All about General anesthesia

Definition

A controllable and reversible loss of consciousness induced by the intoxication of the central nervous system. Lowered sensitivity to external stimuli (hyporeflexia), analgesia, unconsciousness, muscle relaxation, and amnesia are significant features of general anesthesia.

Tree stages of general anesthesia

  • Induction of anesthesia
  • Maintenance of anesthesia
  • Recovery of anesthesia

Inhalational anesthesia

Inhalation anesthetics are substances that are brought into the body via the lungs and are distributed with the blood into the different tissues. The main target of inhalation anesthetics (or so-called volatile anesthetics) is the brain.

MAC

 Definition: MAC is the “minimum alveolar concentration” of an inhaled anesthetic at atmospheric pressure with 100%O2required to prevent movement in response to a noxious stimulus in 50% of subjects.

§  MAC is analogous to the plasma EC50 (concentration for 50% effect) for intravenous anesthetics.

the alveolar concentration of an anesthetic (Fa)

§   ventilation the first of five factors that govern the pulmonary inhaled anesthetic concentration

§   blood passing through the lung opposes the effect of ventilation by drawing anesthetic from the lung.

§   An increased inspired concentration of anesthetic decreases the effect of uptake (the concentration effect), and at 100% inspired concentration, uptake no longer opposes the effect of ventilation.

the alveolar concentration of an anesthetic (Fa)

§  Metabolism of anesthetics can increase uptake.

§  Anesthetic uptake may be enhanced by movement of anesthetic between tissues (intertissue diffusion)

§  Three factors determine uptake by blood: solubility (the blood-gas partition coefficient),

§  pulmonary blood flow (cardiac output),

§   the difference in anesthetic partial pressure between the lungs and venous blood returning to the lungs

The toxicity of inhaled anesthetics

§   Halothane, enflurane, isoflurane, and desflurane have been reported to induce liver injury in susceptible patients. halothane (20%) enflurane (2.5%) isoflurane (0.2%) > desflurane (0.02%). Sevoflurane does not produce acylated protein adducts.

§   inorganic fluoride levels50umol/L, fluoride-associated renal injury has not been reported.

Common inhaled anesthetics

§   Nitrous oxide: weak inhaled anesthetic potency, have no significant effect on cardiac output, heart rate, and blood pressure. Clinical concentration 50%-70%, oxygen concentration must be higher than 0.3, so as to prevent hypoxemia. To prevent diffused hypoxemia,100% oxygen should be inhaled for 5-10 min after stopping nitrous oxide. increase the pressure of the sealed cavity.

§  Enflurane: higher inhaled anesthetic potency, have an effect on EEG, depress the cardiovascular system, depress the respiratory system, but have no irritation to the airway. To maintain anesthesia with a concentration 0.5%-2%, be careful to use on the patient with epilepsy.

§  Isoflurane: high inhaled anesthetic potency, mildly depress the cardiovascular system and the respiratory system,  have no irritation to the airway. To maintain anesthesia with concentration 0.5%-2% can be used for controlled hypotension.

§  sevoflurane: higher inhaled anesthetic potency, mildly depress the cardiovascular system,  severely depress the respiratory system,  have no irritation to the airway. To maintain anesthesia with a concentration of 1.5%-2.5%.

Intravenous Anesthesia

Intravenous anesthetics are administered via the intravenous route - that is, directly into the patient's bloodstream. This allows them to reach a therapeutic level quickly and affect the brain quickly.

Common intravenous anesthetics

§   Thiopental:  rapid onset of action and short duration, water-soluble barbiturate salts in alkaline solutions PH10-11, usual concentration 2.5%. action on the GABA receptor, decrease cerebral metabolism, depress the cardiovascular system,  the respiratory system, and the sympathetic system.

§   Side effect: larygospasm bronchospasm

§   Induction:4-6mg/kg

§   Treat convulsions:1-2mg/kg

§   Ketamine: significant analgesic effect; It usually does not depress the cardiovascular and respiratory systems, but it does possess some of the adverse psychological effects ;

§   dissociative anesthesia; increase ICP; increase in intraocular pressure; increase salivation; a bronchial smooth muscle relaxant

§   Induction:1-2mg/kg iv,duration 15-20min

§   Basel anesthesia:5-10mg/kg im for children ,duration 30min

§   Etomidate: Etomidate is used primarily for the induction of anesthesia, especially in elderly patients and patients who have a cardiovascular compromise. It has a rapid onset of effect and a rapid offset even after a continuous infusion. Prolonged infusion results in inhibition of adrenocortical synthesis. The major advantage of etomidate is its minimal effect on the cardiovascular and respiratory systems. It is associated with a high incidence of burning on injection, thrombophlebitis, and postoperative nausea and vomiting (PONV). The induction dose is 0.2 to 0.3 mg/kg.

§ propofol: propofol provides rapid onset and offset with context-sensitive decrement times of approximately 10 minutes when infused for less than 3 hours and less than 40 minutes when infused for up to 8 hours. Its mechanism of action of γ-aminobutyric acid (GABA). At therapeutic doses, propofol produces a moderate depressant effect on ventilation. It causes a dose-dependent decrease in blood pressure primarily through a decrease in cardiac output and systemic vascular resistance. A unique action of propofol is its antiemetic effect.

§    induction : 1 to 2 mg/kg

§    maintenance: infusion of 100 to 200 µg/kg/min.

Muscle relaxants

§   This class of drugs has its effect at the neuromuscular junction by preventing the effects of acetylcholine. Normally, when a nerve stimulus acts to contract a muscle, it releases acetylcholine. The binding of this acetylcholine to receptors causes the muscle to contract

Different Mechanism between nondepolarizing and depolarizing relaxants

§   Nondepolarizing muscle relaxants produce neuromuscular blockade by competing with acetylcholine for postsynaptic receptors.  Depolarizing ones produces prolonged depolarization that results in decreased sensitivity of the postsynaptic nicotinic acetylcholine receptor and inactivation of sodium channels so that the propagation of the action potential across the muscle membrane is inhibited.

Depolarizing muscle relaxants

§   Succinylcholine is the only available neuromuscular blocker with a rapid onset of effect and an ultrashort duration of action.

§   Induction:1-2mg/kg peak time:60sec

§   Side effect:sinus bradycardia; increase plasma potassium;increase intragastric pressure, increase ICP; increase in intraocular pressure

Nondepolarizing muscle relaxants

§   Pancuronium: onset time:3-6min;duration :100-120min; Induction:0.1-0.15mg/kg

§   Vecuronium: onset time:2-3min;duration :25-30min; Induction:0.07-0.15mg/kg

§   Rocuronium: onset time:1-1.5min;duration :25-30min; Induction:0.6-1.2mg/kg

§   Cisatracurium: onset time:2-3min;duration :50-60min; Induction:0.15-0.2mg/kg,hofmann elimination