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- 1. Prepared by :Nurul Najwa Mustapa Supervisor: Dr Azhar EMERGENCY DRUGS IN ANESTHESIA
- 2. CONTENT • ATROPINE • PHENYLEPHRINE •EPHEDRINE • ADRENALINE • NORADRENALINE
- 3. ATROPINE • antimuscarinic agent/ ‘parasympatholytic’ agents - reduce the activity of the PNS • Synthetic tertiary amine • MOA : Act as competitive antagonists of acetylcholine (ach) at muscarinic acetylcholine receptors (mACHr) • located in - post-ganglionic target tissues innervated by the parasympathetic nervous system - in the sympathetically innervated sweat glands.
- 4. ATROPINE USES • Premed todecrease secretions • Treatment of symptomatic bradycardia (0.5 mg IV every 3 to 5 minutes, max 3mg) • Treatment of organophosphate poisoning • METABOLISM AND EXCRETION • Hepatic metabolism • excreted in urine
- 5. EFFECTS • Tachycardia •Effect last 2–3 hours • May precipitate arrhythmias by decreasing AV conduction time CVS • Bronchodilation • ↑RR RS • Crosses BBB causing central anticholinergic syndrome • Antiemetic • Antiparkinsonian effects CNS • Antisialagogue • ↓Tone lower oesophageal sphincter GI • Inhibits sweating may cause hyperpyrexia in children METABOLIC • Dry mouth • Urinary retention • Blurred vision ANTIMUSCARINIC
- 6. ADRENERGIC DRUG Catecholamines • Adrenaline •Noradrenaline • Dopamine Non Catecholamines • Ephedrine • Phenylephrine • Amphetamine & etc
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- 10. PHENYLEPHRINE • Direct-acting sympathomimeticamine with potent α1-agonist actions. • No effect on β receptors
- 11. EFFECT • Increase systemicvascular resistance and blood pressure and may result in a reflex bradycardia, all of which results in a drop in cardiac output. It is not arrhythmogenic. Cardiovascular • Blood low falls in a manner similar to that demonstrated by noradrenaline. Renal • use as a nasal decongestant and mydriatic agent. Others
- 12. PHENYLEPHRINE How to use •Peripheral line • Dilute into 100ml NS – 100mcg/ml • Infusion dose: 0.1-10mcg/kg/min • Bolus: 50 to 100 mcg METABOLISM AND EXCRETION • Hepatic metabolism by monoamine oxidase
- 13. EPHEDRINE • Synthetic noncatecholamine agonist at α, β1, and β2 receptors with both direct and indirect actions • MOA : Indirect sypathomimetic, i.e. causes release of noradrenaline from nerve terminals • Direct stimulation of α and β receptors • Inhibits monoamine oxidase • USES : Hypotension • Nasal decongestant • Nocturnal enuresis • DOSE : Oral: 30 mg t.d.s. • IV: given as boluses of 3 mg, titrate to effect
- 14. EFFECTS • ↑ HR• ↑ CO • ↑ BP • ↑ Coronary artery blood flow • ↑ Myocardial O2 consumption CVS • Bronchodilation • RS • ↓ Renal blood flow • ↓ GFR Renal • Caution with MAOIs can precipitate hypertensive crisis NB Tachyphylaxis occurs as noradrenaline stores are depleted. Usually seen after ～30 mg given Others
- 15. EPHEDRINE METABOLISM AND EXCRETION •Minimal hepatic metabolism • 65% excreted unchanged in urine
- 16. ADRENALINE • α andβ adrenoreceptor agonist • Effects are mediated by stimulation of adenylyl cyclase increase in CAMP Alpha 1 increase SVR increase BP Beta 1 increase HR CO Beta 2 bronchodilation, reduce mast cell release
- 17. ADRENALINE Pharmacokinetics • Administration :IV /IM • Elimination : degraded by conjugation with glucuronic and sulphuric acids and excreted in the urine. Smaller part oxidised by amine oxidase and inactivated by o-methyl-transferase Dose • Infusion dose : 0.01-1.5 mcg/kg/min • Single strength: 3mg in 50cc (0.06mg/ml) • Double strength: 6mg in 50cc (0.12mg/ml)
- 18. EFFECTS •Low Dose –β effects predominate • ↑ CO • ↑ Cardiac oxygen consumption • Coronary artery vasodilation • ↓ Diastolic BP • ↓ Peripheral vascular resistance High Dose – α effects predominate • ↑ SVR CVS •Potent bronchodilator • Slight ↑ minute volume • ↑ Pulmonary vascular resistance RS •↑ BMR • ↑ Glycogenolysis and plasma glucose • ↑ Initial insulin secretion ( β effect) followed by reduction (α effect) • ↑ Glucagon secretion • ↑ Lactate • ↑ Lipase causing fatty acid oxidation and ketogenesis • ↑ Renin and aldosterone secretion METABOLIC • Reduce renal blood flow and urine output RENAL •Intestinal muscle relaxed, pyloric and ileocolic sphincter constricted GIT
- 19. EPINEPHRINE USES • Severe septicshock Added as 2nd vasoactive agent when noradrenaline dose > 15-20mcg/min does not achieve the target • ACLS 1mg 3-5min push IV • Anaphylaxis Administered adrenaline in boluses of 0.05-0.1mg. If no response, administered infusion adrenaline at 0.1mcg/kg/min. Adrenaline is preferred as it reverses peripheral vasodilation and reduces oedema • Viral croup • Asthma Use 1:1000 solution and (if required) make up to a total of 5ml using normal saline prior to administration • Used locally to decrease the spread of LA and to reduce surgical blood loss
- 20. NORADRENALINE • Direct andindirect α1 agonist, some small action at β receptors Uses • Vasoactive agent of choice • Sepsis • Cardiogenic shock • Neurogenic shock Dose • Infusion dose : 0.01-1.5 mcg/kg/min • Infusion (1 vial 4mg/4ml) • Single strength: dilute 1 vial in 50ml (0.08mg/ml) • Double strength: dilute 2 vials in 50ml (0.16mg/ml)
- 21. EFFECTS S/E • NE vasoconstrictsthe pulmonary, renal and mesenteric circulation, infusion must be monitored to prevent injury to vital organs. • Prolonged infusion can cause ischaemia in the fingers because of marked peripheral vasoconstriction • ↑BP and SVR (CO may ↓) • Peripheral vasoconstriction • ↑ Myocardial O2 consumption • Coronary artery vasodilation • ↑ Pulmonary vascular resistance CVS • ↓Renal blood flow • ↓Splanchnic blood flow GI
- 22. NORADRENALINE METABOLISM AND EXCRETION •Exogenous noradrenaline metabolised by: • • Mitochondrial monoamine oxidase (in liver, brain and kidney) • • Cytoplasmic COMT • Excreted in urine, main product is VMA (3-methoxy, 4-hydroxymandelic acid) • Endogenous noradrenaline metabolised by: • Uptake 1: active uptake back in to nerve terminals where reused, or metabolised by MAO • Uptake 2: diffusion away from the nerve and metabolised by COMT to VMA, or normetadrenaline
- 23. DRUG ALPHA 1BETA 1 BETA 2 DOPAMINERGIC PREDOMINANT CLINICAL EFFECTS PHENYLEPHRINE *** 0 0 0 SVR , CO / NOREPINEPHRINE *** ** 0 0 SVR , CO / ADRENALINE *** *** ** 0 CO , SVR (Low dose) , SVR
- 24. REFERENCES • The PrimaryFRCA Structured Oral Examination Study Guide 2. Second Edition. Kate McCombe and Lara Wijayasiri • Pharmacology for Anaesthesia and Intensive Care. Fourth Edition. T.E Peck, S.A Hill
Editor's Notes
- #16 Tolerance: larger doses required to produce the same effect. Pharmacokinetic clearance: increased drug clearance induced by repeat doses Pharmacodynamic tolerance: changes in receptor number or function due to exposure to the drug Physiological tolerance: homeostatic adaptation of unrelated systems to compensate for drug effect Behavioural tolerance: learned compensation for the effect of the drug which diminishes its effects. Tachyphylaxis: a rapid decrease in response to repeated doses over a short time period Not dose-dependent (i.e. giving a larger dose of the drug may not restore the maximum effect) Rate-sensitive (i.e. requires frequent dosing) After a relatively short period of withholding the drug, its effect is restored (i.e tachyphylaxis resolves rapidly)