Increased myocardial oxygen consumption

Introduction The amount of oxygen consumed by the organization per unit time. Also known as oxygen uptake (oxygen uptake). Under normal circumstances, it is mainly determined by the function of the human circulation system. The oxygen consumption of the myocardium changes only when it is in urgent need of oxygen. Oxygen consumption is high and it is prone to hypoxia. This change may be reversible. Myocardial oxygen consumption is 27ml/min in a quiet state, accounting for 12% of the total oxygen consumption of the whole body. It is one of the organs with the most oxygen consumption in the human body and one of the organs with the least resistance to hypoxia. The aerobic rhythm movement of the heart is also the process of exercise consumption. The oxygen consumption of the moving myocardium of the body is more than doubled.

Cause

There are 6 factors that determine myocardial oxygen consumption, including 3 major factors and 3 secondary factors.

Three main factors: First, ventricular wall tension during systole (systolic ventricular volume × intracardiac pressure ventricular wall thickness); second, wall tension duration (heart rate × systolic ejection time); third is myocardial contractility .

3 secondary factors: one is basal metabolism; the second is electro-acupuncture; the third is the shortening of myocardial fibers.

an examination

Related inspection

Serum adenosine deaminase serum adenosine deaminase (ADA) Doppler echocardiography

The myocardial oxygen consumption is large, and the amount of oxygen taken up by the unit volume of blood is large. In the case of myocardial hypoxia, the rate of oxygen uptake per unit volume of blood is further limited, mainly relying on dilating coronary vessels to increase myocardial oxygen supply. Coronary dilatation is caused by local metabolites (adenosine, H+, K+, PGI2, etc.) and -adrenergic receptors in coronary smooth muscle, and the role of adenosine is the most important. When cardiomyocytes are hypoxic, AMP produced by ATP and ADP increases, and AMP dephosphorizes under the action of 5-nucleotidase to form adenosine. Adenosine easily penetrates into the tissue fluid through the cell membrane and acts on the coronary vessels to expand. Most of the adenosine in the tissue fluid usually enters the cell, rephosphorylates to form AMP, and a part is inactivated by adenosine deaminase. Adenosine deaminase activity may be reduced during hypoxia, which is also a cause of local adenosine increase.

Myocardial oxygen consumption is about 7ml ~ 9ml / 100g, accounting for 12% of systemic oxygen consumption. The distribution of myocardial oxygen consumption mainly has the following aspects:

1. Myocardial electrical activity, accounting for 0.05%;

2. The essential metabolism that maintains cell survival when the heart muscle stops beating, accounting for 19%;

3. Myocardial tension is one of the main determinants of myocardial oxygen consumption;

4. Heart rate is another important factor in determining myocardial oxygen consumption. Increased oxygen consumption when heart rate increases;

5. Myocardial contraction strength;

6. In the loaded state, the shortening of the myocardial fibers consumes more oxygen than the isometric contraction under the same tension.

Among the above factors, myocardial tension, heart rate and myocardial contractility are factors that determine oxygen consumption, accounting for more than 70% of myocardial oxygen consumption.

Differential diagnosis

Myocardial hypoxia: The heart is deprived of oxygen due to insufficient blood supply. The main manifestations are: palpitations, heart discomfort, sometimes heart pain or appreciation of colic; shortness of breath, exercise, fullness or agitation is more serious, the body is weak; in severe cases, short-term shock.

The myocardial oxygen consumption is large, and the amount of oxygen taken up by the unit volume of blood is large. In the case of myocardial hypoxia, the rate of oxygen uptake per unit volume of blood is further limited, mainly relying on dilating coronary vessels to increase myocardial oxygen supply. Coronary dilatation is caused by local metabolites (adenosine, H+, K+, PGI2, etc.) and -adrenergic receptors in coronary smooth muscle, and the role of adenosine is the most important. When cardiomyocytes are hypoxic, AMP produced by ATP and ADP increases, and AMP dephosphorizes under the action of 5-nucleotidase to form adenosine. Adenosine easily penetrates into the tissue fluid through the cell membrane and acts on the coronary vessels to expand. Most of the adenosine in the tissue fluid usually enters the cell, rephosphorylates to form AMP, and a part is inactivated by adenosine deaminase. Adenosine deaminase activity may be reduced during hypoxia, which is also a cause of local adenosine increase.

Myocardial oxygen consumption is about 7ml ~ 9ml / 100g, accounting for 12% of systemic oxygen consumption.

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