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Volume overload

Volume overload, also known as fluid overload or hypervolemia, is a medical condition in which the body accumulates excess extracellular fluid, leading to increased blood volume, tissue swelling, and potential impairment of organ function such as the heart, lungs, and kidneys.^[1]^[2] This imbalance disrupts normal fluid homeostasis, where the body typically maintains a balance between fluid intake, output, and distribution across intravascular, interstitial, and intracellular compartments.^[3] Clinically, it is often identified by a weight gain of 5-10% or more due to positive fluid balance, particularly in hospitalized or critically ill patients.^[2] Volume overload is prevalent in patients with chronic conditions such as congestive heart failure and chronic kidney disease, affecting up to 43% of individuals with advanced CKD. In critically ill patients, it occurs in approximately 35% upon ICU discharge and is associated with increased morbidity and mortality.^[4]^[5] The primary causes of volume overload include underlying chronic conditions that impair fluid excretion, such as congestive heart failure, chronic kidney disease, and liver cirrhosis, which reduce the body's ability to eliminate excess sodium and water.^[1]^[3] Iatrogenic factors, like excessive intravenous fluid administration during medical treatment or surgery, can also contribute, as can hormonal changes during pregnancy or high dietary sodium intake that promotes fluid retention.^[6]^[1] In critically ill individuals, inflammation and capillary permeability alterations further exacerbate the shift of fluid from blood vessels to tissues, worsening edema formation.^[2] Symptoms typically manifest as peripheral edema (swelling in the legs, ankles, or abdomen), rapid weight gain, bloating, and discomfort, with more severe cases involving shortness of breath from pulmonary edema or irregular heart rhythms due to cardiac strain.^[1]^[7] Diagnosis involves a combination of clinical assessment, including physical examination for edema and daily weight monitoring, alongside laboratory tests for electrolyte levels (e.g., sodium) and imaging like ultrasound to evaluate fluid status in veins or the lungs.^[2]^[3] Management focuses on addressing the root cause while promoting fluid removal, often through diuretics like furosemide to increase urine output, dietary restrictions on sodium and fluids, and in severe cases, dialysis or ultrafiltration to mechanically extract excess volume.^[1]^[2] Early intervention improves prognosis, with mild cases resolving in days through conservative measures, though untreated volume overload is linked to higher morbidity and mortality, especially in intensive care settings where it correlates with prolonged ventilation and organ failure.^[2] Prevention strategies emphasize monitoring fluid balance in at-risk patients, such as those with cardiovascular or renal disease, and adhering to low-sodium diets.^[1]

Introduction

Definition

Volume overload is defined as an abnormal expansion of the extracellular fluid volume, with a particular emphasis on the intravascular compartment, leading to increased circulating blood volume and elevated cardiac preload. This state arises from an imbalance in fluid homeostasis, often involving excess total body sodium and water retention that expands the extracellular space.^[8]^[9]^[10] Clinically, volume overload is indicated by elevated hemodynamic parameters, such as central venous pressure exceeding 12 mmHg, which reflects right-sided filling pressure overload, or pulmonary capillary wedge pressure greater than 18 mmHg, signaling left-sided congestion and potential pulmonary edema risk. These thresholds help distinguish pathological volume states from normal physiology, where central venous pressure typically ranges from 2 to 8 mmHg and pulmonary capillary wedge pressure from 4 to 12 mmHg.^[11]^[12]^[13]^[14] Unlike euvolemia, which maintains a balanced extracellular fluid volume essential for adequate tissue perfusion without congestion, volume overload represents a pathological excess that impairs cardiac efficiency. Hypervolemia serves as a broader synonym encompassing total body fluid surplus, including both vascular and interstitial components, whereas volume overload in cardiological contexts specifically highlights the circulatory burden and preload augmentation.^[1]^[15] The recognition of volume overload traces back to early 20th-century cardiology, when fluid retention was increasingly linked to heart failure symptoms, evolving from 19th-century observations of edema in cardiac disease to a formalized understanding of its role in hemodynamic compromise.^[16]

Epidemiology

Volume overload is a common complication in patients with heart failure (HF), particularly in those hospitalized for acute decompensation, where the majority present with symptoms and signs of fluid congestion. In chronic HF, intravascular and interstitial volumes can expand by 33% to 35% above normal levels in untreated symptomatic patients with reduced ejection fraction. Among patients with stage 3-5 chronic kidney disease (CKD), the prevalence of volume overload reaches approximately 52%, defined as overhydration exceeding 7% of body weight. The majority (approximately 80-90%) of patients hospitalized for acute decompensated heart failure present with symptoms and signs of volume overload, with higher rates observed in elderly populations over 65 years, where HF incidence itself rises dramatically due to age-related cardiac vulnerabilities.^[17] Demographic patterns reveal disproportionate impacts in certain groups; for instance, volume overload is more prevalent in males with CKD, comprising about 69% of affected cohorts, and is exacerbated by comorbidities such as diabetes (prevalence 62% in overloaded vs. 28% in euvolemic patients) and hypertension. In regions with high salt intake or limited access to dialysis, such as low-resource settings, the risk escalates due to poorer management of fluid balance and hypertension control. Cardiovascular disease further compounds these risks, with overloaded CKD patients showing elevated systolic blood pressure (142 mm Hg vs. 133 mm Hg in euvolemic individuals). Trends indicate a rising incidence of volume overload, driven by global aging populations and increasing obesity rates, which contribute to HF development and fluid retention. Obesity prevalence among adults over 60 has nearly doubled in recent decades, reaching 43% in the United States, and is projected to fuel a 20-46% increase in HF cases by 2030 in developed countries, indirectly amplifying volume overload burdens. In CKD, sustained fluid overload heightens the risk of progression to end-stage renal disease (adjusted hazard ratio 2.45). Mortality statistics underscore the severity, with volume overload linked to 20-30% in-hospital mortality in severe HF cases involving cardiogenic shock or critical illness. In CKD cohorts, cardiovascular mortality is over five times higher in overloaded patients (6.3% vs. 1.2% in euvolemic), and fluid overload exceeding 10% of body weight at renal replacement therapy initiation triples the 90-day mortality risk. These outcomes highlight the need for targeted interventions to mitigate population-level impacts.

Pathophysiology

Fluid Dynamics

In volume overload, the biophysical foundation of fluid accumulation lies in the imbalance of Starling forces governing transcapillary exchange. The net rate of fluid movement across the capillary endothelium is described by the Starling equation:

J_v = K_f \left[ (P_c - P_i) - \sigma (\pi_c - \pi_i) \right]

where J_v represents the volume flux of fluid, K_f is the filtration coefficient, P_c and P_i are the hydrostatic pressures in the capillary and interstitium, \sigma is the reflection coefficient for proteins, and \pi_c and \pi_i are the corresponding oncotic pressures. Under normal conditions, this equation maintains equilibrium between intravascular and interstitial compartments by balancing hydrostatic forces that drive fluid out of capillaries against oncotic forces that pull fluid back in.^[18] In states of volume overload, elevated capillary hydrostatic pressure (P_c), often due to expanded plasma volume, shifts the equation toward net filtration, promoting excessive fluid extravasation into the interstitial space and resulting in tissue edema. This disruption is exacerbated if oncotic pressure (\pi_c) is reduced, such as from hypoalbuminemia, further impairing reabsorption at the venous end of capillaries. The process underlies the distribution of excess fluid from the intravascular to extracellular compartments, with sustained overload leading to widespread interstitial accumulation.^[10] A key driver of this fluid expansion is renal sodium retention, mediated by hormones such as aldosterone and antidiuretic hormone (ADH). Aldosterone acts on the principal cells of the cortical collecting ducts to upregulate epithelial sodium channels and Na+/K+-ATPase activity, enhancing Na+ reabsorption and creating an osmotic gradient for water follow-up. Concurrently, ADH, or vasopressin, increases the insertion of aquaporin-2 channels in the collecting duct epithelium, directly boosting water permeability and reabsorption independent of sodium. This coordinated mechanism expands extracellular fluid volume, perpetuating the cycle of overload by increasing total body sodium content and osmotic water retention.^[19] These dynamics induce shifts across fluid compartments, with initial intravascular expansion drawing from and mobilizing interstitial reserves to maintain circulating volume. In mild volume overload, total body water typically increases by 5-10%, reflecting proportional gains in both intravascular (about 25% of extracellular fluid) and interstitial (about 75%) spaces, though chronic cases can see disproportionate interstitial growth exceeding 30% above baseline. The time course varies: acute overload manifests within hours, as in excessive intravenous fluid administration overwhelming renal excretion capacity, whereas chronic forms build gradually over weeks through persistent neurohormonal activation and subtle daily retention. This expanded volume elevates cardiac preload, influencing ventricular loading dynamics.^[2]^[10]^[20]

Cardiac and Vascular Responses

In volume overload, the left ventricle experiences significant dilation as a compensatory response, with end-diastolic volume typically increasing by 20-50% to accommodate excess preload via the Frank-Starling mechanism. This mechanism enhances sarcomere stretch and contractility, initially boosting stroke volume and maintaining cardiac output despite the hemodynamic burden. However, prolonged dilation promotes eccentric hypertrophy, characterized by cardiomyocyte lengthening and addition of sarcomeres in series, which normalizes wall stress but risks maladaptive remodeling and eventual systolic dysfunction.^[21]^[22]^[23] Pulmonary hypertension often develops secondarily due to elevated left atrial pressure from left ventricular overload, transmitting backpressure to the pulmonary vasculature and raising mean pulmonary artery pressure above 20 mmHg (the current diagnostic threshold since 2018). This postcapillary hypertension initially arises from passive venous congestion but can progress to reactive changes, including vascular remodeling and increased pulmonary vascular resistance, further straining right ventricular function.^[24]^[25]^[26] Vascular adaptations in volume overload involve endothelial dysfunction, impairing nitric oxide bioavailability and promoting vasoconstriction through renin-angiotensin-aldosterone system activation. This shift exacerbates afterload and contributes to sustained hypertension and remodeling, often accompanied by increased arterial stiffness.^[27]^[28] Compensatory neurohormonal activation, particularly sympathetic nervous system surge, increases heart rate to support cardiac output, alongside enhanced contractility and vasoconstriction. While acutely beneficial, this chronic sympathoexcitation leads to β-adrenergic receptor downregulation, myocardial remodeling, and worsened volume retention, accelerating decompensation.^[29]

Etiology

Primary Causes

Volume overload primarily arises from intrinsic medical conditions that disrupt normal fluid homeostasis, leading to excessive accumulation of extracellular fluid. These conditions directly impair the body's ability to regulate volume through cardiac, renal, or vascular mechanisms, resulting in systemic congestion. Key examples include heart failure, chronic kidney disease, valvular heart disease, and cirrhosis, each contributing to volume expansion via distinct pathophysiological pathways. Heart failure, characterized by systolic or diastolic dysfunction, is a leading intrinsic cause of volume overload. In systolic heart failure, reduced ejection fraction impairs forward blood flow, causing blood to back up into the pulmonary and systemic circulations, which triggers renal sodium and water retention and subsequent congestion. Diastolic dysfunction, often seen in heart failure with preserved ejection fraction, limits ventricular filling during diastole, elevating end-diastolic pressures and promoting fluid extravasation into tissues. Approximately 6.7 million adults in the United States are affected by heart failure as of 2024, with advanced stages (New York Heart Association classes III and IV) representing a significant proportion that experience pronounced volume overload due to these mechanisms.^[30] Chronic kidney disease (CKD) contributes to volume overload through progressive decline in glomerular filtration rate (GFR), particularly when GFR falls below 30 mL/min/1.73 m² in stage 4 CKD. This reduction impairs the kidneys' excretory capacity, leading to uremic retention of sodium and water, which manifests as hypervolemia, hypertension, and edema. Fluid overload in advanced CKD is exacerbated by activation of the renin-angiotensin-aldosterone system, further promoting renal sodium reabsorption and interstitial fluid accumulation. Valvular heart disease, especially regurgitant lesions such as mitral regurgitation, imposes a chronic volume load on the heart by allowing backward flow of blood during systole. In mitral regurgitation, a portion of the left ventricular stroke volume regurgitates into the left atrium instead of ejecting forward, increasing preload and effective circulating volume, which over time leads to left ventricular dilation and eccentric hypertrophy. This regurgitant burden substantially elevates total stroke volume, contributing to systemic volume overload in affected patients. Cirrhosis induces volume overload via portal hypertension, which splanchnic vasodilation reduces effective arterial blood volume despite total body fluid expansion. This perceived hypovolemia activates compensatory mechanisms, including the renin-angiotensin-aldosterone system and antidiuretic hormone release, resulting in avid renal sodium and water retention. The ensuing ascites and peripheral edema exemplify the secondary hyperaldosteronism-driven fluid accumulation characteristic of decompensated cirrhosis.

Secondary Causes

Secondary causes of volume overload encompass external and iatrogenic factors that disrupt fluid balance, often exacerbating underlying vulnerabilities without originating from intrinsic organ failure. These triggers are typically modifiable and arise from therapeutic interventions, dietary habits, or physiological states like pregnancy. Excessive fluid administration, particularly through intravenous saline in intensive care unit (ICU) settings, is a leading iatrogenic cause of volume overload. In critically ill patients, liberal fluid resuscitation can result in positive fluid balance, increasing risks of organ dysfunction and prolonged ICU stays. For instance, approximately 40% of post-surgical patients admitted to the ICU exhibit fluid overload upon arrival, associated with higher morbidity and mortality due to interstitial edema and impaired tissue perfusion.^[31] Medication-induced volume overload commonly stems from drugs that promote renal sodium retention. Nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit renal prostaglandins, which normally facilitate natriuresis and diuresis, leading to extracellular fluid expansion and edema, especially in patients with heart failure or renal impairment. Similarly, corticosteroids enhance sodium reabsorption in the distal tubules by mimicking mineralocorticoid effects, contributing to hypertension and fluid retention in susceptible individuals.^[32]^[33] Nutritional factors, notably high-sodium intake, accelerate volume overload in at-risk populations by overwhelming renal excretory capacity. Diets exceeding 5 g of sodium per day promote osmotic fluid retention and elevate blood pressure, particularly in patients with chronic kidney disease or heart failure, where salt sensitivity amplifies extracellular volume expansion. The European Society of Cardiology guidelines recommend restricting sodium to below this threshold in heart failure to mitigate such risks.^[34]^[35] Pregnancy-related volume overload often manifests in preeclampsia, a condition affecting 5-8% of pregnancies worldwide, characterized by endothelial dysfunction and vascular leakiness. This leads to generalized edema and potential pulmonary congestion due to increased capillary permeability and sodium retention, independent of primary cardiac or renal pathology. Fluid management in these cases must be cautious to avoid iatrogenic overload.^[36]^[37]

Clinical Presentation

Symptoms

Volume overload manifests through various patient-reported symptoms, primarily reflecting the effects of excess fluid on the cardiopulmonary and systemic systems. These subjective experiences often prompt medical evaluation and are key to early recognition of the condition. Dyspnea, or shortness of breath, is the hallmark symptom, occurring on exertion or at rest due to pulmonary congestion from elevated left atrial pressure and fluid transudation into the alveoli. It is reported in approximately 80% to 90% of patients presenting with acute heart failure exacerbated by volume overload.^[38]^[39] Orthopnea and paroxysmal nocturnal dyspnea represent positional variants of dyspnea, characterized by difficulty breathing when lying flat that improves upon sitting upright, resulting from gravitational redistribution of intravascular volume to the pulmonary circulation during recumbency. These symptoms are common in moderate to severe cases and often awaken patients from sleep in paroxysmal nocturnal dyspnea.^[40]^[41] Fatigue and weakness are prevalent complaints arising from diminished cardiac output, which impairs oxygen delivery and nutrient perfusion to peripheral tissues despite compensatory mechanisms. Patients describe a profound sense of exhaustion that limits daily activities, even without exertion.^[39]^[42] Abdominal discomfort, often presenting as early satiety or a sensation of fullness after small meals, stems from hepatic congestion due to elevated right-sided filling pressures that engorge the liver and stretch its capsule. This can also include vague pain in the right upper quadrant, reflecting splanchnic venous congestion.^[43]^[44]

Signs

Volume overload manifests through several objective clinical signs detectable during physical examination, primarily reflecting fluid retention and elevated venous pressures in the cardiovascular system. Elevated jugular venous pressure (JVP), typically exceeding 8 cm H₂O when measured at a 45-degree torso angle, serves as a key indicator of right heart overload and systemic venous congestion.^[45] This finding, observed as distension of the internal jugular vein above the sternal angle, correlates with increased central venous pressure and is particularly reliable in older patients with heart failure.^[46] In advanced cases, the JVP may fail to decline with respiration (Kussmaul's sign), further signifying right-sided heart strain.^[46] Peripheral edema, often pitting in nature and predominantly affecting the lower extremities such as the ankles and legs, arises from fluid extravasation due to elevated hydrostatic pressures.^[47] It is graded on a scale from 1+ (mild, 2 mm depression rebounding immediately) to 4+ (severe, >8 mm depression lasting >2 minutes), helping clinicians quantify the extent of volume retention.^[48] This sign requires approximately 5 liters of extracellular fluid accumulation to become evident and is more pronounced in dependent areas.^[46] Pulmonary rales, manifesting as fine crackles on auscultation, are audible in the basal lung fields and result from interstitial fluid accumulation in the alveoli.^[41] These adventitious sounds, often bilateral and more prominent in moderate-to-severe cases, indicate left-sided volume overload leading to pulmonary congestion.^[46] In acute decompensation, they may accompany wheezing or diminished breath sounds if pleural effusions develop.^[46] In advanced volume overload, particularly with predominant right-sided involvement, hepatomegaly presents as an enlarged, possibly tender liver due to hepatic congestion from backward transmission of elevated venous pressures.^[41] Ascites, the accumulation of fluid in the peritoneal cavity, accompanies this as a sign of chronic systemic venous hypertension, often noted on abdominal percussion or palpation.^[46] These abdominal findings underscore the progression of biventricular failure in longstanding cases.^[49]

Diagnosis

History and Physical Examination

The initial clinical assessment for volume overload begins with a thorough history-taking to identify potential contributors and risk factors. Patients are queried about recent fluid intake, including adherence to any prescribed restrictions, as excessive oral fluids can precipitate overload in those with underlying cardiac or renal impairment.^[50] Inquiry into weight gain is essential, particularly a rapid increase exceeding 2 kg per week, which signals fluid retention and correlates with decompensation in heart failure.^[50] Medication history is reviewed to assess compliance with diuretics, cardiac glycosides, or other agents, as nonadherence often underlies acute episodes.^[39] If heart failure is suspected as the underlying cause, risk stratification may employ the Framingham criteria, which estimate heart failure probability through major factors (e.g., paroxysmal nocturnal dyspnea, jugular venous distention) and minor factors (e.g., extremity edema, tachycardia); diagnosis requires two major or one major plus two minor criteria.^[39] Physical examination follows a systematic sequence starting with vital signs to detect early indicators of hemodynamic stress. Tachycardia exceeding 100 beats per minute is a common finding, reflecting compensatory increased cardiac output in response to overload.^[51] Subsequent systemic inspection evaluates for signs of congestion, such as bilateral lower extremity pitting edema, which has high specificity (>95%) for volume excess in heart failure contexts, though asymmetry may suggest localized issues like venous thrombosis.^[50] Bedside estimation of volume status uses a "wet versus dry" framework prevalent in critical care: "wet" features include elevated jugular venous pressure (>8 cm H₂O, likelihood ratio 3.9-5.1), hepatojugular reflux, and pulmonary rales, while "dry" indicates absence of these with normal peripheral perfusion.^[50] This approach guides initial management while confirmatory tests like echocardiography provide further validation.^[39]

Diagnostic Tests

Laboratory tests play a crucial role in confirming volume overload by assessing electrolyte imbalances and underlying etiology. General tests include serum electrolytes (e.g., sodium levels below 135 mEq/L indicating dilutional hyponatremia due to fluid retention) and etiology-specific panels, such as renal function tests (creatinine, blood urea nitrogen) for chronic kidney disease or liver function tests (albumin, bilirubin) for cirrhosis.^[1] ^[2] If heart failure is suspected, B-type natriuretic peptide (BNP) serves as a key biomarker, released from cardiac ventricles in response to volume expansion and pressure overload; levels exceeding 100 pg/mL indicate significant cardiac strain and support the diagnosis of heart failure associated with volume overload.^[52]^[53] Cumulative fluid balance monitoring, via intake/output records (often requiring urinary catheterization), and daily weight measurements are gold standards for quantifying positive fluid balance, with gains of 5-10% body weight signaling overload.^[2] Point-of-care ultrasound provides non-invasive assessment of volume status, including inferior vena cava (IVC) diameter and collapsibility to estimate central venous pressure, and lung ultrasound for B-lines indicating interstitial edema.^[2] Echocardiography offers targeted imaging when cardiac involvement is suspected, revealing left ventricular ejection fraction below 40% (defining heart failure with reduced ejection fraction) alongside dilated cardiac chambers reflecting chronic volume expansion; it may also show normal ejection fraction in heart failure with preserved ejection fraction.^[54]^[55] Doppler imaging further evaluates regurgitant blood flows across valves, such as in mitral or aortic regurgitation, which contribute to volume overload by increasing preload and ventricular dilation.^[56]^[57] Chest X-ray offers a non-invasive initial assessment of pulmonary congestion. Cardiomegaly is evident when the cardiothoracic ratio exceeds 0.5, indicating ventricular dilation from sustained volume overload.^[58]^[59] Kerley B lines, short horizontal septal lines in the lung periphery, signify interstitial pulmonary edema secondary to elevated left atrial pressure in volume-overloaded states.^[60] Invasive hemodynamic monitoring via Swan-Ganz catheterization delivers precise measurements for severe or unclear cases, particularly with suspected cardiac etiology. Pulmonary capillary wedge pressure (PCWP) greater than 18 mmHg confirms left ventricular filling pressures consistent with volume overload and pulmonary congestion, guiding therapeutic decisions in critical settings.^[61]^[14]

Management

Management of volume overload depends on the underlying etiology and severity, with the goal of addressing the root cause while promoting fluid removal and preventing complications. Common strategies across causes include diuretics, fluid and sodium restriction, and monitoring, but specific interventions vary.^[1]

Acute Interventions

In acute settings related to heart failure, the primary goal of interventions for volume overload is to achieve rapid decongestion and hemodynamic stabilization, typically in patients hospitalized for acute decompensated heart failure or similar conditions. Loop diuretics, such as furosemide, form the cornerstone of therapy, administered intravenously to promote natriuresis and diuresis. An initial dose of 40-80 mg IV furosemide is commonly used, equivalent to 0.5-1.0 mg/kg or at least twice the patient's daily oral home dose, with escalation via bolus or continuous infusion if needed to achieve adequate response.^[62]^[63] The target is typically 1-2 L of urine output per day to relieve congestion without excessive volume depletion, monitored closely to maintain euvolemia and prevent electrolyte imbalances.^[62]^[64] Fluid restriction is recommended as an adjunct to diuretic therapy in patients with significant volume overload, particularly those with hyponatremia or severe symptoms, to limit further expansion of extracellular fluid. Guidelines suggest restricting intake to less than 1.5 L per day, individualized based on clinical status and serum sodium levels, though evidence for broad outcome benefits remains limited.^[62]^[65] For patients with volume overload complicated by hypertension or elevated preload, vasodilators such as nitroglycerin are indicated to reduce cardiac filling pressures and alleviate pulmonary congestion. Intravenous nitroglycerin infusion, starting at 10-20 mcg/min and titrated upward as tolerated, is recommended in cases with adequate perfusion and systolic blood pressure above 100 mm Hg, providing symptomatic relief in heart failure with reduced ejection fraction.^[62] Tachyphylaxis may develop within 24 hours, necessitating dose adjustments or alternative agents like nitroprusside in select scenarios.^[62] In refractory cases where diuretics fail to resolve congestion despite escalation, ultrafiltration via extracorporeal devices offers a mechanical alternative for fluid removal. This therapy, classified as a reasonable option (Class 2b), involves removing 1-2 L of isotonic fluid over 4-6 hours through a semipermeable membrane, guided by hemodynamic monitoring to avoid hypotension.^[62] Clinical trials, such as the UNLOAD study, demonstrate greater net fluid loss and reduced rehospitalizations with ultrafiltration compared to intensified diuretic regimens, though it carries risks of vascular access complications and requires specialized settings. For acute volume overload in chronic kidney disease, particularly with acute kidney injury, loop diuretics may be used if residual renal function exists, but renal replacement therapy such as hemodialysis or continuous venovenous hemofiltration is often required for rapid fluid removal when diuretics are ineffective.^[8]^[66] In liver cirrhosis with acute decompensation, initial management includes intravenous diuretics and albumin infusion alongside large-volume paracentesis for tense ascites, with transjugular intrahepatic portosystemic shunt (TIPS) considered for refractory cases.^[67]

Chronic Therapies

Chronic therapies for volume overload target the underlying mechanisms, with approaches tailored to the specific condition. In heart failure with reduced ejection fraction (HFrEF), where persistent fluid retention and hemodynamic imbalances contribute to recurrent congestion, these treatments focus on neurohormonal modulation to reduce afterload, prevent cardiac remodeling, and counteract sodium retention, thereby minimizing episodes of decompensation following initial stabilization. Guideline-directed medical therapy (GDMT) forms the cornerstone, with specific agents titrated to evidence-based targets while monitoring renal function and electrolytes.^[62] Angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) are foundational in chronic management, as they inhibit the renin-angiotensin-aldosterone system (RAAS), reducing afterload and suppressing renin activation to alleviate volume overload. In the Studies of Left Ventricular Dysfunction (SOLVD) trial, enalapril at 10-20 mg daily reduced mortality by 16% and hospitalizations for heart failure in patients with symptomatic HFrEF.^[68] ARBs, such as valsartan, provide similar benefits for ACE inhibitor-intolerant patients, with class I recommendations in guidelines for reducing morbidity and mortality.^[62] Beta-blockers, particularly carvedilol, are recommended to control heart rate, prevent adverse remodeling, and improve survival in chronic HFrEF with volume overload. The Carvedilol Prospective Randomized Cumulative Survival (COPERNICUS) trial demonstrated that carvedilol, initiated at 3.125 mg twice daily and titrated to 25 mg twice daily, reduced all-cause mortality by 35% in patients with severe chronic heart failure.^[69] This agent also decreases hospitalizations for worsening symptoms, supporting its role in long-term maintenance.^[62] Aldosterone antagonists, such as spironolactone, directly counter sodium retention and fibrosis, addressing persistent volume overload in HFrEF. Administered at 25 mg daily, spironolactone reduced the risk of death by 30% in the Randomized Aldactone Evaluation Study (RALES) among patients with severe heart failure on standard therapy.^[70] These agents are indicated for New York Heart Association class II-IV symptoms, with careful monitoring for hyperkalemia.^[62] For high-risk patients with chronic HFrEF and volume overload, device therapy including implantable cardioverter-defibrillators (ICDs) prevents sudden cardiac death, a common complication in this population. The Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT) showed that ICDs reduced all-cause mortality by 23% in patients with ejection fraction ≤35% and class II-III symptoms, independent of amiodarone use.^[71] ICD implantation is recommended post-optimization of GDMT, with expected survival exceeding one year.^[62] In chronic kidney disease, management emphasizes sodium and fluid restriction, loop diuretics to the maximum tolerated dose if glomerular filtration rate allows, and regular dialysis sessions (e.g., hemodialysis 3 times weekly) to control volume in end-stage disease, with ultrafiltration adjusted to achieve dry weight.^[72]^[8] For liver cirrhosis, chronic therapy involves sodium restriction to less than 2 g/day, combination diuretic therapy with spironolactone (starting at 100 mg daily) and furosemide (40 mg daily) in a 100:40 mg ratio, and repeated large-volume paracentesis with albumin replacement for recurrent ascites, with TIPS or liver transplantation for refractory ascites.^[67]

Complications and Prognosis

Acute Complications

Volume overload can precipitate several immediate complications due to hemodynamic instability and organ stress, particularly when encountered in acute decompensated heart failure, but also in other conditions such as chronic kidney disease and liver cirrhosis. These short-term risks arise from excessive fluid accumulation leading to increased cardiac preload, pulmonary congestion, and reduced effective circulating volume, potentially resulting in multi-organ dysfunction if not promptly addressed.^[49] Pulmonary edema represents a primary acute complication, manifesting as rapid fluid transudation into the alveoli from elevated left atrial pressure. In severe cases, this progresses to acute respiratory failure, necessitating endotracheal intubation and mechanical ventilation in 7-20% of patients despite initial medical therapy.^[73] This respiratory compromise stems from profound hypoxemia and hypercapnia, exacerbating overall hemodynamic burden.^[74] In non-cardiac contexts, such as chronic kidney disease, volume overload may lead to hypertensive emergencies or exacerbated uremia, while in liver cirrhosis, it can contribute to abdominal compartment syndrome from tense ascites or increased risk of spontaneous bacterial peritonitis.^[3] Cardiac arrhythmias, particularly atrial fibrillation, frequently emerge from mechanical atrial stretch induced by volume expansion. Atrial dilatation promotes electrophysiological heterogeneity and triggers ectopic foci, with new-onset atrial fibrillation occurring in 10-20% of acute heart failure episodes associated with volume overload.^[75] This arrhythmia further impairs cardiac output, perpetuating the cycle of decompensation.^[76] Renal hypoperfusion, despite systemic volume excess, occurs due to reduced renal perfusion pressure from elevated venous congestion and neurohormonal activation in volume-overloaded states. This prerenal azotemia culminates in acute kidney injury, defined by a serum creatinine rise exceeding 0.3 mg/dL within 48 hours per KDIGO criteria, affecting approximately 20-25% of patients with acute decompensated heart failure.^[77] Early recognition is critical, as worsening renal function amplifies fluid retention and electrolyte imbalances.^[78] Thromboembolic events arise from blood stasis in dilated cardiac chambers and peripheral veins amid reduced contractility and immobility. In volume-overloaded heart failure, this stasis predisposes to deep vein thrombosis or left atrial thrombi, increasing the risk of pulmonary embolism or ischemic stroke, with venous thromboembolism incidence elevated 2- to 3-fold compared to non-heart failure populations.^[79] Anticoagulation strategies may overlap with acute interventions to mitigate these risks.^[80]

Long-term Outcomes

Patients with volume overload face substantial long-term mortality risks, with a 5-year mortality rate of approximately 50% in the context of decompensated heart failure.^[81] This prognosis reflects the progressive nature of the underlying cardiac dysfunction and recurrent episodes of congestion, despite advances in guideline-directed medical therapy.^[62] In chronic kidney disease, persistent volume overload is associated with accelerated progression to end-stage renal disease, while in cirrhosis, it correlates with higher rates of hepatic decompensation and need for transplantation. Quality of life assessments, such as New York Heart Association (NYHA) functional class, often show improvement following effective decongestive therapies and optimization of heart failure management, indicating reduced symptoms and enhanced daily functioning.^[82] Readmission rates remain a significant concern, with 20-30% of patients experiencing rehospitalization within 30 days, frequently due to recurrent volume overload and incomplete resolution of congestion.^[83] These events contribute to ongoing healthcare burden and further deterioration in clinical status. Prognostic factors, including the timing of interventions, play a critical role in outcomes. Early implementation of therapies, such as beta-blockers and renin-angiotensin-aldosterone system inhibitors, can enhance left ventricular recovery, improving ejection fraction by 10-15% in responsive patients.^[82] This recovery correlates with better overall survival and fewer decompensations over time.

Prevention

Risk Factor Modification

Risk factor modification is essential for preventing volume overload across various underlying conditions, including heart failure, chronic kidney disease (CKD), liver cirrhosis, and iatrogenic exposures. Common strategies focus on lifestyle adjustments to maintain fluid balance, tailored to the specific etiology. Dietary sodium restriction remains a cornerstone, with guidelines recommending less than 2.3 g (2300 mg) per day for at-risk individuals, such as those with heart failure or CKD, to reduce fluid retention.^[62] In heart failure, pilot randomized controlled trials suggest intakes of 1.5–2.3 g per day may improve quality of life and support fluid balance.^[62] For patients with liver cirrhosis, sodium intake should be limited to 2 g or less per day to manage ascites and prevent symptomatic overload.^[84] In CKD, low-sodium diets (<2 g per day) combined with fluid restriction help prevent volume expansion, particularly in those with hypertension or proteinuria.^[85] Adherence to these restrictions counters sodium retention in sodium-avid states common across these conditions. Daily self-weighing is a key preventive measure for early detection of fluid accumulation, applicable to heart failure, CKD, and cirrhosis patients. Individuals should weigh themselves each morning under consistent conditions and seek medical attention for gains exceeding 2 kg over three days, as this may indicate early decompensation.^[86]^[62] In dialysis-dependent CKD, regular interdialytic weight monitoring helps adjust ultrafiltration to avoid overload.^[87] Medication adherence and avoidance of nephrotoxic or fluid-retaining agents are crucial for preserving organ function and preventing secondary volume overload. Nonsteroidal anti-inflammatory drugs (NSAIDs) should be avoided due to their promotion of sodium and water retention, which can blunt diuretic efficacy across heart failure, CKD, and cirrhosis.^[62] Thiazolidinediones are contraindicated in heart failure because of fluid retention risks, while nondihydropyridine calcium channel blockers like diltiazem and verapamil are discouraged for their negative inotropic effects.^[62] In CKD and cirrhosis, additional caution is needed with agents that impair renal or hepatic function, such as certain antibiotics or contrast media. For patients with mild cardiac or overall impairment, structured lifestyle changes like exercise programs can enhance physiological resilience. In stable heart failure, supervised aerobic exercise improves functional capacity and reduces decompensation risk.^[62] Similar moderate activities may benefit CKD patients without advanced disease, supporting cardiovascular health without exacerbating fluid issues.^[85] To prevent iatrogenic volume overload in hospitalized or perioperative patients, conservative intravenous fluid administration is recommended, guided by dynamic assessments like fluid responsiveness rather than fixed volumes, to minimize excess accumulation during treatment or surgery.^[88]

Monitoring Strategies

Monitoring strategies for volume overload emphasize surveillance tailored to the underlying condition, integrating clinical, biomarker, and technological approaches to enable early intervention and prevent decompensation. In heart failure and CKD patients, home-based B-type natriuretic peptide (BNP) testing allows serial measurements to track cardiac stress and volume status. Feasible with point-of-care devices, guidelines support assessments every 3 to 6 months in stable cases to optimize therapy and detect emerging congestion.^[89]^[62] For cirrhosis, monitoring includes regular assessment of serum sodium and albumin to guide fluid management. Implantable hemodynamic sensors, such as the CardioMEMS device, provide continuous pulmonary artery pressure monitoring primarily for heart failure patients with prior hospitalizations, reducing events by approximately 30% through remote diuretic adjustments.^[90]^[62] In CKD on dialysis, bioimpedance or lung ultrasound can monitor interdialytic volume.^[87] Telemedicine facilitates remote monitoring of vital signs, including daily weight, blood pressure, and heart rate, for chronic conditions like heart failure, CKD, and cirrhosis. Patients use apps or wearables to transmit data, alerting providers to patterns like weight gain exceeding 2 kg in 3 days. Structured telemonitoring reduces rehospitalizations, though efficacy varies by method.^[91]^[92] Echocardiography at clinically indicated intervals assesses cardiac function in patients with heart failure or cardiovascular risks contributing to volume overload. In stable cases without recent changes, it is recommended selectively to evaluate left ventricular ejection fraction and diastolic parameters, rather than routinely, to detect remodeling responses to therapy.^[62] For cirrhosis-related cardiac strain, echo may guide management of cirrhotic cardiomyopathy.^[54]

References

[1]
Hypervolemia Symptoms, Causes & Treatment - Cleveland Clinic
May 10, 2022 · Hypervolemia is a condition where your body has too much fluid. Another name for hypervolemia is “fluid overload” or “volume overload.”
[2]
Fluid Overload - PMC - PubMed Central - NIH
Causes of FO ... Clinically, FO is usually defined by some combination of edema, excessive weight gain, or excessively positive fluid balance in a patient that ...
[3]
Fluid imbalance: MedlinePlus Medical Encyclopedia
Nov 19, 2023 · This is called fluid overload (volume overload). This can lead to edema (excess fluid in the skin and tissues). Many medical problems can cause ...<|control11|><|separator|>
[4]
Hypervolemia (Fluid Overload): Symptoms, Causes, Treatment
Jan 18, 2023 · Hypervolemia, or fluid overload, happens when there is too much fluid in your body. It can raise blood pressure, cause swelling, and impact organ function.Symptoms · Causes · Diagnosis
[5]
Hypervolemia: Symptoms, treatment, and diagnosis
Hypervolemia is a condition in which there is too much fluid in the blood. It is also known as fluid overload. Learn more about the causes.Causes · Symptoms · Diagnosis · Treatment
[6]
Volume Overload - Endocrine and Metabolic Disorders
Volume overload generally refers to expansion of the extracellular fluid (ECF) volume. ECF volume expansion typically occurs in heart failure, acute or chronic ...
[7]
Fluid Volume Overload and Congestion in Heart Failure | Circulation
Jul 19, 2016 · Volume overload and fluid congestion remain primary issues for patients with chronic heart failure. The pathophysiology is complex.
[8]
Central Venous Pressure (CVP) Reduction Associated With Higher ...
In the VASST study, Boyd et al. (7) found that fluid overload and increased CVP (>12 mmHg) caused an increase in mortality in critically ill patients. Danziger ...Introduction · Materials and Methods · Results · Discussion
[9]
Bedside ultrasound to assess acute central venous pressure change ...
CVP higher than 10 mmHg indicates volume overload and values <10 mmHg represent normal volume state. This finding is based on the biomechanical properties ...
[10]
Haemodynamic implications of cardiovascular magnetic resonance ...
Patients with high CMR PCWP (≥18 mmHg) exhibited greater myocardial scar burden (28.5% vs. 17.2%, P = 0.0008) and microvascular obstruction (7.6% vs. 2.5%, P < ...<|separator|>
[11]
Pulmonary Capillary Wedge Pressure - StatPearls - NCBI Bookshelf
The normal pulmonary capillary wedge pressure is between 4 to 12 mmHg. Elevated levels of PCWP might indicate severe left ventricular failure or severe mitral ...Introduction · Anatomy and Physiology · Equipment · Technique or Treatment
[12]
Physiology, Central Venous Pressure - StatPearls - NCBI Bookshelf
Elevated CVP is indicative of myocardial contractile dysfunction and/or fluid retention. On the other hand, low central venous pressure is indicative of volume ...Missing: threshold | Show results with:threshold
[13]
History and epidemiology - PMC - NIH
In the 19th and early 20th centuries, heart failure associated with fluid retention was treated with Southey's tubes, which were inserted into oedematous ...
[14]
Fluid Movement Across the Endothelial Barrier - NCBI - NIH
Not only can fluid flow influence solute flux but solute flux can influence fluid movement. Starling's Law of Filtration, Jv = LpS(ΔP − σΔπ), is a non-steady ...
[15]
Physiology, Aldosterone - StatPearls - NCBI Bookshelf - NIH
Aldosterone causes sodium to be absorbed and potassium to be excreted into the lumen by principal cells. In alpha intercalated cells, located in the late distal ...
[16]
Fluid overload in the ICU: evaluation and management
Aug 2, 2016 · In this study patients were classified in three groups according to their CVP value: low (0 to 3 mmHg); medium (4 to 12 mmHg); and high (13 to ...
[17]
Effects of left ventricular volume overload produced by mitral ...
Data are means +/- SD. MR caused LV dilation; end-diastolic dimension increased from 4.3 +/- 0.4 in baseline to 4.7 +/- 0.5 in acute MR and 5.8 +/- 0.1 cm in ...
[18]
Heart Plasticity in Response to Pressure- and Volume-Overload
Feb 13, 2020 · Likewise, the Frank-Starling mechanism – that is, an increase in contractile output per unit of preload, seems to be preserved in compensated ...Pressure-Overload · Cardiac Hypertrophy · Volume-Overload
[19]
Left Ventricular Response to Mitral Regurgitation | Circulation
Nov 25, 2008 · LV preload reserve is exploited, and the Frank-Starling mechanism contributes to an increase in the total stroke volume.Mitral Regurgitant Volume · Afterload-Shortening... · Chronic Mr<|separator|>
[20]
Secondary Pulmonary Hypertension - StatPearls - NCBI - NIH
Pulmonary hypertension is a persistent increase in the mean pulmonary arterial pressure of more than 25 mm Hg at rest and greater than 30 mm Hg during exercise ...
[21]
Pulmonary hypertension in left heart disease - ERS Publications
PH is defined by a mean pulmonary arterial pressure (Ppa) ≥25 mmHg; in the case of PH associated with LHD, otherwise defined as Group 2 [2], this is associated ...
[22]
Endothelial Cell Dysfunction and Increased Cardiovascular Risk in ...
Apr 13, 2023 · In multiple studies, macro- and microvascular endothelial dysfunction could independently predict cardiovascular events in patients at risk for ...
[23]
Physiology: hemodynamics, endothelial function, renin–angiotensin ...
... volume to the tubules under conditions of moderate variations in cardiovascular function. ... endothelial dysfunction, and increased arterial stiffness. The ...
[24]
Sympathetic nervous system activation and heart failure - PMC - NIH
These compensatory mechanisms are initially able to compensate for impaired myocardial function, however, they inflict deleterious effects on cardiac structure ...
[25]
Association of perioperative weight-based fluid balance with 30-day ...
Mar 27, 2019 · Further, approximately 40% of patients admitted to the ICU after surgery are in a state of fluid overload [15], which might be associated with ...<|control11|><|separator|>
[26]
Non-steroidal anti-inflammatory drugs and risk of heart failure ...
NSAIDs are known to cause salt and fluid retention which could trigger exacerbation of heart failure (HF). In fact, this possible adverse effect has long been ...Missing: overload | Show results with:overload
[27]
Corticosteroid Adverse Effects - StatPearls - NCBI Bookshelf
Jul 3, 2023 · [19] The use of NSAIDs and glucocorticoids is associated with a 4-fold increased risk of a GI adverse effect compared with the use of either ...Missing: volume | Show results with:volume
[28]
Dietary sodium and fluid intake in heart failure. A clinical consensus ...
Apr 12, 2024 · The 2021 European Society of Cardiology (ESC) HF guidelines recommend avoiding excessive salt intake (>5 g/day) in all patients with HF, ...<|control11|><|separator|>
[29]
Volume Overload and Adverse Outcomes in Chronic Kidney Disease
May 5, 2015 · Volume overload is frequently encountered and is associated with cardiovascular risk factors in patients with chronic kidney disease (CKD).Missing: incidence | Show results with:incidence
[30]
Preeclampsia and Eclampsia - Women's Health and Education Center
The exact incidence of preeclampsia is unknown but it has been reported to be approximately 5-8%. Preeclampsia is primarily a disorder of first pregnancies.
[31]
Preeclampsia: Clinical features and diagnosis - UpToDate
Aug 12, 2025 · Generalized edema in preeclampsia may be due to capillary leak from endothelial damage and/or increased sodium retention that may be related ...
[32]
Relation of Dyspnea Severity on Admission for Acute Heart Failure ...
Of 48,616 patients with acute HF and dyspnea, 4022 (8.3%) had dyspnea with moderate activity, 19,619 (40.3%) with minimal activity, and 24,975 (51.4%) at rest.
[33]
Heart Failure (Congestive Heart Failure) - StatPearls - NCBI Bookshelf
Feb 26, 2025 · For stage C and stage D HF patients, the following NYHA classification of HF symptoms should be used: Class I: Symptom onset with more than ...
[34]
Dyspnea, Orthopnea, and Paroxysmal Nocturnal ... - NCBI - NIH
Orthopnea is caused by pulmonary congestion during recumbency. In the horizontal position there is redistribution of blood volume from the lower extremities and ...
[35]
Diagnosis and Evaluation of Heart Failure - AAFP
Jun 15, 2012 · Heart failure is a common clinical syndrome characterized by dyspnea, fatigue, and signs of volume overload, which may include peripheral edema ...
[36]
Heart Failure with Preserved Ejection Fraction: Diagnosis ... - AAFP
Nov 1, 2017 · Heart failure with preserved ejection fraction should be suspected in patients with typical symptoms (e.g., fatigue, weakness, dyspnea, ...
[37]
Gastrointestinal and Liver Issues in Heart Failure | Circulation
Apr 26, 2016 · Common gastrointestinal manifestations of HF include anorexia, early satiety, and abdominal pain; in patients with advanced HF, ascites, protein ...
[38]
Cardiohepatic Interactions in Heart Failure: An Overview and ...
Furthermore, HF patients may present with liver-related symptoms including abdominal distention, intermittent right upper quadrant discomfort, nausea, early ...
[39]
Physiology, Jugular Venous Pulsation - StatPearls - NCBI Bookshelf
Jan 30, 2023 · Normally, the JVP is between 6 to 8 cm H2O. Go to: Mechanism. The tracings of the jugular venous pulse wave, which can be observed using cardiac ...
[40]
Heart Failure Clinical Presentation - Medscape Reference
Sep 25, 2025 · Common noncardiac signs and symptoms of heart failure include anorexia, nausea, weight loss, bloating, fatigue, weakness, oliguria, nocturia, and cerebral ...History · Predominant Right-Sided... · Heart Failure in Children
[41]
Peripheral Edema - StatPearls - NCBI Bookshelf
Apr 5, 2025 · Pitting edema is associated with fluid overload conditions. Non-pitting edema is commonly linked to lymphatic obstruction, myxedema, lipedema.
[42]
Peripheral Edema: Evaluation and Management in Primary Care
Pitting edema has been classically graded on a 1 to 4 scale based on depth and rebound time; however, this scale lacks reliability and reproducibility.
[43]
Congestive Heart Failure and Pulmonary Edema - StatPearls - NCBI
Sep 19, 2022 · Heart failure is a chronic, progressive condition where the heart is unable to pump blood effectively to meet the body's needs, leading to fluid buildup.Continuing Education Activity · History and Physical · Treatment / Management
[44]
Assessment of Volume Status in Hospitalized Patients With Chronic ...
Assessment of volume status in hospitalized patients with heart failure is a critically important diagnostic skill that clinicians utilize frequently.
[45]
09. Heart Failure (HF) - UCSF Hospitalist Handbook
Review old TTE, stress tests, ECGs, and cath reports. · History: · Physical examination: · Evaluate perfusion (cold vs warm): altered mental status, Cheyne-Stokes ...
[46]
B-Type Natriuretic Peptide Levels: Diagnostic and Prognostic in ...
B-type natriuretic peptide (BNP) is a neurohormone secreted mainly in the cardiac ventricles in response to volume expansion and pressure overload.
[47]
Natriuretic Peptide B Type Test - StatPearls - NCBI Bookshelf
Aug 2, 2025 · Therefore, a normal BNP level (<100 pg/mL) effectively rules out heart failure and should prompt a search for noncardiac causes of dyspnea. An ...Missing: strain | Show results with:strain
[48]
Hyponatremia in Heart Failure: Pathogenesis and Management - PMC
Hyponatremia, defined as a serum sodium concentration <135 mEq/L, is the most common electrolyte abnormality in the hospitalized patients associated with a ...
[49]
Management of Hyponatremia in Heart Failure - PubMed Central - NIH
Hyponatremia, defined as serum sodium level below 135 mEq/L, is the most common electrolyte disorder in patients with heart failure [1]. For one in five ...
[50]
Echocardiography in the Assessment of Heart Failure Patients - PMC
Dec 4, 2024 · Patients with HF are classified according to ejection fraction (EF) as follows: reduced EF (HFrEF), where EF is ≤40%, mildly reduced EF ...
[51]
Role of Cardiac Imaging: Echocardiography - Dilated Cardiomyopathy
May 18, 2019 · Echocardiography has crucial importance in the diagnosis of dilated cardiomyopathy (DCM). Echocardiographic features of DCM are left ventricular (LV) dilation ...
[52]
Mitral Regurgitation - StatPearls - NCBI Bookshelf - NIH
Apr 30, 2024 · Mitral regurgitation leads to left ventricular volume overload due to increased stroke volume, caused by increased blood volume within the ...
[53]
Echocardiographic assessment of aortic regurgitation: a narrative ...
Jan 3, 2024 · This narrative review summarises the epidemiology of AR, reviews current practices and recommendations with regards to the echocardiographic assessment of AR.
[54]
Cardiomegaly - StatPearls - NCBI Bookshelf - NIH
Nov 20, 2022 · A chest X-ray with an enlarged cardiac silhouette and a cardiothoracic ratio of more than 50% suggests cardiomegaly.[29] Further delineation of ...Missing: >0.5 | Show results with:>0.5
[55]
Diagnosing Lung Abnormalities Related to Heart Failure in Chest ...
Feb 23, 2023 · ... pulmonary trunk; D: Interstitial oedema (Kerley B lines); E: Increased CTR > 0.5. B and C may signify the presence of pulmonary hypertension.
[56]
Cardiogenic Pulmonary Edema - StatPearls - NCBI Bookshelf - NIH
Chest X-ray (It is one of the most important investigations required for the evaluation of pulmonary edema and overload states. Early Stage. In the early ...<|control11|><|separator|>
[57]
the story of left atrial and pulmonary artery pressure monitors - PMC
Oct 7, 2015 · ... catheter into a sub-selected pulmonary artery (PA) branch. An elevated PCWP, exceeding 18–22 mmHg, indicates pulmonary edema and congestion.<|control11|><|separator|>
[58]
2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines | Circulation
Below is a merged response that consolidates all the information from the provided segments into a single, dense representation. To maximize detail and clarity, I’ve organized the data into tables where appropriate, focusing on symptoms, prevalence, and useful URLs. The response retains all information mentioned while ensuring a concise and structured format.
[59]
Lasix, Furoscix (furosemide) dosing, indications, interactions ...
0.5-1 mg/kg (or 40 mg) IV over 1-2 minutes; may be increased to 80 mg if there is no adequate response within 1 hour;not to exceed 160-200 mg/dose.
[60]
How do we maximize diuresis in acute decompensated heart failure?
Oct 1, 2022 · The initial goal should always be to maximize loop diuretic therapy using urine output or urinary sodium for guidance. Combination therapy can ...
[61]
Fluid Restriction Recommendations in Heart Failure: Dry as a Bone ...
Aug 14, 2022 · The ESC guidelines state, “fluid restriction of 1.5 to 2 liters a day may be considered in patients with severe heart failure or hyponatremia to relieve ...
[62]
Effect of Enalapril on Survival in Patients with Reduced Left ...
Aug 1, 1991 · Overall, enalapril therapy reduced mortality by 16 percent, an effect that is both clinically important and statistically significant. Besides ...
[63]
Effect of Carvedilol on Survival in Severe Chronic Heart Failure
May 31, 2001 · Patients with severe chronic heart failure as a result of ischemic or nonischemic cardiomyopathy were enrolled at 334 centers in 21 countries.
[64]
The Effect of Spironolactone on Morbidity and Mortality in Patients ...
Sep 2, 1999 · Spironolactone also improved the symptoms of heart failure, as measured by changes in the NYHA functional class. The reductions in the risk of ...
[65]
Amiodarone or an Implantable Cardioverter–Defibrillator for ...
Jan 20, 2005 · Patients with congestive heart failure (CHF) can die suddenly and unpredictably from arrhythmia despite the use of proven medical therapies, ...
[66]
Risk factors for treatment failure in patients with severe acute ...
Intubation is necessary in 7 to 20% of patients with severe acute cardiogenic pulmonary oedema despite optimal treatment. This study evaluated the ...
[67]
Pulmonary Edema - StatPearls - NCBI Bookshelf
Apr 7, 2023 · More than 1 million patients are admitted each year with a diagnosis of pulmonary edema secondary to cardiac causes (heart failure).[4] An ...
[68]
Heart Failure and Atrial Fibrillation: From Basic Science to Clinical ...
Jan 30, 2015 · Among HF trials and registries, the prevalence of AF ranged from 13% to 41%, depending in part upon age and the severity of HF [5,6], with no ...
[69]
Relationship of Paroxysmal Atrial Tachyarrhythmias to Volume ...
Oct 1, 2009 · Further, clinical experience suggests that AT may be triggered by periods of volume overload in such patients. In part, AT episodes in this ...
[70]
Acute Kidney Injury - StatPearls - NCBI Bookshelf - NIH
Nov 25, 2023 · Acute kidney injury (AKI), previously known as acute renal failure, denotes a sudden and often reversible reduction in kidney function.
[71]
Fluid Overload and Acute Kidney Injury - PMC - PubMed Central - NIH
Inadequate fluids give rise to hypoperfusion and organ injury and overzealous fluid therapy can give rise to fluid overload and related consequences.Introduction · Pathophysiology Of... · Hypervolemia...Missing: creatinine | Show results with:creatinine
[72]
Venous Thromboembolism in Hospitalized Patients With Heart Failure
Jan 1, 2010 · Hospitalized patients with HF are at increased risk for VTE, most commonly presenting as DVT and PE, which are associated with significant ...Missing: overload | Show results with:overload
[73]
Pulmonary Embolism in Heart Failure | Circulation
Oct 7, 2008 · The increased risk of VTE observed with heart failure itself has been attributed to reduced flow caused by low cardiac output and abnormalities ...
[74]
https://www.ncbi.nlm.nih.gov/books/NBK557611/
[75]
Improvement in Left Ventricular Ejection Fraction in Outpatients With ...
Jun 25, 2020 · In this large study of patients receiving treatment for chronic HFrEF in routine practice, improvements in LVEF ≥5% during intermediate duration ...
[76]
Trends in 30- and 90-Day Readmission Rates for Heart Failure
Apr 19, 2021 · Nearly 1 in 4 heart failure (HF) patients are readmitted within 30 days of discharge and approximately half are readmitted within 6 months. It ...
[77]
Early Indication of Decompensated Heart Failure in Patients ... - NIH
Feb 18, 2016 · ... daily weight monitoring. The ESC recommends that patients experiencing a weight increase of 2 kg or more in 3 days should alert healthcare ...Missing: weigh | Show results with:weigh
[78]
Exercise Training in Heart Failure: Clinical Benefits and Mechanisms
Jul 3, 2025 · Exercise training improves exercise capacity and diastolic function in patients with heart failure with preserved ejection fraction: results ...Missing: overload | Show results with:overload
[79]
Primary results of the HABIT Trial (heart failure assessment with ...
Apr 23, 2013 · This pilot study demonstrates that home BNP testing is feasible and that trials using home monitoring for guiding therapy are justifiable in high-risk patients.
[80]
CardioMEMS Heart Sensor Allows Monitoring of Pressures to ...
Heart failure management guided by this home pulmonary artery pressure monitoring system significantly reduced the rate of HF hospitalizations by 30% in the ...Introduction · Methods · Results
[81]
Heart Failure Management through Telehealth: Expanding Care and ...
Apr 28, 2024 · The major randomized controlled trials that compare remote monitoring (RM) to traditional in-office follow-ups for heart failure patients with ...
[82]
Remote Monitoring for Heart Failure Management at Home - JACC
Jun 5, 2023 · Early telemonitoring of weights and symptoms did not decrease heart failure hospitalizations but helped identify steps toward effective monitoring programs.