SUSHEEL YESHALA

HISTORY OF INHALATIONAL ANAESTHETICS
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1800 ² Humphry Davy described analgesic effect of Nitrous oxide. 1824 ² Henry Hill Hickman described anaesthesia using an inhaled substance(CO2). 1846 ² WTG Morton did successful public demonstration of anaesthesia using Ether. 1846- James Young Simpson used Chloroform.

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HISTORY OF INHALATIONAL ANAESTHETICS
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1930 ² Cyclopropane. 1956 ² Halothane. 1966 ² Enflurane. 1968 ² Isoflurane. 1990 ² Sevoflurane. 1992 ² Desflurane.

Properties of an ideal inhalation anaesthetic
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Non-inflammable or explosive. Not metabolized in the body . Stable with soda lime (CO2 absorbent). Potent to use as a sole agent. Rapid induction & recovery.

Properties of an ideal inhalation anaesthetic
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Easy to control depth of Anaesthesia. Non-irritant to smell (smooth induction). anaesthetics effect: analgesia,amnesia,hypnosis. No CNS excitation, no CVS or respiratory effect, No organ specific toxicity
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Nitrous Oxide, N2O ("Laughing Gas")
Physical Properties ` colorless ` odorless ` Non-inflammable but, like O2, supports combustion
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gas at room temp and ambient pressure; liquid under pressure Only inorganic gas used in modern anaesthestic practice.

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Nitrous Oxide
Cardiovascular
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direct myocardial depressant effect balanced by sympathetic nervous system stimulation so cardio stable in normal person. myocardial depression may be unmasked by - Coronary artery disease. - hypovolemia pulmonary vasoconstriction -> increased pulmonary vascular resistance.

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Nitrous Oxide
Respiratory ` tachypnea + decreased tidal volume = stable minute volume and PaCO2
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BEWARE: inhibits carotid body hypoxic drive ( potent respiratory depressant).

CNS ` mildly increases CBF, CBV and ICP ` increases CMRO2 ` analgesia

Nitrous Oxide
Biotransformation and Toxicity ` eliminated mainly by exhalation
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irreversibly oxidizes cobalt atom of vitamin B12, inhibiting B12-dependent enzymes: methionine synthetase (myelin formation) thymidylate synthetase (DNA synthesis) so prolonged exposure # Bone marrow depression (megaloblastic anemia) # Peripheral neuropathy

# pernicious anemia

Nitrous Oxide
Controversial: ` Emetogenic ` Teratogenic (maybe not, but better avoided in early pregnancy)

Nitrous Oxide
Contraindications 35 times more soluble in blood than nitrogen.. So fills and expands any air-containing cavities:
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air embolism pneumothorax intracranial air

Nitrous Oxide
Contraindications ` lung cysts
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intraocular air bubbles Tympanoplasty pulmonary hypertension

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Halothane, CF3-CHBrCl
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Introduced in 1956 Most commonly used in India ` cost-effective
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Halothane
Physical Properties ` halogenated ethane ` spontaneous oxidative decomposition on exposure to light ` retarded by -thymol preservative -amber-colored bottle

Halothane

Organ System Effects:
Cardiovascular` `

direct myocardial depressant depresses cardiac output and lowers arterial BP depresses myocardial O2 demand

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Halothane
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depresses SA-node function - bradycardia. - AV nodal rhythm. depresses baroreceptor reflex enhances myocardial sensitivity to the dysrhythmogenic effects of epinephrine.

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Halothane
Respiratory ` fast, shallow breathing.
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Increased PaCO2 severe depression of hypoxic ventilatory drive potent bronchodilator depresses mucociliary function.

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Halothane
CNS ` cerebral vasodilator
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increases CBF, ICP Decreases CMRO2. blunts cerebrovascular autoregulation

Halothane
Biotransformation and Toxicity
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Mainly eliminated by exhalation but 20-30% is oxidized in liver by cytochrome P-450 enzyme system to trifluroacetic acid. In the absence of O2, hepatotoxic reduction products may arise.

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Halothane
Halothane hepatitis
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extremely rare (1:35,000 cases). {Diagnosis by exclusion} factors that increase risk: -multiple exposures to halothane over a short interval -middle-aged, obese women -familial predisposition -personal history of toxicity

Halothane
Halothane hepatitis
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centrilobular necrosis antibody that binds to halothane-exposed hepatocytes.

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Halothane
Contraindications/Precautions
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malignant hyperthermia susceptibility unexplained liver dysfunction after previous halothane exposure intracranial mass lesion

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Isoflurane, CF3CHCl-O-CF2H
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Introduced in 1981. One of the most commonly administered volatile anesthetic today.

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Isoflurane
Physical Properties
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pungent ethereal odour chemical isomer of enflurane

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Isoflurane

Organ System Effects
Cardiovascular
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minimal cardiac depression carotid baroreflexes relatively intact heart rate increases 10-20%.

Isoflurane
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dilates coronary arteries several large studies failed to show convincing evidence of clinically significant coronary steal syndrome

Isoflurane
Respiratory ` tachypnea, but less pronounced
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blunts hypoxic drive bronchodilator

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Isoflurane
CNS ` increases CBF and ICP
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decreases CMRO2

Isoflurane
Hepatic
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hepatic oxgenation maintained better than with halothane or enflurane

Isoflurane
Biotransformation and Toxicity
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minor part is metabolized (principally to trifluoroacetic acid)

Isoflurane
Contraindications ` malignant hyperthermia susceptibility
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severe hypovolemia Coronary artery disease (?)

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Sevoflurane, (CF3)2-cH-O-CF2H

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Introduced in 1990. Agent of choice in paediatric patients because of its faster induction & recovery.

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Sevoflurane
Physical Properties ` Relatively low solubility ` non-pungent makes it an excellent choice for inhalational induction.

Sevoflurane
Organ System Effects Cardiovascular ` mild negative inotrope ` little or no tachycardia ` so cardiac output not as well maintained as with isoflurane or desflurane

Sevoflurane
Respiratory ` depresses respiration
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bronchodilator

Sevoflurane
CNS
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slightly increases CBF and ICP decreases CMRO2

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Sevoflurane

Biotransformation and Toxicity
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rate of metabolism - 5% (ten times that of isoflurane) Compound A is a metabolic product with soda lime, which is nephrotoxic.

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Sevoflurane
Contraindications ` Malignant hyperthermia susceptibility
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Hypovolemia Elevated ICP

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Desflurane, CF3-CFH-O-CF2H
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Introduced in 1992.

Physical Properties -boils at room temperature at altitudes

high

Desflurane
Physical Properties
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low solubility permits rapid changes in partial pressure in alevoli and brain. Thus rapid induction and recovery. pungent and irritating to the airway

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Desflurane

Organ System Effects
Cardiovascular
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similar to isoflurane (but does NOT increase coronary artery blood flow) cardiac output only slightly depressed rapid increase in alevolar partial pressure -> pronounced tachycardia and hypertension

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Desflurane
Respiratory ` fast, shallow breathing ` Increased salivation ` airway irritation
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breath-holding coughing laryngospasm

Desflurane
CNS
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cerebral vasodilator, increases CBF and ICP marked decrease in CMRO2

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Desflurane

Biotransformation and Toxicity
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minimal metabolism in vivo degraded (more than other agents) to carbon monoxide by carbon dioxide absorbent especially with barium hydroxide lime ( prolong use with barium hydroxide can lead to CO poisoning)

Desflurane
Contraindication ` Intracranial hypertension
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malignant hyperthermia susceptibility hypovolemia

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Enflurane, CFClH-CF2-O-CF2H
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Introduced in 1966.

Physical Properties ` halogenated ether
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mild, sweet,ethereal oder

Enflurane
Organ System Effects Cardiovascular ` negative cardiac inotrope ` lowers cardiac output, arterial blood pressure, myocardial oxygen consumption ` heart rate usual increases

Enflurane
Respiratory
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rapid, shallow breathing with increased PaCO2 abolishes hypoxic drive bronchodilator depresses mucocillary function marked respiratory depression so that at 1 MAC, paCO2 = 60 mmHg

Enflurane
CNS ` increases CBF and ICP ` increases CSF secretion ` deep enflurane aneshthesia -> EEG spike-and-wave pattern -> tonic-clonic seizures.

Enflurane
Biotransformation and Toxicity
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fluoride is produced, which causes mild reduction in renal concentrating ability

Enflurane
Contraindications/Pre-cautions ` malignant hyperthermia susceptibility ` preexisting kidney disease

` seizure
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disorder

intracranial hypertension

STAGES OF ANAESTHESIA
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Described by Arthur Guedel. He described it for Ether. All stages are not seen in modern anaesthesia where combination of inhalation and intravenous agents are used.

STAGES OF ANAESTHESIA
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Stage I (ANALGESIA): Analgesia to loss of

consiousness

Respiration: Rhythm- Irregular volume- Small Pupil: Size- Small Position- Divergent Reflexes depressed: Nil

STAGES OF ANAESTHESIA
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Stage II (EXCITEMENT): Loss of

consciousness to rhythmical respiration Respiration: Rhythm- Irregular Volume- Large Pupil: Size- Large Position- Divergent Reflexes depressed: Eyelash, Eyelid

STAGES OF ANAESTHESIA
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Stage III (Surgical anaesthesia):

Plane 1- Rhythmical respiration to cessation of eye movement Respiration: Rhythm- Regular volume- Large Pupil: Size- Small Position- Divergent Reflexes depressed: Skin, Vomiting, Conjunctival, Pharyngeal.

STAGES OF ANAESTHESIA
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Stage III:

Plane 2: Cessation of eye movement to start of respiratory muscle paresis (excl.diaphragm) Respiration: Rhythm- regular Volume- medium Pupil: Size- ½ dilated Position- fixed centrally Reflexes depressed: Corneal

STAGES OF ANAESTHESIA
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Stage III:
Respiration: Rhythm- regular pause after expiration Volume- medium Pupil: Size- 3\4 dilated Position- fixed centrally Reflexes depressed: Laryngeal, Peritoneal.

Plane 3: Respiratory muscle paresis to paralysis

STAGES OF ANAESTHESIA
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Stage III:
Respiration: Rhythm-Jerky, Irregular, Quick inspiration, prolonged expiration i.e. ´See-sawµ Volume- Small Pupil: Size- fully dilated Position- fixed centrally Reflexes depressed: Anal sphincter, Carinal

Plane 4: Diaphragmatic paresis to paralysis

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Stage IV: (Apnoea)

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