Cardiac insufficiency occurs when a person’s heart disease continues to worsen and cardiac decompensation exceeds its compensatory function. In the early stages of cardiac insufficiency, the compensatory acceleration of the heart rate helps to increase the cardiac output to normal or near normal level, however, the acceleration of the heart rate also increases the myocardial oxygen consumption and shortens the coronary artery supply and ventricular filling time, which decreases the cardiac output per beat instead. What are the causes of cardiac decompensation? 1, accelerated heart rate, reduced cardiac output: early cardiac insufficiency, compensatory acceleration of the heart rate, although it helps to increase the amount of cardiac output to reach or near the normal level, however, the accelerated heart rate also increases myocardial oxygen consumption, and coronary artery blood supply and ventricular filling time is shortened, and the volume of blood per beat decreases cardiac output instead. 2, water, sodium retention: the reduction of cardiac blood volume, causing the redistribution of blood, the reduction of renal blood flow. The reduction of renal blood flow can cause the glomerular filtration rate to decrease or renin secretion to increase, which in turn acts on the angiotensinogen produced by the liver to form angiotensin I. Angiotensin I passes through the pulmonary and renal circulation and, under the action of converting enzymes, forms tubotensin II, which, in addition to causing systemic and small renal artery spasm to aggravate renal ischemia, also induces the adrenal cortex to secrete more aldosterone, which increases sodium retention and plasma osmolality, stimulating the osmotic pressure receptors near the hypothalamic supraoptic nucleus and reflexively increasing the secretion of antidiuretic hormone in the posterior pituitary gland, thus causing sodium, water This causes sodium and water retention, increased blood volume, venous and capillary congestion and increased pressure. 3. Increased ventricular end-diastolic pressure: In heart failure, myocardial contractility is weakened, heart beat output is reduced, residual blood volume in the ventricular cavity is increased, ventricular end-diastolic pressure is elevated, venous return is obstructed, causing venous stasis and increased venous pressure, and when the increase in intracapillary hydrostatic pressure exceeds plasma osmolarity and tissue pressure, intracapillary fluid extravasates and tissue edema.