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Cardiovascular Pharmacology Concepts

Richard E. Klabunde, PhD

Clinical Disorders:

Therapeutic Classes:

Mechanism Classes:


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Click here for information on Cardiovascular Physiology Concepts, 2nd edition, a textbook published by Lippincott Williams & Wilkins (2011)

 

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Click here for information on Normal and Abnormal Blood Pressure, a textbook published by Richard E. Klabunde (2013)

 



The Pharmacologic Treatment of Angina

Causes of Angina

Angina, which is sometimes called angina pectoris, is chest pain that is caused by inadequate coronary blood flow to the myocardium.

Angina (chest pain) Causes

When coronary blood flow cannot deliver sufficient oxygen to support cardiac oxidative metabolism (reduced oxygen supply/demand ratio), the myocardium becomes hypoxic. This triggers pain receptors within the heart, which lead to the classical presentation of chest pain and the sensation of substernal heaviness or pressure.

As described below and in the above figure, coronary blood flow can be decreased by 1) transient constriction of the coronar arteries (i.e., vasospasm), 2) chronic narrowing of a coronary artery (i.e., fixed stenosis) caused by atherosclerosis, or 3) the formation of a blood clot within the vessel lumen (i.e., coronary thrombosis). Angina can also be precipitated by increased oxygen consumption, especially if the coronary blood flow is already compromised.  Increases in heart rate, contractility (inotropy), afterload (e.g., elevated arterial pressure, aortic valve stenosis, ventricular dilation), and preload, the latter of which stimulates the Frank-Starling mechanism to increase the force of cardiac contraction. Decreasing either coronary flow or increasing oxygen demand, or a combination of the two, will decrease the oxygen supply/demand ratio and lead to myocardial hypoxia and the stimulation of pain receptors within the myocardium.

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Types of Angina

Revised 03/14/07

DISCLAIMER: These materials are for educational purposes only, and are not a source of medical decision-making advice.