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General Anesthesia
Dr. Amany Mohamed
Dr. Engy Reda
Dr. Rana Hassan
Doaa Mahmoud Othman
Id 201817210
GENERAL ANESTHESIA :
- Is a state characterized by unconsciousness, analgesia, amnesia,
skeletal muscle relaxation, and loss of reflexes
- Drugs used as general anesthetics are CNS depressants with
actions that can be induced and terminated more rapidly than
those of conventional sedative-hypnotics
Triad of General anesthesia
Mechanism of action of general anesthesia
1- Old theory the anesthetic agent bind with lipid matrix of the
nerve membrane , this lead to secondary changes in ion flux and
interaction with membrane of the ligand – gated ion channel .
2- Facilitation GABA receptor function.
3- Antagonize the action of the excitatory neurotransmitter
glutamic acid on the N-methyl-aspartate (NMDA) receptor.
4- Causes membrane hyperpolarization (inhibitory action) by
their activation of potassium channel.
5- Anesthetic decease the duration of opening nicotinic receptor
– an action that decrease the excitatory effect of acetylcholine
synapse
Classic Stages of Anesthesia
Stage 1: Analgesia
decreased awareness of pain, amnesia ,without loss of consciousness
Stage 2 : excitation
delirium & excitation, enhanced reflexes, retching, incontinence,
irregular respiration
Stage 3: Surgical Anesthesia
unconscious, no pain reflexes, regular respiration, BP is maintained
Stage 4: Medullary Depression
respiratory & CV depression requiring ventilation & pharmacologic
support.* Seen mainly with Ether. Not all stages are observed with
modern GAs.
Pre-anesthetic medication
General anesthesia usually involves the administration of
different drugs for premedication, induction of anesthesia
and maintenance of anesthesia
Premedication has two main aims:
1- The prevention of the parasympathomimetic effect of
anesthesia (bradicardia, brochial secretion)
2- The reduction of anxiety or pain
Pre-anesthetic medication
It is the use of drugs prior to anesthesia to make it more safe and
pleasant.
To relieve anxiety – benzodiazepines.
To prevent allergic reactions – antihistaminics.
To prevent nausea and vomiting – antiemetics.
To provide analgesia – opioids.
To prevent Bradycardia and secretion – atropine.
The aim is to relieve apprehension and facilitate smooth induction.
To supplement analgesic, amnesic action of anesthetics.To prevent
bradycardia and secretion.
Phases of Anesthesia
1) Induction: putting the patient to sleep
2) Maintenance: keeping the patient asleep
3) Recovery: waking the patient up
Classification of general anaesthesia
Inhaled Anesthetics
Easily vaporized liquid halogenated
hydrocarbons
Administered as gases .
Properties of Inhaled
anesthetics
Nitrous Oxide (N2O) laughing gas
Good analgesia
Weak anesthesia
Less effect on respiratory and cardiovascular
system.
Rapid onset & recover
Used along w/ other anesthetic; fast induction &
recovery
Properties of Inhaled
anesthetics
Enflurane
- Rapid induction and recovery
- Used for maintenance of anesthesia
- Less potent than halothen
- good muscle relaxation
- less sanitization to the myocardium -
- Metabolize into fluoride ion
- Decrease BP
Parenteral Anesthetics (IV)
Most commonly used drugs to induce anesthesia
Barbiturates (Thiopental* & Methohexital)
Benzodiazepines (Midazolam)
Opioids (Morphine & Fentanyl)
Propofol
*Etomidate
Ketamin
Ketamine
A “dissociative anesthetic”
Characterized by:
analgesia, amnesia, eyes open, involuntary limb
movement,.(unconscious appear to be awake)
Rapid onset and last for5-10 min.(short acting)
It is bind to NMDA (N-methyl-D-aspartate receptor )
and also stimulate the central sympathetic outflow
which cause heart stimulation, increased blood
pressure and cardiac output.
Mechanism of action
Used in children & young adults for short
procedures
Side Effects:
1-salivation,
2-hallucinations
3- & vivid dreams(adult)
4- stimulation of sympathetic nervous system
cause tachycardia, increase blood pressure
5- reach to stage two of anesthesia only
Ketamine
 It is used in veterinary medicine for many diagnostic
and surgical procedures.
 It is α2 sympathomimetic agent, it act by activation
of central α2 receptors which will cause reduction or
depression in release of dopamine and
norepinphrine.
Xylazine
 CNS depression and sedation (30-90 min).
 Analgesia which last (15-30 min).
 Muscle relaxation.
 Emesis
 Hypotension and brady cardia
 Decreased respiratory rate.
recovery from effect usually takes 2-4 hr.
Pharmacological effects
The speed of induction of anesthetic effects
depends on several factors
1. Solubility
The more rapidly a drug equilibrates with the blood, the more quickly the
drug passes into the brain to produce anesthetic eflects
2.Inspired gas partial pressure
3.Ventilation rate
4. Pulmonary blood flow
5. Arteriovenous concentration gradient
A high partial pressure of the gas in the lungs results in more rapid
achievement of anesthetic levels in the blood.
The greater the ventilation, the, more rapid is the rise in alveolar and blood
partial presure of the agent and the onset of anesthesia
At high pulmonary blood flows, the gas partial pressure rises at a slower rate,
thus, the speed of onset of anesthesia is reduced. At low flow rates, onset is
faster.
General anathesia  (1).pptx

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General anathesia (1).pptx

  • 1. General Anesthesia Dr. Amany Mohamed Dr. Engy Reda Dr. Rana Hassan Doaa Mahmoud Othman Id 201817210
  • 2. GENERAL ANESTHESIA : - Is a state characterized by unconsciousness, analgesia, amnesia, skeletal muscle relaxation, and loss of reflexes - Drugs used as general anesthetics are CNS depressants with actions that can be induced and terminated more rapidly than those of conventional sedative-hypnotics
  • 3. Triad of General anesthesia
  • 4. Mechanism of action of general anesthesia 1- Old theory the anesthetic agent bind with lipid matrix of the nerve membrane , this lead to secondary changes in ion flux and interaction with membrane of the ligand – gated ion channel . 2- Facilitation GABA receptor function. 3- Antagonize the action of the excitatory neurotransmitter glutamic acid on the N-methyl-aspartate (NMDA) receptor. 4- Causes membrane hyperpolarization (inhibitory action) by their activation of potassium channel. 5- Anesthetic decease the duration of opening nicotinic receptor – an action that decrease the excitatory effect of acetylcholine synapse
  • 5. Classic Stages of Anesthesia Stage 1: Analgesia decreased awareness of pain, amnesia ,without loss of consciousness Stage 2 : excitation delirium & excitation, enhanced reflexes, retching, incontinence, irregular respiration Stage 3: Surgical Anesthesia unconscious, no pain reflexes, regular respiration, BP is maintained Stage 4: Medullary Depression respiratory & CV depression requiring ventilation & pharmacologic support.* Seen mainly with Ether. Not all stages are observed with modern GAs.
  • 6.
  • 7. Pre-anesthetic medication General anesthesia usually involves the administration of different drugs for premedication, induction of anesthesia and maintenance of anesthesia Premedication has two main aims: 1- The prevention of the parasympathomimetic effect of anesthesia (bradicardia, brochial secretion) 2- The reduction of anxiety or pain
  • 8. Pre-anesthetic medication It is the use of drugs prior to anesthesia to make it more safe and pleasant. To relieve anxiety – benzodiazepines. To prevent allergic reactions – antihistaminics. To prevent nausea and vomiting – antiemetics. To provide analgesia – opioids. To prevent Bradycardia and secretion – atropine. The aim is to relieve apprehension and facilitate smooth induction. To supplement analgesic, amnesic action of anesthetics.To prevent bradycardia and secretion.
  • 9. Phases of Anesthesia 1) Induction: putting the patient to sleep 2) Maintenance: keeping the patient asleep 3) Recovery: waking the patient up
  • 11. Inhaled Anesthetics Easily vaporized liquid halogenated hydrocarbons Administered as gases .
  • 12. Properties of Inhaled anesthetics Nitrous Oxide (N2O) laughing gas Good analgesia Weak anesthesia Less effect on respiratory and cardiovascular system. Rapid onset & recover Used along w/ other anesthetic; fast induction & recovery
  • 13. Properties of Inhaled anesthetics Enflurane - Rapid induction and recovery - Used for maintenance of anesthesia - Less potent than halothen - good muscle relaxation - less sanitization to the myocardium - - Metabolize into fluoride ion - Decrease BP
  • 14. Parenteral Anesthetics (IV) Most commonly used drugs to induce anesthesia Barbiturates (Thiopental* & Methohexital) Benzodiazepines (Midazolam) Opioids (Morphine & Fentanyl) Propofol *Etomidate Ketamin
  • 15. Ketamine A “dissociative anesthetic” Characterized by: analgesia, amnesia, eyes open, involuntary limb movement,.(unconscious appear to be awake) Rapid onset and last for5-10 min.(short acting)
  • 16. It is bind to NMDA (N-methyl-D-aspartate receptor ) and also stimulate the central sympathetic outflow which cause heart stimulation, increased blood pressure and cardiac output. Mechanism of action
  • 17. Used in children & young adults for short procedures Side Effects: 1-salivation, 2-hallucinations 3- & vivid dreams(adult) 4- stimulation of sympathetic nervous system cause tachycardia, increase blood pressure 5- reach to stage two of anesthesia only Ketamine
  • 18.  It is used in veterinary medicine for many diagnostic and surgical procedures.  It is α2 sympathomimetic agent, it act by activation of central α2 receptors which will cause reduction or depression in release of dopamine and norepinphrine. Xylazine
  • 19.  CNS depression and sedation (30-90 min).  Analgesia which last (15-30 min).  Muscle relaxation.  Emesis  Hypotension and brady cardia  Decreased respiratory rate. recovery from effect usually takes 2-4 hr. Pharmacological effects
  • 20. The speed of induction of anesthetic effects depends on several factors 1. Solubility The more rapidly a drug equilibrates with the blood, the more quickly the drug passes into the brain to produce anesthetic eflects 2.Inspired gas partial pressure 3.Ventilation rate 4. Pulmonary blood flow 5. Arteriovenous concentration gradient A high partial pressure of the gas in the lungs results in more rapid achievement of anesthetic levels in the blood. The greater the ventilation, the, more rapid is the rise in alveolar and blood partial presure of the agent and the onset of anesthesia At high pulmonary blood flows, the gas partial pressure rises at a slower rate, thus, the speed of onset of anesthesia is reduced. At low flow rates, onset is faster.