Why do heart failure patients have edema

Discover the different causes and their associated…. Following a heart-healthy diet, which includes fruits, vegetables, nuts, whole grains, and beans, may help prevent or address heart failure. There are many explanations for why a person may have swollen feet. Some causes, such as a twisted or sprained ankle, are obvious. Others might be…. Swollen ankles, or edema, are a common symptom of a variety of conditions.

Learn more about the causes of swollen ankles, including lymphedema…. Can heart failure cause swollen feet? Medically reviewed by Dr. Payal Kohli, M. Explanation Other symptoms Treatment Contacting a doctor Other possible causes Summary Heart failure can cause swelling in the feet. About swollen feet. Other symptoms. When to contact a doctor.

Beta blockers will help reduce your blood pressure. Heart rate medications will help regulate your heartbeat. Our Quality Testimonials Appointments. View Doctors. Not finding the treatment you're looking for? Serial NP assessment at home is feasible with a finger-stick test and this approach in high-risk patients might detect possible decompensation early. Invasive devices have potential as tools to predict congestion.

After the first 3 months, treatment was personalised based on the readings, which led to a fall in LA pressure Congestion is an important cause of symptoms in patients with HF. The discomfort of swollen legs and ascites precipitates hospitalisation. Congestion is associated with the sensation of breathlessness, particularly when patients develop pulmonary oedema and pleural effusions.

Congestion reduces hepatic function, and the congested liver can itself be a source of discomfort. As described above, congestion causes renal dysfunction by reducing the transrenal pressure gradient. Anaemia, which is highly prevalent among HF patients, can be made worse by congestion through dilution, and can further exacerbate symptoms and cardiac dysfunction. The commonest cause for hospitalisation in patients with CHF is fluid retention and congestion.

Congestion is a powerful marker of an adverse prognosis and it is thus potentially an important therapeutic target. Diuretics are the mainstay of management for patients with congestion. It has become a truism to state that their use is based on empirical judgement and subjective clinical evaluation, rather than evidencebased medicine.

Different classes of diuretics are used in patients with chronic HF, although loop diuretics furosemide, bumetanide and torasemide are the most widely prescribed. They exert their effect primarily by inhibiting the sodium—potassium—chloride co-transporter in the thick ascending limb of the Loop of Henle, by preventing the re-absorption of these ions, a subsequent diuresis occurs.

The loop diuretics mediate their effect from the luminal side of the tubule, and so some glomerular filtration is essential to allow them to work. The beneficial effects of a loop diuretic on JVP, pulmonary congestion, peripheral oedema and body weight have been known for years; diuretics also improve cardiac function, symptoms, and exercise tolerance in patients with HF. Particularly in patients with severe renal dysfunction, a reduced response to them is frequently observed and their use alone may be insufficient.

For those responding poorly to a loop diuretic alone, the combination with a thiazide or thiazide-like diuretic can be very potent. Although metolazone is often used in this scenario, there is little evidence that it is superior to other agents, such as bendroflumethiazide. Mineralocorticoid receptor antagonists MRAs are, of course, also diuretics. Two large trials 39,40 have shown that adding spironolactone or eplerenone to standard treatment in symptomatic patients with reduced LVEF either chronically or after a recent myocardial infarction produces morbidity and mortality benefits.

Whether the beneficial effects are due to a reduction in congestion is not at all clear given the wide range of actions of MRAs. The clinical benefits observed following the introduction of loop diuretics are counterbalanced by a more marked activation of the renin— angiotensin system. Francis and colleagues showed that the acute injection of a loop diuretic furosemide 1.

Other reports suggest that using diuretics unnecessarily when there is no evidence of congestion for a longer period of time might decrease systolic and diastolic blood pressure and increase circulating levels of renin compared with placebo. Retrospective studies have raised concerns about a possible detrimental effect of the long-term use of loop diuretics in HF patients, possibly caused by chronic and sustained adverse neuroendocrine activation.

A small number of studies have attempted to identify patients who might be able to tolerate diuretic withdrawal. Patients with HF have raised vasopressin AVP , which causes water re-absorption in the collecting ducts of the nephrons.

Vaptans block the action of vasopressin on its receptors, thus leading to loss of water alone without a natriuresis — a so-called aquaresis. In patients with severe HF symptoms, and compared with placebo, a single intravenous dose of conivaptan 20 or 40 mg significantly reduced pulmonary capillary wedge pressure and right atrial pressure during the first hours following administration, also increasing urine output at a dose-dependent amount.

Enthusiasm for the routine use of vaptans has thus waned, but they could certainly be helpful in patients who have hyponatraemia. It is possible that vaptans might be better than a loop diuretic as standard care. Tolvaptan, or tolvaptan plus furosemide, were well tolerated and produced a similar increase in urine output, greater than furosemide or placebo, without affecting blood pressure or other electrolytes apart from sodium, which increased although within normal values.

The role of vaptans in routine practice is still uncertain, but several trials are on the way. At the moment, European Society of Cardiology ESC guidelines only recommend that tolvaptan may be used for patients with acute HF and resistant hyponatraemia; in the US, vasopressin antagonists have a class IIb recommendation for the short treatment of acute HF with congestion and persistent severe hyponatremia, at risk of or having active cognitive symptoms.

ACE-inhibitors are the first-line treatment for chronic HF patients with reduced systolic function, unless contraindicated. They have a wide range of effects including the promotion of diuresis and the renal excretion of sodium, principally by blocking the effects of angiotensin II in the kidney and angiotensin II-mediated aldosterone secretion.

In turn, ACE-inhibitors reduce the circulating blood volume, and both venous and arterial pressures; moreover, they not only improve the peak oxygen consumption but also decrease NP plasma levels in symptomatic 55 or asymptomatic patients.

In a trial that pre-dates modern therapy, patients whose symptoms and congestion were well-controlled were unable to maintain clinical stability for long periods on diuretics alone. The risk of clinical decompensation was decreased when diuretics were combined with digoxin or an ACE-I. LCZ combines angiotensin receptor blockade with valsartan and inhibition of neprilysin, an enzyme that degrades NPs, with sacubitril.

LCZ decreases the risk of death and hospitalisation for HF in patients with stable chronic HF compared with enalapril. It has long been known that digoxin used alone in patients with severe congestion — particularly those with atrial fibrillation — can cause a profound diuresis.

Levosimendan causes vasodilation of the coronary arteries and systemic resistance vessels, decreasing preload and afterload. Some recent reports suggest that short, intermittent courses of intravenous levosimendan might decrease NPs and possibly HF hospitalisation. The long-term education of patients with HF is of fundamental importance, to emphasise medication adherence and monitor symptoms indicating progression of disease.

It might be that some patients remain congested just because they do not take their prescribed medications. During times of severe fluid retention, simple interventions, such as continuous bed rest, might enhance diuresis and significantly reduce body weight compared with bed rest during night only; 68 also diurnal postural changes might influence the diuretic action, which is enhanced by supine position compared to the erect.

The role of sodium restriction is not clear, although part of the traditional management of HF and recommended in guidelines albeit with an acknowledged low grade of evidence to support the recommendations. In the most severe cases of HF, renal dysfunction and diuretic resistance often occur, and limit the available therapeutic resources to decrease congestion.

While ultrafiltration is an invasive solution usually reserved for patients with severe acute HF, peritoneal dialysis PD is a home-based, intermittent, therapeutic option in which the removal of the excess fluid takes place using the peritoneum as a filter.

Two recent studies of patients with advanced HF complicated by renal failure have reported that PD is feasible, and that it might decrease body weight, and improve symptoms and functional status.

Congestion is a cardinal clinical feature of chronic HF, and is linked to adverse outcomes. Although several interventions might improve congestion, it often remains underdiagnosed. Little is known about the effects of the anti-congestive drugs par excellence, the diuretics, on hard outcome measures, such as mortality.

Pierpaolo Pellicori ,. Kuldeep Kaur ,. Andrew L Clark ,. Abstract Congestion, or fluid overload, is a classic clinical feature of patients presenting with heart failure patients, and its presence is associated with adverse outcome.

Keywords Diuretics , congestion , chronic heart failure , treatment , review ,. Open access: The copyright in this work belongs to Radcliffe Medical Media. How Do We Identify Congestion? The left side of the heart is responsible for pumping blood out of the heart to the rest of the body.

Left-sided heart failure can develop when the left ventricle lower left chamber of heart can no longer pump enough blood out of the heart and into circulation. Left-sided heart disease sometimes involves edema in the lungs. When blood returns to the heart, it enters the right atrium top right chamber and then moves to the right ventricle bottom chamber , which pushes blood into the lungs to receive oxygen.

When the right side of the heart weakens, blood coming in from the veins can start to back up. This is called right-sided heart failure , which usually results in edema in the lower extremities. The term congestive heart failure is often used interchangeably with heart failure.

But it really just refers to a state of heart failure in which fluid buildup in the body is serious enough to require medical attention. This can result in both pulmonary edema and edema of the abdomen, lower legs, and feet. Treating edema usually means treating the underlying cause of the swelling. In the case of heart failure, that could involve the use of medications like:.

And in the most severe cases of heart failure, a heart transplant may be necessary. This is due to a weakening or stiffening of the heart muscle. If you notice swelling, but know of no underlying medical reason for it, see a doctor soon. Read this article in Spanish.