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Anaesthetic drugs & drugs used with anaesthesia

Anaesthetic drugs & drugs used with anaesthesia. We have the following groups of drugs used to give & supplement anaesthesia: 1- Intravenous anaesthetic agents. 2- Inhalational anaesthetic agents. 3- Muscle relaxants & their reversal. 1- Intravenous anaesthetic agents :

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Anaesthetic drugs & drugs used with anaesthesia

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  1. Anaesthetic drugs & drugs used with anaesthesia

  2. We have the following groups of drugs used to give & supplement anaesthesia: 1- Intravenous anaesthetic agents. 2- Inhalational anaesthetic agents. 3- Muscle relaxants & their reversal. 1- Intravenous anaesthetic agents : Uses of I.V. anaesthetic agents : 1. Induction , maintenance of anaesthesia. 2 . Sedation during regional anaesthesia. 3 . Sedation in I.C.U. 4 . Treatment of status epilepticus.

  3. Classification of I.V. anaesthetic agents • 1- Rapidly acting agents A : Barbiturates :- Thiopentone sodium , Methohexitone. B : Imidazole compounds :- Etomidate. C : Alkyl phenols :- propofol 2-Slower acting agents A : Ketamine HCL B : Benzodiazepines : e.g. Midazolam C : Large doses opiods : Fentanyl , Alfentanyl , Sufentanyl D : Neurolept combination ( opiod + neuroleptics )

  4. Thiopentone sodium Pharmacodynamics : C.N.S. * anaesthesia within 30 seconds. There is progressive depression of CNS & spinal reflexes. *Potent hypnotic action *Poor analgesic effect & in small doses it has anti analgesic effect & depresses pain threshold. * Decrease : cerebral blood flow , cerebral blood volume , cerebral metabolic rate , cerebral O2 consumption , free radicles ,& I.C.P. * Consciousness regained in 5 – 10 min

  5. C.V.S. * Depresses the myocardium which leads to decreased cardiac out put as the plasma concentration increases. * Mild initial decrease in blood pressure which returns to normal within few minutes , but if injected rapidly or large doses leads to severe decreases in blood pressure. * Reflex tachycardia RESPIRATORY SYSTEM Markedly depressed ( decrease rate and depth). * It causes short period of apnoea. * There is mild degree of bronchial constriction. EYE : Decrease I.O.P. Hepatorenal function : no effect but in large doses or prolonged infusion , there may be a transient impairment in them.

  6. Pharmacokinetics It is metabolized in the liver and excreted mainly by the kidney. Small proportion of it is excreted unchanged in the kidney. Dosage & adminstration 2.5% I.V. 3-5 mg / kg

  7. Adverse effects 1- Hypotension. 2- Respiratory depression. 3 – Tissue necrosis at the site of injection ( if extravasation occurs). 4 – If intra-arterial injection occurs ,profound constriction may results. 5 – Laryngeal spasm. 6 – Bronchospasm in asthmatics. 7 – Allergic reactions. 8 – Thrombophlebitis.

  8. Indications 1 – Induction of anaesthesia 2 – Maintenance of anaesthesia , for short procedures. 3 – Basal narcosis by rectal adminstration 4 – Treatment of status epilepticus 5 – To decrease I.C.P. Absolute contraindication : 1 – Airway obstruction. 2 – Porphyria. 3 – Previous hypersensitivity reaction 4 – Status asthmaticus

  9. Ketamine HCL Pharmacodynamics C.N.S. * It produces ( dissociative anaesthesia ): the patient appear to be awake but does not responed to stimuli , even painful ones. * Potent analgesic at subanaesthetic blood concentration. *Amnesic effect , may last for 1 hour after recovery. *Smooth induction but with emergence delerium , restlessness , disorientation & agitation. *Un pleasant nightmares & hallucination may occur during recovery for up to 24 hours , it is decreased by avoidance of verbal , visual & tactile stimulation during recovery period or by adminstration of opiods or benzodiazepine.They are less in children & elderly. *It increases CMR,CBF,ICP.

  10. C.V.S. *Increase bl.pr , h.rate , c.o.p. & myocardial O2 consumption. Respiratory system : * Ventilation is well maintained. *Broncheal muscles are dilated *Increase broncheal secretion Skeletal muscles : increase muscle tone , spontaneous movements may occur. Eye : increase I.O.P. , persistance of eye movement during surgical anaesthesia. Pharmacokinetics It is metabolized in the liver & excreted by the kidney. Dosage : 1-2 mg /kg i.v. , 8-10 mg / kg i.m.

  11. Adverse effects 1- Emergence delerium , nystagmus & hallucination. 2- Hypertension & tachycardia ;harmful in hypertesive & I.H.D. patients 3- Prolonged recovery . 4- Salivation. 5- Increase I.C.P. Indication 1- Shocked patient 2- Paediatric anaesthesia (minor surgery , investigation like cardiac catheterization , ophthalmic examination or radiotherapy ) 3- Difficult locations , sites of accidents , analgesia & anaesthesia in casualities of war . 4- Analgesia & sedation 5- Developing countries Absolute contraindication: 1- Airway obstruction 2- Increase I.C.P.

  12. INHALATIONAL ANAESTHETIC AGENTS This includes : halothane , isoflurane , enflurane , desflurane & sevoflurane. Halothane : Halothane is a colourless liquid with a sweat , non irritant odour.It is non inflammable & non explosive. Pharmacodynamic : C.N.S. * It induces CNS depression * It increases cerebral blood flow & I.C.P., more marked in space occupying lesion. C.V.S.: 1- Reduction in bl.pr proportional to the depth of anaesthesia due to myocardial depression. 2- Decreases myocardial contractility , stroke volume , &C.O.P. 3- Increases right atrial pressure 4- Bradycardia may be associated with hypotension 5- May induce arrythmia , the most common are nodal rhythm & ventricular extrasystoles. 6- Sensitizes the myocardium to the dysrrhythmic effect of circulating catecholamines.

  13. Respiratory system Decrease tidal volume and increase respiratory rate. Uterus The contractility of the uterus is inhibited rapidly by inspired concentration of 2-3 % , the myometrium regains its normal tone soon after withdrawal of halothane Pharmacokinetics : Halothane is metabolized in the liver

  14. Muscle Relaxants & Their Reversal Depolarizing M.R. Suxamethonium : It is short acting depolarizing M.R. ,when givwn i.v. it act within 30 sec , with duration of effect up to 3-5 min depending on the dose. Pharmacodynamic : C.N.S. : NO ACTION C.V.S. : It has no direct action on the heart , but it has vagal stimulation leading to bradycardia & decrease in bl.pr Arrythmia & temporary cardiac arrest may occur especially after large or repeated doses , treated by atropine. *Circulatory arrest may occur due to hyperkalaemia in burned pt. Muscular system : rapid & profound neuromuscular block of skeletal muscle usually proceeded by fasciculation due to depolarization of motor end plate. Pharmacokienetic : It is hydrolysed by plasma cholinestrase Dosage & admin : I.V. for adult 0.75 – 1 mg /kg I.V. for children 1 mg/kg I.V. for infant and small children 2 mg/kg

  15. PRECAUTIONS 1- In advanced myasthenia gravis. 2- In uraemic patient. 3- Penterating eye injury. CONTRAINDICATION 1- SEVERE LIVER DISEASE 2- BURNED PATIENT 3- LARGE DEGENERATING MUSCLE DISEASE e.g. paraplagia of recent onset , major limb trauma. 4- MALIGNANT HYPERTHERMIA

  16. SCOLINE APNOEAThe drug is matabolized in the plasma by an enzyme called (plasma cholinestrase ,pseudocholinestrase),at a very rapid rate.Recovery from neuromuscular block may start to occur within 3 minutes and completed within 12-15 minutes.If plasma cholinestrase is structurally abnormal because of inherited factors or if its concentration is reduced by an acquired factors, then the duration of action of the drug may be altered significantly.INHERITED FACTORSThe exact structure of plasma cholinestrase is determined genetically by autosomal genes.Several abonormalities in the amino acids sequence of the normal enzyme can developed but the most common abnormalities of the enzyme is called (atypical enzyme).Thus a patient who has heterozygote of atypical(E1u,E1a) will have longer effect of suxamethonium in standered dose(about 30 minutes).Homozygote of atypical(E1a,E1a) will have an effect over 2 hours.

  17. Acquired Factors This is due to decrease quantity of the enzyme but not due to structural change in the enzyme. Causes 1-Liver disease: because decrease synthesis of the enzyme. 2-Carcinomatosis. 3 -Starvation. 4-Pregnancy:for 2 reasons ,a: increase circulating volume(dilutional effect) , b: decrease synthesis of enzyme. 4-Anticholinestrase drugs: edrophonium, neostigmine, organophosphorus. 5-Other drugs wich are metabolized by plasma cholinestrase and thus decrease the availability of the enzyme. e.g, etomidate , ester local anaesthetics , MAO inhibitors , esmolol( short acting beta antagonist). 6-Hypothermia. 7-Cardiopulmonary bypass , plasmapheresis. 8-Renal disease.

  18. TREATMENT 1-keep the patient anaesthetized and the lung ventilated artificially. 2-Monitor neuromuscular transmission accuretly untill full recovery from residual neuromuscular block. 3-Fresh frozen plasma because it is a source of this enzyme.

  19. PANCURONIUM It is a long acting non depolarizing muscle relaxant. It act after 1.5 minute and last for 30 – 40 minutes. PHARMACODYNAMIC C.V.S. : RESPIRATORY ; has low histamine releasing properties and its use is prefered in high bronchial reactivity. moderate increase in pulse rate , blood pressure and cardiac out put due to vagolytic effect. PHARMACOKINETICS : It is metabolized by the liver, and mainly excreted by the kidney.Small percentage is excreted by the bile.Its elimination is slowed and neuromuscular blockade is prolonged by renal failure. Dosage ; 0.08 -0.1 mg /kg

  20. REVERSAL OF MUSCLE RELAXANTS Depolarizing muscle relaxants : They diffuses away from the neuromuscular junction and are hydrolyzed in the plasma by pseudocholinestrase ( plasma cholinestrase ) enzyme. This is very rapid process ,since no specific agent to reverse these relaxants. Non depolarizing muscle relaxants Reversal of these drugs depends upon redistribution , gradual metabolism and excretion of the relaxant by the body, or administration of specific reversal agents ( cholinestrase inhibitors ) which inhibit acetylcholinestrase enzyme activity (this enzyme is responsible for the degredation of acetylcholine ).This inhibition will increase the amount of acetylcholine at the neuromuscular junction and regain muscular contractility.

  21. Cholinestrase inhibitor These are: 1- Edrophonium 2- Neostigmine 3- Pyridostigmine 4- Physostigmine NEOSTIGMINE :It is given prior to or at the same time with atropine to reverse its muscarinic effects. Pharmacodynamics : C.V.S.:1- peripheral vagal stimulation will cause bradycardia , some degree of vasodilatation and a fall in blood pressure , these are reversed by atropine. 2- cardiac arrythmia and arrest may follow large doses. RESPIRATORY S. : bronchoconstriction and increase bronchial secretion SKELETAL MUSCLE :increasing the number of acetylcholine molecules at the motor end plate.Asmall dose will increase the muscle contraction but in large or repeated doses , it may cause depression to the muscle contraction. SMOOTH MUSCLES : stimulation of smooth m.,perstalsis of the stomach , intestine & bile duct are increase and may cause colic.other effect include sweating , salivation & increase mucous sec.

  22. INDICATION : 1- Reverse the action of the non depol.M.R. 2- Treatment of paralytic ileus, atony of the bladder. 3- myasthenia gravis. 4- Glaucoma 5- Sinus tachycardia DOSAGE :0.04 – 0.08 mg / kg .

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