General Anesthesia
General Anesthesia Definition:The word
anaesthesia is derived from the Greek: meaning insensible or without feeling
Is the loss of response to & perception of all external stimuli.
General anaesthetics are the drugs which causes reversible loss of all the sensations and consciousness
Components of General Anesthesia:
1.Unconsciousness 2. Analgesia 3. Muscle relaxation
ROLE OF ROLE OF ANAESTHESIOLOGIST ANAESTHESIOLOGIST
So we can summarize the role of anaesthesiologist in:1. Knowing physiology of body well.2. Knowing the pathology of patient disease and co-existing
disease3. Study well the pharmacology of anaesthetic drugs and
other drugs which may be used intra-operatively.4. Use anaesthetics in the way and doses which is adequate to
patient condition and not modified by patient pathology with no drug toxicity.
5. Lastly but most importantly administrate drug to manipulate major organ system, to maintain homeostasis and protect patient from injury by surgeon or theatre conditions.
APPROACH TO APPROACH TO ANAESTHESIAANAESTHESIA
The empirical approach to anaesthetic drug administration consists of selecting an initial anaesthetic dose {or drug} and then titrating subsequent dose based on the clinical responses of patients, without reaching toxic doses.
The ability of anaesthesiologist to predict clinical response and hence to select optimal doses is the art of anaesthesia
Knowing physiology, pathology ,and pharmacology is not enough to communicate safe anesthesia
But there is need for two important tools:
1. Anaesthetic machine.
2. Monitoring system.
TOOLS OF TOOLS OF ANAESTHESIAANAESTHESIA
1. Oxygen gas supply.
2. Nitrous oxide gas supply.
3. Flow meter
4. Vaporizer specific for every agent
5. Mechanical ventilator
6. Tubes for connection.
ANAESTHETIC MACHINEANAESTHETIC MACHINE
1. Pulse, ECG
2. Blood pressure
3. Oxygen saturation.
4. End tidal CO2
5. Temperature
6. Urine output, CVP, EEG, bispectral index, muscle tone, ECHO, drug concentration.
MONITORINGMONITORING
Phases of Anesthesia
Induction: keeping the patient to sleep
Maintenance: keeping the patient asleep
Emergence: waking the patient up
STAGES OF GENERAL ANESTHESIA
STAGE 1 (Analgesia): From induction of anesthesia to loss of conciousness (loss of eyelid reflex). Pain is progressively abolished in this stage.
STAGE 2 (Delirium/Excitement): From loss of consiousness to beginning of regular respiration.Characterized by uninhibited excitation. Pupils are dilated and eyes divergent. Agitation, delirium, irregular respiration, and breatholding are commonly seen. Potentially dangerous responses can occur during this stage including vomiting, laryngospasm, HTN, tachycardia, and uncontrolled movement.
STAGE 3 (Surgical Anesthesia):
Regular respiration to caessation of spontaneous breathing
Central gaze, constricted pupils, and regular respirations. Target depth of anesthesia is sufficient when painful stimulation does not elicit somatic reflexes or deleterious autonomic reflexes.
Plane 1 From the return of regular respirations to the cessation of REM.
Plane 2 The Surgical Plane From the cessation of REM to the onset of
paresis of the intercostal muscles.
Plane 3 From the onset to the complete paralysis of the intercostal muscles.
Plane 4 From the paralysis of the intercostal of
this plane the patient will be apneic.
STAGE 4 (Impending Death/Overdose):
Onset of apnea, dilated and nonreactive pupils, and hypotension to complete circulatory failure.
Classic Stages of Anesthesia*
Stage 1: Analgesia
– decreased awareness of pain, amnesia Stage 2: Disinhibition
– 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.
Mechanisms of Action1. Enhanced GABA effect on GABAA Receptors
– Inhaled anesthetics - Etomidate– Barbiturates - Propofol– Benzodiazepines
2. Block nicotinic receptor subtypes (analgesia) – Moderate to high conc’s of inhaled anesthetics
3. Activate K channels (hyperpolarize )– Nitrous oxide, ketamine, xenon
4. Inhibit NMDA (glutamate) receptors – Nitrous oxide, ketamine, xenon, high dose barbiturates
5. Enhance glycine effect on glycine R’s (immobility)
Immobilization in response to surgical incision
(spinal cord)
Sedation, loss of consciousness (thalamic firing)
Amnesia (hippocampal neurotransmission)
Regional Effects
CLASSIFICATION
INTRAVENOUS
INDUCING AGENTSThiopentone sodium
MethohexitalPropofol
Etomidate
SLOWER ACTINGDiazepamLorazepamMidazolam
DISSOCIATIVE ANAESTHESIAKetamine
OPIOID ANALGESIAFentanyl
INHALATIONAL
GASNitrous oxide
LIQUIDEther
HalothaneEnfluraneDesfluraneSevoflurane
Parenteral Anesthetics (Intravenous)
Most commonly used drugs to induce anesthesia– Barbiturates (Thiopental* & Methohexital)– Benzodiazepines (Midazolam)– Opioids (Morphine & Fentanyl)– Propofol*– Etomidate
* Most commonly used for induction
Barbiturates & Benzodiazepines MOA:Barbiturate
BZDS
GABA
1) Both bind to GABAA
receptors, at different sites• Both cause increase Cl- influx in presence of GABA• BNZ binding can be blocked by flumazenil.
2) Barbs at high doses - are also GABA mimetic, block Na channels NMDA/glutamate R
CN
S E
ffec
ts
Increasing dose
Coma Barbiturates
Benzodiazepines
Hypnosis
Sedation, disinhibition, anxiolysis
Possible selective anticonvulsant & muscle-relaxing activity
Dose Response Relationships
Anesthesia
Medullary depression
Barbiturates
Thiopental & methohexital are highly lipid soluble & can produce unconsciousness & surgical anesthesia in <1 min.
Rx: induction of anesthesia & short procedures
Actions are terminated by redistribution
With single bolus - emergence from GA occurs in ~ 10 mins
Hepatic metabolism is required for elimination
Thiopental (3-5mg/kg)
Barbs are respiratory & circulatory depressants (Contraindicated: hypovolemia, cardiomyopathy, beta-blockade,etc.)
Psychomotor impairment may last for days after use of a single high dose
Taste of garlic prior to anesthesia
Potentially fatal attacks of porphyria in pts with a history of acute or intermittent porphyria.
Delay giving other drugs (e.g. NMJ blockers) until barb has cleared the i.v. line to avoid precipitation.
Propofol
Propofol is a diisopropylphenol intravenous hypnotic agent that produces rapid induction of anesthesia with minimal excitatory activity
It undergoes extensive distribution and rapid elimination by the liver
Propofol Produces anesthesia as rapidly as i.v. barb’s & but recovery is
more rapid than barb’s.
Recovery is not delayed after prolonged infusion (due to more rapid clearance).**
Patients are able to ambulate sooner & patients “feel better” in the post-op period compared to other i.v. anesthetics.
Antiemetic effects (pts w/ risk of nausea), marked hypotension (>barbs)
Commonly used as component of “balanced anesthesia” for maintenance of anesthesia following induction of anesthesia.
** More rapid discharge from the recovery room
INDICATIONS
Conscious sedation Induction agent of anesthesiaMaintenance of anesthesiaAntiemetic
DOSE AND ROUTES
Conscious sedation25 - 50 mg IV, Titrate slowly to desired effect(on set of slurred speech) Induction2 - 2.5 mg/kg IV, given slowly over 30seconds in 2 - 3 divided doses Maintenance25 - 50 mg IV bolusInfusion 100 - 200 mcg/kg/min Antiemetic10mg IV
ADVERSE REACTIONS, PRECAUTIONS, AND INTERACTIONS
Reduce doses in elderly, hypovolemic, high risk surgical patients and with use of narcotics and sedative hypnotics
Minimize pain by injecting into a large vein and/or mixing IV lidocaine (0.1 mg/kg) with the induction dose of Propofol
ADVERSE REACTIONS, PRECAUTIONS, AND INTERACTIONS
Not recommended for patient with increased intracranial pressure
Should be administered with caution to patients with a history of epilepsy or seizures disorder
Etomidate Rapid induction (~1 min), Short duration of action (3-5
mins)
Used as a supplement with nitrous oxide for short surgical procedures
Hypnotic, but not analgesic
Little effect on CV & Respiration
Can cause post-op nausea & decrease cortisol production w/ long term infusion*.
Primarily used in pts w/ limited cardiac or respiratory reserve (safer than barbs or propofol in pts w/ coronary artery dx., cardiomyopathy, etc.)
Benzodiazepines
Midazolam (> Diazepam & Lorazepam)
– Used to produce anxiolysis, amnesia & sedation prior to induction of GA w/ another agent.
– Sedative doses achieved w/in 2 min, w/ 30 min duration of action (short duration).
– Effects are reversed with flumazenil.
INDICATIONS Midazolam
pre-op sedative induction of anesthesiaConscious sedationcommonly used for short diagnostic or
endoscopic procedures
DOSE AND ROUTES Midazolam
may be given IM, PO, or IVPre-op sedation: 0.07-0.08 mg/kg IM 1 hr
prior Induction of anesthesia: 0.050 - 0.350
mg/kg IVBasal sedation: 0.035 mg/kg initially, then
titrated slowly to a total dose of 0.1 mg/kg
• Recovery half times from anesthesia can be “Context Sensitive”
150
100
50
0
Rec
over
y H
alf
Tim
e (m
ins)
Infusion Duration (hours)0 2 4 6 8 10
DiazepamThiopental*
Midazolam
Propofol
Etomidate
*Unconsciousness can last for days after prolonged administration
Opioids (Fentanyl & Remifentanil*) GAs do not produce effective analgesia (except for ketamine).
Given before surgery to minimize hemodynamic changes produced by painful stimuli. This reduces GA requirements.
High doses can cause chest wall rigidity & post-op respiratory depression
Therapeutic doses will inhibit respiration (CO2)
Used for post-op analgesia, supplement anesthetic in balanced anesthesia.
Remifentanil is an ester opioid metabolized by plasma esterases. It is very potent but w/ a short t1/2 (3-10 mins).
Ketamine
Nonbarbiturate, rapid acting general anesthetic
Dissociated from the environment, immobile, and unresponsive to pain
Profound analgesic
Ketamine
Selectively blocks the associative pathways producing sensory blockade
Preserved pharyngeal-laryngeal reflexesNormal or slightly enhanced skeletal
muscle toneCardiovascular and respiratory stimulation
INDICATIONS Ketamine
Sole agent for procedures that do not require skeletal muscle relaxation
Induction of anesthesia prior to the administration of other anesthetic agents
Supplementation of low potency agents
DOSE AND ROUTES Ketamine
may be injected IM or IV Induction: 1-2 mg/kg Slow IVMaintenance: 30-90 mcg/kg/min IV drip Intramuscular: 6.5-13 mg/kg IM10 mg/kg IM will produce approximately
12-25 min of surgical plane.
ADVERSE REACTIONS, PRECAUTIONS, AND INTERACTIONS Ketaminecontraindicated in pts. with known
hypersensitivity or can't tolerate a significant increase in blood pressure
IV dose should be administered over 60 seconds. Rapid administration may cause respiratory depression or apnea
ADVERSE REACTIONS, PRECAUTIONS, AND INTERACTIONS Ketamine
BP, pulse rate, and respiratory rate are often stimulated
Concomitant use of barbiturates or narcotics prolong recovery time
Ketamine (1.5mg/kg)
A “dissociative anesthetic” that produces a cataleptic state that includes intense analgesia, amnesia, eyes open, involuntary limb movement, unresponsive to commands or pain.
Increases heart rate & blood pressure (opposite of other GAs)
Can be used in shock states (hypotensive) or patients at risk for bronchospasm.
Used in children & young adults for short procedures
Side Effects: nystagmus, pupillary dilation, salivation, hallucinations & vivid dreams
Inhaled Anesthetics
Inhaled Anesthetics Easily vaporized liquid halogenated hydrocarbons Administered as gases
(gas)
Inhaled Anesthetics
Partial pressure or “tension” in inspired air is a measure of their concentration
The speed of induction of anesthesia depends on:
– Inspired gas partial pressure (GA concentration)
– Ventilation rate
– GA solubility (less soluble GAs equilibrate more quickly with blood & into tissues such as the brain)
Minimum Alveolar Concentration
The minimum alveolar anesthetic concentration required to eliminate the response to a painful stimulus in 50% of patients
A measure of GA potency.
It’s “a population average”.
1.3 MAC - 100% will not respond to stimuli.
When several GAs are mixed, their MAC values are additive (e.g. nitrous oxide is commonly mixed w/ other anesthetics).
Elimination Anesthesia is most commonly terminated by redistribution
of drug from brain to the blood & out through the lungs.
The rate of recovery from anesthesia for GAs with low blood: gas PCs is faster than for highly soluble Gas.
Time is $$ in the O.R. & recovery roomBlood: Gas P. Coeff– Haltothane 2.30– Desflurane 0.42– Sevoflurane 0.69
Halothane & methoxyflurane undergo hepatic metabolism & can cause liver toxicity.
Properties of Inhaled anesthetics
Nitrous Oxide
– MAC > 100% : Incomplete anesthetic
– Good analgesia
– No metabolism
– Rapid onset & recovery
– Used along w/ other anesthetic; fast induction & recovery
* fewer side effects also seen in children
Halothane
•The first halogenated inhalational anesthetic
•Not pungent (use for induction w/ children)*
•Medium rate of onset & recovery
•Although inexpensive, its use has declined
•Sensitizes the heart to epi-induced arrhythmias
•Rare halothane induced hepatitis
Desflurane– Most rapid onset of action & recovery of
the halogenated GAs – Widely used for outpatient surgery– Irritating to the airway in awake patients & causes coughing, salivation &
bronchospasm (poor induction agent)– Used for maintenance of anesthesia
Sevoflurane– Very low blood:gas partition coefficient w/ relatively rapid onset of action &
recovery *– Widely used for outpatient surgery*– Not irritating to the airway– Useful induction agent, particularly in children
* Similar to Desflurane
Isoflurane
– Medium rate of onset & recovery– Used for induction & maintenance of anesthesia– Isoflurane “was” the most commonly used inhalational GA in the US. Has been largely replaced
by Desflurane
Methoxyflurane
– Now widely considered obsolete– Slow onset & recovery– Extensive hepatic/renal metabolism, w/ release of F- ion causing renal dysfunction
Toxicity Malignant Hyperthermia
– Esp. when halogenated GA used with succinylcholine– Rx: dantrolene (immediately)
Halothane:– Halothane undergoes >40% hepatic metabolism– Rare cases of postoperative hepatitis occur– Halothane can sensitize the heart to Epi (arrhythmias)
Methoxyflurane– F release during metabolism (>70%) may cause renal insufficiency after prolonged
exposure.
Nitrous oxide– Megaloblastic anemia may occur after prolonged exposure due to decreases in methionine
synthase activity(Vit B12 deficiency).
PREANAESTHETIC MEDICATION Opioids: Morphine-10 mg
Pethidine 50-100mg i.m.
Sedatve antianxiety : Diazepam 5-10mg orallyLorazepam 2mg i.m.
Anticholinergics : Atropine 0.6mg i.m./ i.v Glycopyrolate 0.1-0.3mg i.m
Neuroleptics: Chlorpramazine 25mg
H2 blockers : Ranitidine 150mg Famotidine 40mg
Antiemetics : Metoclopramide 10-20mg i.m
Airway Alveoli Blood Brain
Airway Alveoli Blood Brain
Nitrous Oxide
Halothane
• Why induction of anesthesia is slower with more soluble anesthetic gases. In this schematic diagram, solubility in blood is represented by the relative size of the blood compartment (the more soluble, the larger the compartment). Relative partial pressures of the agents in the compartments are indicated by the degree of filling of each compartment. For a given concentration or partial pressure of the two anesthetic gases in the inspired air, it will take much longer for the blood partial pressure of the more soluble gas (halothane) to rise to the same partial pressure as in the alveoli. Since the concentration of the anesthetic agent in the brain can rise no faster than the concentration in the blood, the onset of anesthesia will be slower with halothane than with nitrous oxide.
Blood:Gas PC
0.47
2.30
Nitrous Oxide
Methoxyflurane
Halothane
Time (min)
Art
eria
l an
esth
etic
ten
sio
n(%
of i
nsp
ire
d te
nsi
on
)
• Tensions of three anesthetic gases in arterial blood as a function of time after beginning inhalation. Nitrous oxide is relatively insoluble (blood:gas partition coefficient = 0.47); methoxyflurane is much more soluble (coefficient = 12); and halothane is intermediate (2.3).
Solubility Effects Arterial Anesthetic Levels
Blood:Gas PC
0.47
2.30
12
Equilibration with a soluble GA may take hoursto achieve. Time is $$ in the O.R.
Ventilation Rate’s Effect on Arterial Anesthetic Tension
Nitrous Oxide
Halothane
Ventilation (L/min)
Art
eria
l an
esth
etic
ten
sio
n(%
of i
nsp
ire
d te
nsi
on
)
Time (min)
Hyperventilation increases the speed ofinduction for Gas with normally slow onset
• Ventilation rate and arterial anesthetic tensions. Increased ventilation (8 versus 2 L/min) has a much greater effect on equilibration of halothane than nitrous oxide.
NMJ BlockersSuccinylcholine, PancuroniumUsed to:
– relax skeletal muscle – facilitate intubation**– insure immobility
Reversed by neostigmine* & glycopyrrolate* during post-op period
* quaternary drugs; * intubation is usually needed for airway maintenance & to prevent aspiration.
Dantrolene Interfers with the release of calcium from the sarcoplasmic
reticulum through the SR calcium channel complex.
Used to prevent or reverse malignant hyperthermia (which is otherwise fatal in ~50% of cases w/o dantrolene).
Given by i.v. push at the onset of symptoms (e.g. an unexpected rise in CO2 levels)
Supportive measures & 100% O2 are also used to treat malignant hyperthermia
Nausea & Vomiting
General anesthetics effect the chemoreceptor trigger zone & brainstem vomiting center (cause nausea & vomiting)
Rx: - Ondansetron (5-HT3 antagonist) to prevent
- Avoidance of N2O
- Propofol for induction- Keterolac vs. opioid for analgesia- Droperidol, metaclopromide & dexamethasone
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