An inotrope is an agent that alters the force or energy of muscular contractions. Negatively inotropic agents weaken the force of muscular contractions. Positively inotropic agents increase the strength of muscular contraction.
The term inotropic state is most commonly used in reference to various drugs that affect the strength of contraction of heart muscle. However, it can also refer to pathological conditions. For example, enlarged heart muscle can increase inotropic state, whereas dead heart muscle can decrease it. Cardiac inotropes Both positive and negative inotropes are used in the management of various cardiovascular conditions. The choice of agent depends largely on specific pharmacological effects of individual agents with respect to the condition. One of the most important factors affecting inotropic state is the level of calcium in the cytoplasm of the muscle cell. Positive inotropes usually increase this level, while negative inotropes decrease it. However, not all positively and negatively drugs affect calcium release, and, among those that do, the mechanism for manipulating the calcium level can differ from drug to drug.
Positive inotropic agents Positive inotropic agents increase myocardial contractility, and are used to support cardiac function in conditions such as decompensated congestive heart failure, cardiogenic shock, septic shock, myocardial infarction, cardiomyopathy, etc. Examples of positive inotropic agents include: Amiodarone Berberine Calcium Calcium sensitisers Levosimendan Cardiac myosin activators Omecamtiv Catecholamines Dopamine Dobutamine Dopexamine Epinephrine Isoprenaline Norepinephrine Angiotensin II Digoxin Digitalis Eicosanoids Prostaglandins Phosphodiesterase inhibitors Enoximone Milrinone Amrinone Theophylline Glucagon Insulin Negative inotropic agents Negative inotropic agents decrease myocardial contractility, and are used to decrease cardiac workload in conditions such as angina. While negative inotropism may precipitate or exacerbate heart failure, certain beta blockers have been believed to reduce morbidity and mortality in congestive heart failure. Quite recently, however, the effectiveness of beta blockers has come under renewed critical scientific scrutiny. Beta blockers Calcium channel blockers Diltiazem Verapamil Clevidipine Class IA antiarrhythmics such as Quinidine Procainamide disopyramide Class IC antiarrhythmics such as Flecainide See also Pressors Bathmotropic Dromotropic References.
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