General anaesthesia principles
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This document provides an introduction to general anaesthesia. It discusses the stages of anaesthesia according to the Guedel classification system and describes various drugs used in anaesthesia including intravenous agents like thiopentone, propofol, and benzodiazepines. It also discusses inhalational agents such as nitrous oxide, ether, halothane, isoflurane, and sevoflurane. Finally, it covers muscle relaxants, distinguishing between depolarizing agents like suxamethonium and non-depolarizing agents. The document provides an overview of the pharmacodynamics and uses of these different drug classes for anaesthesia.
General anaesthesia principles
- 1. Introduction to General anaesthesia By: Dr. Radhwan Alkhashab Consultant anaesthesia & ICU 2020
- 2. General anaesthesia : Term used to describe the process of producing unconsciousness during surgery. Induction of anaesthesia produces an unconscious patient. Reflexes are depressed. The patient is entirely dependent on the anaesthetist for their safety. Most complications occur during induction and extubation. Which includes hypotension, arrhythmias, hypoventilation apnoea, hypoxia, aspiration, laryngospasm and adverse drug reactions
- 3. Pharmacodynamic of general anaesthesia: Drugs acting on CNS & pass blood stream & then transport to brain , where they penetrate BBB & enter specific cell in the central nervous system, here they exert their effects which are usually reversible effect .
- 4. Stages of anaesthesia: Also called (Guedel classification ), was described at 1937 with diethyl ether. Stage 1( Analgesia) : begin with the beginning of induction & end at time of loss of consciousness ,here the patient have regular & small volume respiration, the pupil are normal & patient can feel with intact airway reflexes. Stage 2 (Excitement) : start from the LOC to automatic breathing , patient have irregular respiration, dilated pupils ,abolished eyelash reflex.
- 5. Stages of anaesthesia (cont.) Stage 3 (Surgical anaesthesia) : start at automatic respiration to respiratory paralysis. This divided into four planes: Plane 1:pin point pupils, cessation eye ball movement, loss of eyelid reflex. Plane 2:loss of corneal & pharyngeal reflex. Plane 3:loss of laryngeal reflex, paralysis of intercostal muscles & respiration become diaphragmatic. Plane 4:diaphragmatic paralysis , dilated pupils ,depressed carinal reflex. Stage 4 (coma): characterize by apnoea , hypotension, cold extremities, weak pulse, in this stage cardiovascular & respiratory centre collapse & may lead to death .
- 6. Induction of anaesthesia Routes : -I.V. -Inhalational. -I.M. -Rectal.
- 7. Intravenous anaesthesia Uses: 1. Induction of anaesthesia. 2. TIVA. 3. Supplement inhalational or regional anaesthesia. 4. Sedation.
- 8. Criteria of I.V. anaesthesia: Advantages Rapid onset Dose titratable Depression of pharyngeal reflexes allows early insertion of LMA Anti-emetic and anti-convulsive properties Disadvantages Venous access required Risk of hypotension Apnoea common Loss of airway control Anaphylaxis
- 9. Types of I.V. drugs Barbiturates : Thiopentone : Hypnotic & anticonvulsant. High lipid soluble. Rapid onset(30 seconds). Short duration (6-8 minutes)& patient awake within 20 minutes. Can be use as I.V. induction agent & rectal route induction agent in children. Dose 4-7mg/kg as induction dose , 0.5-1.5mg/kg as sedation dose. CVS: decrease BP & increase heart rate. Respiratory system: respiratory centre depression, cause apnoea ,upper airway obstruction, bronchospasm in asthmatic patient, laryngospasm in light anaesthesia. CNS : decrease cerebral blood flow, intracranial pressure, oxygen consumption. this give brain protection against focal ischemia. Cause histamine release , & precipitate acute intermittent porphyria.
- 10. Ketamine Cause dissociative anaesthesia: in which patient appear awake (eye open,swallowing,moving limbs) but unable to respond to pain. I.V & I.M. routes. Cause hallucination . Painless & not irritant to vein. Onset of anaesthesia is slower than Thiopentone. Longer duration (10-15 minutes). Muscle rigidity. CVS: stimulant leading to tachycardia & hypertension. Respiratory system: bronchodilator.
- 11. Propofol 1) Rapid onset within 30 seconds. 2) Short duration up to 5 minutes. 3) Irritant at site of infusion. 4) Uses in outpatient clinic. 5) CVS: hypotension . 6) Good laryngeal reflex useful for LMA insertion
- 12. Benzodiazepine Diazepam.midazolam,lorazepam. Use as sedation & as induction agents. Can be given oral,I.V., I.M., routes. Induction dose 0.25-0.5mg/kg of diazepam intravenous route. Slower onset than other I.V. agent. Cause more stable cardiovascular effect so can be use for poor cardiac performance. Respiratory arrest & reduce respiratory response to CO2 . Decrease cerebral blood flow& intracranial pressure& oxygen consumption , can be use to control grand mal seizure. Can produce ante grade amnesia. No analgesic property.
- 13. Opioids Use for Premedication, induction, maintenance of anaesthesia & postoperative analgesia. Cause respiratory depression. Do not seriously impaired cardiovascular function. Slowing gastric empty. Decrease cerebral blood flow, ICP,& cerebral oxygen consumption
- 14. Inhalational drugs Useful as induction agent in paediatric group. Can use to maintain anaesthesia. Oxygenation can be assured, so can use in patient suspected upper airway obstruction. Slow onset of induction , so it avoided in patient with full stomach.
- 15. Types of inhalational agents
- 16. Nitrous oxide N2O Use as carrier gas in mixture with O2 & up to 70% conc. Weak anaesthetic agent & can supplement with inhalational agents. Good analgesic property. Teratogen. Irreversible oxidizing cobalt atom in vitamin B12 so prolong exposure to anaesthetic concentration of N2O can result in megaloplatic anaemia & peripheral neuropathy. N2O is 35 time more soluble than N2 in the blood, thus it tend to diffuse into air containing cavities more rapidly than N2 , so cause expanding air containing cavity or may cause increase pressure inside the cavity, e.g.: • air embolism. • pneumothorax. • Acute intestinal obstruction. • Intracranial air, e.g. air encephalography. • Pulmonary air cyst. • Intraocular air bubbles.
- 17. Ether (diethyl ether) -1st volatile agent. -It is flammable. -Irritant. Safe but unpleasant agent for inhalational. Cumulative effect lead to prolong postoperative drowsiness. Bronchodilator.
- 18. Halothane Non flammable, non irritant. Potent, rapid induction & recovery. Respiratory depressant & bronchodilator effect. CVS: cardiac depressant, decrease cardiac output by decrease heart rate & contractility & BP. Sensitize myocardium to dysrhythmogenic effect of epinephrine. Increase cerebral blood flow, ICP, this can be prevented by hyperventilation before halothane administration. Cause relaxation of pregnant uterus in conc. More than 0.5%. It is poor analgesic. 20% metabolized in liver, it's reductive form can cause halothane hepatitis in 1:35000.
- 19. Isoflurane More potent than halothane & more irritant at inhalation. Respiratory depressant. Less cardiac depressant & doesn't precipitate dysrhythmias, but produce hypotension by peripheral vasodilatation. 0.2% metabolized & have no significant hepatic or renal toxicity.
- 20. Sevoflurane Cardiovascular effect similar to isoflurane but less tachycardia. Does not precipitate dysrhythmias. Respiratory depressant similar to isoflurane. Non irritant to upper respiratory tract. Faster induction & elimination than halothane. 2% metabolized, renal or hepatic toxicity are reported.
- 21. Muscle relaxant
- 22. Neuromuscular blocking agents Transmission of nerve impulse to the muscle at the neuromuscular junction (NMJ) of voluntary muscle is accomplished by acetylcholine (Ach). That large amount of Ach are released when an impulse is conducted down the motor nerve fibre to the nerve ending. Ach cross myoneural junctionl cleft & become attached to the paired lipoprotein receptors grouped around ion channels in the membrane. this makes the membrane of the motor end plate permeable to an inward flow of sodium ion & calcium ion & the exit of potassium ion. depolarization thus occur, an electrical potential is produced & propagated lead to a muscle contraction. The Ach is rapidly hydrolyzed by acetyl cholinesterase, which is present in the vicinity of motor end plate.
- 23. Two types of muscle relaxant: 1.Depolarizing (short acting) (non competitive) muscle relaxant:- suxamethonium: Act similar to Ach by causing depolarization, but instead of repolarisation occurring immediately, the depolarization persist& the muscle remain flaccid until suxamethonium are destroyed by another enzyme serum cholinesterase (pseudo cholinesterase). The action is not reversed by neostigmin. Dose 1mg/kg, onset of action within 45 seconds & last up to 3 minutes.
- 24. 2. Non depolarizing (competitive) muscle relaxant These typified by tubocurarine, which accompany end plate without causing depolarization. These drugs are reversed by neostigmin by inhibition of Ach-esterase leading to increase concentration of Ach & compete the drug at end plat & restore normal muscle activity. Types of NDMR depending on duration of action: Short-acting compounds with a duration of action of up to 15 min (mivacurium). Medium-acting compounds which are effective for approximately 40 min (atracurium, vecuronium, rocuronium, cis-atracurium). Long-acting compounds which have a clinical effect for 60 min (pancuronium, d-tubocurarine).
- 25. Indication of muscle relaxant 1.Facilitate tracheal intubation. 2.Maintain the relaxation state during IPPV.
- 26. Suxamethonium Suxamethonium is the only depolarizing relaxant in clinical use today and is metabolized by plasma cholinesterase. Onset of action start within 45-60 seconds & last up to 3 minutes. Suxamethonium have many side effects: Postoperative muscle pains. Raised intra-ocular pressure. Hyperkalaemia. Bradycardias, particularly in children. Malignant hyperthermia.
- 27. Tubocurarine (1935) Intubating dose 0.3 to 0.5 mg/kg, duration of action 30 to 40 minutes, it cause histamine release leading to hypotension , bronchospasm. *Atracurium (1980) Intubating dose 0.3 to 0.6 mg/kg, duration of action 20 to 40 minutes, Atracurium may cause histamine release and has caused anaphylaxis. At body temperature and pH it undergoes spontaneous “breakdown” (Hofmann elimination) to laudanosine. Up to 50% may also be hydrolyzed by blood esters. This makes atracurium very predictable and may be the drug of choice for patients with renal or liver failure.
- 28. Pancuronium (1967) Intubating dose 0.1 mg/kg, duration of action 30 to 60 minutes, supplementary doses 0.01 to 0.02 mg/kg. The onset of action is about 3 minutes. Pancuronium may cause an increase in heart rate, blood pressure and cardiac output. Traditionally used in shocked patients. It rarely causes histamine release. Elimination may be prolonged in renal and liver failure.
- 29. *Vecuronium (1983) Intubating dose 0.08 to 0.1 mg/kg, duration of action 20 to 30 minutes, supplementary doses 0.03 to 0.05 mg/kg. The onset of action is about 2 to 3 minutes. Vecuronium has minimal effect on blood pressure or pulse rate and does not cause histamine release. *Rocuronium (1994) Intubating dose 0.6 mg/kg, duration of action 30 to 40 minutes, supplementary doses 0.15 mg/kg. The onset of action is about 1 minute. Rocuronium is similar to vecuronium but may cause some tachycardia.
- 30. Thank you Any Q