the immediate post-intubation hemodynamic parameters among the study
participants in the two groups. The findings show that, except for central
venous pressure, there were statistically significant differences in all other
hemodynamic parameters. Mean heart rate, systolic blood pressure, diastolic
blood pressure and mean arterial pressure were higher in group 2 (10%
lignocaine spray), compared to group 1 (2% intravenous lignocaine). Figure 9 shows
the diagrammatic representation of the hemodynamic parameters in the study
subjects across the two groups, immediately post-intubation.
Figure 9. Hemodynamic
parameters, immediately post intubation, in the study subjects in the two study
groups
Table 10. Hemodynamic
parameters, 1-minute post intubation, in the study subjects in the two study
groups
|
|
|
HR |
SBP |
DBP |
MAP |
CVP (mm Hg) |
|
|
|
Beats/minute |
MmHg |
MmHg |
mmHg |
|
|
1
minute post-intubation |
Group 1 |
102.5 (12.6) * |
140.1 (17.5) * |
89.5 (14.4) * |
106.4 (14.7) * |
5.7 (1.6) |
|
|
Group 2 |
109.7 (15.3) * |
149.4 (17.3) * |
97.3 (12.2) * |
114.7 (12.8) * |
6.1 (1.4) |
Group
1 (2% intravenous lignocaine); Group 2 (10% lignocaine spray); * Statistically
significant
Table
10 shows the 1 minute post-intubation hemodynamic parameters among the study
participants in the two groups. The findings show that, except for central
venous pressure, there were statistically significant differences in all other
hemodynamic parameters. Mean heart rate, systolic blood pressure, diastolic
blood pressure and mean arterial pressure were higher in group 2 (10%
lignocaine spray), compared to group 1 (2% intravenous lignocaine). Figure 10
shows the diagrammatic representation of the hemodynamic parameters in the
study subjects across the two groups, 1-minute post-intubation.
Figure 10. Hemodynamic
parameters, 1-minute post intubation, in the study subjects in the two study
groups
Table 11. Hemodynamic parameters, 3 minutes post
intubation, in the study subjects in the two study groups
|
|
|
HR |
SBP |
DBP |
MAP |
CVP (mm Hg) |
|
|
|
Beats/minute |
MmHg |
MmHg |
mmHg |
|
|
3
minutes post-intubation |
Group
1 |
100.9 (13.6) |
129.7 (19.2) |
85.7 (13.3) |
100.8 (14.0) |
5.9 (2.0) |
|
|
Group
2 |
106.4 (15.5) |
136.4 (18.6) |
89.6 (10.6) |
105.8 (12.4) |
6.7 (1.5) |
Group
1 (2% intravenous lignocaine); Group 2 (10% lignocaine spray)
Table
11 shows the 3 minutes’ post-intubation hemodynamic parameters among the study
participants in the two groups. The findings show that there were no
statistically significant differences in these hemodynamic parameters. Figure
11 shows the diagrammatic representation of the 3 minutes post-intubation
hemodynamic parameters in the study subjects across the two groups.
Figure 11. Hemodynamic parameters, 3 minutes post
intubation, in the study subjects in the two study groups
Table 12. Hemodynamic parameters, 5 minutes post
intubation, in the study subjects in the two study groups
|
|
|
HR |
SBP |
DBP |
MAP |
CVP (mm Hg) |
|
|
|
Beats/minute |
MmHg |
MmHg |
mmHg |
|
|
5
minutes post-intubation |
Group
1 |
93.7 (13.2) |
126.3 (21.1) |
81.7 (14.8) |
96.7 (16.1) |
5.9 (1.2) |
|
|
Group
2 |
100.9 (14.9) |
133.0 (19.6) |
85.2 (11.7) |
101.1 (13.7) |
6.6 (1.6) |
Group
1 (2% intravenous lignocaine); Group 2 (10% lignocaine spray)
Table
12 shows the 5 minutes post-intubation hemodynamic parameters among the study
participants in the two groups. The findings show that there were no
statistically significant differences in these hemodynamic parameters. Figure
12 shows the diagrammatic representation of the 5 minutes’ post-intubation
hemodynamic parameters in the study subjects across the two groups.
Figure 12. Hemodynamic parameters, 5 minutes post
intubation, in the study subjects in the two study groups
Table 13. Hemodynamic parameters, 7 minutes post
intubation, in the study subjects in the two study groups
|
|
|
HR |
SBP |
DBP |
MAP |
CVP (mm Hg) |
|
|
|
Beats/minute |
MmHg |
MmHg |
mmHg |
|
|
7
minutes post-intubation |
Group
1 |
93.6 (11.8) |
126.3 (19.1) |
79.7 (11.9) |
95.2 (13.3) |
6.0 (1.4) |
|
|
Group
2 |
95.9 (14.8) |
129.6 (15.6) |
83.4 (12.0) |
98.9 (12.4) |
6.3 (1.5) |
Group
1 (2% intravenous lignocaine); Group 2 (10% lignocaine spray)
Table
13 shows the 7 minutes post-intubation hemodynamic parameters among the study
participants in the two groups. The findings show that there were no
statistically significant differences in these hemodynamic parameters. Figure
13 shows the diagrammatic representation of the 7 minutes post-intubation
hemodynamic parameters in the study subjects across the two groups.
Figure 13. Hemodynamic parameters, 7 minutes’ post
intubation, in the study subjects in the two study groups
Table 14. Hemodynamic parameters, 10 minutes post
intubation, in the study subjects in the two study groups
|
|
|
HR |
SBP |
DBP |
MAP |
CVP (mm Hg) |
|
|
|
Beats/minute |
MmHg |
MmHg |
mmHg |
|
|
10
minutes post-intubation |
Group
1 |
89.5 (10.1) |
127.3 (15.3) |
82.9 (12.6) |
97.7 (12.5) |
7.3 (1.6) |
|
|
Group
2 |
91.7 (15.9) |
127.5 (13.6) |
83.3 (10.2) |
98.0 (10.4) |
6.9 (1.3) |
Group
1 (2% intravenous lignocaine); Group 2 (10% lignocaine spray)
Table
14 shows the 10 minutes post-intubation hemodynamic parameters among the study
participants in the two groups. The findings show that there were no
statistically significant differences in these hemodynamic parameters. Figure
14 shows the diagrammatic representation of the 10 minutes post-intubation
hemodynamic parameters in the study subjects across the two groups.
Figure 14. Hemodynamic parameters, 10 minutes post
intubation, in the study subjects in the two study groups
Table 15. Hemodynamic parameters, 15 minutes post
intubation, in the study subjects in the two study groups
|
|
|
HR |
SBP |
DBP |
MAP |
CVP (mm Hg) |
|
|
|
Beats/minute |
MmHg |
MmHg |
mmHg |
|
|
15
minutes post-intubation |
Group
1 |
87.0 (7.7) |
123.2 (12.5) |
81.0 (11.4) |
95.5 (10.2) |
6.7 (1.4) |
|
|
Group
2 |
91.5 (10.4) |
127.9 (12.4) |
84.8 (11.0) |
99.2 (10.5) |
6.6 (1.7) |
Group
1 (2% intravenous lignocaine); Group 2 (10% lignocaine spray)
Table
15 shows the 15 minutes post-intubation hemodynamic parameters among the study
participants in the two groups. The findings show that there were no
statistically significant differences in these hemodynamic parameters. Figure
15 shows the diagrammatic representation of the 15 minutes post-intubation
hemodynamic parameters in the study subjects across the two groups.
Figure15. Hemodynamic parameters, 15 minutes post
intubation, in the study subjects in the two study groups
Table 16. Hemodynamic parameters, 20 minutes post
intubation, in the study subjects in the two study groups
|
|
|
HR |
SBP |
DBP |
MAP |
CVP (mm Hg) |
|
|
|
Beats/minute |
MmHg |
MmHg |
mmHg |
|
|
20
minutes post-intubation |
Group
1 |
87.3 (12.4) |
125.6 (10.9) |
82.4 (8.2) |
96.7 (7.5) |
6.2 (1.4) |
|
|
Group
2 |
88.3 (12.5) |
125.4 (10.5) |
82.7 (7.6) |
96.9 (7.9) |
6.6 (1.3) |
Group
1 (2% intravenous lignocaine); Group 2 (10% lignocaine spray)
Table
16 shows the 20 minutes’ post-intubation hemodynamic parameters among the study
participants in the two groups. The findings show that there were no
statistically significant differences in these hemodynamic parameters. Figure
16 shows the diagrammatic representation of the 20 minutes post-intubation
hemodynamic parameters in the study subjects across the two groups.
Figure 16. Hemodynamic parameters, 20 minutes post
intubation, in the study subjects in the two study groups
DISCUSSION
Rationale
for conducting the study
Laryngoscopy
and tracheal intubation are one of the commonest procedures done by
anaesthesiologists. Tracheal intubation following laryngoscopy is a potent
stimulus that increases heart rate and blood pressure. Various measures like
heavy premedication, high-dose narcotics, deep inhalational anesthesia and
potent vasoactive drugs have been used so as to mask these hemodynamic
responses of laryngoscopy and intubation. These measures have potential
cardiovascular side-effects and may also prolong recovery, hence are not
suitable for short procedures. Lignocaine is the most frequently used local
anesthetic. It is also routinely used for local, peripheral and epidural
anesthesia. Lignocaine has been evaluated in numerous trials as a spray or gel
to suppress response associated with laryngoscopy. It has also been used to
reduce the incidence of postoperative sore throat, cough, and hoarseness of
voice. More commonly, lignocaine inhalation has been utilized to reduce the
frequency of chronic cough in patients with asthma and chronic obstructive lung
disease (COPD). Similarly, lignocaine has been used intravenously to modulate
the physiological response following laryngoscopy and tracheal intubation.
Currently, there is limited literature on comparison between lignocaine spray
and intravenous lignocaine in alleviation of cardiovascular response following
tracheal intubation. Therefore, this study was conducted among patients with
ejection fraction <50% and undergoing CABG, to compare the efficacy of
lignocaine spray (10%) and intravenous (2%, 1.5mg/kg) route in attenuating the
sympathoadrenal response on hemodynamic parameters due to laryngoscopy and
endotracheal intubation. The study looked at hemodynamic response such as heart
rate, systolic and diastolic blood pressure, mean arterial pressure and central
venous pressure. Additionally, data on arrhythmias and post-operative sore
throat was also collected.
The administration of anesthesia in patients with cardiac disease,
especially those undergoing CABG, demands an absolutely steady haemodynamics
during induction of general endotracheal anesthesia [46]. Any hemodynamic
perturbation during this phase of presurgery medical management by the
anesthesiologist is very poorly tolerated. This requires a great deal of
experience, training, and understanding of individual cardiac lesions and their
response to various anesthetic drug regime and interventions [46]. Many of
these patients also have fixed cardiac output (CO) and their compensatory
mechanisms are not fully functional [46,47]. Therefore, any increase or
decrease in systemic vascular resistance (SVR) and heart rate, which occurs
during laryngoscopy and tracheal intubation due to sympathetic activation, can
adversely affect the hemodynamics [47]. The cardiopulmonary interactions
resulting from the underlying pathophysiology pose additional challenges for
safe airway management. Patients with poor cardiopulmonary reserve have the
potential to desaturate during induction [47]. This can be attributed to
insufficient apnea time in this subset of patients as opposed to normal healthy
individuals. Thus, it is important to ensure an adequate preoxygenation in
these patients before obtunding their respiratory efforts [47,48]. The current
guidelines for difficult airway (DA) management recognize this problem and
recommends the use of supplemental oxygenation (para-oxygenation) during airway
procedures [48]. While the anatomic DA is one in which obtaining a good
glottic view or passing an endotracheal tube (ETT) is challenging, the
physiologic DA is one where physiological derangements subject the patient to a
higher risk of cardiovascular collapse with intubation and positive pressure
ventilation (IPPV) [46-48]. These physiologic abnormalities should be taken
into consideration while planning for intubation even if no anatomic airway
difficulty is anticipated.
Congenital cardiac and valvular lesions with
increased pulmonary blood flow and consequent pulmonary arterial hypertension,
right ventricular dysfunction/failure leading to preexisting
ventilation-perfusion (V/Q) mismatch present physiologic hindrances to
ventilation [49]. It is not rare to encounter a combined anatomical and
physiological difficulty, and any mismanagement of the airway is poorly
tolerated and can even be fatal. The preexisting risk gets exaggerated when
intubation requires multiple attempts with difficult intubation being an
independent predictor of death [49,50]. Essentially, there are four physiologic
difficulties encountered in cardiac patients while securing airway before
mechanical ventilation. These are hypoxemia, severe acidosis, hypotension
and right ventricular failure [50].
Lignocaine stabilizes the neuronal membrane by inhibiting the
ionic fluxes required for the initiation and conduction of impulses, thereby
effecting local anesthetic action [51]. The onset of action is rapid. Lidocaine
may be absorbed following topical administration to mucous membranes, its rate
and extent of absorption depending upon concentration and total dose
administered, the specific site of application, and duration of exposure [51].
In general, the rate of absorption of local anesthetic agents following topical
application occurs most rapidly after intratracheal administration [51].
Lidocaine is also well-absorbed from the gastrointestinal tract, but little
intact drug appears in the circulation because of biotransformation in the
liver. Lidocaine is metabolized rapidly by the liver, and metabolites and
unchanged drug are excreted by the kidneys [51]. Approximately 90% of lidocaine
administered is excreted in the form of various metabolites, and less than 10%
is excreted unchanged. Studies have shown that peak blood levels of lidocaine
may occur as early as 5 and as late as 30 minutes after endotracheal
administration of a 4% lidocaine HCI solution [51]. Studies of lidocaine
metabolism following intravenous bolus injections have shown that the
elimination half-life of this agent is typically 1.5 to 2 hours [51]. The
half-life may be prolonged two-fold or more in patients with liver dysfunction.
Diabetes is associated with an increased risk of CVD, which is
exaggerated with coexistent hypertension [52]. Many of the underlying molecular
mechanisms, including oxidative stress, inflammation, and fibrosis causing
microvascular and macrovascular complications of diabetes, also cause vascular
remodelling and dysfunction in hypertension [52,53]. Moreover, patients
with hypertension often exhibit insulin resistance and are at greater risk of
diabetes developing than are normotensive individuals [52,53]. Diabetes and
hypertension are closely interlinked because of similar risk factors, such as
endothelial dysfunction, vascular inflammation, arterial remodelling,
atherosclerosis, dyslipidemia, and obesity, thereby, leading to cardiac
diseases [54, 55]. Reports from Framingham and from other studies have
established diabetes mellitus (DM) and hypertensions as a strong risk factor
for cardiovascular morbidity and mortality [52-54]. In addition, several
studies suggest that DM and hypertension have direct adverse effects on the
heart, independent of obstructive coronary artery disease. Specifically,
the Framingham Heart Study identified an association between DM/hypertension
and increased left ventricular (LV) wall thickness [52-54]. These
observations may be important in view of the strong relation between LV
hypertrophy and adverse cardiovascular outcomes.
Key
findings of the study
The
study did not find any baseline differences between the study groups in terms
of age, sex, weight , mean left ventricular ejection fraction and presence or
absence of diabetes. In the group receiving 2% intravenous lignocaine, none of
the subjects developed arrythmia whereas in the group receiving 10% lignocaine
spray, 13.3% developed arrythmia and this difference was statistically
significant (P=0.04), reason group 1(2% lignocaine) didn’t develop arrythmia
because these subjects received anti-arrythmic dose of 2% lignocaine i.e
1.5mg/kg. Subjects who developed arrythmia in group 2, among all 3 subject
developed atrial fibrillation and one developed ventricular tahycardia. Further, in the group receiving 2%
intravenous lignocaine, 46.7% of the subjects developed sore throat whereas in
the group receiving 10% lignocaine spray, a lower proportion i.e. 23.3%
developed sore throat (P=0.02), group 2 subjects experienced sore throat lesser
than group 1 due to the topical action of 10% lignocaine spray which was given
to group 2 subjects . The pre-intubation
hemodynamic parameters were similar across the two groups. However, immediately
upon intubation the heart rate (mean 103.7 vs.111.8), systolic blood pressure
(mean 140.8 vs.155.4 mm Hg), diastolic blood pressure (mean 91.9 vs. 103.7 mm
Hg) and mean arterial pressure (mean 108.1 vs. 120.9 mm Hg) were higher in the group receiving 10% lignocaine spray,
compared to the group that received 2% intravenous lignocaine. Similarly, at 1
minute after intubation, the heart rate
(mean 102.5 vs.109.7), systolic blood pressure (mean 140.1 vs.149.4 mm Hg),
diastolic blood pressure (mean 89.5 vs. 97.3 mm Hg) and mean arterial pressure
(mean 106.4 vs. 114.7 mm Hg) were higher in
the group receiving 10% lignocaine spray, compared to the group that
received 2% intravenous lignocaine. Thereafter, these differences remained
non-significant at 3 min, 7 min, 10 min, 15 min and 20 min post-intubation. 10
minutes post-intubation all vital parameters came to base line values in group
1 and 15 minutes post intubation all vital parameters came to its baseline
values in group 2.
These findings indicate that intravenous
lignocaine is more efficacious in preventing immediate sympathoadrenal response
to laryngoscopy and tracheal intubation than lignocaine spray and is associated
with comparatively lesser incidence of arrythmia but the incidence of
post-operative sore throat was lesser with lignocaine spray.
Comparison of the findings with previous studies
Jokar A et al (2018) conducted a study aimed to evaluate the effects
of lignocaine spray on hemodynamic response of endotracheal intubation
patients. This was a randomized clinical trial on a study population
comprising patients admitted to the ICU. The patients were divided into
three groups. In Group 1, inhaled nebulized lignocaine 4% (75.0 mg/kg) was
sprayed around the patients' epiglottis and larynx. In Group 2, intravenous
(IV) lignocaine 2% (75.0/mg/kg) was injected. No lignocaine was prescribed for or
administered to the control group. One and four minutes after intubation, the
patients' hemodynamic and vital signs were measured. Although the mean arterial
blood pressure (MAP) of Group 1 (inhaled nebulized lignocaine) was smaller than
that of Group 2 (IV lignocaine), there was no significant difference between
the two groups. In terms of the average number of pulses, a significant
difference was observed between the inhaled and IV lignocaine groups. The
average number of pulses in Group 1 (inhalation) was lower than that of Group 2
(IV injection). The study investigators concluded that inhaled nebulized
lignocaine can control the hemodynamic changes of intubation more effectively
than IV lignocaine. This is very much similar to the findings and observations
of the current study.
UI
Islam M et al (2014) conducted a randomized control trial
involving 60 patients scheduled for elective CABG. The study had two groups-
group A (IV morphine 0.1mg/kg & IV lignocaine 1.5mg/kg) and group B (IV
morphine 0.1mg/kg & lignocaine spray 1.5mg/kg). There were no baseline
differences in the study participant characteristics among the two groups. The
authors found that lignocaine spray was as efficacious as intravenous
lignocaine on attenuation of hemodynamic changes to laryngoscopy and
intubation. This is similar to the findings of our study where lignocaine spray
had similar efficacy, compared to intravenous lignocaine and moreover, led to
reduced incidence of arrythmia and post-operative sore throat.
Agrawal A et al (2016)
conducted a prospective randomized cross over study. Sixty patients requiring
tracheal suction through an endotracheal tube received 1.5 mg/kg of lignocaine
in the nebulized form or as an intravenous injection on two different
occasions. Heart rate (HR), mean arterial pressure (MAP), systolic and
diastolic blood pressure (SBP and DBP) and peripheral capillary oxygen
saturation (SPO2) were recorded at baseline, after the administration of
lignocaine, after two successive suctions and once in two minutes for the next
16 minutes. The study found that the changes in the SPO2 were not significant
when compared between the groups. Similarly, the changes in HR, SBP, DBP and
MAP were not significantly different between the two routes of lignocaine
administration. These findings are again similar to the
findings of our study where lignocaine spray had similar efficacy, compared to
intravenous lignocaine, in providing hemodynamic stability during and
post-intubation.
Jalali A et al (2017) performed a study to compare of
intravenous and oropharyngeal spray of lidocaine and high dose of fentanyl on
systolic and diastolic blood pressures and heart rate of patients over 65 years
during tracheal intubation. In this clinical trial, 160 patients were randomly
divided into five groups of 32 patients. For group one, lidocaine spray 10%;
group two, intravenous lidocaine 1.5 mg/kg; group three, lidocaine spray along
with intravenous lidocaine 0.75 mg/kg; and for group four fentanyl 5╬╝g/kg were
administered and group five patients were controls which were given 1 mg of
midazolam along with 2 ╬╝g/kg fentanyl. Study results showed no significant
difference between groups in terms of systolic and diastolic blood pressures
and heart rate among groups. The authors concluded that all methods were effective for efficient blood pressure control during
laryngoscopy and tracheal intubation.
Kim SY et al (2002) conducted a study to evaluate the effects of
intralaryngotracheal 10% lidocaine spray on hemodynamic responses to
endotracheal intubation for patients with a cerebral aneurysm. Sixty patients with a cerebral
aneurysm were randomly divided into three groups by lidocaine administration
methods before endotracheal intubation: Group 1 (Control, 2% lidocaine 1.5 mg/kg,
intravenous injection); Group 2 (10% lidocaine 1 mg/kg, intralaryngotracheal
spray); Group 3 (10% lidocaine 1.5 mg/kg, intralaryngotracheal spray). Blood
pressure and heart rate were measured preinduction, before laryngoscopy,
immediately after epiglottis elevation, immediately after intubation and 3
minutes after intubation. Immediately after intubation, the increase in blood
pressure and heart rate were blunted significantly in the groups 2 and 3
compared to the intravenous lidocaine injection group (P < 0.01). The
authors concluded that the elevation of
blood pressure and heart rate after endotracheal intubation can be prevented by
intralaryngotracheal spray of 1 mg/kg of 10% lidocaine 3 minutes before
endotracheal intubation. But in my study that suggest intravenous lignocaine to
be more efficacious than lignocaine spray in attenuation of immediate
sympathoadrenal response of laryngoscopy and endotracheal intubation.
Limitations of the study
1.
The sample
size was limited to only 60 subjects and therefore, the study was not
adequately powered to detect small differences in the hemodynamic variables
that might have been present in the two groups
2.
The
findings of the study are applicable to patients undergoing CABG. We do not
fully understand the expected differences between lignocaine spray and
intravenous lignocaine in different sets of patients undergoing surgery for
other indications
3.
The study
did not test the effects of different doses of lignocaine, both in spray and
intravenous forms.
SUMMARY
Following ethical committee approval, a prospective,
randomized and comparative study was conducted to compare hemodynamic response
such as heart rate, systolic and diastolic blood pressure, mean arterial
pressure and central venous pressure during laryngoscopy and tracheal
intubation between patients receiving lignocaine spray (10%) and intravenous
(2%, 1.5mg/kg) lignocaine. Additional comparisons were done on incidence of
arrhythmias and post-operative sore throat. 60 patients of aged between 30-75
years, of either gender, with ejection fraction of <50% and undergoing CABG
under general anaesthesia were selected for the study. The patients were
randomly allocated into two groups:
GROUP 1: After standard induction, this group of
patients received intravenous 2% Lignocaine (preservative free) 3 minutes prior
to laryngoscopy.
GROUP 2: Patients vocal cords were sprayed with 10%
lignocaine spray as soon as the vocal cords were visualized by direct
laryngoscopy.
Automated recordings (Datascope) of heart rate (HR) and
systolic (SBP), diastolic (DBP), and mean (MBP) blood pressures were recorded
at 0 min, 1 min, 3 min, 7 min, 10 min, 15 min and 20 min from induction. The
standard monitors were used to eliminate variability in recording data.
The key study findings are as follows:
·
The study did not find any baseline
differences between the study groups in terms of age (P=0.12), sex (P=0.75),
weight (P=0.23) and mean left ventricular ejection fraction (P=0.45).
·
In the group receiving 2% intravenous
lignocaine, none of the subjects developed arrythmia whereas in the group
receiving 10% lignocaine spray, 13.3% developed arrythmia. These differences
were statistically significant (P=0.04).
·
In the group receiving 2% intravenous
lignocaine, 23.3% of the subjects developed sore throat whereas in the group
receiving 10% lignocaine spray, a higher proportion i.e. 46.7% developed sore
throat. The proportion of study subjects developing sore throat among the two
groups was statistically significant (P=0.02).
·
The pre-intubation hemodynamic parameters
were similar across the two groups.
·
However, immediately upon intubation the
heart rate (mean 103.7 vs.111.8), systolic blood pressure (mean 140.8 vs.155.4
mm Hg), diastolic blood pressure (mean 91.9 vs. 103.7 mm Hg) and mean arterial
pressure (mean 108.1 vs. 120.9 mm Hg) were higher in the group receiving 10% lignocaine spray,
compared to the group that received 2% intravenous lignocaine.
·
Similarly, at 1 minute after
intubation, the heart rate (mean 102.5
vs.109.7), systolic blood pressure (mean 140.1 vs.149.4 mm Hg), diastolic blood
pressure (mean 89.5 vs. 97.3 mm Hg) and mean arterial pressure (mean 106.4 vs.
114.7 mm Hg) were higher in the group
receiving 10% lignocaine spray, compared to the group that received 2%
intravenous lignocaine.
·
Thereafter, these differences remained
non-significant at 3 min, 7 min, 10 min, 15 min and 20 min post-intubation.
These
findings indicate that intravenous lignocaine is more efficacious in preventing
immediate sympathoadrenal response to laryngoscopy and endotracheal intubation
than lignocaine spray and is associated with comparatively lesser incidence of
arrythmia and post-operative sore throat.
CONCLUSION
Considering the increase in Heart rate, SBP, DBP
and MAP immediately upon intubation in those receiving lignocaine spray
compared to those receiving intravenous lignocaine spray, it seems that
intravenous lignocaine is actually more efficient and should be used to prevent
sympathoadrenal stimulation and hemodynamic changes caused during intubation.
Intravenous lignocaine seems to be an effective
and practical method that can be used for critical elderly patients with
reduced ejection fraction who are at a greater risk of hemodynamic
perturbations. This method is also efficient in preventing cardiac arrythmia
during intubation but shows more incidence of post-intubation sore throat.
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PROFORMA
Name
of the participant:
Age:
Gender:
Date
of surgery:
Diagnosis:
Name
of Surgery:
Airway
Examination:
MPC:
TM
Distance:
Neck
Movement:
ASA Grade:
Randomization
into: ‘GROUP A’ or ‘GROUP B’
Parameters
recorded:
|
Variables |
Pre induction |
0 min |
1 min |
3 Mins |
5 mins |
7 mins |
10 mins |
15 mins |
20 mins |
|
Heart
rate |
|
|
|
|
|
|
|
|
|
|
Systolic
BP |
|
|
|
|
|
|
|
|
|
|
Diastolic
BP |
|
|
|
|
|
|
|
|
|
|
Mean
arterial pressure |
|
|
|
|
|
|
|
|
|
|
CVP |
|
|
|
|
|
|
|
|
|
|
ECG for arrhythmias |
|
|
|
|
|
|
|
|
|
Sore throat: Present / Absent
PATIENT
CONSENT FORM
“EFFECTS OF INTRAVENOUS LIGNOCAINE 2%
AND LIGNOCAINE SPRAY 10% FOR INTUBATION RESPONSE IN PATIENTS WITH EJECTION
FRACTION <50%-
COMPARATIVE
STUDY.”
Name of the Institution: Dr DY Patil
University, School Of Medicine, Nerul, New Mumbai
I have read the information in this
form (or it has been read to me). I was
free to ask any questions and they have
been answered. I am over 18 years of age and, exercising my free power of
choice, hereby give my consent to include me as a participant in “EFFECTS OF INTRAVENOUS LIGNOCAINE 2% AND
LIGNOCAINE SPRAY 10% FOR INTUBATION RESPONSE IN PATIENTS WITH EJECTION FRACTION
<50%- COMPARATIVE STUDY.”
I have read and understood this consent
form and the information provided to me.
(1) I
have had the consent document explained to me.
(2) I
have been explained about the nature of the
study.
(3) My
rights and responsibilities have been explained to me by the investigator.
(4) I
agree not to restrict the use of any data or results that arise from this study
provided such a use is only for scientific purpose.
(5)
I agree to cooperate with the investigator
and I will inform him immediately if I or my patient suffers unusual symptoms.
(6)
I am aware of the fact that I myself/ my
patient can opt out of the study at any time without having to give any reason
and this will not affect me or my patient’s
future treatment in the hospital.
(7)
I am also aware that the investigators may
terminate my patients or my participation
in the study at any time, for any reason, without my consent.
(8)
I hereby give permission to the
investigators to release the information obtained from me as result of
participation in this study to the ethics committee. I understand that they may
inspect my original records.
(9) My
identity will be kept confidential if my data are publicly presented.
(10) I
have had my questions answered to my satisfaction.
(11) I
have decided to include myself or my patient in the research study.
I
am aware, that if I have any questions during this study, I should contact at
one of the addresses listed above. By signing this consent from, I attest that
the information given in this document. I will be given a copy of this consent
document.
Participant’s
initials:
Name and signature / thumb impression
of the participant (or legal representative if participant incompetent):
(Name)
(Signature)
Date:
Time:
Name and signature of impartial
witness (required for illiterate patients):
(Name)
(Signature)
Date:
Time:
Address
and contact number of the impartial witness:
Name and signature of the
Investigator or his representative obtaining consent:
(Name)
(Signature)
Date: Time: ________
рдкेрдЯंрдЯ
рдХॉрди्рд╕ेрди्рдЯ рдлॉрд░्рдо
“рдЙрдж्рдШाрдЯрдиाрдЪ्рдпा рднाрдЧाрд╕рд╣ рдкेрдЯंрдЯ्рд╕ рдордзीрд▓
рдк्рд░рд╡ेрд╢ाрдЪ्рдпा рдк्рд░рддिрд╕ाрджाрд╕ाрдаी рдЗंрдЯ्рд░ाрд╡ेрдирд╕ рд▓िрдЧ्рдиोрдХाрдЗрди 2% рдЖрдгि рд▓िрдЧ्рдиोрдХाрдЗрди
рд╕्рдк्рд░े 10% - рдПрдХрдд्рд░ рдЕрдн्рдпाрд╕. ”
рд╕рд╣рднाрдЧीрдЪे рдиाрд╡ः рдк्рд░рдзाрди рдЕрди्рд╡ेрд╖рдХांрдЪे рдиाрд╡: рдкूрдирдо рдЧुрдк्рддा
рд╕ंрд╕्рдеेрдЪे рдиाрд╡: рдбॉ рдбी рд╡ाрдп
рдкाрдЯीрд▓ рд╡िрдж्рдпाрдкीрда, рд╕्рдХूрд▓ рдСрдл рдоेрдбिрд╕िрди, рдиेрд░ूрд│,
рдирд╡ी рдоुंрдмрдИ
рдоी рдпा рдлॉрд░्рдордордзीрд▓ рдоाрд╣िрддी рд╡ाрдЪрд▓ी рдЖрд╣े (рдХिंрд╡ा рддी рдорд▓ा рд╡ाрдЪрд▓ी рдЧेрд▓ी рдЖрд╣े). рдоी рд╣ोрддो
рдХोрдгрддेрд╣ी рдк्рд░рд╢्рди рд╡िрдЪाрд░рдг्рдпाрд╕ рдоोрдХрд│े рдЖрдгि рдд्рдпांрдиा рдЙрдд्рддрд░
рджिрд▓े рдЧेрд▓े. рдоाрдЭे рд╡рдп рез 18 рд╡рд░्рд╖ांрд╣ूрди
рдЕрдзिрдХ рдЖрд╣े рдЖрдгि рдоी рдоाрдЭ्рдпा рдиिрд╡рдбीрдЪ्рдпा рд╡िрдиाрдоूрд▓्рдп рд╢рдХ्рддीрдЪा рдЙрдкрдпोрдЧ рдХрд░ीрдд рдЖрд╣े, рдпाрдж्рд╡ाрд░े рдорд▓ा рдпाрдд рд╕рд╣рднाрдЧी рд╣ोрдг्рдпाрд╕ाрдаी рдорд▓ा рд╕ंрдорддी рджेрдИрд▓
"рдЗंрдЯрд░ेрд╡्рд╣рдирд╕ рд▓िрдЧ्рдиोрдХाрдЗрдирдЪे рдкрд░िрдгाрдо
2% рдЖрдгि рдПрдЬ्рдпुрдХेрд╢рди рд░ेрд╕्рдкॉрди्рд╕ рдЗрди рдПрдЬ्рдпुрдХेрд╢рди рд░ेрд╕्рдкॉрди्рд╕ рдЗрди рдПрдЬ्рдпुрдХेрд╢рди рдл्рд░ॅрдХ्рд╢рди
<50% - рдПрдХрдд्рд░िрдд рдЕрдн्рдпाрд╕ाрд╕рд╣ 10% рд▓िрдЧ्рдиोрдХाрдЗрди рд╕्рдк्рд░े."
рд╣ा рд╕ंрдорддी рдлॉрд░्рдо рдЖрдгि рдорд▓ा рдк्рд░рджाрди рдХेрд▓ेрд▓ी рдоाрд╣िрддी рдоी
рд╡ाрдЪрд▓ी рдЖрдгि рд╕рдордЬрд▓ी рдЖрд╣े.
(рез) рдорд▓ा рд╕ंрдорддी
рджрд╕्рддрдРрд╡рдЬ рдорд▓ा рд╕рдордЬाрд╡ूрди рд╕ांрдЧिрддрд▓े.
(реи) рдорд▓ा рдЕрдн्рдпाрд╕ाрдЪे
рд╕्рд╡рд░ूрдк рдХрд╕े рдЖрд╣े рдпाрдмрдж्рджрд▓ рд╕्рдкрд╖्рдЯ рдХेрд▓े рдЖрд╣े.
()) рдоाрдЭे рдЕрдзिрдХाрд░ рд╡ рдЬрдмाрдмрджाрд░्рдпा рдорд▓ा рдЕрди्рд╡ेрд╖рдХांрдж्рд╡ाрд░े рд╕्рдкрд╖्рдЯ рдХेрд▓्рдпा рдЖрд╣ेрдд.
()) рдпा рдЕрдн्рдпाрд╕ाрдоुрд│े рдЙрдж्рднрд╡рд▓ेрд▓्рдпा рдХोрдгрдд्рдпाрд╣ी
рдбेрдЯाрдЪा рдХिंрд╡ा рдкрд░िрдгाрдоाрдЪा рд╡ाрдкрд░ рдорд░्рдпाрджिрдд рди рдаेрд╡рдг्рдпाрд╕ाрдаी рдоी рд╕рд╣рдордд рдЖрд╣े рдкрд░ंрддु рдЕрд╢ा рдк्рд░рдХाрд░рдЪ्рдпा
рд╡ाрдкрд░ाрдЪा рдЙрдкрдпोрдЧ рдХेрд╡рд│ рд╡ैрдЬ्рдЮाрдиिрдХ рд╣ेрддूрд╕ाрдаी рдХेрд▓ा рдЬाрдИрд▓.
()) рдоी рдЕрди्рд╡ेрд╖рдХांрдиा рд╕рд╣рдХाрд░्рдп рдХрд░рдг्рдпाрд╕
рд╕рд╣рдорддी рджेрддो рдЖрдгि рдорд▓ा рдХिंрд╡ा рдоाрдЭ्рдпा рд░ूрдЧ्рдгाрдд рдЕрд╕ाрдоाрди्рдп рд▓рдХ्рд╖рдгे рдЖрдврд│рд▓्рдпाрд╕ рдоी рдд्рдпाрд▓ा рддाрдмрдбрддोрдм
рд╕ूрдЪिрдд рдХрд░ीрди.
()) рдорд▓ा рд╣े рдоाрд╣िрдд рдЖрд╣े рдХी рдоी
/ рдоाрдЭे рд░ुрдЧ्рдг рдХोрдгрдд्рдпाрд╣ी рдХाрд░рдгाрд╢िрд╡ाрдп рдХोрдгрддेрд╣ी рдХाрд░рдг рди рд╕ांрдЧрддा рдЕрдн्рдпाрд╕ाрдЪी
рдиिрд╡рдб рдХрд░ू рд╢рдХрддो рдЖрдгि рдпाрдЪा рдорд▓ा рдХिंрд╡ा рдоाрдЭ्рдпा рд░ूрдЧ्рдгाрд▓рдпाрдЪ्рдпा рднрд╡िрд╖्рдпाрддीрд▓ рдЙрдкрдЪाрд░ांрд╡рд░ рдкрд░िрдгाрдо
рд╣ोрдгाрд░ рдиाрд╣ी.
()) рдорд▓ा рд╣े рджेрдЦीрд▓ рдоाрд╣िрдд рдЖрд╣े рдХी рддрдкाрд╕рдХрд░्рддा
рдоाрдЭ्рдпा рд░ूрдЧ्рдгांрдиा рдХिंрд╡ा рдоाрдЭ्рдпा рдЕрдн्рдпाрд╕ाрдордз्рдпे рдоाрдЭा рд╕рд╣рднाрдЧ рдХोрдгрдд्рдпाрд╣ी рдХाрд░рдгाрд╕्рддрд╡,
рдХोрдгрдд्рдпाрд╣ी рд╕ंрдорддीрдиे рдоाрдЭ्рдпा рд╕ंрдорддीрд╡िрдиा рд╕рдоाрдк्рдд рдХрд░ू рд╢рдХрддाрдд.
()) рдпा рдЕрдн्рдпाрд╕ाрдд рднाрдЧ рдШेрддрд▓्рдпाрдоुрд│े рдоाрдЭ्рдпाрдХрдбूрди
рдоिрд│ाрд▓ेрд▓ी рдоाрд╣िрддी рдиीрддिрд╢ाрд╕्рдд्рд░ рд╕рдоिрддीрд▓ा рд╕ोрдбрдг्рдпाрд╕ाрдаी рдоी рдпाрдж्рд╡ाрд░े рддрдкाрд╕ рдпंрдд्рд░рдгांрдиा рдкрд░рд╡ाрдирдЧी
рджेрддो. рдорд▓ा рд╕рдордЬрд▓े рдЖрд╣े рдХी рддे рдоाрдЭ्рдпा рдоूрд│ рдиोंрджींрдЪी рддрдкाрд╕рдгी рдХрд░ू рд╢рдХрддाрдд.
()) рдоाрдЭा рдбेрдЯा рд╕ाрд░्рд╡рдЬрдиिрдХрдкрдгे рд╕ाрджрд░ рдХेрд▓्рдпाрд╕
рдоाрдЭी рдУрд│рдЦ рдЧोрдкрдиीрдп рдаेрд╡рд▓ी рдЬाрдИрд▓.
(резреж) рдоाрдЭ्рдпा
рдк्рд░рд╢्рдиांрдЪी рдЙрдд्рддрд░े рдоी рд╕рдоाрдзाрдиाрд▓ा рджिрд▓ी рдЖрд╣ेрдд.
(резрез) рдоी рд╕्рд╡рдд:
рд▓ा рдХिंрд╡ा рдоाрдЭ्рдпा рд░ुрдЧ्рдгाрд▓ा рд╕ंрд╢ोрдзрди рдЕрдн्рдпाрд╕ाрдордз्рдпे рд╕рдоाрд╡िрд╖्рдЯ рдХрд░рдг्рдпाрдЪा рдиिрд░्рдгрдп
рдШेрддрд▓ा рдЖрд╣े.
рдорд▓ा рдоाрд╣िрддी рдЖрд╣े рдХी рдпा рдЕрдн्рдпाрд╕ाрджрд░рдо्рдпाрди рдорд▓ा рдХाрд╣ी рдк्рд░рд╢्рди
рдЕрд╕рд▓्рдпाрд╕,
рдоी рд╡рд░ рд╕ूрдЪीрдмрдж्рдз рдХेрд▓ेрд▓्рдпा рдПрдХा рдкрдд्рдд्рдпाрд╡рд░ рд╕ंрдкрд░्рдХ рд╕ाрдзाрд╡ा. рдХрдбूрди рдпा рд╕ंрдорддीрд╡рд░ рд╕्рд╡ाрдХ्рд╖рд░ी рдХрд░ूрди, рдоी рдпा рджрд╕्рддрдРрд╡рдЬाрдд рджिрд▓ेрд▓्рдпा
рдоाрд╣िрддीрдЪी рдЦाрддрд░рдЬрдоा рдХрд░рддो. рдорд▓ा рдпा рд╕ंрдорддी рджрд╕्рддрдРрд╡рдЬाрдЪी рдПрдХ рдк्рд░рдд рджिрд▓ी
рдЬाрдИрд▓.
рд╕рд╣рднाрдЧीрдЪे рдЖрдж्рдпाрдХ्рд╖рд░े:
рд╕рд╣рднाрдЧीрдЪे рдиाрд╡ рдЖрдгि рд╕्рд╡ाрдХ्рд╖рд░ी / рдЕंрдЧрдаा рдард╕ा (рдХिंрд╡ा рд╕рд╣рднाрдЧी рдЕрд╕рдорд░्рде рдЕрд╕рд▓्рдпाрд╕ рдХाрдпрджेрд╢ीрд░ рдк्рд░рддिрдиिрдзी):
_______________ (рдиाрд╡)
____________ (рд╕्рд╡ाрдХ्рд╖рд░ी)
рддाрд░ीрдЦ рд╡ेрд│: __________________
рдиाрд╡ рдЖрдгि рдиिःрдкрдХ्рд╖ рд╕ाрдХ्рд╖ीрдЪी рд╕рд╣ी (рдиिрд░рдХ्рд╖рд░ рд░ुрдЧ्рдгांрд╕ाрдаी рдЖрд╡рд╢्рдпрдХ):
______________ (рдиाрд╡)
________________ (рд╕्рд╡ाрдХ्рд╖рд░ी)
рддाрд░ीрдЦ рд╡ेрд│: ___________
рдиिрд╖्рдкрдХ्рд╖ рд╕ाрдХ्рд╖ीрдЪा рдкрдд्рддा рдЖрдгि рд╕ंрдкрд░्рдХ рдХ्рд░рдоांрдХः
рдЕрди्рд╡ेрд╖рдХ рдХिंрд╡ा рдд्рдпाрдЪ्рдпा рдк्рд░рддिрдиिрдзीрдЪी рд╕ंрдорддी рдк्рд░ाрдк्рдд
рдХрд░рдгाрд░े рдпांрдЪे рдиाрд╡ рдЖрдгि рд╕्рд╡ाрдХ्рд╖рд░ी:
___________ (рдиाрд╡)
________________(рд╕्рд╡ाрдХ्рд╖рд░ी)
рддाрд░ीрдЦ: _________ рд╡ेрд│:
________
рд░ोрдЧी рд╕рд╣рдорддि рдлाрд░्рдо
"рдЗंрдЯрд░्рдирд╡्рдпूрд╕ рд▓ोрдирдХॉрдЗрди рдХे рдк्рд░рднाрд╡
2% рдФрд░ рд▓ेрдЬोрдирдХाрдЗрди рд╕्рдкैрдиी 10% рдХे рд╕ाрде рд╕ंрдпोрдЬрди рдХे рдкрд░िрдгाрдоों
рдоें рд╕ंрдЪрд░िрдд рдлрд▓рди рдХे рд▓िрдП <50% - рддुрд▓рдиाрдд्рдордХ рдЕрдз्рдпрдпрди।"
рдк्рд░рддिрднाрдЧी рдХा рдиाрдо: рдк्рд░рдзाрди
рдЕрди्рд╡ेрд╖рдХ рдХा рдиाрдо: рдбॉ। рдкोрдирдо рдЧुрдк्рддा
рд╕ंрд╕्рдеा рдХा рдиाрдо: рдбॉ рдбी рд╡ाрдИ
рдкाрдЯिрд▓ рд╡िрд╢्рд╡рд╡िрдж्рдпाрд▓рдп, рд╕्рдХूрд▓ рдСрдл рдоेрдбिрд╕िрди, рдиेрд░ुрд▓, рдирдИ рдоुंрдмрдИ
рдоैंрдиे рдЬाрдирдХाрд░ी рдХो рдЗрд╕ рд░ूрдк рдоें рдкрдв़ा рд╣ै (рдпा рдпрд╣ рдоुрдЭे рдкрдв़ा рдЧрдпा рд╣ै)। рдоैं рдеा
рдХिрд╕ी рднी рд╕рд╡ाрд▓ рдкूрдЫрдиे рдХे рд▓िрдП рд╕्рд╡рддंрдд्рд░ рд╣ैं рдФрд░ рд╡े рдЬрд╡ाрдм
рджिрдпा рдЧрдпा рд╣ै। рдоेрд░ी рдЖрдпु 18 рд╡рд░्рд╖ рд╕े рдЕрдзिрдХ рд╣ै, рдФрд░ рдЕрдкрдиी рдкрд╕ंрдж рдХी рдоुрдл्рдд рд╢рдХ्рддि рдХा рдк्рд░рдпोрдЧ рдХрд░рддे рд╣ुрдП, рдЗрд╕рдоें
рдоुрдЭे рдПрдХ рдк्рд░рддिрднाрдЧी рдХे рд░ूрдк рдоें рд╢ाрдоिрд▓ рдХрд░рдиे рдХे рд▓िрдП рдЕрдкрдиी рд╕рд╣рдорддि рджेрддे рд╣ैं
"рдЗंрдЯ्рд░ाрд╡ेрдирд╕ рд▓ूрд╕ोрдХेрди рдХा рдк्рд░рднाрд╡
2% рдФрд░ рд▓ेрдЬोрдирдХाрдЗрди рд╕्рдкैрдиी 10% рд╣ै, рдЬो рдЗрдЬेрдХ्рд╢рди рдл्рд░ैрдХ्рд╢рди рдХे рд╕ाрде рдорд░ीрдЬों рдоें рдЗंрдЯ्рдпूрд╢рди рд░िрд╕्рдкॉрди्рд╕ рдХे рд▓िрдП рд╣ै
<50% - рдХॉрдо्рдкिрдЯिрдЯिрд╡ рд╕्рдЯрдбी।"
рдоैंрдиे рдЗрд╕ рд╕рд╣рдорддि рдлॉрд░्рдо рдХो рдФрд░ рдоुрдЭे рдк्рд░рджाрди рдХी рдЧрдИ рдЬाрдирдХाрд░ी
рдХो рдкрдв़ рдФрд░ рд╕рдордЭ рд▓िрдпा рд╣ै।
(рез) рдоेрд░े рдкाрд╕
рд╕рд╣рдорддि рдкрдд्рд░ рдоुрдЭे рд╕рдордЭाрдпा рдЧрдпा рд╣ै।
(реи) рдоुрдЭे рдЕрдз्рдпрдпрди
рдХी рдк्рд░рдХृрддि рдХे рдмाрд░े рдоें рд╕рдордЭाрдпा рдЧрдпा рд╣ै।
(рей) рдЕрди्рд╡ेрд╖рдХ
рдж्рд╡ाрд░ा рдоुрдЭे рдоेрд░े рдЕрдзिрдХाрд░ों рдФрд░ рдЬिрдо्рдоेрджाрд░िрдпों рдХो рд╕рдордЭाрдпा рдЧрдпा рд╣ै।
(4) рдоैं рдЗрд╕ рдЕрдз्рдпрдпрди рд╕े рдЙрдд्рдкрди्рди рдХिрд╕ी
рднी рдбेрдЯा рдпा рдкрд░िрдгाрдоों рдХे рдЙрдкрдпोрдЧ рдХो рдк्рд░рддिрдмंрдзिрдд рдирд╣ीं рдХрд░рдиे рдХे рд▓िрдП рд╕рд╣рдордд рд╣ूं, рдмрд╢рд░्рддे рдРрд╕ा рдЙрдкрдпोрдЧ рдХेрд╡рд▓ рд╡ैрдЬ्рдЮाрдиिрдХ рдЙрдж्рджेрд╢्рдп рдХे рд▓िрдП рд╣ो।
(рел) рдоैं рдЕрди्рд╡ेрд╖рдХ
рдХे рд╕ाрде рд╕рд╣рдпोрдЧ рдХрд░рдиे рдХे рд▓िрдП рд╕рд╣рдордд рд╣ूं рдФрд░ рдпрджि рдоैं рдпा рдоेрд░ा рдорд░ीрдЬ рдЕрд╕ाрдоाрди्рдп рд▓рдХ्рд╖рдгों рд╕े рдкीрдб़िрдд
рд╣ै рддो рдоैं рдЙрд╕े рддुрд░ंрдд рд╕ूрдЪिрдд рдХрд░ूंрдЧा।
(рем) рдоुрдЭे рдЗрд╕
рддрде्рдп рдХी рдЬाрдирдХाрд░ी рд╣ै рдХि рдоैं рд╕्рд╡рдпं / рдоेрд░ा рд░ोрдЧी рдмिрдиा рдХिрд╕ी рдХाрд░рдг
рдХे рдХिрд╕ी рднी рд╕рдордп рдЕрдз्рдпрдпрди рд╕े рдмाрд╣рд░ рд╣ो рд╕рдХрддा рд╣ै рдФрд░ рдЗрд╕рд╕े рдЕрд╕्рдкрддाрд▓ рдоें рдоेрд░े рдпा рдоेрд░े рд░ोрдЧी рдХे
рднрд╡िрд╖्рдп рдХे рдЙрдкрдЪाрд░ рдкрд░ рдХोрдИ рдк्рд░рднाрд╡ рдирд╣ीं рдкрдб़ेрдЧा।
(() рдоुрдЭे рдпрд╣ рднी рдкрддा рд╣ै рдХि рдЬांрдЪрдХрд░्рддा
рдоेрд░ी рд╕рд╣рдорддि рдХे рдмिрдиा, рдХिрд╕ी рднी рд╕рдордп, рдХिрд╕ी
рднी рд╕рдордп, рдоेрд░े рд░ोрдЧिрдпों рдпा рдЕрдз्рдпрдпрди рдоें рдоेрд░ी рднाрдЧीрджाрд░ी рдХो рд╕рдоाрдк्рдд
рдХрд░ рд╕рдХрддे рд╣ैं।
(() рдоैं рдЬाँрдЪрдХрд░्рддाрдУं рдХो рдЗрд╕ рдЕрдз्рдпрдпрди
рдоें рднाрдЧीрджाрд░ी рдХे рдкрд░िрдгाрдорд╕्рд╡рд░ूрдк рдк्рд░ाрдк्рдд рдЬाрдирдХाрд░ी рдХो рдиैрддिрдХрддा рд╕рдоिрддि рдХो рдЬाрд░ी рдХрд░рдиे рдХी рдЕрдиुрдорддि
рджेрддा рд╣ूँ। рдоैं рд╕рдордЭрддा рд╣ूं рдХि рд╡े рдоेрд░े рдоूрд▓ рдЕрднिрд▓ेрдЦों рдХा рдиिрд░ीрдХ्рд╖рдг рдХрд░ рд╕рдХрддे рд╣ैं।
(9) рдпрджि рдоेрд░ा рдбेрдЯा рд╕ाрд░्рд╡рдЬрдиिрдХ рд░ूрдк рд╕े
рдк्рд░рд╕्рддुрдд рдХिрдпा рдЬाрддा рд╣ै рддो рдоेрд░ी рдкрд╣рдЪाрди рдЧोрдкрдиीрдп рд░рдЦी рдЬाрдПрдЧी।
(резреж) рдоेрд░ी рд╕ंрддुрд╖्рдЯि
рдХे рд▓िрдП рдоेрд░े рд╕рд╡ाрд▓ों рдХा рдЬрд╡ाрдм рджिрдпा рд╣ै।
(резрез) рдоैंрдиे рд╢ोрдз
рдЕрдз्рдпрдпрди рдоें рдЦुрдж рдХो рдпा рдЕрдкрдиे рдорд░ीрдЬ рдХो рд╢ाрдоिрд▓ рдХрд░рдиे рдХा рдлैрд╕рд▓ा рдХिрдпा рд╣ै।
рдоुрдЭे рдкрддा рд╣ै, рдХि рдпрджि рдЗрд╕ рдЕрдз्рдпрдпрди
рдХे рджौрд░ाрди рдоेрд░े рдХोрдИ рдк्рд░рд╢्рди рд╣ैं, рддो рдоुрдЭे рдКрдкрд░ рд╕ूрдЪीрдмрдж्рдз рдПрдХ рдкрддे рдкрд░
рд╕ंрдкрд░्рдХ рдХрд░рдиा рдЪाрд╣िрдП। рд╕े рдЗрд╕ рд╕рд╣рдорддि рдкрд░ рд╣рд╕्рддाрдХ्рд╖рд░ рдХрд░рдХे, рдоैं рдЗрд╕ рджрд╕्рддाрд╡ेрдЬ़
рдоें рджी рдЧрдИ рдЬाрдирдХाрд░ी рдХी рдкुрд╖्рдЯि рдХрд░рддा рд╣ूं। рдоुрдЭे рдЗрд╕ рд╕рд╣рдорддि рджрд╕्рддाрд╡ेрдЬ рдХी рдПрдХ рдк्рд░рддि рджी рдЬाрдПрдЧी।
рдк्рд░рддिрднाрдЧी рдХे рд╢ुрд░ुрдЖрддी:
рдк्рд░рддिрднाрдЧी рдХा рдиाрдо рдФрд░ рд╣рд╕्рддाрдХ्рд╖рд░ / рдЕंрдЧूрдаे рдХा рдиिрд╢ाрди (рдпा рдХाрдиूрдиी рдк्рд░рддिрдиिрдзि рдпрджि рднाрдЧीрджाрд░ рдЕрдХ्рд╖рдо
рд╣ो):
______ (рдиाрдо) ______(рд╣рд╕्рддाрдХ्рд╖рд░)
рджिрдиांрдХ: ________________ рд╕рдордп: __________________
рдиिрд╖्рдкрдХ्рд╖ рдЧрд╡ाрд╣ рдХा рдиाрдо рдФрд░ рд╣рд╕्рддाрдХ्рд╖рд░ (рдЕрдирдкрдв़ рд░ोрдЧिрдпों рдХे рд▓िрдП рдЖрд╡рд╢्рдпрдХ):
_____________ (рдиाрдо)
____________(рд╣рд╕्рддाрдХ्рд╖рд░)
рджिрдиांрдХ рд╕рдордп: ___________
рдиिрд╖्рдкрдХ्рд╖ рдЧрд╡ाрд╣ рдХा рдкрддा рдФрд░ рд╕ंрдкрд░्рдХ рдиंрдмрд░:
рдЕрди्рд╡ेрд╖рдХ рдпा рдЙрд╕рдХे рдк्рд░рддिрдиिрдзि рдХा рдиाрдо рдФрд░ рд╣рд╕्рддाрдХ्рд╖рд░ рд╕рд╣рдорддि
рдк्рд░ाрдк्рдд рдХрд░рдиा:
_______________ (рдиाрдо)
___________ (рд╣рд╕्рддाрдХ्рд╖рд░)
рджिрдиांрдХ: __________________________ рд╕рдордп: ________
PATIENT INFORMATION SHEET
“EFFECTS OF INTRAVENOUS LIGNOCAINE 2% AND LIGNOCAINE SPRAY
10% FOR INTUBATION RESPONSE IN PATIENTS WITH EJECTION FRACTION <50%- COMPARATIVE STUDY.”
Name of Participant:
You are invited to take part in this research
study. The information in this document is meant to help you decide whether or
not to take part in this study. Please feel free to ask if you have any queries
or concerns.
You
are being asked to participate in this study being conducted in D.Y. Patil
Hospital because you satisfy the eligibility criteria to participate in this
study. You will be one of the subjects we plan to recruit in this study.
What
is the purpose of research?
You have been posted for surgery which needs
administration of general anaesthesia. General anaesthesia involves
laryngoscopy (looking into ones oral cavity and upper respiratory tract using
an instrument called laryngoscope) and endotracheal intubation (insertion of a
tube into trachea for assisted ventilation during anaesthesia). This procedures
at times induces increased heart rate, increase in blood pressure as a reflex
reaction. We will be using lignocaine (either spray or intravenous route) to
suppress the above side effects of laryngoscopy and endotracheal intubation.
The purpose of the study
is to assess the effects of lignocaine spray on hemodynamic parameters due to
laryngoscopy and endotracheal intubation and to compare with that of
intravenous lignocaine in patients with ejection fraction <50%.
Study Procedures
All the patients with EF <50% posted for elective
surgery under general anaesthesia will be given eithe lignocaine spray or
intravenous lignocaine before laryngoscopy and endotracheal intubation. The
efficacy of this drug in reducing the vasopressive effects of laryngoscopy and
endotracheal intubation is to be evaluated by this study.
Possible
risks to you
There
is no risk involved in this study.
Possible
benefits to you
Clinical trials in healthy adults undergoing surgery
under general anaesthesia have proved
that prior use of lignocaine has reduced the vasopressor effects of
laryngoscopy and endotracheal intubation has improved the safety and overall outcome
Possible
benefits to other people
The results of the research may provide benefits to
the society in terms of advancement of medical knowledge and/or therapeutic
benefit to future patients.
Cost
to the participant
The tests will be performed free of cost to you. The
tests will be performed at Dr. DY Patil Hospital.
Confidentiality
of the information obtained from you
You have the right to confidentiality regarding the
privacy of your medical information (personal details, results of physical
examinations, investigations, and your medical history). By signing this
document, you will be allowing the treating physician, other study personnel,
hospital ethics committee to view your data, if required. The results of
clinical tests and therapy performed as part of this research may be included
in your medical record. The information from this study, if published in
scientific journals or presented at scientific meetings, will not reveal your identity.
How will your decision to not
participate in the study affect you?
Your decision not to participate in this research
study will not affect your medical care or your relationship with the treating
physician or the institution. Your doctor will still take care of you and you
will not lose any benefits to which you are entitled.
Right
to new information
If the research team gets any new information during
this research study that may affect your decision to continue participating in
the study, or may raise some doubts, you will be told about that information.
Contact
persons
In
case of conflicts, you can contact the chairperson (convener) of our hospital
ethics Committee at the following address:
Dr.
Chairperson,
Institutional Ethics Committee,
D
Y Patil University and School of Medicine, Nerul, Navi Mumbai.
рд░ुрдЧ्рдг
рдоाрд╣िрддी рдкрдд्рд░рдХ
“рдЙрдж्рдШाрдЯрдиाрдЪ्рдпा рднाрдЧाрд╕рд╣ рдкेрдЯंрдЯ्рд╕ рдордзीрд▓
рдк्рд░рд╡ेрд╢ाрдЪ्рдпा рдк्рд░рддिрд╕ाрджाрд╕ाрдаी рдЗंрдЯ्рд░ाрд╡ेрдирд╕ рд▓िрдЧ्рдиोрдХाрдЗрди 2% рдЖрдгि рд▓िрдЧ्рдиोрдХाрдЗрди
рд╕्рдк्рд░े 10% -
рдПрдХрдд्рд░ рдЕрдн्рдпाрд╕. ”
рд╕рд╣рднाрдЧीрдЪे рдиाрд╡:
рдЖрдкрд▓्рдпाрд▓ा рдпा рд╕ंрд╢ोрдзрди рдЕрдн्рдпाрд╕ाрдордз्рдпे рднाрдЧ рдШेрдг्рдпाрд╕ाрдаी
рдЖрдоंрдд्рд░िрдд рдХेрд▓े рдЖрд╣े. рдпा рдЕрдн्рдпाрд╕ाрдд рднाрдЧ рдШ्рдпाрд╡ा рдХी рдиाрд╣ी
рд╣े рдард░рд╡िрдг्рдпाрд╕ рдорджрдд рдХрд░рдг्рдпाрд╕ाрдаी рдпा рджрд╕्рддрдРрд╡рдЬाрдд рдоाрд╣िрддी рдЖрд╣े. рдХृрдкрдпा
рдЖрдкрд▓्рдпाрдХрдбे рдХाрд╣ी рд╢ंрдХा рдХिंрд╡ा рд╢ंрдХा рдЕрд╕рд▓्рдпाрд╕ рд╡िрдЪाрд░ू рдоोрдХрд│्рдпा рдордиाрдиे.
рдЖрдкрд▓्рдпाрд▓ा рдбीрд╡ाрдп рдордз्рдпे рдШेрдд рдЕрд╕рд▓ेрд▓्рдпा рдпा рдЕрдн्рдпाрд╕ाрдордз्рдпे
рднाрдЧ рдШेрдг्рдпाрд╕ाрдаी рд╕ांрдЧिрддрд▓े рдЬाрддे. рдкाрдЯीрд▓ рд░ुрдЧ्рдгाрд▓рдп рдХाрд░рдг рдЖрдкрдг рдпा
рдЕрдн्рдпाрд╕ाрдд рднाрдЧ рдШेрдг्рдпाрд╕ाрдаी рдкाрдд्рд░рддा рдиिрдХрд╖ рдкूрд░्рдг рдХрд░рддा. рдЖрдо्рд╣ी рдпा рдЕрдн्рдпाрд╕ाрдд
рднрд░рддी рдХрд░рдг्рдпाрдЪी рдЖрдордЪी рдпोрдЬрдиा рдЕрд╕рд▓ेрд▓्рдпा рд╡िрд╖рдпांрдкैрдХी рдПрдХ рдЕрд╕ेрд▓.
рд╕ंрд╢ोрдзрдиाрдЪा рд╣ेрддू рдХाрдп рдЖрд╣े?
рдЖрдкрд▓्рдпाрд▓ा рд╢рд╕्рдд्рд░рдХ्рд░िрдпेрд╕ाрдаी рдкोрд╕्рдЯ рдХेрд▓े рдЧेрд▓े рдЖрд╣े рдЬ्рдпाрд╕
рд╕ाрдоाрди्рдп рднूрд▓ рджेрдг्рдпाрд╕ рдЖрд╡рд╢्рдпрдХ рдЖрд╣े. рд╕ाрдоाрди्рдп рднूрд▓ рдордз्рдпे рд▓ॅрд░िрди्рдЧोрд╕्рдХोрдкी
(рддोंрдбी рдкोрдХрд│ी рдЖрдгि рд▓ॅрд░ीрди्рдЧोрд╕्рдХोрдк рдиाрд╡ाрдЪ्рдпा рдЙрдкрдХрд░рдгाрдЪा рд╡ाрдкрд░ рдХрд░ूрди рд╡рд░рдЪ्рдпा
рд╢्рд╡рд╕рдирдоाрд░्рдЧाрдХрдбे рд▓рдХ्рд╖ рджेрдгे) рдЖрдгि рдПंрдбोрдЯ्рд░ाрд╢िрдпрд▓ рдЗрдирдЯ्рдпूрдмेрд╢рди
(рдПрдиेрд╕्рдеेрд╕िрдпा рджрд░рдо्рдпाрди рд╕рд╣ाрдп्рдпрдХ рд╡ेंрдЯिрд▓ेрд╢рдирд╕ाрдаी рд╢्рд╡ाрд╕рдирд▓िрдХेрдд рдПрдХ рдЯ्рдпूрдм рд╕рдоाрд╡िрд╖्рдЯ
рдХрд░рдгे) рд╕рдоाрд╡िрд╖्рдЯ рдЕрд╕рддे. рдпा рдк्рд░рдХ्рд░िрдпेрдоुрд│े
рдХрдзीрдХрдзी рд╣ृрджрдп рдЧрддी рд╡ाрдврддे, рд░рдХ्рддрджाрдм рд╡ाрдвीрд╕ рдк्рд░рддिрдХ्рд╖ेрдк рдк्рд░рддिрдХ्рд░िрдпा
рдо्рд╣рдгूрди рдк्рд░рд╡ृрдд्рдд рдХрд░рддे. рд▓ॅрд░िрди्рдЧोрд╕्рдХोрдкी рдЖрдгि рдПंрдбोрдЯ्рд░ाрд╕ीрдЕрд▓ рдЗрдирдЯ्рдпूрдмेрд╢рдирдЪे
рд╡рд░ीрд▓ рд╕ाрдЗрдб рдЗрдлेрдХ्рдЯ्рд╕ рджाрдмрдг्рдпाрд╕ाрдаी рдЖрдо्рд╣ी рд▓िрдЧ्рдиोрдХेрди (рдПрдХрддрд░ рд╕्рдк्рд░े
рдХिंрд╡ा рдЗंрдЯ्рд░ाрд╡्рд╣ेрдирд╕ рдоाрд░्рдЧ) рд╡ाрдкрд░рдгाрд░ рдЖрд╣ोрдд.
рдЕрдн्рдпाрд╕ाрдЪा рдЙрдж्рджेрд╢ рдо्рд╣рдгрдЬे рд▓ॅрд░िрди्рдХोрд╕्рдХोрдкी рдЖрдгि рдПंрдбोрдЯ्рд░ाрд╕ीрдпрд▓
рдЗрдирдЯ्рдпूрдмेрд╢рдирдоुрд│े рд╣ेрдоोрдбाрдпрдиाрдоिрдХ рдкॅрд░ाрдоीрдЯрд░्рд╕рд╡рд░ीрд▓ рд▓िрдЧ्рдиोрдХेрди рд╕्рдк्рд░ेрдЪ्рдпा рдк्рд░рднाрд╡ांрдЪे рдоूрд▓्рдпांрдХрди
рдХрд░рдгे рдЖрдгि рдЗрдЬेрдХ्рд╢рди рдл्рд░ॅрдХ्рд╢рди <50% рдЕрд╕рд▓ेрд▓्рдпा рд░ूрдЧ्рдгांрдордз्рдпे рдЗंрдЯ्рд░ाрд╡ेрди्рд╕
рд▓िрдЧ्рдиोрдХेрдирдЪ्рдпा рддुрд▓рдиेрдд рддुрд▓рдиा рдХрд░рдгे.
рдЕрдн्рдпाрд╕ рдк्рд░рдХ्рд░िрдпा
рд╕рд░्рд╡рд╕ाрдзाрд░рдг рднूрд▓ рдЕंрддрд░्рдЧрдд рдиिрд╡рдбрдХ рд╢рд╕्рдд्рд░рдХ्рд░िрдпेрд╕ाрдаी рдкोрд╕्рдЯ
рдХेрд▓ेрд▓े рдИрдПрдл <%реж% рдЕрд╕рд▓ेрд▓्рдпा рд╕рд░्рд╡ рд░ूрдЧ्рдгांрдиा
рд▓ॅрд░ींрдЧोрд╕्рдХोрдкी рдЖрдгि рдПंрдбोрдЯ्рд░ॅрд╢िрдпрд▓ рдЗрдирдЯ्рдпूрдмेрд╢рдирдЪ्рдпा рдЖрдзी рд▓िрдеोрдХेрди рд╕्рдк्рд░े рдХिंрд╡ा рдЗंрдЯ्рд░ाрд╡्рд╣ेрдирд╕
рд▓िрдЧ्рдиोрдХेрди рджिрд▓े рдЬाрдИрд▓. рд▓ॅрд░ीрди्рдЧोрд╕्рдХोрдкी рдЖрдгि рдПंрдбोрдЯ्рд░ॅрд╕िрдпрд▓ рдЗрдирдЯ्рдпूрдмेрд╢рдирдЪे
рд╡ाрд╕ोрдк्рд░िрд╡्рд╣ рдк्рд░рднाрд╡ рдХрдоी рдХрд░рдг्рдпाрд╕ाрдаी рдпा рдФрд╖рдзाрдЪी рдХाрд░्рдпрдХ्рд╖рдорддा рдпा рдЕрдн्рдпाрд╕ाрдж्рд╡ाрд░े рдоूрд▓्рдпांрдХрди
рдХेрд▓ी рдЬाрд╡ी.
рдЖрдкрд▓्рдпाрд╕ाрдаी рд╕ंрднाрд╡्рдп рдЬोрдЦीрдо
рдпा рдЕрдн्рдпाрд╕ाрдордз्рдпे рдХोрдгрддाрд╣ी рдзोрдХा рдиाрд╣ी.
рдЖрдкрд▓्рдпाрд▓ा рд╕ंрднाрд╡्рдп рдлाрдпрджे
рд╕ाрдоाрди्рдп рднूрд▓ рджेрдКрди рд╢рд╕्рдд्рд░рдХ्рд░िрдпा рдХрд░рдд рдЕрд╕рд▓ेрд▓्рдпा рдиिрд░ोрдЧी
рдк्рд░ौрдвांрдордзीрд▓ рдХ्рд▓िрдиिрдХрд▓ рдЪाрдЪрдг्рдпांрдоुрд│े рд╣े рд╕िрдж्рдз рдЭाрд▓े рдЖрд╣े рдХी рд▓िрдЧ्рдиोрдХेрдирдЪ्рдпा рдкूрд░्рд╡ीрдЪ्рдпा
рд╡ाрдкрд░ाрдоुрд│े рд▓ॅрд░िрди्рдЧोрд╕्рдХोрдкीрдЪे рд╡्рд╣ॅрд╕ोрдк्рд░ेрд╕рд░ рдк्рд░рднाрд╡ рдХрдоी рдЭाрд▓ा рдЖрд╣े рдЖрдгि рдПंрдбोрдЯ्рд░ॅрд╕िрдпрд▓ рдЗрдирдЯ्рдпूрдмेрд╢рдирдоुрд│े
рд╕ुрд░рдХ्рд╖ा рдЖрдгि рдПрдХूрдгрдЪ рдкрд░िрдгाрдо рд╕ुрдзाрд░рд▓ा рдЖрд╣े.
рдЗрддрд░ рд▓ोрдХांрдиा рд╕ंрднाрд╡्рдп рдлाрдпрджे
рд╕ंрд╢ोрдзрдиाрдЪ्рдпा рдкрд░िрдгाрдоाрдоुрд│े рднрд╡िрд╖्рдпाрддीрд▓ рд░ूрдЧ्рдгांрдиा рд╡ैрдж्рдпрдХीрдп
рдЬ्рдЮाрдиाрдЪी рдк्рд░рдЧрддी рдЖрдгि / рдХिंрд╡ा рдЙрдкрдЪाрд░ाрдд्рдордХ рдлाрдпрдж्рдпाрдЪ्рдпा рджृрд╖्рдЯीрдиे
рд╕рдоाрдЬाрдд рдлाрдпрджा рд╣ोрдК рд╢рдХेрд▓.
рд╕рд╣рднाрдЧीрдЪी рдХिंрдордд
рдпा рдЪाрдЪрдг्рдпा рддुрдо्рд╣ाрд▓ा рд╡िрдиाрдоूрд▓्рдп рджिрд▓्рдпा рдЬाрддीрд▓. рдбॉ. рдбी рд╡ाрдп рдкाрдЯीрд▓ рд░ुрдЧ्рдгाрд▓рдпाрдд рдпा рдЪाрдЪрдг्рдпा рдШेрдг्рдпाрдд рдпेрддीрд▓.
рдЖрдкрд▓्рдпाрдХрдбूрди рдк्рд░ाрдк्рдд рдоाрд╣िрддीрдЪी рдЧोрдкрдиीрдпрддा
рдЖрдкрд▓्рдпाрд▓ा рдЖрдкрд▓्рдпा рд╡ैрдж्рдпрдХीрдп рдоाрд╣िрддीрдЪ्рдпा рдЧोрдкрдиीрдпрддेрд╕ंрджрд░्рднाрдд
рдЧोрдкрдиीрдпрддेрдЪा рд╣рдХ्рдХ рдЖрд╣े (рд╡ैрдпрдХ्рддिрдХ рддрдкрд╢ीрд▓, рд╢ाрд░ीрд░िрдХ рддрдкाрд╕рдгीрдЪा рдиिрдХाрд▓, рддрдкाрд╕рдгी рдЖрдгि рдЖрдкрд▓ा рд╡ैрдж्рдпрдХीрдп рдЗрддिрд╣ाрд╕).
рдпा рджрд╕्рддрдРрд╡рдЬाрд╡рд░ рд╕्рд╡ाрдХ्рд╖рд░ी рдХрд░ूрди, рдЖрд╡рд╢्рдпрдХ рдЕрд╕рд▓्рдпाрд╕
рдЖрдкрдг рдЙрдкрдЪाрд░ рдХрд░рдгाрд░्рдпा рдбॉрдХ्рдЯрд░, рдЗрддрд░ рдЕрдн्рдпाрд╕
рдХрд░्рдордЪाрд░ी, рд░ुрдЧ्рдгाрд▓рдпाрддीрд▓ рдиीрддिрд╢ाрд╕्рдд्рд░ рд╕рдоिрддीрд▓ा рдЖрдкрд▓ा рдбेрдЯा рдкाрд╣рдг्рдпाрдЪी
рдкрд░рд╡ाрдирдЧी рджेрдд рдЖрд╣ाрдд. рдпा рд╕ंрд╢ोрдзрдиाрдЪा рдПрдХ рднाрдЧ рдо्рд╣рдгूрди рдХेрд▓्рдпा рдЧेрд▓ेрд▓्рдпा рдХ्рд▓िрдиिрдХрд▓ рдЪाрдЪрдг्рдпा рдЖрдгि рдеेрд░рдкीрдЪे
рдкрд░िрдгाрдо рдЖрдкрд▓्рдпा рд╡ैрдж्рдпрдХीрдп рдиोंрджीрдордз्рдпे рд╕рдоाрд╡िрд╖्рдЯ рдХेрд▓े рдЬाрдК рд╢рдХрддाрдд. рдпा рдЕрдн्рдпाрд╕ाрдЪी рдоाрд╣िрддी, рдЬрд░ рд╡ैрдЬ्рдЮाрдиिрдХ рдиिрдпрддрдХाрд▓िрдХांрдордз्рдпे
рдк्рд░рдХाрд╢िрдд рдЭाрд▓ी рдЕрд╕ेрд▓ рдХिंрд╡ा рд╡ैрдЬ्рдЮाрдиिрдХ рдмैрдардХींрдордз्рдпे рд╕ाрджрд░ рдХेрд▓ी рдЧेрд▓ी рдЕрд╕ेрд▓ рддрд░ рддी рдЖрдкрд▓ी рдУрд│рдЦ
рдЙрдШрдб рдХрд░рдгाрд░ рдиाрд╣ी.
рдЕрдн्рдпाрд╕ाрдд рднाрдЧ рди рдШेрдг्рдпाрдЪ्рдпा рддुрдордЪ्рдпा рдиिрд░्рдгрдпाрдЪा рддुрдордЪ्рдпाрд╡рд░
рдХрд╕ा рдкрд░िрдгाрдо рд╣ोрдИрд▓?
рдпा рд╕ंрд╢ोрдзрди рдЕрдн्рдпाрд╕ाрдордз्рдпे рднाрдЧ рди рдШेрдг्рдпाрдЪ्рдпा рдЖрдкрд▓्рдпा
рдиिрд░्рдгрдпाрдЪा рдЖрдкрд▓्рдпा рд╡ैрдж्рдпрдХीрдп рд╕ेрд╡ेрд╡рд░ рдХिंрд╡ा рдЙрдкрдЪाрд░ рдХрд░рдгाрд░्рдпा рдбॉрдХ्рдЯрд░ांрд╢ी рдХिंрд╡ा рд╕ंрд╕्рдеेрд╢ी рдЕрд╕рд▓ेрд▓ा рд╕ंрдмंрдз рдк्рд░рднाрд╡िрдд рд╣ोрдгाрд░ рдиाрд╣ी. рддुрдордЪा рдбॉрдХ्рдЯрд░ рдЕрдж्рдпाрдк рддुрдордЪी рдХाрд│рдЬी рдШेрдИрд▓ рдЖрдгि рддुрдо्рд╣ाрд▓ा рд╣рдХ्рдХ рдЕрд╕рдгाрд░े рдХोрдгрддेрд╣ी рдлाрдпрджे
рдЧрдоाрд╡рдгाрд░ рдиाрд╣ीрдд.
рдирд╡ीрди рдоाрд╣िрддीрдЪा рдЕрдзिрдХाрд░
рдпा рдЕрдн्рдпाрд╕ाрдЪ्рдпा рдЕрдн्рдпाрд╕ाрдиुрд╕ाрд░ рдЬрд░ рд╕ंрд╢ोрдзрди рдХाрд░्рдпрд╕ंрдШाрд▓ा
рдХोрдгрддीрд╣ी рдирд╡ीрди рдоाрд╣िрддी рдоिрд│ाрд▓ी рдЬ्рдпाрдоुрд│े рдпा рдЕрдн्рдпाрд╕ाрдордз्рдпे рднाрдЧ рдШेрдг्рдпाрдЪ्рдпा рдЖрдкрд▓्рдпा рдиिрд░्рдгрдпाрд╡рд░
рдкрд░िрдгाрдо рд╣ोрдК рд╢рдХेрд▓ рдХिंрд╡ा рдХाрд╣ी рд╢ंрдХा рдиिрд░्рдоाрдг рд╣ोрдК рд╢рдХрддाрдд рддрд░ рдд्рдпा рдоाрд╣िрддीрдмрдж्рджрд▓ рдЖрдкрд▓्рдпाрд▓ा рд╕ांрдЧिрддрд▓े
рдЬाрдИрд▓.
рд╕ंрдкрд░्рдХ рд╡्рдпрдХ्рддी
рдорддрднेрдж рдЭाрд▓्рдпाрд╕ рдЖрдкрдг рдЖрдордЪ्рдпा рд░ुрдЧ्рдгाрд▓рдпाрдЪ्рдпा рдиीрддिрд╢ाрд╕्рдд्рд░
рд╕рдоिрддीрдЪे рдЕрдз्рдпрдХ्рд╖ (рд╕ंрдпोрдЬрдХ) рдпांрдЪ्рдпाрд╢ी
рдкुрдвीрд▓ рдкрдд्рдд्рдпाрд╡рд░ рд╕ंрдкрд░्рдХ рд╕ाрдзू рд╢рдХрддा:
рдЬ्рдЮाрдиेрд╢ рдмेрд▓ेрдХрд░ рдбॉ
рдЕрдз्рдпрдХ्рд╖, рд╕ंрд╕्рдеाрдд्рдордХ рдиीрддिрд╢ाрд╕्рдд्рд░
рд╕рдоिрддी,
рдбी рд╡ाрдп рдкाрдЯीрд▓ рд╡िрдж्рдпाрдкीрда рд╡ рд╕्рдХूрд▓ рдСрдл рдоेрдбिрд╕ीрди, рдиेрд░ूрд│, рдирд╡ी рдоुंрдмрдИ.
рдкेрдЯेंрдЯ рдХी рд╕ूрдЪрдиा рдкрдд्рд░
"рдЗंрдЯрд░्рдирд╡्рдпूрд╕ рд▓ोрдирдХॉрдЗрди рдХे рдк्рд░рднाрд╡
2% рдФрд░ рд▓ेрдЬोрдирдХाрдЗрди рд╕्рдкैрдиी 10% рдХे рд╕ाрде рд╕ंрдпोрдЬрди рдХे рдкрд░िрдгाрдоों
рдоें рд╕ंрдЪрд░िрдд рдлрд▓рди рдХे рд▓िрдП <50% - рддुрд▓рдиाрдд्рдордХ рдЕрдз्рдпрдпрди।"
рдк्рд░рддिрднाрдЧी рдХा рдиाрдо:
рдЖрдкрдХो рдЗрд╕ рд╢ोрдз рдЕрдз्рдпрдпрди рдоें рднाрдЧ рд▓ेрдиे рдХे рд▓िрдП рдЖрдоंрдд्рд░िрдд
рдХिрдпा рдЧрдпा рд╣ै। рдЗрд╕ рджрд╕्рддाрд╡ेрдЬ़ рдХी рдЬाрдирдХाрд░ी рдЗрд╕ рдЕрдз्рдпрдпрди рдоें рднाрдЧ рд▓ेрдиे рдпा рди рд▓ेрдиे рдоें рдЖрдкрдХी рдорджрдж
рдХрд░рдиे рдХे рд▓िрдП рд╣ै। рдХृрдкрдпा рдмेрдЭिрдЭрдХ рдкूрдЫें рдХि рдХ्рдпा рдЖрдкрдХे рдкाрд╕ рдХोрдИ рдк्рд░рд╢्рди рдпा рдЪिंрддा рд╣ै।
рдЖрдкрдХो рдбी। рд╡ाрдИ рдоें рдЖрдпोрдЬिрдд рдХिрдП рдЬा рд░рд╣े рдЗрд╕ рдЕрдз्рдпрдпрди рдоें
рднाрдЧ рд▓ेрдиे рдХे рд▓िрдП рдХрд╣ा рдЬा рд░рд╣ा рд╣ै। рдкाрдЯिрд▓ рдЕрд╕्рдкрддाрд▓ рдХ्рдпोंрдХि рдЖрдк рдЗрд╕ рдЕрдз्рдпрдпрди рдоें рднाрдЧ рд▓ेрдиे рдХे
рд▓िрдП рдкाрдд्рд░рддा рдоाрдирджंрдбों рдХो рдкूрд░ा рдХрд░рддे рд╣ैं। рдЖрдк рдЗрд╕ рдЕрдз्рдпрдпрди рдоें рднрд░्рддी рд╣ोрдиे рдХी рдпोрдЬрдиा рдмрдиाрдиे
рд╡ाрд▓े рд╡िрд╖рдпों рдоें рд╕े рдПрдХ рд╣ोंрдЧे।
рдЕрдиुрд╕ंрдзाрди рдХा рдЙрдж्рджेрд╢्рдп рдХ्рдпा рд╣ै?
рдЖрдкрдХो рд╕рд░्рдЬрд░ी рдХे рд▓िрдП рддैрдиाрдд рдХिрдпा рдЧрдпा рд╣ै рдЬिрд╕े рд╕ाрдоाрди्рдп
рд╕ंрдЬ्рдЮाрд╣рд░рдг рдХे рдк्рд░рд╢ाрд╕рди рдХी рдЖрд╡рд╢्рдпрдХрддा рд╣ै। рд╕ाрдоाрди्рдп рд╕ंрдЬ्рдЮाрд╣рд░рдг рдоें рд▓ैрд░ींрдЧोрд╕्рдХोрдкी (рд▓ोрдЧों рдоें рдоौрдЦिрдХ рдЧुрд╣ा рдФрд░ рдКрдкрд░ी рд╢्рд╡ाрд╕ рдкрде рдоें рд▓ेрд░िंрдЬोрд╕्рдХोрдк рдиाрдордХ рдПрдХ рдЙрдкрдХрд░рдг рдХा
рдЙрдкрдпोрдЧ рдХрд░рдХे) рдФрд░ рдПंрдбोрдЯ्рд░ैрдЪिрдпрд▓ рдЗंрдЯुрдмैрд╢рди (рдПрдиेрд╕्рдеेрд╕िрдпा рдХे рджौрд░ाрди рд╕рд╣ाрдпрдХ рд╡ेंрдЯिрд▓ेрд╢рди рдХे рд▓िрдП рдЯ्рд░ेрдХिрдЖ рдоें рдПрдХ рдЯ्рдпूрдм рдХा рд╕рдо्рдоिрд▓рди)
рд╢ाрдоिрд▓ рд╣ै। рдпрд╣ рдк्рд░рдХ्рд░िрдпा рдХрдИ рдмाрд░ рджिрд▓ рдХी рдзрдб़рдХрди рдХो рдмрдв़ा рджेрддी рд╣ै,
рд░िрдл्рд▓ेрдХ्рд╕ рдк्рд░рддिрдХ्рд░िрдпा рдХे рд░ूрдк рдоें рд░рдХ्рддрдЪाрдк рдоें рд╡ृрдж्рдзि рд╣ोрддी рд╣ै। рд▓ॅрд░िрди्рдЧोрд╕्рдХोрдкी
рдФрд░ рдПंрдбोрдЯ्рд░ाрд╕ीрдЕрд▓ рдЗंрдЯुрдмैрд╖ेрдг рдХे рдЙрдкрд░ोрдХ्рдд рджुрд╖्рдк्рд░рднाрд╡ों рдХो рджрдмाрдиे рдХे рд▓िрдП рд╣рдо рд▓िрдЧ्рдиोрдХाрдЗрди
(рдпा рддो рд╕्рдк्рд░े рдпा рдЕंрддःрд╢िрд░ा рдоाрд░्рдЧ) рдХा рдЙрдкрдпोрдЧ рдХрд░ेंрдЧे।
рдЕрдз्рдпрдпрди рдХा рдЙрдж्рджेрд╢्рдп рд▓ैрд░ींрдЧोрд╕्рдХोрдкी рдФрд░ рдПंрдбोрдЯ्рд░ैрдЪिрдпрд▓
рдЗंрдЯुрдмैрд╖ेрдг рдХे рдХाрд░рдг рд╣ेрдоोрдбाрдпрдиाрдоिрдХ рдоाрдкрджंрдбों рдкрд░ рд▓िрдЧ्рдиोрдХेрди рд╕्рдк्рд░े рдХे рдк्рд░рднाрд╡ों рдХा рдЖрдХрд▓рди
рдХрд░рдиा рд╣ै рдФрд░ рдЗрд╕рдХी рддुрд▓рдиा рдоें рдл्рд░ॅрдХ्рд╢рди 50% рдХे рд╕ाрде рд░ोрдЧिрдпों
рдоें рдЕंрддःрд╢िрд░ा рд▓िрдЧ्рдиोрдХाрдЗрди рдХी рддुрд▓рдиा рдХрд░рдиा рд╣ै।
рдЕрдз्рдпрдпрди рдХी рдк्рд░рдХ्рд░िрдпाрдПं
рд╕ाрдоाрди्рдп рдПрдиेрд╕्рдеीрд╕िрдпा рдХे рддрд╣рдд рдРрдЪ्рдЫिрдХ рд╕рд░्рдЬрд░ी рдХे рд▓िрдП
рддैрдиाрдд рдИрдПрдл <50% рд╡ाрд▓े рд╕рднी рд░ोрдЧिрдпों рдХो рд▓ेрд░िंрдЬोрд╕्рдХोрдкी рдФрд░
рдПंрдбोрдЯ्рд░ैрдЪिрдпрд▓ рдЗंрдЯुрдмैрд╖ेрдг рд╕े рдкрд╣рд▓े рдИрде рд▓िрдЧ्рдиोрдХाрдЗрди рд╕्рдк्рд░े рдпा рдЕंрддःрд╢िрд░ा рд▓िрдЧ्рдиोрдХाрдЗрди рджिрдпा
рдЬाрдПрдЧा। рд▓ैрд░ींрдЧोрд╕्рдХोрдкी рдФрд░ рдПंрдбोрдЯ्рд░ैрдЪिрдпрд▓ рдЗंрдЯुрдмैрд╖ेрдг рдХे рд╡ाрд╕ोрдк्рд░ेрд╕िрд╡ рдк्рд░рднाрд╡ों рдХो рдХрдо рдХрд░рдиे
рдоें рдЗрд╕ рджрд╡ा рдХी рдк्рд░рднाрд╡рдХाрд░िрддा рдХा рдЗрд╕ рдЕрдз्рдпрдпрди рдж्рд╡ाрд░ा рдоूрд▓्рдпांрдХрди рдХिрдпा рдЬाрдиा рд╣ै।
рдЖрдкрдХे рд▓िрдП рд╕ंрднाрд╡िрдд рдЬोрдЦिрдо
рдЗрд╕ рдЕрдз्рдпрдпрди рдоें рдХोрдИ рдЬोрдЦिрдо рд╢ाрдоिрд▓ рдирд╣ीं рд╣ै।
рдЖрдкрдХो рд╕ंрднाрд╡िрдд рд▓ाрдн
рд╕ाрдоाрди्рдп рд╕ंрдЬ्рдЮाрд╣рд░рдг рдХे рддрд╣рдд рд╕рд░्рдЬрд░ी рдХрд░рдиे рд╡ाрд▓े рд╕्рд╡рд╕्рде
рд╡рдпрд╕्рдХों рдоें рдиैрджाрдиिрдХ рдкрд░ीрдХ्рд╖рдгों рдиे рд╕ाрдмिрдд рдХрд░ рджिрдпा рд╣ै
рдХि рд▓िрдЧ्рдиोрдХेрди рдХे рдкूрд░्рд╡ рдЙрдкрдпोрдЧ рд╕े рд▓ैрд░ींрдЧोрд╕्рдХोрдкी рдФрд░ рдПंрдбोрдЯ्рд░ैрдЪिрдпрд▓ рдЗंрдЯुрдмैрд╢рди рдХे рд╡ैрд╕ोрдк्рд░ेрд╕ोрд░
рдк्рд░рднाрд╡ рдХो рдХрдо рдХрд░ рджिрдпा рд╣ै рдФрд░ рд╕ुрд░рдХ्рд╖ा рдФрд░ рд╕рдордЧ्рд░ рдкрд░िрдгाрдо рдоें рд╕ुрдзाрд░ рд╣ुрдЖ рд╣ै।
рдЕрди्рдп рд▓ोрдЧों рдХो рд╕ंрднाрд╡िрдд рд▓ाрдн
рдЕрдиुрд╕ंрдзाрди рдХे рдкрд░िрдгाрдо рднрд╡िрд╖्рдп рдХे рд░ोрдЧिрдпों рдХो рдЪिрдХिрдд्рд╕ा
рдЬ्рдЮाрди рдФрд░
/ рдпा рдЪिрдХिрдд्рд╕ीрдп рд▓ाрдн рдХी рдЙрди्рдирддि рдХे рд░ूрдк рдоें рд╕рдоाрдЬ рдХो рд▓ाрдн рдк्рд░рджाрди рдХрд░ рд╕рдХрддे
рд╣ैं।
рдк्рд░рддिрднाрдЧी рдХो рд▓ाрдЧрдд
рдкрд░ीрдХ्рд╖рдг рдЖрдкрдХे рд▓िрдП рдиि: рд╢ुрд▓्рдХ рдХिрдП рдЬाрдПंрдЧे। рдкрд░ीрдХ्рд╖рдг рдбॉ। рдбी рд╡ाрдИ рдкाрдЯिрд▓ рдЕрд╕्рдкрддाрд▓ рдоें рдХिрдП рдЬाрдПंрдЧे।
рдЖрдкрд╕े рдк्рд░ाрдк्рдд рдЬाрдирдХाрд░ी рдХी рдЧोрдкрдиीрдпрддा
рдЖрдкрдХो рдЕрдкрдиी рдоेрдбिрдХрд▓ рдЬाрдирдХाрд░ी рдХी рдЧोрдкрдиीрдпрддा (рд╡्рдпрдХ्рддिрдЧрдд рд╡िрд╡рд░рдг, рд╢ाрд░ीрд░िрдХ рдкрд░ीрдХ्рд╖ाрдУं рдХे рдкрд░िрдгाрдо,
рдЬांрдЪ, рдФрд░ рдЖрдкрдХे рдоोрдмाрдЗрд▓ рдбेрдЯा) рдХी рдЧोрдкрдиीрдпрддा рдХे рдмाрд░े рдоें рдЕрдзिрдХाрд░ рд╣ै। рдЗрд╕ рджрд╕्рддाрд╡ेрдЬ़ рдкрд░ рд╣рд╕्рддाрдХ्рд╖рд░ рдХрд░рдиे рд╕े,
рдпрджि рдЖрд╡рд╢्рдпрдХ рд╣ो, рддो рдЖрдк рдЗрд▓ाрдЬ рдХрд░рдиे рд╡ाрд▓े рдЪिрдХिрдд्рд╕рдХ,
рдЕрди्рдп рдЕрдз्рдпрдпрди рдХрд░्рдоिрдпों, рдЕрд╕्рдкрддाрд▓ рдХी рдиैрддिрдХрддा рд╕рдоिрддि
рдХो рдЕрдкрдиे рдбेрдЯा рдХो рджेрдЦрдиे рдХी рдЕрдиुрдорддि рджेंрдЧे। рдЗрд╕ рд╢ोрдз рдХे рднाрдЧ рдХे рд░ूрдк рдоें рдХिрдП рдЧрдП рдиैрджाрдиिрдХ рдкрд░ीрдХ्рд╖рдгों
рдФрд░ рдЪिрдХिрдд्рд╕ा рдХे рдкрд░िрдгाрдоों рдХो рдЖрдкрдХे рдоेрдбिрдХрд▓ рд░िрдХॉрд░्рдб рдоें рд╢ाрдоिрд▓ рдХिрдпा рдЬा рд╕рдХрддा рд╣ै। рдЗрд╕ рдЕрдз्рдпрдпрди
рдХी рдЬाрдирдХाрд░ी, рдЕрдЧрд░ рд╡ैрдЬ्рдЮाрдиिрдХ рдкрдд्рд░िрдХाрдУं рдоें рдк्рд░рдХाрд╢िрдд рдХी рдЬाрддी
рд╣ै рдпा рд╡ैрдЬ्рдЮाрдиिрдХ рдмैрдардХों рдоें рдк्рд░рд╕्рддुрдд рдХी рдЬाрддी рд╣ै, рддो рдЗрд╕рд╕े рдЖрдкрдХी
рдкрд╣рдЪाрди рдЙрдЬाрдЧрд░ рдирд╣ीं рд╣ोрдЧी।
рдЕрдз्рдпрдпрди рдоें рднाрдЧ рдирд╣ीं рд▓ेрдиे рдХा рдЖрдкрдХा рдиिрд░्рдгрдп рдЖрдкрдХो рдХैрд╕े
рдк्рд░рднाрд╡िрдд рдХрд░ेрдЧा?
рдЗрд╕ рд╢ोрдз рдЕрдз्рдпрдпрди рдоें рднाрдЧ рдирд╣ीं рд▓ेрдиे рдХा рдЖрдкрдХा рдиिрд░्рдгрдп
рдЖрдкрдХी рдЪिрдХिрдд्рд╕ा рджेрдЦрднाрд▓ рдпा рдЙрдкрдЪाрд░ рдХрд░рдиे рд╡ाрд▓े рдЪिрдХिрдд्рд╕рдХ рдпा рд╕ंрд╕्рдеाрди рдХे рд╕ाрде рдЖрдкрдХे рд╕ंрдмंрдзों
рдХो рдк्рд░рднाрд╡िрдд рдирд╣ीं рдХрд░ेрдЧा। рдЖрдкрдХा рдбॉрдХ्рдЯрд░ рдЕрднी рднी рдЖрдкрдХी рджेрдЦрднाрд▓ рдХрд░ेрдЧा рдФрд░ рдЖрдк рдХिрд╕ी рднी рд▓ाрдн рдХो
рдирд╣ीं рдЦोрдПंрдЧे рдЬिрд╕рдХे рдЖрдк рд╣рдХрджाрд░ рд╣ैं।
рдирдИ рдЬाрдирдХाрд░ी рдХा рдЕрдзिрдХाрд░
рдпрджि рдЗрд╕ рд╢ोрдз рдЕрдз्рдпрдпрди рдХे рджौрд░ाрди рдЕрдиुрд╕ंрдзाрди рдЯीрдо рдХो рдХोрдИ
рдирдИ рдЬाрдирдХाрд░ी рдоिрд▓рддी рд╣ै рдЬो рдЕрдз्рдпрдпрди рдоें рднाрдЧ рд▓ेрдиे рдХो рдЬाрд░ी рд░рдЦрдиे рдХे рдЖрдкрдХे рдиिрд░्рдгрдп рдХो рдк्рд░рднाрд╡िрдд
рдХрд░ рд╕рдХрддी рд╣ै, рдпा рдХुрдЫ рд╕ंрджेрд╣ рдкैрджा рдХрд░ рд╕рдХрддी рд╣ै, рддो рдЖрдкрдХो рдЙрд╕ рдЬाрдирдХाрд░ी рдХे рдмाрд░े рдоें рдмрддाрдпा рдЬाрдПрдЧा।
рд╕ंрдкрд░्рдХ рдХрд░ें
рдЕрдзिрдХ рдЬाрдирдХाрд░ी / рдк्рд░рд╢्рдиों
рдХे рд▓िрдП, рдЖрдк рд╣рдоें рдиिрдо्рдирд▓िрдЦिрдд рдкрддे рдкрд░ рд╕ंрдкрд░्рдХ рдХрд░ рд╕рдХрддे рд╣ैं:
рдк्рд░рдзाрди рдЕрди्рд╡ेрд╖рдХ:
рд╕ंрдШрд░्рд╖ рдХे рдоाрдорд▓े рдоें, рдЖрдк рдиिрдо्рдирд▓िрдЦिрдд рдкрддे рдкрд░ рд╣рдоाрд░ी рдЕрд╕्рдкрддाрд▓ рдЖрдЪाрд░ рд╕рдоिрддि рдХे рдЕрдз्рдпрдХ्рд╖ (рд╕ंрдпोрдЬрдХ) рд╕े рд╕ंрдкрд░्рдХ рдХрд░ рд╕рдХрддे рд╣ैं:
рдбॉ। рдЬ्рдЮाрдиेрд╢ рдмेрд▓ेрдХрд░
рдЕрдз्рдпрдХ्рд╖, рд╕ंрд╕्рдеाрдЧрдд рдЖрдЪाрд░
рд╕рдоिрддि,
рдбी рд╡ाрдИ рдкाрдЯिрд▓ рдпूрдиिрд╡рд░्рд╕िрдЯी рдФрд░ рд╕्рдХूрд▓ рдСрдл рдоेрдбिрд╕िрди, рдиेрд░ुрд▓, рдирд╡ी рдоुंрдмрдИ।
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