What Is Decompensated Heart Failure?

The compensatory response is a necessary measure for the body to prevent further reduction of oxygen when heart failure occurs, and the intensity of the compensatory response is closely related to whether or not the heart failure occurs, the rate of occurrence, and the severity. If oxygen can still meet the body's metabolic needs, and the patient does not show the performance of heart failure, this is complete compensation. If the cardiac output can only meet the body's metabolic needs in the resting state, the patient has mild heart strength. The manifestation of failure is called incomplete compensation; in severe cases, oxygen cannot even meet the body's metabolic needs in the resting state, and the patient has obvious symptoms and signs of heart failure, which is decompensation.

Compensatory response

(A), heart rate is accelerated

This is a quick compensation. Because the cardiac output = stroke volume × heart rate, within a certain range, and the stroke volume (stroke volume) is constant, the increase in heart rate (heart rate) can increase CO, and can be improved by increasing Diastolic blood pressure and promote coronary blood perfusion. But this compensation method is limited and uneconomical. When the heart rate is too fast (greater than 180 beats / min for adults), CO decreases due to increased myocardial oxygen consumption, shortened diastole, and insufficient heart filling. The degree of heart rate acceleration can be used clinically as an indicator to determine the severity of heart failure.

Increased heart rate is mainly caused by sympathetic nerve excitement and increased catecholamine secretion. The mechanism is: CO decreases during heart failure, arterial blood pressure decreases, and baroreceptor stimulation is weakened, resulting in a rapid heart rate; CO reduction causes the right atrium and vena cava pressure to increase, stimulating pressure or volume sensors, and reflectively Increased catecholamine secretion, through the myocardial cell membrane and / or receptors, accelerates heart rate and enhances myocardial contractility. Hypoxia stimulates the aorta and carotid body chemoreceptors, excites the respiratory center, accelerates the deepening of breathing, and causes the heart rate to increase reflexively.

(2) Self-regulation of heart pump function

1 . Increased stroke volume through self-regulation of cardiac pump function-Staring mechanism (abnormal regulation)

According to Frank-Staring's law, myocardial contractility and stroke volume within a certain range depend on the overlap of myocardial fiber thickness, thinness, and myofilament. When the sarcomere is less than 2.2um, as the sarcomere length increases, the myocardial contractility gradually increases. When it reaches 2.2um, the thick and thin myofilaments are in the best overlap state, with the largest number of effective bridges and the largest contraction. This muscle Section length is optimal. Under normal circumstances, the end-ventricular pressure is about 0 ~ 1.33kPa (0 ~ 10mmHg), and the sarcomere length is between 1.7 ~ 2.1um. When the ventricular end-diastolic pressure reaches 1.6 ~ 2.0 kPa (12 ~ 15mmHg) and the sarcomere length increases to 2.0 ~ 2.2um, the myocardial contractility and stroke volume increase at this time. Such self-regulation of cardiac output changes caused by changes in the initial length of myocardial fibers is called abnormal regulation. This type of cardiac dilatation with increased volume and increased myocardial contractility is also called tension-induced dilation. When the end-ventricular diastolic pressure is greater than 2.4 kPa (18 mmHg), the sarcomere length exceeds the optimal length, the myocardial contractility decreases, and the stroke volume decreases.

2 . Increased stroke volume through increased myocardial contractility (isochronic adjustment)

Myocardial contractility is an intrinsic characteristic of the heart that does not depend on the anterior and posterior loads to change its mechanical activity. Myocardial contractility is affected by various aspects of the excitation-contraction coupling process. When the myocardial contractility decreases and the stroke volume decreases, the sympathetic nerves excite, thereby increasing the concentration of catecholamines in the blood. By activating -adrenergic receptors, increasing the cAMP concentration in the cytoplasm, activating protein kinase A (PKA ), Phosphorylation of myosin calcium channel protein, leading to increase in the rate and amplitude of cytosolic Ca concentration after myocardial excitation, and exert a positive inotropic effect. PKA can also: phosphorylate phospholamban (PLB), weaken its inhibitory effect on the sarcoplasmic reticulum calcium pump, and enhance the ability of sarcoplasmic reticulum to take up Ca; make troponin inhibit subunit (TnI) phosphate The troponin calcium binding subunit (TnC) has a reduced affinity with Ca, so that Ca can be rapidly dissociated from the state of troponin binding, which is conducive to ventricular filling.

(Three) myocardial reconstruction

1 . Cardiac hypertrophy

Myocardial hypertrophy refers to the adaptive response of the myocardium to hemodynamic overload caused by various reasons. From the perspective of cell molecular biology, cardiac hypertrophy involves specific changes in gene expression and changes in cell phenotype. A certain degree of myocardial hypertrophy is compensatory, and excessive myocardial hypertrophy is a manifestation of decompensation.

(1) Types of myocardial hypertrophy: According to changes in ventricular end-diastolic volume and ventricular thickness, myocardial hypertrophy can be divided into two types: eccentric hypertrophy and concentric hypertrophy. Centrifugal hypertrophy refers to an increase in the weight of the heart, an enlarged ventricular cavity, and a slightly thicker wall. The ratio of the wall thickness to the diameter of the ventricle is equal to or less than normal. It is mostly caused by the overload of the heart's long-term volume, which increases the end-diastolic volume, Increased stress caused by tandem hyperplasia. Concentric hypertrophy refers to the increase in the weight of the heart, the thickening of the wall, and the larger or normal volume of the heart cavity, and the ratio of the wall thickness to the diameter of the cavity is greater than normal. The sarcomere was caused by parallel hyperplasia.

(2) Compensatory significance: In the early stage of myocardial hypertrophy, due to the cardiomyocyte hypertrophic growth and non-cardiac cell proliferative growth, there is a proportionally homogeneous change, which shows adaptive cardiac hypertrophy, which has compensatory significance. The two showed disproportionate heterogeneous growth, showing non-adaptive cardiac hypertrophy or pathological hypertrophy, the heart changed from compensatory to decompensated, and even heart failure.

(3) The main manifestations of cardiac compensation: Strengthening the pumping function of the heart: As the total myocardium increases, the total contractile force of the myocardium increases, and the pumping function of the heart strengthens; The oxygen consumption of the myocardium decreases: According to Laplace's law, = pr / 2h (s = ventricular wall stress, p = pressure, r = ventricular radius, h = ventricular wall thickness), myocardial hypertrophy, and increased ventricular wall thickness can reduce ventricular wall tension and reduce myocardial oxygen consumption; Conversion of -MHC to -MHC improves energy efficiency.

2 . Changes in cell phenotype

Phenotype changes, that is, changes in the "quality" of cardiac muscle cells caused by changes in the type of protein synthesized, are mainly achieved through the conversion of cardiac protein isoform families. For example: in myocardial hypertrophy caused by hypertrophic myocardial stimulating factors, genes that are normally expressed only during the embryonic phase (-MHC) are re-expressed and synthesized during the embryonic period; other genes (-MHC) are restricted in expression, thus Isotype conversion occurs that changes the phenotype of the cell. In addition to the above-mentioned isoform conversion, which is a normal gene expression, the molecular reconstruction of the myocardium may also be related to factors such as gene overexpression, deletion, and mutation.

3 Myocardial interstitial network reconstruction

Under the action of circulating and local renin-angiotensin-aldosterone system (RAAS), norepinephrine, cytokines, mechanical stretch, etc., non-cardiac cell proliferation, especially fibroblasts Cells: Type III collagen often increases significantly in the early stages of reconstruction, which is of great significance for the compensation of heart failure, especially in the early stages of myocardial hypertrophy. In the late stage of reconstruction, type collagen is mainly used. Because of its small extensibility and retraction, its increase increases the stiffness of the myocardium and affects the diastolic function of the ventricle.

In the case of heart failure, in addition to the above-mentioned heart itself and the neuro-humoral compensation mechanism, in order to adapt to changes in hemodynamics during heart failure, the body also compensates through the following links.

1. Increased blood volume

2. Whole body blood flow redistribution

3.The oxygen and hemoglobin dissociation curves are shifted to the right

4, enhanced bone marrow hematopoietic function