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INHALATION ANESTHETICS. Prof. Ayman Hussein Kahla Prof. of Anesthesia Technology Public Health & Health Informatics Faculty UMM ALQURA UNIVERSITY. Anesthesia.

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Inhalation anesthetics

INHALATION ANESTHETICS

Prof. Ayman Hussein Kahla

Prof. of Anesthesia Technology

Public Health & Health Informatics Faculty

UMM ALQURA UNIVERSITY


Anesthesia
Anesthesia

  • A state of temporary & reversible loss of awareness and reflex reactions induced by drugs to render surgery painless, possible & comfortable.

  • General anesthesia for surgical procedure to render the patient unaware / unresponsive to the painful stimuli.


Receptor theory of anesthesia
Receptor Theory of Anesthesia

  • GABA: major inhibitory neurotransmitter (point of action of anesthetic drugs)

  • Membrane structure and function: future of the anesthesiology

  • Glutamate: major excitatory neurotransmitter

  • Endorphins: analgesia.

  • Unitary hypothesis of the inhalation agents.


Mechanism of action
MECHANISM OF ACTION

  • Act in different ways at the level of the central nervous system.

  • Disrupt normal synaptic transmission

    - interfering with release of neurotransmitters from pre-synaptic nerve terminal (enhance or depress excitatory or inhibitory transmission).

    - altering re-uptake of neurotransmitters,

    - Changing the binding of neurotransmitters to the post-synaptic receptor sites or

    - Influencing the ionic conductance change that follows activation of the post-synaptic receptor by neurotransmitters.


Inhalation anesthetics

  • Meyer-Overton Theory postulates that it is the number of molecules dissolved in the lipid cell membrane.

  • Protein Receptor Hypothesis postulates that protein receptors in the central nervous system.

  • Activation of GABA receptors.

  • may inhibit certain calcium channels and therefore prevent the release of neurotransmitters and inhibit glutamate channels.


Inhalation anesthetic agents
Inhalation Anesthetic Agents

  • Nitrous oxide

  • Halothane (Fluothane)

  • Methoxyflurane (Penthrane)

  • Enflurane (Ethrane)

  • Isoflurane (Forane)

  • Desflurane (Suprane)

  • Sevoflurane (Ultane)



Inhalation anesthetics

F H

F – C – C* – Br

F Cl

F F F

Cl – C* – C – O – C – H

H F F

N=N=O

Nitrous Oxide

Halothane

Enflurane

F F H H

C

F C O C F

F C H

F F

F H F

F – C – C* – O – C – H

F F F

F H F

F– C – C* – O – C – H

F Cl F

Desflurane

Sevoflurane

Isoflurane


Obsolete v olatile anesthetics
Obsolete Volatile Anesthetics

- Aliflurane - Chloroform

- Cyclopropane - Diethyl ether

- Enflurane - Ethylene

- Halothane - Methoxyflurane

- Methoxypropane - Roflurane

- Teflurane - Trichloroethylene

- Vinyl ether


Definition
DEFINITION

  • It is a chemical compound possessing general anesthetic properties that can be delivered via inhalation.

  • They are administered by anesthetists (anesthesiologists, nurse anesthetists, and anesthesiologist assistants) through an anesthesia mask, LMA or ETT connected to some type of anesthetic vaporizer and an anesthetic delivery system.


Inhalational anesthetic agents
Inhalational Anesthetic Agents

  • Inhalational anesthesia refers to the delivery of gases or vapors from the respiratory system to produce anesthesia

  • Pharmacokinetics-- uptake, distribution, and elimination from the body.

  • Pharmacodyamics- MAC value.


Inhalation anesthetics


History of anesthesia
History of Anesthesia induction of anesthesia.

  • 1845 - Horace Wells- N2O

  • 1846 - William Morton- Ether

  • 1847 - Simpson- Chloroform

  • 1934 - Cyclopropane

  • 1956 - Halothane


Pharmacokinetics and p harmacodymanics
Pharmacokinetics and induction of anesthesia.Pharmacodymanics

  • Pharmacokinetics: how the body affects the drug

  • Pharmacodymanics: how the drugs affects the body


A nesthetic u ptake
A induction of anesthesia.nesthetic Uptake

  • Solubility in blood

  • Alveolar blood flow

  • Differences in partial pressure between alveolar gas and venous blood

  • Therefore: low output states predispose patients to overdosage of the soluble agents


Elimination
ELIMINATION induction of anesthesia.

  • Biotransformation: cytochrome P- 450 (specifically CYP 2EI)

  • Transcutaneous loss or exhalation

  • Alveolus is the most important in elimination of the inhalation agents

  • Diffusion hypoxia” and the nitrous oxide


Elimination1
Elimination induction of anesthesia.

  • Redistribution from brain to blood to air

  • Anesthetics that are relatively insoluble in blood and brain are eliminated faster


Pharmacokinetics
Pharmacokinetics induction of anesthesia.

  • The concentration of a gas in a mixture of gases is proportional to the partial pressure.

  • Inverse relationship between blood : gas solubility and rate of induction.


Pharmacokinetics1
Pharmacokinetics induction of anesthesia.

  • Increase in inspired anesthetic concentration will increase rate of induction

  • Direct relationship between ventilation rate and induction rate

  • Inverse relationship between blood flow to lungs and rate of onset

  • MAC = minimum concentration in alveoli needed to eliminate pain response in 50% of patients


Hallmark of anesthesia
Hallmark of induction of anesthesia.Anesthesia

  • Amnesia / Unconsciousness

  • Analgesia

  • Muscle relaxation


Basic principles of anesthesia
Basic Principles of Anesthesia induction of anesthesia.

  • Anesthesia defined as the abolition of sensation

  • Analgesia defined as the abolition of pain

    “Triad of General Anesthesia”

    • Need for Unconsciousness

    • Need for Analgesia

    • Need for Muscle relaxation


Stages of anesthesia
STAGES OF ANESTHESIA induction of anesthesia.

  • Stage I : Analgesia

  • Stage II : Excitement, combative

    behavior – dangerous state

  • Stage III : Surgical anesthesia

  • Stage IV : Medullary paralysis – respiratory and vasomotor control ceases.


Inhalation anesthetics

  • Anesthetics induction of anesthesia.are associated with

    - Decrease in systemic blood pressure – myocardial depression and direct vasodilatation.

    - Blunting of baroreceptor control and decreased central sympathetic tone.


Side effects
Side induction of anesthesia.Effects

  • Reduce metabolic rate of the brain

  • Decrease cerebral vascular resistance thus increasing cerebral blood flow = increase in intracranial pressure



Inhalation anesthetics

  • The induction of anesthesia.important characteristics of Inhalational anesthetics which govern the anesthesia are :

  • Solubility in the blood

    (blood : gas partition co-efficient)

  • Solubility in the fat (oil : gas partition co-efficient)


Inhalation anesthetics

Agents with low solubility in blood quickly saturate the blood. The additional anesthetic molecules are then readily transferred to the brain.

BLOOD GAS PARTITION COEFFICIENT



Inhalation anesthetics

OIL GAS PARTITION CO-EFFICIENT and recovery

Higher the Oil: Gas Partition Co-efficient lower the MAC . E.g., Halothane

0.8

1.4

220


Inhalation anesthetics

  • Oil and recovery: gas partition co-efficient:

  • It is a measure of lipid solubility.

  • Lipid solubility - correlates strongly with the potency of the anesthetic.

  • Higher the lipid solubility – potent anesthetic. e.g., halothane


Ideal inhaled a nesthetic
Ideal Inhaled and recoveryAnesthetic

  • Pleasant odor

  • Non-irritant

  • Low blood gas solubility.

  • Chemically stable.

  • Non inflammable.

  • Potent.

  • Inert.

  • Not metabolized.

  • Non-toxic.

  • Analgesic.

  • No Cardiovascular & respiratory depression.


Minimal alveolar concentration mac
Minimal and recoveryAlveolar Concentration (MAC)

  • Concentration of inhaled anaesthetics in the alveolar gasthat prevents movements in 50% of patients in response to a standardized stimulus (eg surgical incision)

  • MAC is important to compare the potencies of various inhalational anesthetic agents.

  • 1.2-1.3 MAC prevent movement in 95% of patients.


Inhalation anesthetics
MAC and recovery

  • MAC value is a measure of inhalational anesthetic potency.

  • It is defined as the minimum alveolar anesthetic concentration ( % of the inspired air) at which 50% of patients do not respond to a surgical stimulus.

  • MAC values are additive and lower in the presence of opioids.


Mac types
MAC TYPES and recovery

  • MAC awake:MAC allowing voluntary response to command in 50% of patients

  • MAC 95%: MAC that prevents movement in 95 % of patients

  • MAC intubation:MAC that allows intubation without muscle relaxant, coughing or bucking in 50% of patients.

  • MAC-BAR(1.7-2.0 MAC), which is the concentration required to block autonomic reflexes to nociceptive stimuli.


Increase mac
Increase MAC and recovery

  • Hyperthermia.

  • Chronic drug abuse (Ethanol).

  • Acute use of amphetamines.

  • Hyperthyroidism.

  • Reducing age.


Decrease mac
Decrease and recoveryMAC

  • Increasing Age.

  • Hypothermia.

  • Other anesthetic (Opioids).

  • Acute drug intoxication (Ethanol).

  • Pregnancy.

  • Hypothyroidism.

  • Other drugs ( Clonidine ,Reserpine).


No effect on mac
No Effect on MAC and recovery

  • Gender

  • Duration of anesthesia

  • Carbon dioxide tension (21-95 mmHg)

  • Metabolic Acid base status

  • Hypertension

  • Hyperkalemia


Inhalation anesthetics
MAC and recovery

  • N2O = 105%

  • Halothane = 0.75%

  • Isoflurane = 1.15%

  • Euflurane = 1.68%

  • Sevoflurane = 2%

  • Deslurane = 6%

  • N2O alone is unable to produce adequate anesthesia ( require high conc. )


Inhalational agent reaches the alveoli
Inhalational Agent Reaches The Alveoli and recovery

  • Increasing the delivered concentrations of anesthetic

  • The gas flow rate through the anesthetic machine

  • Increasing minute ventilation

    MV = Respiratory Rate × Tidal volume


Inhalational agent reaches the brain
Inhalational and recoveryAgent Reaches The Brain

  • The rate of blood flow to the brain

  • The solubility of the inhalational agent in the brain

  • The difference in the arterial and venous concentration of the inhalational agent


Inspiratory concentration fi
Inspiratory Concentration (Fi) and recovery

  • Increase FGF rate.

  • Decrease Breathing System Volume.

  • Decrease absorption of the breathing system of the anesthetic machine.

  • All closer inspired gas concentration to the fresh gas concentration.


Alveolar concentration fa
Alveolar Concentration (FA) and recovery

  • The greater uptake of an anesthetic agent; the lower rate of rise of FA

  • The greater difference between Fi and Fa; the slower the rate of induction

  • The higher the blood gas solubility coefficient; the greater the anesthetic solubility, and the slower the onset of induction and recovery.

  • Increased alveolar blood flow increases anesthetic uptake.


Inhalation anesthetics

  • Solubility in blood and recovery

  • Alveolar blood flow

  • Partial pressure difference between alveolar gas & venous blood (PA- PV)


Arterial concentration fa
Arterial Concentration ( and recoveryFa)

  • Mainly ventilation perfusion mismatching

  • Normally, alveolar and arterial anesthetic pressures are assumed to be equal.

  • Presence of ventilation perfusion mismatching increases alveolar arterial differences


Anesthetic delivery to alveoli
Anesthetic delivery to alveoli and recovery

  • Ventilation

  • Concentration

  • Apparatus Dead Space


Nitrous oxide
Nitrous oxide and recovery

  • Safest inhalational anesthetic.

  • Weak anesthetic but a good analgesic.

  • No toxic effect on the heart, liver and kidney.

  • Caution about diffusional hypoxia.

  • Megaloblastic anemia.


Nitrous oxide n 2 o
Nitrous Oxide (N and recovery2O)

Physical Property:

  • laughing

  • Not flammable

  • Odorless

  • Colorless

  • Tasteless


Nitrous oxide1
NITROUS OXIDE and recovery

  • Prepared by Priestly in 1776

  • Anesthetic properties described by Davy in 1799

  • Characterized by inert nature with minimal metabolism

  • Colorless, odorless, tasteless, and does not burn


Nitrous oxide2
NITROUS OXIDE and recovery

  • Simple linear compound

  • Not metabolized

  • Only anesthetic agent that is inorganic


Nitrous oxide systemic effects
Nitrous Oxide and recoverySystemic Effects

  • Minimal effects on heart rate and blood pressure

  • May cause myocardial depression in sick patients

  • Little effect on respiration

  • Safe, effective agent


Nitrous oxide side effects
Nitrous Oxide Side Effects and recovery

  • Manufacturing impurities toxic

  • Hypoxic mixtures can be used

  • Large volumes of gases can be used

  • Beginning of case: second gas effect

  • End of case: diffusion hypoxia


Nitrous oxide side effects1
Nitrous Oxide Side Effects and recovery

  • Major difference is low potency

  • MAC value is 105%

  • Weak anesthetic, powerful analgesic

  • Needs other agents for surgical anesthesia

  • Low blood solubility (quick recovery)


Nitrous oxide side effects2
Nitrous Oxide Side Effects and recovery

  • Inhibits methionine synthetase (precursor to DNA synthesis)

  • Inhibits vitamin B-12 metabolism

  • Dentists, OR personnel, abusers at risk


N 2 o pharmacology
N and recovery2O Pharmacology

  • Good Analgesic

  • Weak anesthetic

  • Excreted via lungs

  • MAC = 105%

  • Lower water solubility

  • Not Metabolized in the body


N 2 o side effects
N and recovery2O Side Effects

  • Diffusion Hypoxia.

  • Closed gas spaces (N2O can diffuse 20 times faster into closed spaces than it can be removed, resulting in expansion of pneumothorax, bowel gas, or air embolismor in an increase in pressure within noncompliant cavities such as thecraniumormiddle ear.

  • CVS depression

  • Toxicity

  • Teratogenic


Diffusion hypoxia
Diffusion and recoveryHypoxia

  • A decrease in PO2 usually observed as the patient is emerging from an inhalational anesthetic where N2O was a component.

  • The rapid outpouring of insoluble N2O can displace alveolar oxygen, resulting in hypoxia.

  • All patients should receive supplemental O2 at the end of an anesthetic and during the immediate recovery period.


Concentration effect
Concentration and recoveryEffect

Concentration effect states that with higher inspired concentrations of an anesthetic, the rate of rise in arterial tension is greater.


Second gas effect
Second and recoveryGas Effect

The ability of the large volume uptake of one gas (first gas) to accelerate the rate of rise of the alveolar partial pressure of a concurrently administered companion gas (second gas).


S econd gas effect
S and recoveryecond Gas Effect

Usually refers to nitrous oxide combined with an inhalational agent. Because nitrous oxide is not soluble in blood, its' rapid absorption from alveoli causes an abrupt rise in the alveolar concentration of the other inhalational anesthetic agent.


Halothane
Halothane and recovery

  • It is a potent anesthetic.

  • Induction is pleasant.

  • It sensitizes the heart to catecholamines.

  • It dilates bronchus – preferred in asthmatics.

  • It inhibits uterine contractions.

  • Halothane hepatitis and malignant hyperthermia can occur.


Enflurane
Enflurane and recovery

  • Sweet and ethereal odor.

  • Generally do not sensitizes the heart to catecholamines.

  • Seizures occurs at deeper levels –contraindicated in epileptics.

  • Caution in renal failure due to fluoride.