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Adrenergic Blockers by Ms. Maida

This document discusses different types of adrenergic antagonists including alpha blockers, mixed antagonists, and beta blockers. It provides details on specific drugs in each category like their mechanisms of action, dosages, side effects and more.

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Shimmering Moon
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30 views23 pages

Adrenergic Blockers by Ms. Maida

This document discusses different types of adrenergic antagonists including alpha blockers, mixed antagonists, and beta blockers. It provides details on specific drugs in each category like their mechanisms of action, dosages, side effects and more.

Uploaded by

Shimmering Moon
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPT, PDF, TXT or read online on Scribd
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ADRENERGIC ANTAGONISTS

By
Maidah Mehtab
2nd Year (2019-2022)
Anaesthesia Technology
Module: Medical Pharmacology
Assigned Facilitator: Maidah
Mehtab
Adrenergic Antagonist
 They bind but do not activate
adrenoceptors.
 They act by preventing adrenergic activity.
 There are three types
1. Alpha blockers
2. Mixed antagonists
3. Beta blockers
Alpha-Blockers

 These are the drugs that block alpha adrenoceptors.

 Blockade of these receptors reduces the sympathetic


tone of the blood vessels, resulting in decreased
peripheral vascular resistance. This induces a reflex
tachycardia resulting from lowering of blood pressure
Alpha-Blockers
 Alpha 1 antagonists
Doxazosin
prazosin
Terazosin
 Alpha 1 & 2 antagonists
phentolamine
phenoxybenzamine
Alpha-Blockers- Phentolamine
 It produces a competitive block of alpha 1
and alpha 2 receptors.
 Direct smooth muscle relaxation are
responsible for peripheral vasodilation
and a decline in arterial blood pressure.
This drop provokes reflex tachycardia
 These CVS effects are usually apparent
within 2 min and last up to 15 min
Alpha-Blockers- Phentolamine
 Dose & packaging:
• It is administered IV as intermittent
bolus-----1 to 5µg in adults
• Or as continuous infusion----10µg in
100ml dextrose water (100µg/ml)
• It is packaged as lyophilized powder.
(5mg)
Alpha-Blockers- Phentolamine
 Side Effects:
• Postural hypotension
• Reflex tachycardia
• Fluid retention
• Epinephrine reversal
 Contraindications:
• Decreased coronary perfusion because it
triggers arrythmias and anginal pain.
Mixed Antagonists---Labetalol

 They block alpha1, beta1 and beta2


receptors.
 The ratio of alpha blockade to beta
blockade has been estimated to be
approx. 1:7 following IV
administration
Mixed Antagonists---Labetalol
 Actions:
The mixed blockade reduces the peripheral
vascular resistance and arterial blood pressure.
The HR and CO are usually slightly depressed
or unchanged
Thus labetalol lowers BP without reflex
tachycardia because of its combination of alpha
and beta effects
Mixed Antagonists---Labetalol
 Actions:
Peak effect usually occur in 5 min
after an IV dose.
They do not alter the serum lipid or
blood glucose levels.
Mixed Antagonists---Labetalol
 Therapeutic Uses:
 it is useful in treating hypertension in whom
increased peripheral vascular resistance is
undesirable.
 It may be employed to treat pregnancy induced
hypertension as an alternative to methyldopa
 IV labetalol can also used to treat hypertensive
emergencies.
Mixed Antagonists---Labetalol

 Adverse Effects:
 Paradoxical hypertension
 Left venticular failure
 Bronchospasm
 Dizziness
Receptor selectivity of adrenergic antagonists

Drug α1 α2 β1 β2
Prazosin - 0 0 0
Phenoxybenzamine - - 0 0
Phentolamine - - 0 0
Labetalol - 0 - -
Metoprolol 0 0 - -
Esmolol 0 0 - -
Propranolol 0 0 - -
Beta-Blockers
 pharm properties
• variations in:
 Cardioselectivity

Those that are more β1 selective have less influence on


bronchopulmonary and vascular β2 receptors
 membrane-stabilizing effects (local anesthesia)
 intrinsic sympathomimetic activity (some are partial agonists)
 lipid solubility
 metabolism

• these variations are generally of little clinical significance


 2 important ones are lipid and agonist properties
Beta-Blockers
 Cardioselectivity
• metoprolol, esmolol, acebutolol, atenolol, betaxolol
• relative selectivity for B1 receptor
• theoretically cause less bronchoconstriction and peripheral
vasodilation
Beta-Blockers
 Membrane stabilizing effect
• Propranolol, labetalol, and pindolol
• Block sodium channels
• Usually not evident at therapeutic doses
• Contribute to toxicity by prolonging QRS duration and
impairing cardiac conduction.
• Seizures are more commonly observed
Beta-Blockers
 B-agonist (“intrinsic sympathomim. activity = ISA)
• pindolol, alprenolol, acebutolol, carteolol, dilevalol, oxprenolol
• cause little or no resting heart rate depression, but block
increased rate due to exercise
 useful if patient is naturally bradycardic at rest
Beta-Blockers
 lipophilic
• propranolol, metoprolol, oxprenolol, bisoprolol, carevdilol
• readily absorbed from GI, metabolized in liver
• large volume of distrib, and penetrate BBB well
 hydrophilic
• acebutolol, atenolol, betaxolol, carteolol, nadolol. sotalol
• less readily absorbed, not extensively metabolized
• long plasma half-lives
 = hepatic failure prolong t1/2 lipo, renal failure prolongs
hydrophilic
Beta-Blockers
 Metabolism
 Some are eliminated by hepatic metabolism e.g
metoprolol
 Some are excreted by kidneys unchanged e.g
atenolol
 Some are hydrolyzed in blood e.g esmolol
Beta-Blockers
 Adverse effects
• CNS effects (sedation, depression, hallucinations)
 seen with hydrophilic as well as lipophilics

• precipitation of heart failure


• aggravation of bronchospasm in asthma
• Worsen myocardial depression of volatile anesthetics
• Unmask negative inotropic chracteristics of indirect cardiac stimulants
• hypoglycemia in diabetes
 due to blockade of catecholamine-mediated counterreg and antagonism of
adrenergic warning signs of hypoglycemia)
• hyperkalemia if K intolerance
• elevation in 3glycerides, depression HDL
• Discontinuation of beta blockade for 24-48 hrs trigger a withdrawl syndrome
characterized by hypertension, tachycardia and angina
Pharmacology of β-blockers
Selectivity for β1- ISA α2- Hepatic t1/2
Receptors Blockade Metabolism
Atenolol + 0 0 0 6-7
Esmolol + 0 0 0 -1/4
Labetalol 0 + + 4
Metoprolol + 0 0 + 3-4
Propranolol 0 0 + 4-6
Thank You

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