Volume overload - Revision history

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 **Reserve for truly refractory cases
 *Early nephrology and/or advanced HF consultation
 ==Disposition==

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Ostermayer: Created page with "''Volume overload is a clinical syndrome of extracellular fluid (ECF) expansion due to excess total body sodium. It is a common ED presentation that requires identification of the underlying cause and targeted decongestion.'' ==Background== *Definition: expansion of extracellular fluid volume due to increased total body sodium content, leading to edema, pulmonary congestion, and/or third-space fluid accumulation **An increase in total body sodium raises plasma osmolalit..."

2026-03-16T18:29:15Z

Created page with "''Volume overload is a clinical syndrome of extracellular fluid (ECF) expansion due to excess total body sodium. It is a common ED presentation that requires identification of the underlying cause and targeted decongestion.'' ==Background== *Definition: expansion of extracellular fluid volume due to increased total body sodium content, leading to edema, pulmonary congestion, and/or third-space fluid accumulation **An increase in total body sodium raises plasma osmolalit..."

New page

''Volume overload is a clinical syndrome of extracellular fluid (ECF) expansion due to excess total body sodium. It is a common ED presentation that requires identification of the underlying cause and targeted decongestion.''

==Background==
*Definition: expansion of extracellular fluid volume due to increased total body sodium content, leading to edema, pulmonary congestion, and/or third-space fluid accumulation
**An increase in total body sodium raises plasma osmolality, triggering compensatory water retention
**Clinically apparent edema typically requires >2.5 L of excess ECF<ref name="Merck">Volume Overload. Merck Manual Professional Edition. Revised May 2024. https://www.merckmanuals.com/professional/endocrine-and-metabolic-disorders/fluid-metabolism/volume-overload</ref>
**Serum sodium concentration can be high, low, or normal in volume-overloaded patients (despite increased total body sodium)
*'''Key distinction''': Volume overload ≠ dehydration. Patients can be total-body volume overloaded but intravascularly depleted (e.g., cirrhosis, nephrotic syndrome)

===Pathophysiology===
*Reduced effective circulating volume (ECF within the arterial system effectively perfusing tissues) triggers neurohormonal activation<ref>Schrier RW. Pathogenesis of sodium and water retention in high-output and low-output cardiac failure, nephrotic syndrome, cirrhosis, and pregnancy. N Engl J Med. 1988;319(16):1065-1072.</ref>
**Activation of RAAS → renal sodium and water retention
**Sympathetic nervous system activation → systemic vasoconstriction
**ADH release → free water retention
**Suppression of natriuretic peptides (ANP, BNP) → reduced sodium excretion
*'''Heart failure''': reduced cardiac output → decreased effective circulating volume → neurohormonal activation → sodium/water retention
*'''Cirrhosis''': splanchnic vasodilation → arterial underfilling → neurohormoral activation → sodium/water retention with third-spacing into peritoneum
*'''Nephrotic syndrome''': hypoalbuminemia → decreased oncotic pressure → edema; also primary renal sodium retention via ENaC activation in collecting duct
*'''Renal failure''': impaired GFR and tubular sodium excretion → direct sodium/water retention

===Epidemiology===
*Heart failure is the most common cause of volume overload presenting to the ED
**>1 million HF hospitalizations annually in the US<ref name="AHF2024">Arrigo M, Jessup M, Mullens W, et al. Acute heart failure. Nat Rev Dis Primers. 2020;6(1):16.</ref>
**In-hospital mortality 4-14%; 1-year post-discharge mortality up to 30%<ref name="PMC2024">Guo A, Gu Y, Wang R, et al. Acute Heart Failure: From The Emergency Department to the Intensive Care Unit. Cardiol Rev. 2024;32(3):217-226.</ref>
*Cirrhosis with ascites, nephrotic syndrome, and ESRD are other major causes

==Clinical Features==
===Symptoms===
*'''Cardiac'''
**Dyspnea (exertional → orthopnea → PND → dyspnea at rest)
**Bendopnea (dyspnea within 30 seconds of bending forward)
**Exercise intolerance, fatigue
**Chest tightness
*'''Systemic'''
**Weight gain (often 2-10 kg over days to weeks)
**Abdominal distension, early satiety, nausea (hepatic/splanchnic congestion)
**Extremity swelling

===Signs===
*'''Pulmonary congestion'''
**Crackles/rales (may be absent in chronic HF due to lymphatic compensation)
**Wheezing ("cardiac asthma")
**Hypoxia, tachypnea
**Pleural effusions (often right-sided or bilateral; isolated left-sided effusion should raise suspicion for non-cardiac cause)
*'''Systemic venous congestion'''
**Elevated JVP (>8 cm H2O)
**Hepatojugular reflux
**Peripheral pitting edema (lower extremities, sacral in bedridden patients)
**Ascites
**Hepatomegaly, RUQ tenderness (hepatic congestion)
*'''Cardiovascular'''
**S3 gallop (volume overload, systolic dysfunction)
**S4 gallop (diastolic dysfunction)
**Displaced PMI
**Tachycardia (compensatory)
**Hypertension (common; SBP >160 in ~50% of ADHF presentations) or hypotension (low-output HF, cardiogenic shock)
*'''Other'''
**Cool extremities, delayed capillary refill (if low cardiac output)
**Jaundice (congestive hepatopathy)

==Differential Diagnosis==
===Cardiac===
*[[CHF]] (HFrEF, HFpEF, HFmrEF)
*[[Acute coronary syndrome]] with LV dysfunction
*[[Valvular heart disease]] (acute MR, acute AR, severe AS)
*Cardiac tamponade (may present with congestion)
*Constrictive pericarditis
*High-output heart failure ([[thyrotoxicosis]], severe [[anemia]], [[AV fistula]], [[Paget disease]], [[beriberi]])

===Hepatic===
*[[Cirrhosis]] with portal hypertension
*[[Budd-Chiari syndrome]]
*Hepatic sinusoidal obstruction syndrome

===Renal===
*[[Acute kidney injury]] (oliguric)
*[[Chronic kidney disease]] / [[ESRD]]
*[[Nephrotic syndrome]]
*[[Acute glomerulonephritis]]

===Other===
*Iatrogenic (IV fluid overload, blood transfusion)
*[[Pregnancy]] / [[preeclampsia]]
*Severe [[hypoalbuminemia]] (malnutrition, protein-losing enteropathy)
*Medication-related (NSAIDs, CCBs, thiazolidinediones, corticosteroids)
*[[DVT]] / venous insufficiency (unilateral edema — not true volume overload)
*[[Lymphedema]] (non-pitting — not true volume overload)
*[[Myxedema]] (hypothyroidism)

==Evaluation==
===Workup===
''Tailor workup to suspected underlying cause''

====All patients====
*'''BNP or NT-proBNP'''
**BNP >400 pg/mL or NT-proBNP >900 pg/mL (age-adjusted) strongly suggests HF as cause<ref>Maisel AS, Krishnaswamy P, Nowak RM, et al. Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure. N Engl J Med. 2002;347(3):161-167.</ref>
**BNP <100 pg/mL or NT-proBNP <300 pg/mL makes HF unlikely
**''Falsely low in obesity; falsely elevated in renal failure, AF, PE, sepsis''
*'''BMP/CMP''' — electrolytes, BUN, creatinine, glucose, calcium
*'''CBC''' — anemia (high-output HF), infection
*'''Urinalysis''' — proteinuria (nephrotic syndrome), casts (GN)
*'''ECG''' — ischemia, arrhythmia, LVH, low voltage (tamponade/effusion)
*'''CXR''' — cardiomegaly, cephalization, Kerley B lines, pleural effusions, pulmonary edema
*'''Pulse oximetry / ABG''' if respiratory distress

====Cardiac suspected====
*'''Point-of-care ultrasound (POCUS)''' — ''high yield in the ED''
**B-lines (≥3 per zone in ≥2 bilateral zones = pulmonary edema; LR+ ~7.4 for ADHF)<ref>Pivetta E, Goffi A, Lupia E, et al. Lung Ultrasound-Implemented Diagnosis of Acute Decompensated Heart Failure in the ED: A SIMEU Multicenter Study. Chest. 2015;148(1):202-210.</ref>
**IVC assessment (dilated >2.1 cm with <50% collapsibility suggests elevated RA pressure)
**LV function (gross EF estimation)
**Pericardial effusion
**Pleural effusions
*[[Troponin]] — rule out ACS as precipitant
*'''Hepatic function panel''' — congestive hepatopathy
*'''Lactate''' — if concern for cardiogenic shock or hypoperfusion
*'''TSH''' — if new HF or tachycardia-mediated

====Hepatic suspected====
*LFTs, albumin, INR
*Abdominal ultrasound with Doppler (portal hypertension, ascites)
*Paracentesis (if new ascites or concern for SBP) — cell count, albumin, culture, total protein, SAAG

====Renal suspected====
*Urine sodium
**<10 mEq/L in HF, cirrhosis, nephrotic syndrome (avid renal sodium retention)
**>20 mEq/L in renal failure (impaired tubular reabsorption)<ref name="Merck"/>
*Urine protein/creatinine ratio or 24-hour urine protein
*Renal ultrasound
*Consider complement levels, ANA, ANCA if GN suspected

===Diagnosis===
*Volume overload is a '''clinical diagnosis''' supported by history, exam, and ancillary testing
*'''Identify the underlying cause''' — this drives specific management
*'''Assess hemodynamic profile''' using the Stevenson/Nohria classification for HF patients:
**'''Warm and wet''' (adequate perfusion + congestion) — most common ADHF presentation (~70%)
**'''Cold and wet''' (poor perfusion + congestion) — cardiogenic shock spectrum
**'''Warm and dry''' (adequate perfusion + euvolemic) — compensated HF
**'''Cold and dry''' (poor perfusion + euvolemic) — low-output state without congestion

==Management==
===General Principles===
*'''Identify and treat the precipitant''' — ACS, arrhythmia, medication nonadherence, dietary indiscretion, infection, PE, renal failure, uncontrolled HTN
*'''Treat respiratory distress first''' (airway management before diuresis)
*Obtain '''daily weights''' — best metric to follow decongestion progress
*Goal: net negative fluid balance of 1-2 L/day (weight loss 0.5-1 kg/day); may be more aggressive in acute pulmonary edema<ref name="Merck"/>
*Sodium restriction (<2 g/day) and fluid restriction (1.5-2 L/day) if hyponatremic or refractory

===Respiratory Support===
*'''Supplemental O2''' — titrate to SpO2 ≥90%
*'''Non-invasive positive pressure ventilation (NIPPV)''' — ''first-line for acute cardiogenic pulmonary edema''
**Reduces work of breathing, decreases preload and afterload, improves oxygenation
**CPAP 5-10 cmH2O or BiPAP 10/5 cmH2O, titrate to effect
**3CPAP RCT demonstrated reduced mortality and intubation rates vs standard O2<ref>Gray A, Goodacre S, Newby DE, et al. Noninvasive ventilation in acute cardiogenic pulmonary edema. N Engl J Med. 2008;359(2):142-151.</ref>
*'''Intubation''' — if NIPPV fails, altered mental status, or inability to protect airway
**Beware hemodynamic compromise with induction agents and positive pressure ventilation in patients with poor cardiac reserve

===Vasodilators===
''For hypertensive volume-overloaded patients (SBP >110-120 mmHg), especially with acute pulmonary edema''
*'''IV Nitroglycerin''' — ''drug of choice in acute cardiogenic pulmonary edema with adequate BP''
**Start 5-20 mcg/min, titrate q3-5 min up to 200 mcg/min
**Reduces preload > afterload; improves coronary blood flow
**High-dose NTG (bolus 200-400 mcg then infusion) can rapidly reduce pulmonary edema symptoms
**Avoid if SBP <90, severe aortic stenosis, recent PDE5 inhibitor use
*'''IV Nitroprusside''' — arteriolar and venous dilation; useful if severe afterload excess
**0.3-0.5 mcg/kg/min; max 2-3 mcg/kg/min
**Risk of cyanide toxicity, coronary steal; generally second-line
*'''Consider nicardipine or clevidipine''' if concomitant [[hypertensive emergency]]

===Diuretics===
''Cornerstone of decongestion therapy''

====Loop Diuretics (First-Line)====
*'''IV furosemide''' is the most commonly used agent
**'''Diuretic-naive patients''': Start 20-40 mg IV bolus
**'''Chronic loop diuretic users''': Give IV dose ≥ home oral daily dose (high-dose strategy preferred)
***The '''DOSE trial''' showed high-dose IV furosemide (2.5× oral dose) provided greater symptom relief, diuresis, and weight loss vs. low-dose (1× oral dose), with only transient increases in creatinine<ref name="DOSE">Felker GM, Lee KL, Bull DA, et al. Diuretic strategies in patients with acute decompensated heart failure. N Engl J Med. 2011;364(9):797-805. doi:10.1056/NEJMoa1005419</ref>
***No significant difference between bolus q12h vs. continuous infusion on primary outcomes<ref name="DOSE"/>
**Reassess urine output at 2 hours; if <100-150 mL/hr, double the dose<ref name="HF2022">Heidenreich PA, Bozkurt B, Aguilar D, et al. 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. Circulation. 2022;145(18):e895-e1032. doi:10.1161/CIR.0000000000001063</ref>
*'''Equivalent doses''': furosemide 40 mg IV = bumetanide 1 mg IV = torsemide 20 mg IV
*'''Bioavailability''': IV furosemide 100%, oral furosemide ~50% (variable; bumetanide and torsemide have more reliable oral absorption)

====Diuretic Resistance (Sequential Nephron Blockade)====
''If inadequate urine output despite escalating loop diuretic dose''
*'''Add thiazide-type diuretic''' for synergistic blockade at distal convoluted tubule
**Metolazone 2.5-5 mg PO (give 30 min before loop diuretic) '''OR'''
**Chlorothiazide 250-500 mg IV (if unable to take PO)
**Monitor closely for hypokalemia, hyponatremia, hypomagnesemia
*'''Add acetazolamide''' — carbonic anhydrase inhibitor; blocks proximal tubular sodium reabsorption
**The '''ADVOR trial''' (n=519) showed IV acetazolamide 500 mg daily added to loop diuretics significantly increased successful decongestion at 3 days (42.2% vs. 30.5%; RR 1.46, 95% CI 1.17-1.82; p<0.001), with shorter hospital stay and no difference in adverse events<ref name="ADVOR">Mullens W, Dauw J, Martens P, et al. Acetazolamide in Acute Decompensated Heart Failure with Volume Overload. N Engl J Med. 2022;387(13):1185-1195. doi:10.1056/NEJMoa2203094</ref>
**Most effective in patients with elevated serum bicarbonate (metabolic alkalosis from chronic diuretic use)
**''Note: ADVOR excluded patients on SGLT2 inhibitors; interaction unknown''
*'''Consider SGLT2 inhibitor''' (empagliflozin, dapagliflozin) — osmotic diuresis via glucosuria and natriuresis at proximal tubule; EMPULSE trial supports in-hospital initiation<ref>Voors AA, Angermann CE, Teerlink JR, et al. The SGLT2 inhibitor empagliflozin in patients hospitalized for acute heart failure: a multinational randomized trial. Nat Med. 2022;28(3):568-574.</ref>

====Monitoring During Diuresis====
*Urine output (Foley if ICU; monitor closely in ED)
*Daily weight (best metric)
*BMP q12-24h (K, Mg, Na, Cr) — replete K >4.0, Mg >2.0
*Reassess volume status clinically (JVP, lung exam, edema, orthopnea)
*Monitor for signs of over-diuresis: hypotension, worsening renal function, muscle cramps
*''Transient rises in creatinine during diuresis ("pseudo-worsening renal function") are generally acceptable if patient is decongesting and hemodynamically stable''<ref name="HF2022"/>

===Inotropes===
''Reserved for "cold and wet" profile (low cardiac output + congestion) — cardiogenic shock spectrum''
*'''Dobutamine''' — beta-1 agonist; increases contractility and cardiac output
**Start 2.5-5 mcg/kg/min, titrate to effect
**Shorter half-life, more easily titratable than milrinone
*'''Milrinone''' — PDE-3 inhibitor; inotrope + vasodilator ("inodilator")
**Load 50 mcg/kg over 10 min (often omitted), then 0.375-0.75 mcg/kg/min
**Renally cleared; accumulates in renal failure
**Greater vasodilation → more hypotension risk than dobutamine
*Do NOT start or newly initiate beta-blockers in acute decompensation<ref name="HF2022"/>

===Disease-Specific Management===
====Heart Failure====
*See [[CHF]]
*Initiate or continue GDMT when hemodynamically stable (ARNI/ACEi/ARB, beta-blocker, MRA, SGLT2i)<ref name="HF2022"/>
*STRONG-HF trial supports rapid up-titration of GDMT post-discharge<ref>Mebazaa A, Davison B, Chioncel O, et al. Safety, tolerability and efficacy of up-titration of guideline-directed medical therapies for acute heart failure (STRONG-HF). Lancet. 2022;400(10367):1938-1952.</ref>

====Cirrhosis with Ascites====
*'''Spironolactone''' is first-line (100 mg/day, max 400 mg/day) ± furosemide in 100:40 ratio
*Sodium restriction (<2 g/day)
*'''Large-volume paracentesis''' for tense ascites or respiratory compromise
**Give albumin 6-8 g per liter removed if >5 L removed
*Avoid NSAIDs (worsen renal sodium retention)
*Avoid ACEi/ARBs (can precipitate hypotension and hepatorenal syndrome)
*Maintain MAP >82 mmHg to prevent hepatorenal syndrome

====Nephrotic Syndrome====
*Treat underlying cause
*Sodium restriction (<3 g/day), fluid restriction
*Loop diuretics (higher doses often needed due to albumin binding in tubular lumen)
*Add thiazide if refractory
*Avoid vigorous diuresis → risk of thromboembolism from hemoconcentration, AKI
*Albumin infusion + furosemide debated; may help in selected patients with severe hypoalbuminemia

====Renal Failure====
*Loop diuretics (higher doses needed as GFR declines)
*Avoid thiazides if GFR <30 (ineffective alone; may work synergistically with loops)
*'''Emergent dialysis/ultrafiltration''' indications:
**Refractory pulmonary edema
**Severe hyperkalemia
**Severe metabolic acidosis
**Uremic symptoms (pericarditis, encephalopathy, bleeding)

====Iatrogenic Volume Overload====
*Reduce or discontinue IV fluids
*Diuresis as above
*Reassess fluid strategy (most hospitalized patients do not need maintenance IVF)

===Refractory Volume Overload===
*Ensure adequate diuretic dosing before declaring refractory
*Maximize sequential nephron blockade (loop + thiazide + acetazolamide)
*Consider hypertonic saline with furosemide (emerging evidence, not yet standard)
*'''Ultrafiltration''' — mechanical fluid removal via venovenous access
**UNLOAD trial showed benefit in fluid removal; CARRESS-HF showed no benefit over stepped pharmacological therapy and more adverse events<ref>Bart BA, Goldsmith SR, Lee KL, et al. Ultrafiltration in decompensated heart failure with cardiorenal syndrome. N Engl J Med. 2012;367(24):2296-2304.</ref>
**Reserve for truly refractory cases
*Early nephrology and/or advanced HF consultation

==Disposition==
===Admit===
*Acute pulmonary edema requiring IV diuretics, NIPPV, or intubation
*Hypotension or cardiogenic shock ("cold and wet")
*New-onset HF (requires workup for etiology)
*Significant electrolyte derangements
*ACS or arrhythmia as precipitant
*Inadequate diuretic response in ED
*Volume overload with renal failure requiring dialysis consideration
*Tense ascites requiring paracentesis with hemodynamic instability

===ICU Admission===
*Cardiogenic shock or need for vasopressors/inotropes
*Respiratory failure requiring intubation
*IV nitroprusside infusion
*Hemodynamically unstable with ongoing need for titrated infusions

===Consider Discharge===
*Mild exacerbation in known HF with preserved hemodynamics
*Adequate diuretic response in ED (symptom improvement, adequate urine output)
*Able to resume oral diuretics
*Reliable follow-up within 24-72 hours (STRONG-HF model supports close post-discharge follow-up)<ref>Mebazaa A, Davison B, Chioncel O, et al. STRONG-HF. Lancet. 2022;400(10367):1938-1952.</ref>
*Stable electrolytes, renal function
*No acute precipitant requiring inpatient management
*''Ensure medication reconciliation, dietary counseling, daily weight monitoring instructions, and clear return precautions''

===Discharge Checklist===
*Restart/optimize GDMT (for HF patients)
*Adjusted diuretic regimen with clear instructions
*Daily weight log with action plan (call if >2 lb gain overnight or >5 lb in a week)
*Low-sodium diet education
*Fluid restriction if indicated
*PCP or cardiology follow-up within 7 days (ideally 24-72 hours post-discharge)

==See Also==
*[[CHF]]
*[[Pulmonary edema]]
*[[Cardiogenic shock]]
*[[Ascites]]
*[[Nephrotic syndrome]]
*[[Acute kidney injury]]
*[[Hypertensive emergency]]
*[[Diuretics]]

==External Links==
*[https://emcrit.org/ibcc/chf/ EMCrit IBCC - Acute Decompensated Heart Failure]
*[https://www.wikijournalclub.org/wiki/DOSE Wiki Journal Club - DOSE Trial]
*[https://www.wikijournalclub.org/wiki/ADVOR Wiki Journal Club - ADVOR Trial]

==References==
<references/>

[[Category:Cardiology]]
[[Category:Renal]]
[[Category:Critical Care]]

← Older revision		Revision as of 09:24, 22 March 2026
Line 132:		Line 132:

	===Diagnosis===		===Diagnosis===
	*Volume overload is a ~~'''~~clinical diagnosis~~'''~~ supported by history, exam, and ancillary testing		*Volume overload is a clinical diagnosis supported by history, exam, and ancillary testing
	*Identify the underlying cause — this drives specific management		*Identify the underlying cause — this drives specific management
	*Assess hemodynamic profile using the Stevenson/Nohria classification for HF patients:		*Assess hemodynamic profile using the Stevenson/Nohria classification for HF patients:
Line 144:		Line 144:
	*Identify and treat the precipitant — ACS, arrhythmia, medication nonadherence, dietary indiscretion, infection, PE, renal failure, uncontrolled HTN		*Identify and treat the precipitant — ACS, arrhythmia, medication nonadherence, dietary indiscretion, infection, PE, renal failure, uncontrolled HTN
	*Treat respiratory distress first (airway management before diuresis)		*Treat respiratory distress first (airway management before diuresis)
	*Obtain ~~'''~~daily weights~~'''~~ — best metric to follow decongestion progress		*Obtain daily weights — best metric to follow decongestion progress
	*Goal: net negative fluid balance of 1-2 L/day (weight loss 0.5-1 kg/day); may be more aggressive in acute pulmonary edema<ref name="Merck"/>		*Goal: net negative fluid balance of 1-2 L/day (weight loss 0.5-1 kg/day); may be more aggressive in acute pulmonary edema<ref name="Merck"/>
	*Sodium restriction (<2 g/day) and fluid restriction (1.5-2 L/day) if hyponatremic or refractory		*Sodium restriction (<2 g/day) and fluid restriction (1.5-2 L/day) if hyponatremic or refractory
Line 176:		Line 176:
	**Diuretic-naive patients: Start 20-40 mg IV bolus		**Diuretic-naive patients: Start 20-40 mg IV bolus
	**Chronic loop diuretic users: Give IV dose ≥ home oral daily dose (high-dose strategy preferred)		**Chronic loop diuretic users: Give IV dose ≥ home oral daily dose (high-dose strategy preferred)
	***The ~~'''~~DOSE trial~~'''~~ showed high-dose IV furosemide (2.5× oral dose) provided greater symptom relief, diuresis, and weight loss vs. low-dose (1× oral dose), with only transient increases in creatinine<ref name="DOSE">Felker GM, Lee KL, Bull DA, et al. Diuretic strategies in patients with acute decompensated heart failure. N Engl J Med. 2011;364(9):797-805. doi:10.1056/NEJMoa1005419</ref>		***The DOSE trial showed high-dose IV furosemide (2.5× oral dose) provided greater symptom relief, diuresis, and weight loss vs. low-dose (1× oral dose), with only transient increases in creatinine<ref name="DOSE">Felker GM, Lee KL, Bull DA, et al. Diuretic strategies in patients with acute decompensated heart failure. N Engl J Med. 2011;364(9):797-805. doi:10.1056/NEJMoa1005419</ref>
	***No significant difference between bolus q12h vs. continuous infusion on primary outcomes<ref name="DOSE"/>		***No significant difference between bolus q12h vs. continuous infusion on primary outcomes<ref name="DOSE"/>
	**Reassess urine output at 2 hours; if <100-150 mL/hr, double the dose<ref name="HF2022">Heidenreich PA, Bozkurt B, Aguilar D, et al. 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. Circulation. 2022;145(18):e895-e1032. doi:10.1161/CIR.0000000000001063</ref>		**Reassess urine output at 2 hours; if <100-150 mL/hr, double the dose<ref name="HF2022">Heidenreich PA, Bozkurt B, Aguilar D, et al. 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. Circulation. 2022;145(18):e895-e1032. doi:10.1161/CIR.0000000000001063</ref>
Line 185:		Line 185:
	''If inadequate urine output despite escalating loop diuretic dose''		''If inadequate urine output despite escalating loop diuretic dose''
	*Add thiazide-type diuretic for synergistic blockade at distal convoluted tubule		*Add thiazide-type diuretic for synergistic blockade at distal convoluted tubule
	**Metolazone 2.5-5 mg PO (give 30 min before loop diuretic) ~~'''~~OR~~'''~~		**Metolazone 2.5-5 mg PO (give 30 min before loop diuretic) OR
	**Chlorothiazide 250-500 mg IV (if unable to take PO)		**Chlorothiazide 250-500 mg IV (if unable to take PO)
	**Monitor closely for hypokalemia, hyponatremia, hypomagnesemia		**Monitor closely for hypokalemia, hyponatremia, hypomagnesemia
	*Add acetazolamide — carbonic anhydrase inhibitor; blocks proximal tubular sodium reabsorption		*Add acetazolamide — carbonic anhydrase inhibitor; blocks proximal tubular sodium reabsorption
	**The ~~'''~~ADVOR trial~~'''~~ (n=519) showed IV acetazolamide 500 mg daily added to loop diuretics significantly increased successful decongestion at 3 days (42.2% vs. 30.5%; RR 1.46, 95% CI 1.17-1.82; p<0.001), with shorter hospital stay and no difference in adverse events<ref name="ADVOR">Mullens W, Dauw J, Martens P, et al. Acetazolamide in Acute Decompensated Heart Failure with Volume Overload. N Engl J Med. 2022;387(13):1185-1195. doi:10.1056/NEJMoa2203094</ref>		**The ADVOR trial (n=519) showed IV acetazolamide 500 mg daily added to loop diuretics significantly increased successful decongestion at 3 days (42.2% vs. 30.5%; RR 1.46, 95% CI 1.17-1.82; p<0.001), with shorter hospital stay and no difference in adverse events<ref name="ADVOR">Mullens W, Dauw J, Martens P, et al. Acetazolamide in Acute Decompensated Heart Failure with Volume Overload. N Engl J Med. 2022;387(13):1185-1195. doi:10.1056/NEJMoa2203094</ref>
	**Most effective in patients with elevated serum bicarbonate (metabolic alkalosis from chronic diuretic use)		**Most effective in patients with elevated serum bicarbonate (metabolic alkalosis from chronic diuretic use)
	**''Note: ADVOR excluded patients on SGLT2 inhibitors; interaction unknown''		**''Note: ADVOR excluded patients on SGLT2 inhibitors; interaction unknown''
Line 239:		Line 239:
	*Loop diuretics (higher doses needed as GFR declines)		*Loop diuretics (higher doses needed as GFR declines)
	*Avoid thiazides if GFR <30 (ineffective alone; may work synergistically with loops)		*Avoid thiazides if GFR <30 (ineffective alone; may work synergistically with loops)
	*~~'''~~Emergent dialysis/ultrafiltration~~'''~~ indications:		*Emergent dialysis/ultrafiltration indications:
	**Refractory pulmonary edema		**Refractory pulmonary edema
	**Severe hyperkalemia		**Severe hyperkalemia