Heart Failure Or Congestive Heart Failure (CHF) And Its Causes In Complete Detail
Heart failure, often called congestive heart failure (CHF), is a common endpoint of various forms of heart disease and is usually a progressive condition with a poor diagnosis. In the United States alone, more than 5 million people are affected by the condition, which results in more than 1 million hospital admissions each year and a financial burden of over $32 billion.
CHF occurs when the heart tissue is unable to produce enough energy to meet its metabolic needs, or can do so at just above normal filling pressure. In rare cases, heart failure results from a significant increase in tissue demand, such as hyperthyroidism, or a decrease in oxygen carrying capacity, such as anemia (heart failure).
The onset of CHF is sometimes sudden, as in a major myocardial infarction or acute valve dysfunction. However, in most cases, CHF develops slowly and carefully due to the cumulative effects of chronic workload or progressive myocardial damage.
Heart failure can be linked to systolic or diastolic dysfunction. Systolic dysfunction is the result of insufficient myocardial contraction, usually as a result of ischemic heart disease or hypertension.
Diastolic dysfunction refers to the failure of the heart to relax and fill properly, which can be caused by large left ventricular hypertrophy, myocardial fibrosis, amyloid accumulation, or constructive pericarditis. About half of CHF cases are related to diastolic dysfunction and are more common in the elderly, diabetics and women.
Heart failure can be caused by valve failure (for example, endocarditis) or by a rapid rise in blood volume or blood pressure, even if the heart is normal. When the diseased heart is unable to pump blood efficiently, the final diastolic pressure in the ventricles increases.
Volume, increasing end-diastolic pressure, and increasing venous pressure. Thus, insufficient cardiac output, called direct reduction, is almost always accompanied by an increase in the stagnation of the venous circulation, ie, insufficient retraction. Although heart problems are often rooted in poor heart function, almost all other organs are eventually affected by some combination back and forward failure of heart disease.
1- The Frank-Starling Mechanism
Increasing the amount of final diastolic filling expands the heart and increases cardiac myofibrillar stretch. These longer fibers shrink more strongly, thus increasing cardiac output. If the aged ventricle is able to maintain cardiac output in this way, the patient may experience compensatory heart failure. However, ventricular dilation occurs at the expense of increasing wall tension and increasing oxygen demand from the already affected myocardium. Over time, weak muscles are unable to pump enough blood to meet the body’s needs, and patients experience unpaid heart failure.
2- Activation Of Neurohumoral System
- The release of the neurotransmitter norepinephrine by the autonomic nervous system increases heart rate and increases myocardial contractility and vascular resistance.
- Activation of renin-angiotensin-aldosterone system stimulates water and salt retention Volume of circulation) and increase in vascular head.
- Release of atrial neutrophilic peptides balances the renin-angiotensin-aldosterone system by diuresis and relaxes vascular smooth muscle.
3- Myocardial Structural Changes Including Augmented Muscle Mass
- In cases of excessive pressure loading (e.g., hypertension or valvular stenosis), new sarcomares are usually parallel to the longitudinal axis of the myocyte adjacent to the existing sarcomars. Thus, an increase in the diameter of the muscle fibers leads to concentrated hypertrophy: the thickness of the ventricular wall increases without increasing the size of the space.
- In case of volume overload (for example, valve or shunt failure), new sarcomers are introduced. Series with pre-existing sarcomares, thus increasing the length of muscle fibers. As a result, the ventricles begin to dilate, and as a result the wall thickness may increase, return to normal, or decrease. Therefore, the weight of the heart, rather than the thickness of the wall, is the best indication of hypertrophy in the volume of a sheep’s liver.
Compensation is the price of a hypertrophy. Hypertrophic myocardium’s oxygen demand is made possible by an increase in myocardial cell mass. Because the myocardial capillary bed does not expand in response to an increase in myocardial oxygen demand, myocardium suffers from ischemic injury.
Hypertrophy is also commonly associated with changes in the expression patterns of genes reminiscent of fetal myocytes, such as changes in the dominant shape of the heavy chain produced by myosin. The expression of altered genes may contribute to changes in the function of myocytes resulting in increased heart rate and compressive strength, which in turn increases cardiac output, but also increases the oxygen consumption by the heart also increases.
In the case of ischemia and a chronic increase in workload, other pathological changes eventually occur, including myocyte apoptosis, cytoskeletal changes, and extracellular matrix (ECM) accumulation.
Pathological Compensatory Cardiac Hypertrophy
In contrast, volume-loading hypertrophy due to regular aerobic exercise (physiological hypertrophy) often accompanies a decrease in capillary density, decreased heart rate, and resting blood pressure.
This physical adaptation reduces overall heart disease and mortality.
Competitively, static exercise (such as weight lifting) is associated with stress hypertrophy and may not have the same beneficial effects.