Managing fluid retention in heart failure

Fluid congestion, also known as fluid overload, is a common clinical symptom in heart failure patients and is linked to a worse prognosis. Although not always clinically obvious, fluid congestion may benefit from more objective measurements than a straightforward clinical evaluation. Despite being the backbone of fluid congestion therapy, diuretics have not been demonstrated in any randomised studies to have any impact on mortality in individuals with chronic heart failure. Furthermore, it is unknown how much diuretics should be used in this population. The effectiveness of a reliable strategy for identifying and then treating subclinical congestion must be investigated.

Fluid retention is linked to the onset of peripheral oedema in heart failure patients. Renal perfusion decreases as the heart begins to fail. Renin production rises as a result of the kidneys' response, which causes an increase in aldosterone synthesis, which in turn causes salt and water retention. Additionally, arginine vasopressin (AVP) is released, which further improves fluid retention and increases thirst. Renin-angiotensin-aldosterone and AVP system activation maintain cardiac preload (more fluids) and afterload (vasoconstriction, mostly owing to angiotensin II), preserving the homeostasis of the cardiovascular system but at the cost of increased systemic venous pressure (VP). The condition of the heart itself deteriorates with time as a result of the left atrium and failed LV expanding, especially if mitral regurgitation occurs. As the gradient between mean renal artery pressure (often itself diminished by the heart failure process) and systemic venous pressure diminishes, the high venous pressure might further restrict renal blood flow. The rate of glomerular filtration decreases, aggravating and maintaining the vicious cycle.

Patients with heart failure often have symptoms of congestion. Having ascites and swollen legs makes going to the hospital necessary. Breathlessness is a common side effect of congestion, especially when patients have pleural effusions and pulmonary oedema. Hepatic function is decreased by congestion, and a congested liver can also cause pain. As previously mentioned, congestion lowers the transrenal pressure gradient, which results in renal impairment. Congestion by dilution can worsen anaemia, which is quite common in heart failure patients, which can further increase symptoms and heart failure.

For individuals with chronic heart failure, fluid retention and congestion are the most frequent reasons for hospitalisation. A hospital stay alone is linked to a bad prognosis, while more stays are linked to progressively worse survival. As a result, it seems that congestion itself, rather than only diminished heart function, is linked to a bad prognosis.

Chronic heart failure's primary clinical characteristic, congestion, has a negative impact on outcomes. Congestion can be alleviated by a variety of therapies, although it is frequently misdiagnosed. Diuretics are the anti-congestive medications of choice, but little is known about how they affect hard outcome indicators like death. Trials are required to test therapeutic decongestive strategies in order to determine whether increased loop diuretic doses, combined diuretics, or more aggressive interventions, such as peritoneal dialysis, might improve the patient's clinical status and, potentially, outcome. More objective measures of congestion, such as raised NPs or dilated vena cava on ultrasound, may allow the identification of higher-risk patients.

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