GeneralAnesthetics and Stages of Anesthesia

8/13/2019 GeneralAnesthetics and Stages of Anesthesia

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By: Naghman Zuberi

General Anesthetics and

Stages of Anesthesia



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Anesthesia

• Allow surgical, obstetrical and diagnostic

procedures to be performed in a manner which is

painless to the patient

• Allow control of factors such as physiologic

functions and patient movement



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General anesthesia

Regional anesthesia

Local anesthesia Conscious Sedation (monitored

anesthesia care)

Anesthetic techniques



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• No universally accepted definition

• Usually thought to consist of:

– Oblivion

– Amnesia

– Analgesia

– Lack of Movement

– Hemodynamic Stability

What is “Anesthesia”



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• Sensory

-Absence of intraoperative pain

• Cognitive:

-Absence of intraoperative awareness

-Absence of recall of intraoperative events

• Motor:

-Absence of movement

-Adequate muscular relaxation

• Autonomic:

-Absence of hemodynamic response

-Absence of tearing, flushing, sweating

What is “Anesthesia”



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Hypnosis (unconsciousness)

Amnesia

Analgesia

Immobility/decreased muscle tone

(relaxation of skeletal muscle)

Inhibition of nociceptive reflexes

Reduction of certain autonomic reflexes

(gag reflex, tachycardia, vasoconstriction)

Goals of General Anesthesia



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Rapid induction

Sleep

Analgesia

Secretion control

Muscle relaxation

Rapid reversal

Desired Effects Of General Anesthesia

(Balanced Anesthesia)



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Induction- initial entry to surgicalanesthesia

Maintenance- continuous monitoring and

medication Maintain depth of anesthesia, ventilation, fluid balance,

hemodynamic control, hoemostasis

Emergence- resumption of normal CNS

function Extubation, resumption of normal respiration

Phases of General Anesthesia Stages Of General Anesthesia



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Stage I: Disorientation, altered consciousness

Stage II: Excitatory stage, delirium, uncontrolled movement, irregular breathing.

Goal is to move through this stage as rapidly as possible.

Stage III: Surgical anesthesia; return of regular respiration.

Plane 1: “light” anesthesia, reflexes, swallowing reflexes.

Plane 2: Loss of blink reflex, regular respiration (diaphragmatic andchest). Surgical procedures can be performed at this stage.

Plane 3: Deep anesthesia. Shallow breathing, assisted ventilation

needed. Level of anesthesia for painful surgeries (e.g.; abdominal

exploratory procedures).

Plane 4: Diaphragmatic respiration only, assisted ventilation is required.

Cardiovascular impairment.

Stage IV: Too deep; essentially an overdose and represents anesthetic crisis.

This is the stage between respiratory arrest and death due to circulatory

collapse.

Phases of General Anesthesia Stages Of General Anesthesia



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•Intravenous

–Safe, pleasant and rapid•Mask

–Common for children under 10

–Most inhalational agents are pungent, evoke coughing and

gagging

•Avoids the need to start an intravenous catheter

before induction of anesthesia

–Patients may receive oral sedation for separation fromparents/caregivers

•Intramuscular

–Used in uncooperative patients

Routes of Induction



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Inhalation anesthesia

Anesthetics in gaseous state are taken up

by inhalation

Total intravenous anesthesia

Inhalation plus intravenous (“Balanced

Anesthesia”)

Most common

Anesthetic Techniques



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Anesthetic drugs have rapid onset and offset

• “Minute to minute” control is the “holy grail” of general anesthesia

• Allows rapid adjustment of the depth of anesthesia

• Ability to awaken the patient promptly at the end of the surgical

procedure

• Requires inhalation anesthetics and short-acting intravenous drugs



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• During the maintenance phase, anesthetic doses are adjustedbased upon signs of the depth of anesthesia

• Most important parameter for monitoring is blood pressure

• There is no proven monitor of consciousness

Anesthetic Depth



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Safest for the patient

Appropriate duration

i.v. induction agents for short procedures

Facilitates surgical procedure

Most acceptable to the patient

General vs. regional techniques

Associated costs

Selection of anesthetic technique



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MAC – Minimal Alveolar Concentration• "The alveolar concentration of an inhaled anesthetic that prevents movement

in 50% of patients in response to a standardized stimulus (eg, surgical

incision)."

• A measure of relative potency and standard for experimental studies.

• MAC values remain constant regardless of stimuli, weight, sex, and even

across species

• Steep DRC: 50% respond at 1 MAC but 99% at 1.3 MAC

• MAC values for different agents are approximately additive. (0.7 MAC N2O +

0.6 MAC halothane = 1.3 MAC total)

• "MAC awake," (when 50% of patients open their eyes on request) is

approximately 0.3.

• Light anesthesia is 0.8 to 1.2 MAC, often supplemented with adjuvant i.v.

drugs



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Circadian rhythm

Body temperature

Age

Other drugs Prior use

Recent use

Factors Affecting MAC



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How do Inhalational Anesthetics Work?

•Membrane Stabilization Theory:

– Site of action in lipid phase of cell membranes (membrane stabilizing

effect) or

– Hydrophobic regions of membrane-bound proteins

– May induce transition from gel to liquid crystalline state ofphospholipids

– Supported by NMR and electron-spin resonance studies

– Anesthesia can be reduced by high pressure



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Potentiation ofinhibitory „receptors‟

GABA A

Glycine

Potassium channels

Inhibition ofexcitatory „receptors‟

NMDA (glutamate)

AMPA (glutamate)

Nicotinic

acetylcholine

Sodium channels

Inferred from demonstration of effect on receptor at clinically relevant

concentrations and lack of effect in absence of receptor

Receptors Possibly Mediating CNS

Effects Of Inhaled Anesthetics



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Inhaled Anesthetics

• Gases

– Nitrous oxide

– Present in the gaseous state at room temperature and pressure

– Supplied as compressed gas



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Volatile anesthetics

Present as liquids at

room temperature

and pressure Vaporized into gases

for administration

Inhaled Anesthetics



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Volatile anesthetics

Present as liquids at

room temperature and

pressure – BUT NOT

ALWAYS!

Vaporized into gases

for administration

Inhaled Anesthetics



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Partial pressure (mmHg) Applies to gas phase or to dissolved gases

Volumes %

Percentage of total gas volume contributed byanesthetic

Percentage of total gas molecules contributed by

anesthetic

Partial pressure/atmospheric pressure

Concentration of Inhaled Anesthetics

Determines Dose



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Ratio of concentration in one phase to that in

a second phase at equilibrium

Important solubility coefficients for inhaledanesthetics

Lower blood-gas partition coefficient leads to

faster induction and emergence

Higher oil-gas partition coefficient leads to

increased potency

Solubility of Inhaled Anesthetics

Determines Dose and Time-course



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•Ether – Slow onset, recovery, explosive

•Chloroform – Slow onset, very toxic

•Cyclopropane – Fast onset, but very explosive

•Halothane (Fluothane) – first halogenated ether (non-flammable)

• 50% metabolism by P450, induction of hepatic microsomal

enzymes; TFA, chloride, bromide released

• Myocardial depressant (SA node), sensitization of myocardium to

catecholamines

• Hepatotoxic

•Methoxyflurane (Penthrane) - 50 to 70% metabolized

• Diffuses into fatty tissue

• Releases fluoride, oxalic acid

• Renotoxic

Inhaled Anesthetics - Historical



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• Enflurane (Ethrane) Rapid, smooth induction and maintenance

• 2-10% metabolized in liver

• Introduced as replacement for halothane, “canabilized” to make

way for isoflurane

• Isoflurane (Forane) smooth and rapid induction and emergence

• Very little metabolism (0.2%)

• Control of Cerebral blood flow and Intracranial pressure

• Potentiates muscle relaxants, Uterine relaxation

• CO maintained, arrhythmias uncommon, epinephrine can be used

with isoflurane; Preferential vasodilation of small coronary vessels

can lead to “coronary steal”

• No reports of hepatotoxicity or renotoxicity

• Most widely employed

Inhaled Anesthetics – Currently



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• Nitrous Oxide is still widely used

• Potent analgesic (NMDA antagonist)

• MAC ~ 120%

• Used ad adjunct to supplement other inhalationals

• Xenon

• Also a potent analgesia (NMDA antagonist)

• MAC is around 80%

• Just an atom – what about mechanism of action?

Inhaled Anesthetics – Currently

Mali nant H perthermia



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Genetic susceptibility-Ca+ channel defect (CACNA1S) or RYR1

(ryanodine receptor)

Excess calcium ion leads to excessive ATP

breakdown/depletion, lactate production, increased CO2 production, increased VO2, and, eventually, to myonecrosis and

rhabdomyolysis, arrhythmias, renal failure

May be fatal if not treated with dantrolene – increases reuptake

of Ca++ in Sarcoplasmic Reticulum

Signs: tachycardia + tachypnea + ETCO2 increasing + metabolicacidosis; also hyperthermia, muscle rigidity, sweating,

arrhythmia

Detection:

Caffeine-halothane contracture testing (CHCT) of biopsied muscle;

Genetic testing for 19 known mutations associated with MH

Malignant Hyperthermia

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).

GeneralAnesthetics and Stages of Anesthesia

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