From the Guidelines
Congestive heart failure causes fluid accumulation due to the heart's inability to pump blood effectively, leading to increased pressure in the blood vessels and subsequent fluid retention, as supported by the 2013 ACCF/AHA guideline for the management of heart failure 1. The heart's weakened state results in decreased cardiac output, causing increased pressure in the blood vessels, which in turn forces fluid out of the blood vessels and into surrounding tissues.
- Key factors contributing to fluid accumulation include:
- Increased pressure in the blood vessels
- Kidney retention of sodium and water in response to decreased blood flow
- Hormonal changes, such as activation of the renin-angiotensin-aldosterone system, which promotes fluid retention 1
- Overactivity of the sympathetic nervous system, causing blood vessel constriction and increased heart rate As stated in the 2013 ACCF/AHA guideline, diuretics are recommended to improve symptoms in patients with heart failure with reduced ejection fraction (HFrEF) who have evidence of fluid retention, unless contraindicated 1.
- The mechanism of diuretics, such as loop diuretics (e.g., bumetanide, furosemide, and torsemide) and thiazide diuretics, involves inhibiting the reabsorption of sodium or chloride at specific sites in the renal tubules, thereby increasing urinary sodium excretion and decreasing physical signs of fluid retention 1. The use of diuretics is crucial in managing fluid retention in heart failure patients, and their appropriate use is a key element in the success of other treatments for heart failure, as emphasized in the guideline 1.
From the Research
Causes of Accumulated Fluid in Congestive Heart Failure
- The pathophysiology of congestion in congestive heart failure is complex and involves the dynamics of interstitial and intravascular fluid compartment interactions and fluid redistribution from venous splanchnic beds to central pulmonary circulation 2
- The resultant reduced blood flow characterizing heart failure promotes activation of neurohormonal systems, which leads to fluid retention, often exhibited as pulmonary congestion, peripheral edema, dyspnea, and fatigue 3
- The interplay between the heart and the kidneys in heart failure involves multiple interdependent mechanisms, including hemodynamic alterations resulting in insufficient peripheral and renal perfusion, which can lead to renal tubule hypoxia 3
- Activation of neurohormonal factors, including renin-angiotensin-aldosterone system (RAAS), sympathetic nervous system (SNS), endothelin-1 (ET-1), and anti-diuretic hormone (ADH), due to reduced cardiac output and renal perfusion, results in sodium and water retention, vasoconstriction, and increased central venous pressure (CVP) 3
Mechanisms Underlying Edema Formation
- The unique relationship between the heart and the kidneys plays a central role in edema formation in heart failure 3
- Persistent activation of deleterious neurohormonal systems, including RAAS, SNS, ET-1, and ADH, leads to sodium and water retention, vasoconstriction, and increased CVP, which is associated with renal venous hypertension/congestion and increased intra-abdominal pressure (IAP) 3
- The supremacy of the deleterious neurohormonal systems over the beneficial natriuretic peptides (NP) in heart failure is evident by persistent sodium and water retention and cardiac remodeling 3
Role of Angiotensin-Converting Enzyme
- Angiotensin-converting enzyme (ACE) inhibitors are a cornerstone treatment for patients with heart failure, targeting the renin-angiotensin-aldosterone system (RAAS) 4, 5
- ACE inhibitors have been shown to improve clinical outcome for patients with overt congestive heart failure, as well as for those with asymptomatic left ventricular dysfunction 5