Drugs for Tachycardia

A daily-taken oral nitrate used to treat angina.

A nitrate alternative that doesn't cause tolerance and may directly activate guanylate cyclase, leading to hyperpolarization.

Drugs that decrease oxygen demand by inhibiting myocardial contractility and reducing afterload, helpful for variant angina.

A type of calcium channel blocker with long duration of action, used when beta-blockers may not work; includes amlodipine and nifedipine.

A dihydropyridine CCB that inhibits L-form calcium channels in all states.

Inhibits the production of active vitamin K, and is a ‘Vitamin K antagonist’.

Increase heart rate by acting on beta-1 adrenoreceptors.

Selective beta-1 adrenoreceptor agonist, increases cAMP, and enhances Ca entry, used for heart failure and shock.

Aspirin inhibits cyclooxygenase (COX-1) in platelets, decreasing cAMP and cGMP, acting as a vasodilator.

Aspirin decreases both cAMP and cGMP levels, a key step in its anti-clotting effect.

Abciximab is a monoclonal antibody that prevents fibrinogen from binding to GPIIb/IIIa receptors, stopping platelet aggregation.

Fibrinolytics promote the breakdown of fibrin strands in blood clots.

Alteplase (a recombinant tPA) is mainly used to treat strokes and acute thrombotic/embolic events, such as post-MI.

Tranexamic acid is a procoagulant that blocks fibrin degradation. It helps create clots.

Statins inhibit HMG-CoA reductase, lowering cholesterol synthesis.

Ezetimibe inhibits cholesterol absorption, reducing cholesterol levels.

Vitamin K is crucial for the production of clotting factors.

Desmopressin stimulates the release of von Willebrand factor (vWF), important for blood clotting.

Diltiazem decreases the amplitude of the nodal action potential (AP) and increases its duration (effective refractory period, ERP).

Diltiazem has a negative inotropic effect on myocytes, decreasing the duration of their AP. This can be risky in ventricular tachycardias.

Digoxin inhibits the Na+/K+ pump, which pumps out 3 Na ions for every 3 K ions pumped in after an action potential (AP). This indirectly increases Ca levels in the heart, leading to increased heart rate.

Digoxin increases heart rate by increasing intracellular Ca in myocytes. This is used for heart failure treatment and relieving ventricular tachycardia.

Adenosine activates A1 receptors and Gi receptors in the AV node, increasing K+ permeability and hyperpolarizing the node. This slows down heart rate.

Atropine is a non-specific muscarinic antagonist used for short-term treatment of bradycardia. It blocks the effects of acetylcholine, which slows down heart rate.

Adrenaline is a non-specific adrenergic agonist used for short-term treatment of bradycardia. It stimulates beta 1 receptors in the heart, increasing heart rate.

Dopamine is a beta 1 receptor agonist used for short-term treatment of bradycardia. It increases heart rate and contractility.

Dobutamine is a selective beta 1 receptor agonist used for short-term treatment of bradycardia. It is more selective for beta 1 than beta 2, making it more specific for heart stimulation.

Drugs used for anticoagulation when warfarin is not suitable, such as Xaban (direct Factor X inhibitor) and Dabigatran (direct thrombin inhibitor).

Anticoagulants that work by binding paradoxical clotting factors for warfarin treatment, activating antithrombin III, and removing clotting factors.

Drugs like Xaban directly inhibit Factor X, preventing the clotting cascade and reducing thromboembolic risk.

Drugs like Dabigatran directly inhibit thrombin, preventing the formation of fibrin clots and reducing thromboembolic events.

Drugs that block platelet activation and aggregation, reducing the formation of blood clots. These include Clopidogrel, Prasugrel, and Ticagrelor.

Antiarrhythmic drugs that effectively treat very fast heart rates, particularly ventricular tachycardia, but have minimal effect on atrial fibrillation or atrial tachycardia. They work primarily on the rapid dissociation phase of the action potential.

A Class 1b antiarrhythmic drug administered intravenously, used to treat ventricular tachycardia. It has minimal impact on slower rhythms like atrial fibrillation.

Potent antiarrhythmic drugs effective for both atrial and ventricular tachycardias. They have a strong negative inotropic effect and are associated with the risk of myocardial infarction if used after a heart attack.

A Class 1c antiarrhythmic drug that effectively treats a variety of tachycardias but increases the risk of myocardial infarction if used after a heart attack.

A Class 1c antiarrhythmic drug that effectively treats atrial and ventricular tachycardias. It also has beta-blocker effects.

Antiarrhythmic drugs that block calcium channels and typically end in 'ol'. They prolong the phase 4 depolarization in the AV node, effectively reduce arrhythmias, and are used post-MI.

A Class II antiarrhythmic drug with both Class II and Class III activity. It prolongs the action potential duration and is used post-MI.

Antiarrhythmic drugs that block potassium channels, extending the effective refractory period and slowing the heart rate. They are effective for slowing heart rate and have a unique mechanism of action.

A Class III antiarrhythmic drug that blocks potassium channels, effectively slows heart rate, and has additional Class I and IV activities. It is extremely lipophilic, leading to possible adverse effects.

Antiarrhythmic drugs that block calcium channels, reducing heart contractility and slowing heart rate. They are used for a variety of arrhythmias and can also be used for other cardiovascular conditions.