Inhalation Anaesthetic.Sy

8/6/2019 Inhalation Anaesthetic.Sy

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SUSHEEL YESHALA


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HISTORY OF INHALATIONAL

ANAESTHETICS

` 1800 Humphry Davy described analgesiceffect of Nitrous oxide.

` 1824 Henry Hill Hickman described

anaesthesia using an inhaled substance(CO2).

` 1846 WTG Morton did successful publicdemonstration of anaesthesia using Ether.

` 1846- James Young Simpson usedChloroform.


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HISTORY OF INHALATIONAL

ANAESTHETICS

` 1930 Cyclopropane.` 1956 Halothane.

` 1966 Enflurane.

` 1968 Isoflurane.

` 1990 Sevoflurane.

` 1992 Desflurane.


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Properties of an ideal inhalationanaesthetic

` 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.


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Properties of an ideal inhalationanaesthetic` 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,N

o organ specific toxicity.


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Nitrous Oxide, N2O ("Laughing Gas")

Physical Properties` colorless` odorless` Non-inflammable but, like O

2

, supportscombustion

` gas at room temp and ambient pressure; liquidunder pressure

` Only inorganic gas used in modernanaesthestic practice.


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Nitrous Oxide

Cardiovascular

` direct myocardial depressant effect balancedby sympathetic nervous system stimulation socardio stable in normal person.

` myocardial depression may be unmasked by- Coronary artery disease.- hypovolemia

` pulmonary vasoconstriction -> increasedpulmonary vascular resistance.


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Nitrous OxideRespiratory` tachypnea + decreased tidal volume = stable

minute volume and PaCO2

` BEWARE: inhibits carotid body hypoxic drive( potent respiratory depressant).

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


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Biotransformation and Toxicity` eliminated mainly by exhalation`

` 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


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Nitrous Oxide

Controversial:` Emetogenic

` Teratogenic (maybe not, but better avoided inearly pregnancy)


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Nitrous Oxide

Contraindications35 times more soluble in blood than nitrogen..So fills and expands any air-containingcavities:

` air embolism

` pneumothorax

` intracranial air


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Nitrous Oxide

Contraindications` lung cysts

`

intraocular air bubbles

` Tympanoplasty

` pulmonary hypertension


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Halothane, CF3-CHBrCl

` Introduced in 1956` Most commonly used in India

` cost-effective


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Halothane

Physical Properties` halogenated ethane

` spontaneous oxidative decomposition on exposureto light

` retarded by

-thymol preservative

-amber-colored bottle


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Halothane

Organ System Effects:

Cardiovascular-

` direct myocardial depressant

` depresses cardiac output and lowers arterialBP

` depresses myocardial O2 demand


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Halothane

` depresses SA-node function- bradycardia.

- AV nodal rhythm.

` depresses baroreceptor reflex

` enhances myocardial sensitivity to thedysrhythmogenic effects of epinephrine.


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Halothane

Respiratory` fast, shallow breathing.

` Increased PaCO2

` severe depression of hypoxic ventilatorydrive

`

potent bronchodilator

` depresses mucociliary function.


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Halothane

CNS` cerebral vasodilator`

` increases CBF, ICP

` Decreases CMRO2.

` blunts cerebrovascular autoregulation


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Halothane

Biotransformation and Toxicity

` Mainly eliminated by exhalation but 20-30% isoxidized in liver by cytochrome P-450 enzyme

system to trifluroacetic acid.

` In the absence of O2, hepatotoxic reductionproducts may arise.


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Halothane

Halothane hepatitis

` extremely rare (1:35,000 cases). {Diagnosis byexclusion}

` factors that increase risk:-multiple exposures to halothane over a

short interval-middle-aged, obese women-familial predisposition-personal history of toxicity


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Halothane

Halothane hepatitis

` centrilobular necrosis

` antibody that binds to halothane-exposedhepatocytes.


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Isoflurane, CF3CHCl-O-CF2H

` Introduced in 1981.

` One of the most commonly administered volatileanesthetic today.


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Isoflurane

Physical Properties

` pungent ethereal odour

` chemical isomer of enflurane


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Isoflurane

Organ System EffectsCardiovascular` minimal cardiac depression

` carotid baroreflexes relatively intact

` heart rate increases 10-20%.


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Isoflurane

` dilates coronary arteriesseveral large studies failed to show

convincing evidence of clinically

significant coronary steal syndrome


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Isoflurane

Respiratory` tachypnea, but less pronounced

` blunts hypoxic drive

` bronchodilator


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Isoflurane

CNS` increases CBF and ICP

` decreases CMRO2


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Isoflurane

Hepatic

` hepatic oxgenation maintained better than withhalothane or enflurane


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Isoflurane


` minor part is metabolized (principally totrifluoroacetic acid)


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Isoflurane

Contraindications` malignant hyperthermia susceptibility

` severe hypovolemia

` Coronary artery disease (?)


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


` Agent of choice in paediatric patients becauseof its faster induction & recovery.


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Sevoflurane

Organ System EffectsCardiovascular

` mild negative inotrope

` little or no tachycardia

` so cardiac output not as well maintained as withisoflurane or desflurane


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Sevoflurane

Respiratory` depresses respiration

` bronchodilator


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Sevoflurane

CNS

` slightly increases CBF and ICP

` decreases CMRO2


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Sevoflurane


` rate of metabolism - 5% (ten times that of

isoflurane)

` Compound A is a metabolic product with sodalime, which is nephrotoxic.


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Sevoflurane

Contraindications` Malignant hyperthermia susceptibility

` Hypovolemia

` Elevated ICP


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Desflurane, CF3-CFH-O-CF2H


Physical Properties

-boils at room temperature at highaltitudes


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Desflurane

Physical Properties

` low solubility permits rapid changes in partialpressure in alevoli and brain. Thus rapid induction

and recovery.

` pungent and irritating to the airway


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Desflurane

Organ System EffectsCardiovascular` 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` breath-holding

` coughing

` laryngospasm


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Desflurane

CNS

` cerebral vasodilator, increases CBF and ICP

` marked decrease in CMRO2


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Desflurane

Biotransformation and Toxicity` minimal metabolism in vivo

` degraded (more than other agents) tocarbon monoxide by carbon dioxideabsorbent especially with barium hydroxidelime ( prolong use with barium hydroxidecan lead to CO poisoning)


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Desflurane

Contraindication` Intracranial hypertension

` malignant hyperthermia susceptibility

` hypovolemia


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

Physical Properties

` halogenated ether

` mild, sweet,ethereal oder


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Enflurane

Organ System EffectsCardiovascular

` negative cardiac inotrope

` lowers cardiac output, arterial blood pressure,

myocardial oxygen consumption` heart rate usual increases


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Enflurane

Respiratory

` rapid, shallow breathing with increased PaCO2` abolishes hypoxic drive

` bronchodilator` depresses mucocillary function` marked respiratory depression so that at 1

MAC, paCO2 = 60 mmHg


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Enflurane

CNS` increases CBF and ICP

` increases CSF secretion

` deep enflurane aneshthesia ->EEG spike-and-wave

pattern -> tonic-clonic seizures.


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Enflurane

Contraindications/Pre-cautions` malignant hyperthermia susceptibility

` preexisting kidney disease

`

seizure disorder` intracranial hypertension


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STAGES OFANAESTHESIA

` Stage II (EXCITEMENT): Loss ofconsciousness to rhythmical respiration

Respiration: Rhythm- IrregularVolume- Large

Pupil: Size- LargePosition- Divergent

Reflexes depressed: Eyelash, Eyelid


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`

Stage III (Surgical anaesthesia):Plane 1- Rhythmical respiration to cessation ofeye movement

Respiration: Rhythm- Regularvolume- LargePupil: Size- Small

Position- Divergent

Reflexes depressed: Skin, Vomiting,Conjunctival, Pharyngeal.


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` Stage III:Plane 3: Respiratory muscle paresis to paralysis

Respiration: Rhythm- regularpause after expiration

Volume- medium

Pupil: Size- 3\4 dilated

Position- fixed centrally

Reflexes depressed: Laryngeal, Peritoneal.


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`

Stage III:Plane 4: Diaphragmatic paresis to paralysis

Respiration: Rhythm-Jerky, Irregular, Quickinspiration, prolonged expiration i.e. See-saw

Volume- Small

Pupil: Size- fully dilatedPosition- fixed centrally

Reflexes depressed: Anal sphincter, Carinal

` Stage IV: (Apnoea)


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