4 topics with concise reviews: definitions, key facts, and class questions.
In this section, we analyze drugs capable of increasing blood pressure by increasing cardiac output — cardiotonic agents. This is a fundamental topic for understanding the principles of therapy for acute and chronic heart failure.
The section builds from physiology to pharmacology. First, we review the mechanism of cardiomyocyte contraction — without understanding the function of ion channels and the role of calcium, learning the mechanisms of drug action will be impossible. Then we examine in detail two key groups: classical cardiac glycosides and modern non-glycoside inotropes using levosimendan as an example.
What is most frequently asked in class? Professors love to quiz students on the mechanism of action of cardiac glycosides (blockade of Na⁺/K⁺-ATPase), signs of digitalis intoxication, and antidotes. Also, be prepared to explain how levosimendan increases myocardial contractility without increasing its oxygen demand.
What is inotropism and how is it related to cardiotonics?
Inotropism is the basic function of working cardiomyocytes, ensuring myocardial contractility. Cardiotonic agents possess a positive inotropic effect, meaning they purposefully stimulate and enhance this contractile activity.
Which proteins directly provide cardiomyocyte contraction?
The physiological basis of contraction is the association of two main contractile proteins — actin and myosin.
What is the main pharmacological effect characteristic of cardiac glycosides?
The primary effect is a positive inotropic effect, that is, an increase in myocardial contractility due to an elevation in cytosolic calcium ion concentration within cardiomyocytes.
What is the main difference between levosimendan and dobutamine/milrinone?
Dobutamine and milrinone exert their effect at the first stage of the intracellular cycle, enhancing the influx of calcium ions through plasma membrane channels. Levosimendan, on the other hand, does not increase the amount of incoming calcium, but rather modulates the binding process of already available free cytosolic calcium to troponin C.
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