Name Class Clinical Indications Receptor Action Mechanism of Action Adverse Effects and Interactions Administration + PK
Irreversible, non-competitive binding to alpha 1 and 2 receptors. Binds to a different site than catecholamines Hypotension, headache, nasal congestion,
Post-synaptic Hypertension Non-selective
Phenoxybenzamine causing a change in shape so catecholamines can’t bind. Inhibits Gq second messenger system in the fatigue, sexual dysfunction, tachycardia and Oral
anti-adrenergic Pheochromocytoma ⍺-antagonist smooth muscle of vessels causing vasodilation, lowering the blood pressure arrhythmia
Alpha blockers
Doxazosin Post-synaptic Selective ⍺1-antagonist Antagonises ⍺1 receptors on vascular smooth muscle, inhibiting the Gq second messenger system
Hypotension, tachycardia, headache and nasal
Hypertension causing decreased Ca2+ release leading to vasodilation, lowering the blood pressure. Oral
Prazosin anti-adrenergic congestion
Alpha agonist Resistant hypertension Selective ⍺2-agonist Agonises ⍺2 receptors in presynaptic neurons. This activates the Gi second messenger system causing a
Hypotension, constipation, dizziness,
Alpha agonists Clonidine decrease of Ca2+ flow into the neuron. This polarises the cell and prevents the release of noradrenaline.
drowsiness, and dry mouth
Oral
hypotensive agent Overall it reduces sympathetic outflow from the CNS reducing heart rate and relaxing vascular smooth muscle.
Antagonises 𝛃1 receptors in the heart, inhibiting the Gs second messenger system leading to decreased
Atenolol Hypertension
release of Ca2+ from sarcoplasmic reticulum leading to decreased force of contraction. Also antagonises 𝛃1
Heart failure after MI Bradycardia, hypotension, fatigue, wheeze,
Bisoprolol Class II antiarrhythmic Atrial flutter and fibrillation
Selective 𝛃1-antagonist receptors in pacemaker cells, decreasing the inflow of Ca2+ and therefore delaying the action potential,
nausea, dizziness
Oral
Metoprolol slowing the heart rate and AV conduction. Also antagonises 𝛃1 receptors in the kidneys decreasing renin
Ventricular arrhythmias
production and therefore preventing vasoconstriction, reducing blood pressure.
Beta blockers
Hypertension Non-selective Same mechanism of action as above for 𝛃1 antagonisation. 𝛃2 antagonisation in vascular and respiratory
Bradycardia, hypotension, not to be given to
Propranolol Angina 𝛃-antagonist smooth muscle inhibits the Gs second messenger system causing vasoconstriction and
Class II antiarrhythmic Atrial flutter and fibrillation bronchoconstriction. The vasoconstriction settles down however, due to the decreased renin effect of 𝛃1
patients with respiratory illness as it can cause Oral
Timolol bronchoconstriction
Ventricular arrhythmias antagonisation.
Agonises 𝛃1 receptors in cardiac muscle cells activating the Gs second messenger system, this increases
the release of Ca2+ from the sarcoplasmic reticulum and therefore increases the force of contraction. It also
Beta agonists Dobutamine Inotropic agent Cardiogenic shock Selective 𝛃1-agonist agonises 𝛃1 receptors in the pacemaker cells of the heart, increasing the inflow of Ca2+ accelerating the
Headache, nausea, vomiting and palpitations Oral
action potential leading to increased heart rate and AV nodal conduction.
Non-dihydropyridine Blocks depolarised Ca2+ channels mainly in the heart (small effect on smooth muscle). Main effect is on
Angina
Verapamil L-type calcium channel the heart. They prevent depolarisation of cardiac myocytes by blocking the entry of Ca2+. This delays phase Bradycardia, hypotension and peripheral
Class IV Atrial flutter/fibrillation
4 of the action potential in AV and SA nodes and in cardiac myocytes, slowing the heart rate and decreasing oedema
Oral
Diltiazem PSVT blocker (-ve inotropic)
antiarrhythmic force of contraction.
Calcium CB’s
Hypertension Blocks depolarised Ca2+ channels on the cell membrane of vascular smooth muscle preventing the influx of
Dihydropyridine /
Amlodipine Vasospastic angina L-type calcium channel Ca2+ causing smooth muscle relaxation and therefore vasodilation. This increases the flow of blood through
Class IV Atrial flutter/fibrillation the coronary arteries and therefore blood supply to the heart. Also relaxes peripheral smooth muscle reducing Fatigue, gastrointestinal disorders and oedema Oral
Nifedipine blocker (vasodilation)
antiarrhythmic PSVT peripheral resistance and therefore blood pressure.
Atrial flutter/fibrillation K+ channel antagonist in the cardiac myocytes and pacemaker cells. Blocks the efflux of K+ from the cell
Class III Ventricular tachycardia Potassium channel during the repolarization phase, slowing the repolarization. This prolongs the duration of the action potential
Amiodarone without altering phase 0 or the resting membrane potential. This results in negative inotropic, chronotropic
Arrhythmias Oral
antiarrhythmic blocker
and dromotropic effects.
Potassium CB’s
Atrial flutter/fibrillation K+ channel antagonist in the cardiac myocytes and pacemaker cells. Blocks the efflux of K+ from the cell
Class III Ventricular tachycardia Potassium channel during the repolarization phase, slowing the repolarization. This prolongs the duration of the action potential
Sotalol without altering phase 0 or the resting membrane potential. This results in negative inotropic, chronotropic
Arrhythmias Oral
antiarrhythmic blocker
and dromotropic effects. Also has beta blocking properties
Quinidine Atrial flutter/fibrillation Binds to fast sodium channels in their open or inactive state preventing the influx of Na+ into myocytes
Class IA PSVT Open or inactive sodium and Purkinje fibers in the heart. In the myocytes which slows the phase 0 depolarization resulting in a
Procainamide Ventricular tachycardia negative inotropic effect. In the purkinje fibers, it antagonises HCN channels, slowing the funny current
Arrhythmias which can lead to VF Oral
antiarrhythmic channel blocker
Disopyramide Digoxin induced arrhythmias suppressing the automaticity of the cells.
Atrial flutter/fibrillation Repeatedly binds and unbinds with fast sodium channels in their open or inactive state preventing the
Class IB PSVT Weak open or inactive influx of Na+ into myocytes and Purkinje fibers in the heart. In the myocytes which slows the phase 0 Arrhythmias, anxiety, hypotension, and
Lidocaine Ventricular tachycardia depolarization resulting in a negative inotropic effect. In the purkinje fibers, it antagonises HCN channels, headache
IV
Sodium CB’s antiarrhythmic sodium channel blocker
Digoxin induced arrhythmias slowing the funny current suppressing the automaticity of the cells.
Atrial flutter/fibrillation Strongly binds to fast sodium channels in their open or inactive state preventing the influx of Na+ into
Arrhythmias, dizziness and oedema
Class IC Supraventricular tachycardia Potent open or inactive myocytes and Purkinje fibers in the heart. In the myocytes which slows the phase 0 depolarization resulting in
Flecainide Ventricular tachycardia a negative inotropic effect. In the purkinje fibers, it antagonises HCN channels, slowing the funny current
Do not use in patients with structural cardiac Oral
antiarrhythmic sodium channel blocker defects.
Digoxin induced arrhythmias suppressing the automaticity of the cells.
