Cardiovascular Physiology and Pathophysiology
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Physiology
Structure and Function4 Topics -
Lymphatics and Edema Formation
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The Microcirculation
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Vascular Control3 Topics
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The Cardiac Cycle
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Determinants of Myocardial Performance7 Topics
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Neuro-Control of Heart and Vasculature4 Topics
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Electro-Mechanical Association4 Topics
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Electrical Side of the Heart4 Topics
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PathophysiologyDefining Heart Failure
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Causes of Heart Failure
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MVO2 and Heart Failure
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Cardiac Output and Heart Failure7 Topics
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Compensation for Circulatory Failure
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Vascular Tone in Heart Failure
MVO2 and Heart Failure
Myocardial oxygen consumption (MVO2) refers to the amount of oxygen consumed (required) by the heart muscle for contraction and relaxation.
MVO2 is increased when:
- HR is increased
- Contractility is increased
- Ventricular volume is increased (increase in preload)
- Ventricular pressure is increased (increase in afterload)
- Ventricular thickness is decreased (an increase in afterload)
MVO2 is decreased when the opposite conditions occur.
Changes in myocardial oxygen consumption and cardiac performance
Under normal conditions, at rest, myocardial oxygen supply and myocardial oxygen demand are roughly equal. Therefore, there is little to no oxygen reserve for the heart muscle.
Any situation that increases the myocardial oxygen consumption must also cause an increase in cardiac output and coronary flow (myocardial oxygen supply) or else demand for O2 will outstrip supply and anaerobic conditions will prevail. This anaerobic state results in less efficient cardiac performance (reduced contractility) and dysrhythmias which can result in a further reduction in cardiac output with further reductions in coronary flow (myocardial O2 supply). A vicious cycle occurs.