Heart failure is when the heart is not pumping as it should be. With congestive heart failure you have to seek immediate medical care. Your body depends on the heart’s pumping action to transfer oxygenated blood to the body’s cells. The body can work properly when the cells are sufficiently sustained. Heart failure becomes pronounced when the weakened heart cannot supply the cells with enough blood and this results in tiredness and shortness of breath and a hacking cough. Regular exercises, like walking, or climbing stairs can turn out to be exceptionally difficult.
The two types of heart failure are systolic and diastolic. With systolic heart failure, also known as heart failure with reduced ejection fraction or (HFrEF), the left ventricle loses its capacity to contract regularly. The heart cannot pump with enough power to push enough blood into the flow. The ejection fraction is less than 40 percent and the most common causes are cardiomyopathies coronary artery disease, usually been preceded by a myocardial infarction (heart attack), although these often occur silently.
Heart failure with preserved ejection fraction (HFpEF), also known as the diastolic failure (or diastolic dysfunction): The left ventricle loses its capacity to relax regularly (because the muscle is hardened). The heart cannot appropriately load up with blood during the resting time frame between each beat. EF is higher than 40 percent, although not always in the normal range of 55 to 70 percent. Most indications of diastolic heart failure are connected to chronic shortness of breath during exertion. Peripheral swelling may be seen sooner in the course of diastolic heart failure than in systolic heart failure.
Some problems of heart failure are irregular heart rhythm, heart valve problems, kidney damage or failure, anemia, liver injury, lung complications, life-threatening weight loss, and muscle loss. If your heart is frail, the higher and lower chambers probably won’t squeeze at the same period. Your heart may beat too slowly, too quickly, or in an irregular pattern. When the rhythm is off, that’s when your heart can’t adequately direct blood out to your body.
In conditions of strain, neurohumoral responses support increase heart function and keep blood pressure and organ perfusion, but continuing stimulation of these responses is damaging to the standard balance between myocardial-stimulating and vasoconstricting hormones and between myocardial-relaxing and vasodilating hormones.
The heart comprised of many neurohumoral receptors such as angiotensin II type 1 (AT1) and type 2 (AT2), serotonin, adenosine, and natriuretic peptides. The parts of all these receptors are not completely clear. In patients with heart failure, beta-1 receptors (which constitute 70% of cardiac beta receptors) are downregulated, possibly in response to excessive sympathetic activation. The result of downregulation is impaired myocyte contractility and increased heart rate.
Plasma norepinephrine levels are enlarged, mainly reflecting sympathetic nerve stimulus making it impossible for plasma epinephrine levels to increase. Damaging effects consist of vasoconstriction with increased preload and afterload, direct myocardial damage including apoptosis, reduced renal blood flow, and activation of other neurohumoral systems, including the renin-angiotensin-aldosterone- vasopressin system.
Vasopressin is free in response to a fall in blood pressure by many neurohormonal stimuli. Increased vasopressin reduces renal excretion of free water, probably contributive to hyponatremia in heart failure. Vasopressin levels in patients with heart failure and normal blood pressure fluctuate.