Pandazi Ageliki Assistant Professor 2 nd Department of Anaesthesiology, Attikon Hospital, University of Athens
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1 Pandazi Ageliki Assistant Professor 2 nd Department of Anaesthesiology, Attikon Hospital, University of Athens
2 Sympatholytic drugs (antagonists): Bind to beta-adrenoceptors Block norepinephrine and epinephrine binding Inhibit normal sympathetic effects. Minimal effect on resting subjects, they reduce the effect of excitement/physical exertion
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4 Type of b- receptors Site Effects of stimulation b1 (E=NE) Heart (predominant, although there are also b2) Adipose tissue Kidney heart rate (SA node) conduction velocity myocardial contractility oxygen consumption automaticity (AV node and muscle) renin release Lipolysis b2 (E > NE) Skeletal muscle Skeletal muscle vasculature Bronchial smooth muscle Uterus Liver Bladder (detrusor muscle) Intestinal smooth muscle Pancreas b3 Brown adipose tissue Heat production Tremors Vasodilatation in skeletal muscle Bronchodilatation Uterine relaxation (Pregnant) Hypokalaemia and hepatic glycogenolysis Relaxation Relaxation Increase insulin secretion b1/b2 Blood 1. Anti inflammatory effect 2. Platelet aggregation
5 Catecholamines (1st messenger transmitter) Attachment over b-receptor causes b-receptor stimulation Stimulation of G-protein Stimulation of adenyl cyclase Increase Cyclic AMP (2nd messenger transmitter) Stimulation of protein kinase-a Cardiac effects Bronchial dilatation Skeletal vasodilatation Release of glucose and potassium from liver
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9 Resemblance to isoproterenol (potent b- receptor agonist) Benzene ring with various substitutions
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11 Beta-blockers with intrinsic sympathomimetic activity (ISA): Partial activation of receptor + prevention of catecholamine binding background sympathetic activity, normal and enhanced sympathetic activity prevented (useful in bradycardia) Beta-blockers with membrane stabilizing activity (MSA)= effect similar to the membrane stabilizing activity of sodium channel blockers (Class I antiarrhythmics, local anaesthetics). Beta blockers with α 1 -Receptor antagonism: additional arterial vasodilation
12 Name Pot. Beta -1 ISA MSA t1/2 (h) Lipid Sol. 1 st Pass % Abs. % Bioav. Elim Propranolol (Inderal) Nadolol (Blocadren) Timolol (Blocadren) Metoprolol (Lopressor) Atenolol (Tenormin) Esmolol (Brevibloc) Pindolol (Visken) Acebutalol (Sectral) Sotalol * (Sotapor) Labetalol # (Normodyne) High Yes >90 30 Hep; Weak Ren Mod Little >90 75 Ren Mod Yes >90 50 Hep Weak Ren min Weak NA NA Blood esterases High >90 90 Ren/Hep Mod Little Ren/Hep ;AM Weak Ren Mod Yes >90 33 Hep AM *: Class III antiarrhythmic; #: an alpha-1 blocker also. ISA: intrinsic sympathomimetic activity; MSA: membrane stabilizing activity. AM: active metabolite. Many other Beta blockers available.
13 1st generation: non-selective, they block both β 1 and β 2 adrenoceptors. 2 nd generation: relatively selective for β 1 adrenoceptors (dose-related selectivity, can be lost at higher drug doses) 3 rd generation: also possess vasodilator actions through blockade of vascular a- adrenoceptors
14 1 st generation (non-selective) 2 nd generation ( cardioselective ) 3 rd generation carteolol acebutolol Labetalol carvedilol labetalol nadolol penbutolol pindolol propranolol sotalol timolol atenolol betaxolol bisoprolol esmolol metoprolol nebivolol
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16 All the drugs are well absorbed after oral administration. Peak concentration occurs 1-3 hours after ingestion. Bioavailability after oral administration limited to varying degrees for most b-blockers (except betaxolol, penbutol, pindolol and sotalol), mainly because of hepatic (first-pass) metabolism. Bioavailability is very low and increases as the dose is increased Oral administration: lower blood concentrations than intravenous of the same dose
17 Large volumes of distribution Most have half-life of 3-10 hours, except: Esmolol: half life of 8-10 minutes and Nadolol: longest half life of 24 hrs (excerted unchanged in the urine) Propranolol, Penbutol: cross blood-brain barrier (lipophilic) Propranolol, Metoprolol: hepatic metabolism. polymorphism of P450 2D6: interindividual differences of plasma clearance, poor metabolisers 3fold-10fold higher plasma concentrations Hepatic failure, diminished hepatic blood flow, hepatic enzyme inhibition prolongs the half life Renal failure prolongs the half life of hydrophilic drugs.
18 Randomized controlled trials and meta-analyses provide conflicting guidance on the role of b-blockers in reducing perioperative complications. Pharmacological properties of -blockers may contribute to heterogeneous trial results: The extent of -blocker metabolism by CYP2D6 The time available to titrate b-blocker dosage preoperatively, and variations in b-blocker selectivity for the b-1 receptor may contribute to the heterogeneous results. Metoprolol should probably not be used for perioperative b-blockade when there is insufficient time to titrate its dose.
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20 Some level of basal sympathetic tone exists on the heart Beta-blockers reduce sympathetic influences that normally stimulate: Chronotropy (heart rate) Inotropy (contractility), Dromotropy (electrical conduction) and Lusitropy (relaxation). Beta-blockers cause decreases in: Heart rate, (Slowed SA node) Contractility, Conduction velocity (Slowed AV conduction with an increased PR interval) Relaxation rate. Even greater effect when there is elevated sympathetic activity.
21 Reduces myocardial O2 demand by reducing heart rate and force of contraction. Longer diastolic filling time increases coronary perfusion time. Reduces peripheral resistance Decreases the slope of phase 4 depolarisation as well as spontaneous firing rate of sinus or ectopic pacemakers. Reduces cardiac output. Reduces plasma renin
22 β 2 -adrenoceptors:only a small modulatory role on basal vascular tone little vascular effect B-blockers: remove a small β 2 -adrenoceptor vasodilator influence that is normally opposing the more dominant alpha-adrenoceptor mediated vasoconstrictor influence Acutely: rise in peripheral vascular resistance from unopposed α-receptor-mediated effects. Chronic use: decrease in peripheral vascular resistance in patients with hypertension. Mechanism unknown.
23 Impair relaxation of bronchial muscle (mediated by b-2) increase in airway resistance, particularly in asthmatics b-1 selective blockers: some advantages, but they do not avoid completely interactions with b-2 receptors Avoided in patients with asthma Better tolerated in patients with COPD
24 Decrease nocturnal melatonin release sleep disturbance Protect against social anxiety Lower aqueous humor secretion decrease intraocular pressure treatment of glaucoma Increase of VLDL, decrease of HDL and HDL/LDL (the same for selective, non-selective, less with blockers with ISA) Inhibition of glycogenolysis in liver (b2-blockade) impairement of recovery from hypoglycemia: Mask tachycardia (sign of hypoglycemia) Caution in insulin-dependent diabetics (preferred b1-selective) Better tolerance in patients with diabetes type II
25 Coronary artery disease (angina, myocardial infarction) Hypertension Arrhythmias Atrial fibrillation Essential tremor Symptomatic control (tachycardia, tremor) in anxiety, hyperthyroidism Migraine -prophylaxis Glaucoma (topical)
26 Hypertrophic obstructive cardiomyopathy Acute dissecting aortic aneurysm Pheochromocytoma,in conjunction with α-blocker Marfan syndrome (treatment with propranolol slows progression of aortic dilation and its complications) Prevention of variceal bleeding in portal hypertension Possible mitigation of hyperhidrosis
27 Respiratory disease : Cardio selective b-blockers are used. Cardio vascular disease : In sick sinus syndrome b-blockers are dangerous Active peripheral vascular disease : e.g. Raynaud s - b-blockers are relatively contraindicated. Renal disease : b-blockers may reduce GFR. They are excreted by kidney so in renal failure doses are changed. Liver disease : Avoid b-blockers with high first pass metabolism like propranolol.
28 Pregnancy : It may depress vitals of foetus and causes uterine artery vasoconstriction. Labetolol and Atenolol can be used. Alpha methyldopa preferred Surgical : It is prophylactically used to prevent anaesthetic tachycardia Smokers : b-blockers are less effective in reducing coronary events. Diabetes mellitus : Cardio selective agents are preferred.
29 In asthma In diabetes mellitus In peripheral vascular disease
30 The side effects result from excessive blockade of normal sympathetic influences on the heart and include: Bradycardia Exacerbating heart failure or precipitating heart failure in those with preexisting myocardial dysfunction Hypotension Hypertension in phaeochromocytoma (due to preexisting a-effect) AV nodal block Decrease in exercise tolerance (due to decreased cardiac output) Therefore: Contraindicated in patients with sinus bradycardia and partial AV block. Considerable care if given in conjunction with cardiac selective calcium-channel blockers (e.g., verapamil) (additive effects in electrical and mechanical depression). Beta-blockers in heart failure: at present only carvedilol and metoprolol have been approved by the FDA for this indication.
31 CNS : Sedation, sleep disturbances, depression, psychotic reactions, nightmares, impotence, lethargy, headache. Bronchospasm Rash Fever Drug allergy Hyperkalaemia in diabetics Uraemia, Hyperuricaemia Decrease HDL/LDL ratio Rare side effects : uveitis, sclerosing cholangitis, peritonitis, purpura, agranulocytosis.[ Abrupt withdrawal syndrome : exacerbation of MI angina, arrhythmias. Patients on chronic b-blockers therapy should be tapered of this therapy slowly.
32 Bradycardia, heart block, hypotension and low output shock. Death is more likely with agents having membrane stabilizing action Bronchoconstriction can be severe, even fatal.
33 Atropine (1-2 mg iv ):eliminates the unopposed vagal activity. For long lasting bradycardia: TPI Glucagon: cardiac inotropic and chronotropic actions independent of the b-adrenoceptors (dose 5-10 mg iv, infusion of 1-10 mg/hr) No response: iv injection or infusion of a b- adrenoceptor agonist is used, e.g. isoprenaline (4 mcg/min, increasing at 1-3 min intervals until the heart rate is beats/min) Other sympathomimetics : e.g. dobutamine, dopamine, dopexamine, noradrenaline, adrenaline For bronchoconstriction: salbutamol
34 Prototypical agent Low and dose-dependent bioavailability Long-acting form: prolonged absorbion over 24 hours No effect at a, muscarinic receptors No ISA Blocks brain serotonin receptors (unknown clinical significance)
35 B-1 selective, intravenous, ultra-short acting Ester linkage : rapid metabolism by red blood cell esterases to a metabolite with low affinity for b- receptors About 10-minute half-life, suitable for continuous infusion Rapid clinical onset and offset of action Ability to titrate the drug to changing circumstances Use in specific clinical settings: Supraventricular arryhthmias Arrhythmias associated with thyrotoxicosis Perioperative hypertension Myocardial ischemia in acutely ill patients
36 Dosage schedules: micrograms/kg/min with a loading dose or bolus. The most frequently reported adverse effect with esmolol infusion: hypotension. Adverse effects due to beta-blockade can be corrected by down-titrating or discontinuing the infusion with complete disappearance of clinical effects in minutes. Relatively safe in patients with congestive heart failure or chronic obstructive lung disease Careful titration and monitoring of the patient Barbier GH et al. Clinical rationale for the use of an ultra-short acting beta-blocker: esmolol. Int J Clin Pharmacol Ther Apr;33(4):212-8
37 Racemic mixture: (S,S) and (R,S)-isomers: relatively inactive (S,R)-isomer: potent a-blocker (a-1 selective) (R,R)-isomer: potent b-blocker Hypotension accompanied with less tachycardia than a-blockers Clinical use: hypertension of pregnancy
38 Hoffman BB. Adrenoceptor Antagonist Drugs. In Katzung B: Basic & Clinical Pharmacology. 10th Edition, Westfall TC, Westfall DP. Adrenergic Agonists and Antagonists. Section II Goodman & Gilman s The Pharmacological Basis of Therapeutics. 11th Edition. 2006
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