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PRESENTED BY:
HAFSA JAMIL
Facilitator :
Dr.Muhammad Asadullah
shahzad
Anesthesia
ANESTHESIA:
• Is a temporary state consisting of
unconsciousness, loss of memory, lack of pain,
and muscle relaxation.
• A patient under the effects of anesthesia is said
to be anesthetized.
• Types of Anesthesia
• Local anesthesia
• General anesthesia
Pre-Anesthetic Medication :
• Drugs administered before an anesthetic to decrease
anxiety and to obtain:
 Smoother induction.
 Maintenance.
 Emergence from anesthesia.
These drugs are
• Sedative hypnotic ::
• To subside worry and tension e.g Diazepam .
• Analgesics:
• For smooth induction and decrease post operative pain
e.g Morphine.
• Anticolinergic::
• To reduce bronchial secretion e.g Atropine .
• Antiemetics:
• To prevent nausea and vomiting e.g Promathiazine .
General Anesthesia:
•A drug that brings about a
reversible loss of sensation along
with the loss of consciousness .
8
General Anaesthesia (GA)
unconsciousness
amnesiaanalgesia.
• A variety of drugs are given
to the patient that have
different effects with the
overall aim of ensuring
unconsciousness, amnesia
and analgesia.
Stage I: Analgesia
decreased awareness of pain . Consciousness may be
impaired but not lost..
Stage II: Disinhibition
Excitatory stage, uncontrolled movement, irregular
breathing.
Goal is to move through this stage as rapidly as possible.
Stage III: Surgical anesthesia
return of regular respiration.
Loss of blink reflex, regular respiration . Surgical
procedures can be performed at this stage.
Stage IV: Medullary Depression
This is the stage between respiratory arrest and death due
to circulatory collapse..
Stages Of General Anesthesia
•CLASSIFICATION
General Anesthetics divide into 2 classes
Inhalation
Anesthetics
• Gasses or
Vapors
• Halogenated
Intravenous
Anesthetics
• Barbiturates
• Dissociative
• Opioids
• Benzodiazepines
Inhalation Anesthetics
• Nitrous oxide
• Cycloprapane
Gas
• Halothane
• Isoflurane
• Sevoflurane
• Enflurane
Halogenated
agents:
Intravenous Anesthesia:
• Thiopental
• Thiamylal
• MethohexitalBarbiturates
• Ketamine
Dissociative
agents
• Morphine
• Fentanyl
citrate
Opioids
• Midazolam
• Lorazepam
• Diazepam
Benzodiazipines
Mechanism of Action
• Interaction with protein receptors.
• Volatile A – increase GABA and Glycine.
( inhibitory neurotransmitters).
MECHANISM OF
ACTION :
MAC(minimum alveolar concentration)
•A measure of potency of
inhaled anesthetics.
.
Pharmacokinetics of Inhaled
Anesthetics
1. Amount that reaches the brain
Indicated by oil:gas ratio (lipid solubility)
2. Solubility of gas into blood
The lower the blood:gas ratio, the more anesthetics will arrive at
the brain
Rate of Entry into the Brain: Influence of Blood
and Lipid Solubility
General Actions of Inhaled Anesthetics
• Respiration
• Depressed respiration and response to CO2.
• Kidney
• Depression of renal blood flow and urine output.
• Muscle
• High enough concentrations will relax skeletal muscle.
Cont’
• Cardiovascular System
• Generalized reduction in arterial pressure and peripheral vascular
resistance.
• Isoflurane maintains CO and coronary function better than other
agents.
• Central Nervous System
• Increased cerebral blood flow and decreased cerebral metabolism.
Nitrous oxide
• Merits
• Rapid induction and
recovery
• No adverse effects on
circulation and
respiration
• Good analgesia
• Demerits
• Diffusion hypoxia
• Post operative nausea
and vomiting
• Ineffective anesthetic
alone.
• Inadequate muscle
relaxation
Nitrous Oxide
Halothane
• MERITS
• Non irritating
• Safe for children
• Can be given in
asthmatics.
• DEMERITS
• Weak analgesia and
inadequate muscle
relaxation.
• Hepatotoxicity
• CVS and respiratory
disturbances .
• Expensive
•Malignant hyperthermia (MH) is a
pharmacogenetic hypermetabolic
state of skeletal muscle induced in
susceptible individuals by
inhalational anesthetics and/or
succinylcholine (and maybe by
stress or exercise).
Malignant Hyperthermia
•Signs: tachycardia, hyperthermia,
muscle rigidity, sweating, arrhythmia.
•May be fatal.
•Treated with Dantrolene.
Malignant Hyperthermia
ENFLURANE
• Merits
• Rapid inhalation and
recovery .
• DEMERITS
• CNS excitation
• May cause seizures
ISOFLURANE
• Merits
• Rapid and smooth
anesthesia
• No hepatic/renal
toxicity
• Demerits
• Uterine relaxation
• Progressive regulatory
depression
Intravenous Anesthetics
• Most exert their actions by potentiating
GABAA receptor.
• GABAergic actions may be similar to
those of volatile anesthetics, but act at
different sites on receptor.
• Most decrease cerebral metabolism and intracranial
pressure.
• Most cause respiratory depression.
• May cause apnea after induction of anesthesia.
Organ Effects
•They cause cardiovascular
depression.
Cardiovascular Effects
Ketamine
• Merits
• Short acting
• Dissociative
anesthesia
• Can be used in
children
• Very good analgesic
• Demerits
• Post operative
hallucination
• Increase cerebral
blood flow
Propofol
• Merits
• Rapid and smooth
onset and recovery
• Reduce intracranial
pressure
• Demerits
• Poor analgesic
• Excreted through
kidney
Local Anaesthesia
• DEFINITION: Local anaesthesia is drug-induced
reversible local blockade of nerve conduction in a specific
part of the body that does not alter consciousness.
Prosperities of ideal LA
• Reversible action.
• Non-irritant.
• No allergic reaction.
• No systemic toxicity.
• Rapid onset of action.
• Sufficient duration of action.
• Potent.
• Stable in solutions.
• Not interfere with healing of tissue.
• Have a vasoconstrictor action or compatible with VC.
• Not expensive
Surface/topical
anesthesia
Local
infiltration
Peripheral
nerve block
Bier block (IV
regional
anesthesia)
Epidural
anesthesia
Spinal
anesthesia
Six Placement Sites
Esters vs Amides
• The ester linkage is more easily broken so the ester drugs
are less stable in solution and cannot be stored for as
long as amides.
• Amide anaesthetics are also heat-stable.
• The metabolism of most esters results in the production of
para-aminobenzoate (PABA) which is associated with
allergic reaction.
• Amides, in contrast, very rarely cause allergic
phenomena. For these reasons amides are now more
commonly used than esters.
The mechanism of action of local
anaesthetics
• Disruption of ion
channel function via
specific binding to
sodium channels,
holding them in an
inactive state.
• Disruption of ion
channel function by the
incorporation of local
anaesthetic molecules
into the cell membrane
.
• Small nerve fibres are more sensitive than large nerve
fibres
• Myelinated fibres are blocked before non-myelinated
fibres of the same diameter.
• Thus the loss of nerve function proceeds as loss of pain,
temperature, touch, proprioception, and then skeletal
muscle tone. This is why people may still feel touch but
not pain when using local anaesthesia.
Absorption and distribution
• Some of the drug will be absorbed into the systemic
circulation: how much will depend on the vascularity of the
area to which the drug has been applied.
• The distribution of the drug is influenced by the degree of
tissue and plasma protein binding of the drug. the more
protein bound the agent, the longer the duration of action
as free drug is more slowly made available for
metabolism.
Metabolism and excretion
• Esters (except cocaine) are broken down rapidly by
plasma esterases to inactive compounds and
consequently have a short half life. Cocaine is hydrolysed
in the liver. Ester metabolite excretion is renal.
• Amides are metabolised hepatically by amidases. This is
a slower process, hence their half-life is longer and they
can accumulate if given in repeated doses or by infusion.
Uses:
• Local anesthesia.
• Ventricular arrhythmia.
• Decrease haemodynamic response to tracheal intubation
also decrease cough.
• Treatment of epileptic fits.
Advantages of local anaesthesia
• Non inflammable.
• Excellent muscle relaxant effect.
• During local anesthesia the patient remains conscious.
• It requires less skilled nursing care as compared to other
anesthesia like general anesthesia.
• Maintains his own airway.
• Less pulmonary complication.s
• Aspiration of gastric contents unlikely.
• Less nausea and vomiting.
• Contracted bowel so helpful in abdominal and pelvic
surgery.
• Postoperative analgesia.
• There is reduction surgical stress.
• Earlier discharge for outpatients.
Advantage of using adrenaline:
•Epinephrine vasoconstricts arteries reducing bleeding and also
delays the resorption of lidocaine, almost doubling the duration of
anaesthesia.
•Bupivacaine has caused several deaths when the epidural
anaesthetic has been administered intravenously accidentally.
Adverse Effects
• CNS: excitation followed by
dépression (drowsiness to
unconsciousness and death due to
respiratory depression.
• Cardiovascular System: bradycardia,
heart block, vasodilation
(hypotension)
• Allergic reactions: allergic dermatitis
to anaphylaxis (rare, but occur most
often by ester-type drugs).
Causes :
• Accidental rapid
intravenous injection.
• Rapid absorption, such
as from a very vascular
site ie mucous
membranes.
• Overdose .
Factors reducing toxicity:
• Decide on the concentration of the local anaesthetic that
is required for the block to be performed. Calculate the
total volume of drug that is allowed according to the table
below.
Hope you all get it…

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Anesthesia

  • 1.
  • 2. PRESENTED BY: HAFSA JAMIL Facilitator : Dr.Muhammad Asadullah shahzad
  • 4. ANESTHESIA: • Is a temporary state consisting of unconsciousness, loss of memory, lack of pain, and muscle relaxation. • A patient under the effects of anesthesia is said to be anesthetized. • Types of Anesthesia • Local anesthesia • General anesthesia
  • 5. Pre-Anesthetic Medication : • Drugs administered before an anesthetic to decrease anxiety and to obtain:  Smoother induction.  Maintenance.  Emergence from anesthesia.
  • 6. These drugs are • Sedative hypnotic :: • To subside worry and tension e.g Diazepam . • Analgesics: • For smooth induction and decrease post operative pain e.g Morphine. • Anticolinergic:: • To reduce bronchial secretion e.g Atropine . • Antiemetics: • To prevent nausea and vomiting e.g Promathiazine .
  • 7. General Anesthesia: •A drug that brings about a reversible loss of sensation along with the loss of consciousness .
  • 8. 8 General Anaesthesia (GA) unconsciousness amnesiaanalgesia. • A variety of drugs are given to the patient that have different effects with the overall aim of ensuring unconsciousness, amnesia and analgesia.
  • 9. Stage I: Analgesia decreased awareness of pain . Consciousness may be impaired but not lost.. Stage II: Disinhibition Excitatory stage, uncontrolled movement, irregular breathing. Goal is to move through this stage as rapidly as possible. Stage III: Surgical anesthesia return of regular respiration. Loss of blink reflex, regular respiration . Surgical procedures can be performed at this stage. Stage IV: Medullary Depression This is the stage between respiratory arrest and death due to circulatory collapse.. Stages Of General Anesthesia
  • 11. General Anesthetics divide into 2 classes Inhalation Anesthetics • Gasses or Vapors • Halogenated Intravenous Anesthetics • Barbiturates • Dissociative • Opioids • Benzodiazepines
  • 12. Inhalation Anesthetics • Nitrous oxide • Cycloprapane Gas • Halothane • Isoflurane • Sevoflurane • Enflurane Halogenated agents:
  • 13. Intravenous Anesthesia: • Thiopental • Thiamylal • MethohexitalBarbiturates • Ketamine Dissociative agents
  • 14. • Morphine • Fentanyl citrate Opioids • Midazolam • Lorazepam • Diazepam Benzodiazipines
  • 15. Mechanism of Action • Interaction with protein receptors. • Volatile A – increase GABA and Glycine. ( inhibitory neurotransmitters).
  • 17. MAC(minimum alveolar concentration) •A measure of potency of inhaled anesthetics. .
  • 18. Pharmacokinetics of Inhaled Anesthetics 1. Amount that reaches the brain Indicated by oil:gas ratio (lipid solubility) 2. Solubility of gas into blood The lower the blood:gas ratio, the more anesthetics will arrive at the brain
  • 19. Rate of Entry into the Brain: Influence of Blood and Lipid Solubility
  • 20. General Actions of Inhaled Anesthetics • Respiration • Depressed respiration and response to CO2. • Kidney • Depression of renal blood flow and urine output. • Muscle • High enough concentrations will relax skeletal muscle.
  • 21. Cont’ • Cardiovascular System • Generalized reduction in arterial pressure and peripheral vascular resistance. • Isoflurane maintains CO and coronary function better than other agents. • Central Nervous System • Increased cerebral blood flow and decreased cerebral metabolism.
  • 22. Nitrous oxide • Merits • Rapid induction and recovery • No adverse effects on circulation and respiration • Good analgesia • Demerits • Diffusion hypoxia • Post operative nausea and vomiting • Ineffective anesthetic alone. • Inadequate muscle relaxation
  • 25. • MERITS • Non irritating • Safe for children • Can be given in asthmatics. • DEMERITS • Weak analgesia and inadequate muscle relaxation. • Hepatotoxicity • CVS and respiratory disturbances . • Expensive
  • 26. •Malignant hyperthermia (MH) is a pharmacogenetic hypermetabolic state of skeletal muscle induced in susceptible individuals by inhalational anesthetics and/or succinylcholine (and maybe by stress or exercise). Malignant Hyperthermia
  • 27. •Signs: tachycardia, hyperthermia, muscle rigidity, sweating, arrhythmia. •May be fatal. •Treated with Dantrolene. Malignant Hyperthermia
  • 28. ENFLURANE • Merits • Rapid inhalation and recovery . • DEMERITS • CNS excitation • May cause seizures
  • 29. ISOFLURANE • Merits • Rapid and smooth anesthesia • No hepatic/renal toxicity • Demerits • Uterine relaxation • Progressive regulatory depression
  • 30. Intravenous Anesthetics • Most exert their actions by potentiating GABAA receptor. • GABAergic actions may be similar to those of volatile anesthetics, but act at different sites on receptor.
  • 31. • Most decrease cerebral metabolism and intracranial pressure. • Most cause respiratory depression. • May cause apnea after induction of anesthesia. Organ Effects
  • 33. Ketamine • Merits • Short acting • Dissociative anesthesia • Can be used in children • Very good analgesic • Demerits • Post operative hallucination • Increase cerebral blood flow
  • 34. Propofol • Merits • Rapid and smooth onset and recovery • Reduce intracranial pressure • Demerits • Poor analgesic • Excreted through kidney
  • 35.
  • 36. Local Anaesthesia • DEFINITION: Local anaesthesia is drug-induced reversible local blockade of nerve conduction in a specific part of the body that does not alter consciousness.
  • 37. Prosperities of ideal LA • Reversible action. • Non-irritant. • No allergic reaction. • No systemic toxicity. • Rapid onset of action. • Sufficient duration of action. • Potent. • Stable in solutions. • Not interfere with healing of tissue. • Have a vasoconstrictor action or compatible with VC. • Not expensive
  • 38.
  • 39. Surface/topical anesthesia Local infiltration Peripheral nerve block Bier block (IV regional anesthesia) Epidural anesthesia Spinal anesthesia Six Placement Sites
  • 40. Esters vs Amides • The ester linkage is more easily broken so the ester drugs are less stable in solution and cannot be stored for as long as amides. • Amide anaesthetics are also heat-stable. • The metabolism of most esters results in the production of para-aminobenzoate (PABA) which is associated with allergic reaction. • Amides, in contrast, very rarely cause allergic phenomena. For these reasons amides are now more commonly used than esters.
  • 41. The mechanism of action of local anaesthetics • Disruption of ion channel function via specific binding to sodium channels, holding them in an inactive state. • Disruption of ion channel function by the incorporation of local anaesthetic molecules into the cell membrane .
  • 42. • Small nerve fibres are more sensitive than large nerve fibres • Myelinated fibres are blocked before non-myelinated fibres of the same diameter. • Thus the loss of nerve function proceeds as loss of pain, temperature, touch, proprioception, and then skeletal muscle tone. This is why people may still feel touch but not pain when using local anaesthesia.
  • 43. Absorption and distribution • Some of the drug will be absorbed into the systemic circulation: how much will depend on the vascularity of the area to which the drug has been applied. • The distribution of the drug is influenced by the degree of tissue and plasma protein binding of the drug. the more protein bound the agent, the longer the duration of action as free drug is more slowly made available for metabolism.
  • 44. Metabolism and excretion • Esters (except cocaine) are broken down rapidly by plasma esterases to inactive compounds and consequently have a short half life. Cocaine is hydrolysed in the liver. Ester metabolite excretion is renal. • Amides are metabolised hepatically by amidases. This is a slower process, hence their half-life is longer and they can accumulate if given in repeated doses or by infusion.
  • 45. Uses: • Local anesthesia. • Ventricular arrhythmia. • Decrease haemodynamic response to tracheal intubation also decrease cough. • Treatment of epileptic fits.
  • 46. Advantages of local anaesthesia • Non inflammable. • Excellent muscle relaxant effect. • During local anesthesia the patient remains conscious. • It requires less skilled nursing care as compared to other anesthesia like general anesthesia. • Maintains his own airway.
  • 47. • Less pulmonary complication.s • Aspiration of gastric contents unlikely. • Less nausea and vomiting. • Contracted bowel so helpful in abdominal and pelvic surgery. • Postoperative analgesia. • There is reduction surgical stress. • Earlier discharge for outpatients.
  • 48. Advantage of using adrenaline: •Epinephrine vasoconstricts arteries reducing bleeding and also delays the resorption of lidocaine, almost doubling the duration of anaesthesia. •Bupivacaine has caused several deaths when the epidural anaesthetic has been administered intravenously accidentally.
  • 49. Adverse Effects • CNS: excitation followed by dépression (drowsiness to unconsciousness and death due to respiratory depression. • Cardiovascular System: bradycardia, heart block, vasodilation (hypotension) • Allergic reactions: allergic dermatitis to anaphylaxis (rare, but occur most often by ester-type drugs).
  • 50. Causes : • Accidental rapid intravenous injection. • Rapid absorption, such as from a very vascular site ie mucous membranes. • Overdose .
  • 51. Factors reducing toxicity: • Decide on the concentration of the local anaesthetic that is required for the block to be performed. Calculate the total volume of drug that is allowed according to the table below.
  • 52.
  • 53. Hope you all get it…