L16 - ADHF

What is acute decompensated heart failure (ADHF)?

New or worsening HF signs/symptoms requiring additional medical care; may involve systemic volume overload, acute pulmonary edema, or hypoperfusion; occurs with impaired or preserved LV function.

What are the major precipitating factors of ADHF?

Medication or sodium restriction nonadherence; cardiotoxic drugs; ACS/MI; atrial fibrillation or other arrhythmias; acute valvular insufficiency; pneumonia/infection; hypertensive crisis; alcohol/illicit drugs; anemia; thyroid disorders.

Which medications can precipitate or worsen ADHF?

Anthracyclines (cardiotoxic); NSAIDs; thiazolidinediones (TZDs); non-dihydropyridine CCBs; steroids/glucocorticoids.

What are the causes of de novo ADHF?

Large MI, acute BP elevation with LV dysfunction, or severe progressive LV systolic dysfunction with worsening cardiac output refractory to therapy.

What symptoms and signs indicate pulmonary congestion?

Symptoms: dyspnea, orthopnea, paroxysmal nocturnal dyspnea (PND), tachypnea. Signs: rales, pulmonary edema, pleural effusions, hypoxemia, left-sided S3 gallop.

What symptoms and signs indicate systemic congestion?

Edema, abdominal/hepatic swelling or pain, JVD, hepatojugular reflux, hepatomegaly/tenderness, ascites, right-sided S3 gallop.

What symptoms and signs indicate hypoperfusion?

Extreme fatigue, poor appetite, nausea, early satiety, mental status changes; low BP, low CO, worsening renal function, cool extremities.

What physical examination findings should be evaluated in ADHF?

HR, BP, RR, oxygen saturation, weight, JVD, S3/S4, lung rales, abdominal fluid overload, pitting edema, and cool extremities.

What diagnostic tests are used in ADHF and what do they show?

Chest X-ray: pulmonary edema/pleural effusions. Echocardiogram: EF and structural/functional abnormalities. ECG: arrhythmias (AFib) or MI.

Which laboratory tests should be evaluated in ADHF?

CBC; electrolytes (Na, K, Mg); renal function (BUN, SCr); cardiac troponin for myocardial injury/possible MI; BNP or NT-proBNP to support HF assessment.

What BNP and NT-proBNP thresholds are listed in the lecture?

BNP >100 pg/mL; NT-proBNP >450 pg/mL if under 50 years; >900 pg/mL if older than 50. Interpret alongside signs and symptoms.

What do warm, cold, wet, and dry mean?

Warm = adequate perfusion/no hypoperfusion. Cold = hypoperfusion. Wet = pulmonary/systemic congestion or volume overload. Dry = no evidence of congestion.

What do cardiac index (CI) and PCWP measure?

CI = CO/BSA, a measure of perfusion; lecture cutoff 2.2 L/min/m². PCWP = measure of preload/volume status; lecture cutoff 18 mmHg.

What are the four hemodynamic subsets of ADHF?

I = warm/dry (adequate perfusion, no congestion); II = warm/wet (adequate perfusion, congestion); III = cold/dry (hypoperfusion, no congestion); IV = cold/wet (hypoperfusion plus congestion).

How is warm and dry (Subset I) managed?

Perfusion and volume status optimized; lowest mortality. Maximize oral guideline-directed medical therapy (GDMT) and monitor.

How is warm and wet (Subset II) managed?

Goal: relieve congestion/decrease preload while maintaining CO. FIRST LINE IV loop diuretics; consider IV nitroglycerin or nitroprusside if no symptomatic hypotension. Sodium/fluid restriction and oxygen as needed.

What should be done if warm/wet patients have diuretic resistance?

Increase IV loop diuretic dose; add metolazone or another synergistic diuretic; use continuous IV loop infusion; consider vasodilator if BP permits. Ultrafiltration for refractory congestion.

How is cold and dry (Subset III) managed?

Goal: increase CO and vital-organ perfusion. If too dry, give IV fluids and reassess. If volume status already optimized but hypoperfusion persists, give IV inotrope (dobutamine or milrinone).

How is cold and wet (Subset IV) managed?

Goal: improve CO/perfusion AND remove congestion. Individualized combination of IV positive inotropes and IV diuretics, with vasodilators when appropriate and BP allows; careful monitoring.

What are the overall goals of ADHF treatment?

Relieve congestion; improve low CO/perfusion; minimize medication risks; identify/treat precipitating causes; optimize oral therapy before discharge; educate patient.

Which diuretics are preferred for ADHF volume overload and how do they work?

IV loop diuretics (furosemide, bumetanide, torsemide), Class I recommendation. Promote sodium/water excretion and functional venodilation, decreasing preload and congestion.

What are the lecture's initial IV furosemide dosing rules?

If on home furosemide: one strategy is total home dose as IV bolus (maximum 200 mg). If not on home furosemide: SCr

What are the urine-output goals after initial IV furosemide?

SCr

What should be done if initial IV furosemide fails the urine-output goal?

Double initial IV bolus dose and give within 2–4 hours of previous dose; reassess urine output and congestion.

What causes diuretic resistance in ADHF?

Reduced absorption/peak drug concentration; reduced responsiveness; high distal tubular sodium delivery; low CO/renal perfusion reducing drug delivery to kidneys.

How can diuretic resistance be overcome?

Higher IV loop bolus doses, continuous IV infusion, adding metolazone, sodium/fluid restriction, or ultrafiltration after failure of medical therapy.

What adverse effects should be monitored with IV loop diuretics?

Hypokalemia, hypomagnesemia, hyponatremia, hypotension, reduced CO from overdiuresis, and worsening renal function. Correct significant electrolyte abnormalities.

What should be monitored at least daily during IV diuresis?

Fluid intake/output, daily weight, congestion symptoms, BUN/SCr, K/Mg/Na, HR and BP; CI/PCWP when invasive monitoring is indicated.

What is the role of IV vasodilators in ADHF?

Class IIb option added to diuretics to relieve dyspnea when symptomatic hypotension is absent. Avoid when SBP <90 mmHg.

What is the difference between arterial and venous vasodilation?

Arterial dilation decreases afterload and can increase CO. Venodilation decreases preload and pulmonary congestion. Mixed agents do both.

What are nitroprusside's effects, administration, and toxicities?

Mixed arterial/venous vasodilator; decreases SVR, BP, preload and increases CO. Continuous IV infusion, taper slowly, protect from light; invasive hemodynamic monitoring. Risks: hypotension, headache, increased ICP, cyanide toxicity (liver impairment), thiocyanate toxicity (renal impairment).

What are nitroglycerin's effects, administration, contraindications, and adverse effects?

Predominantly venodilator (decreases preload) with mild arterial dilation. Continuous IV infusion using glass/special containers and tubing. Risks: hypotension, tachycardia, headache, excessive preload reduction, tolerance. Avoid with hypotension, PDE-5 inhibitors, riociguat, or corn-product allergy per lecture.

When are IV positive inotropes indicated?

Cold/hypoperfused patients, particularly cardiogenic shock (SBP <90 mmHg PLUS hypoperfusion). Maintain systemic perfusion and end-organ function; long-term intermittent infusions without indications may be harmful.

How do dobutamine, dopamine, and milrinone increase contractility?

Dobutamine/dopamine: beta agonism activates adenylate cyclase and increases cAMP. Milrinone: phosphodiesterase inhibition prevents cAMP breakdown. Increased intracellular cAMP enhances contractility and relaxation.

What are dobutamine's effects, administration, and adverse effects?

Beta-1 inotropy plus beta-2 vasodilation; increases CO, may decrease preload, often minimal MAP change (MAP = CO × SVR). Continuous IV infusion. Monitor tachycardia, arrhythmias (ECG), headache.

What are milrinone's effects, administration, and adverse effects?

PDE inhibitor/inodilator with positive inotropy and arterial/venous dilation; decreases preload and may decrease MAP, causing reflex tachycardia. Continuous IV infusion; HF half-life ~3 hours; reduce dose in renal impairment. Risks: arrhythmias, hypotension, thrombocytopenia, headache.

What are dopamine's role and adverse effects?

Reserved in lecture for marked hypotension/cardiogenic shock; increases inotropy and MAP via continuous IV infusion. Risks: tachycardia, arrhythmias, increased myocardial O2 demand, reduced myocardial blood flow.

Is digoxin used for acute ADHF management?

No. Lecture states digoxin is not used for acute management.

What monitoring is especially important for inotropes and vasodilators?

BP/MAP, HR, ECG/arrhythmias, perfusion, urine output, renal function, and invasive hemodynamics when indicated. Milrinone: renal dosing and platelets. Nitroprusside: cyanide/thiocyanate toxicity.

When should preadmission GDMT be continued during ADHF hospitalization?

Continue ARNI/ACE-I/ARB, evidence-based beta blocker, MRA, and SGLT2 inhibitor if no hemodynamic instability or contraindication.

When should GDMT be initiated in patients not already taking it?

Before hospital discharge, after volume status is optimized and IV diuretics, vasodilators, and inotropes have been successfully discontinued.

What are the four GDMT medication pillars for HFrEF?

ARNI (or ACE-I/ARB), evidence-based beta blocker, MRA, and SGLT2 inhibitor.

What discharge counseling is required after ADHF?

Diet/sodium restriction, discharge medications and adherence, daily weights, activity, follow-up appointments, worsening symptom action plan; follow-up clinic visit usually within 7 days.

Case: A patient has rales, JVD, pitting edema, warm extremities, and adequate BP. Which subset?

Subset II: warm and wet. Congestion is present, but no clear hypoperfusion. Treat with IV loop diuretic.

Case: A patient has cool extremities, low BP, worsening renal function, and no edema/congestion. Which subset and treatment?

Subset III: cold and dry. Evaluate if too dry: IV fluids if volume depleted; if volume optimized and hypoperfusion persists, IV dobutamine or milrinone.

Case: A patient has pulmonary edema, JVD, cool extremities, low BP, and hypoperfusion. Which subset and treatment?

Subset IV: cold and wet. Carefully combine IV inotrope for perfusion and IV loop diuretic for congestion; individualize treatment.

Case: CD is 70, has SOB/orthopnea/edema, JVD/rales, warm extremities, BP 150/80, NT-proBNP 3000, EF 30%, and new AFib. Identify subset and triggers.

Subset II (warm/wet). Possible triggers: recent ibuprofen (NSAID), new atrial fibrillation, and lack of optimized chronic HF therapy.

Case: CD has SCr 0.9 mg/dL and no home furosemide. What initial dose and urine-output goal?

Furosemide 40 mg IV push once. Target >500 mL urine in first 2 hours; if goal not met, double to 80 mg IV within 2–4 hours of previous dose.

Case: CD meets the urine-output goal after furosemide 40 mg IV. What next?

Per lecture case, schedule furosemide 40 mg IV every 12 hours (8–16-hour interval noted), reassess congestion and continue until volume optimized. Monitor I/O, weight, K/Mg/Na, BUN/SCr and BP.

Case: CD is stabilized and changed to furosemide 40 mg PO daily. What must be addressed before discharge?

Optimize the four HFrEF GDMT pillars as tolerated; review inappropriate/precipitating drugs (ibuprofen), address new AFib, provide medication/diet/daily-weight counseling and arrange follow-up (usually 7 days).

CASE 1: BJ has BP 88/60, JVD, bilateral rales, pitting edema, and cold clammy extremities. What hemodynamic subset is he?

D. Cold and wet (Subset IV). Wet = pulmonary/systemic congestion; cold = hypoperfusion (hypotension and cold extremities).

CASE 1: BJ recently attended a barbecue and has not refilled his 30-day supply of furosemide for 2 months. Which factors precipitated ADHF? Select ALL: A. Losartan B. Furosemide C. Medication nonadherence D. Dietary nonadherence

C and D. Missing furosemide doses and excessive sodium intake can precipitate fluid overload and ADHF.

CASE 1: BJ has BP 88/60 with hypoperfusion and takes losartan 25 mg daily. Should losartan be continued, increased, or held during acute management?

Hold/discontinue losartan until hypoperfusion and hypotension resolve. Do not initiate or increase chronic GDMT during hemodynamic instability.

CASE 1: BJ takes furosemide 40 mg PO daily at home. Which initial IV regimen is recommended? A. 40 mg IV once B. 80 mg IV once C. Metolazone 2.5 mg PO once D. Chlorothiazide 500 mg IV once

A. Furosemide 40 mg IV bolus once, then check urine output after 2 hours. The lecture case uses the total home dose as the initial IV bolus.

CASE 1: BJ receives furosemide 40 mg IV and produces only 250 mL urine after 2 hours. SCr is 1.5 mg/dL. What is the next step?

Inadequate response: goal is >500 mL in 2 hours because SCr <2.5. Double to furosemide 80 mg IV bolus once and reassess in 2 hours; if adequate, schedule 80 mg IV Q12H.

CASE 1: BJ is cold/wet with SBP 88 mmHg. Which additional acute therapy is most appropriate? A. Digoxin IV B. Nitroglycerin IV C. Dobutamine D. Milrinone E. None

C. Dobutamine. Hypoperfusion requires positive inotropic support; hypotension makes IV vasodilators inappropriate.

CASE 1: What is the prescribed dobutamine regimen for BJ's hypoperfusion?

Dobutamine 5 mcg/kg/min IV continuous infusion; titrate up to 20 mcg/kg/min according to response. Monitor BP, HR, and ECG continuously.

CASE 1: What are BJ's goals of acute ADHF treatment?

Relieve pulmonary/systemic congestion and improve perfusion/CO. IV furosemide treats wet; IV dobutamine treats cold.

CASE 1: What monitoring is required during BJ's IV furosemide and dobutamine therapy?

Daily: signs/symptoms, weight, urine output/I&O, SCr/BUN, K, Mg, Na. Continuous: BP, HR, ECG during unstable hypoperfusion and dobutamine treatment.

CASE 1: BJ improves by Day 3: BP 130/86, SCr 1.0, K 4.0, HR 80, volume optimized. Which options are appropriate? A. Continue IV furosemide B. Furosemide 40 mg PO BID C. Losartan 25 mg daily D. Entresto 24/26 mg BID E. Metoprolol succinate 25 mg daily F. Empagliflozin 10 mg daily G. Spironolactone 50 mg daily

B, D, E, F. Transition to oral diuretic; initiate ARNI, evidence-based beta blocker, and SGLT2 inhibitor. Spironolactone is appropriate at 12.5 mg daily in the case, NOT the listed 50 mg dose.

CASE 1: Once BJ is stable, what is the complete chronic HFrEF pharmacotherapy plan?

Furosemide 40–80 mg PO daily to BID; replace losartan with Entresto 24/26 mg PO BID; initiate metoprolol succinate 25 mg PO daily (or carvedilol 3.125 mg BID or bisoprolol 1.25 mg daily); empagliflozin 10 mg PO daily; spironolactone 12.5 mg PO daily. Titrate GDMT gradually.

CASE 1: Why is spironolactone 50 mg daily not the preferred initiation dose for BJ?

The case specifies starting spironolactone 12.5 mg PO daily after stabilization, with adequate renal function and K <5 mEq/L. The listed 50 mg dose is not the recommended starting regimen.

CASE 1: What follow-up and monitoring should BJ receive after discharge?

Follow up with PCP in approximately 1 week; reassess symptoms, BP, HR, daily weights, K, Na, and SCr. Titrate chronic HF medications toward targets as tolerated.

CASE 1: What counseling is important for BJ's new medications?

Furosemide: morning dosing, daily weights, photosensitivity. Beta blocker: fatigue, orthostatic symptoms, never stop abruptly. Entresto: angioedema warning. Empagliflozin: urinary/genital infection symptoms. Spironolactone: avoid potassium salt substitutes/excessive K intake. Stress sodium restriction and adherence.

CASE 2: DM has BP 140/90, JVD, rales, ascites, pitting edema, and warm extremities. Which subset? A. Warm/dry B. Warm/wet C. Cold/dry D. Cold/wet

B. Warm and wet (Subset II). She has congestion but no signs of hypoperfusion.

CASE 2: DM takes pioglitazone, lisinopril, and metoprolol succinate. Which medication may have precipitated ADHF? A. Pioglitazone B. Lisinopril C. Metoprolol succinate D. All

A. Pioglitazone, a TZD, can cause fluid retention and worsen HF. Discontinue and select alternative diabetes therapy.

CASE 2: During acute treatment, which chronic medication actions are appropriate? A. Start Entresto B. Continue lisinopril 40 mg C. Continue metoprolol succinate 50 mg D. Continue pioglitazone E. Stop pioglitazone F. Increase lisinopril G. Increase metoprolol

B, C, E. Continue stable GDMT (lisinopril and metoprolol succinate), discontinue pioglitazone, and postpone GDMT changes until volume status is optimized.

CASE 2: DM has SCr 2.4 mg/dL and is not taking furosemide at home. Which initial dose? A. 40 mg IV B. 80 mg IV C. Metolazone 2.5 mg PO D. Chlorothiazide 500 mg IV

B. Furosemide 80 mg IV bolus once because SCr >2 mg/dL and no home loop diuretic; reassess urine output after 2 hours.

CASE 2: According to the provided practice-case answer key, what is the urine-output goal after DM's initial IV furosemide dose?

The case answer key specifies >500 mL in 2 hours; if inadequate, double the dose. NOTE: This conflicts with the lecture's SCr-based rule, which specifies >250 mL in 2 hours when SCr is below? No: when SCr >2.5 mg/dL. DM's SCr is 2.4, so >500 mL is consistent.

CASE 2: DM is warm/wet with BP 140/90. Which additional therapy is required? A. Digoxin IV B. Nitroglycerin IV C. Dobutamine D. Milrinone E. None

E. No additional therapy needed initially. IV loop diuretic is first-line. IV vasodilator may be considered if needed and BP permits, but is not required.

CASE 2: Why does DM not require dobutamine or milrinone?

She is warm/wet, meaning adequate perfusion. Inotropes are for cold/hypoperfused patients, especially cardiogenic shock.

CASE 2: DM has SCr 2.4 and eGFR approximately 23 mL/min. Which chronic HF agents are not appropriate per the case, and which SGLT2 inhibitor can be considered?

Per the supplied case: do not initiate spironolactone (eGFR <30) or dapagliflozin at eGFR 23; empagliflozin 10 mg PO daily can be considered.

CASE 2: DM is stable after diuresis. Which options are appropriate? A. Furosemide 40 mg PO BID B. Continue lisinopril C. Continue metoprolol 50 mg D. Stop lisinopril E. Start Entresto 49/51 mg BID after washout F. Increase metoprolol to 100 mg G. Spironolactone 12.5 mg H. Dapagliflozin 10 mg

A, D, E, F. The case recommends oral furosemide, switching ACE-I to ARNI after 36-hour washout, and beta-blocker titration. It separately recommends empagliflozin, which is not listed among these choices.

CASE 2: What is DM's complete chronic HF medication plan after volume optimization?

Furosemide 40–80 mg PO daily to BID; discontinue lisinopril and after 36-hour washout start Entresto 49/51 mg PO BID; increase metoprolol succinate to 100 mg PO daily as tolerated; initiate empagliflozin 10 mg PO daily. No spironolactone with eGFR 23 per case.

CASE 2: Why is a 36-hour washout required when switching DM from lisinopril to Entresto?

Entresto contains sacubitril (neprilysin inhibitor); overlap with an ACE inhibitor increases angioedema risk. Stop ACE inhibitor and wait at least 36 hours before starting Entresto.

CASE 2: What monitoring and follow-up are recommended after DM's medication changes?

PCP follow-up in 1 week; assess HF symptoms, BP, HR, SCr, K, and Na. Monitor renal function and potassium closely after ARNI changes; monitor volume status and infections with empagliflozin.

CASE 2: What is DM's CKD stage based on eGFR ~23 mL/min/1.73 m²?

CKD G4 (Stage 4). HTN and diabetes are progression factors; obtain urine albumin assessment and evaluate CKD complications.

CASE 2: What counseling should DM receive before discharge?

Furosemide in morning, daily weights, sun protection; metoprolol fatigue/orthostasis and do not stop abruptly; Entresto angioedema; empagliflozin urinary/genital infection risk; emphasize medication/diet adherence and follow-up.

CASE CD: A 70-year-old man has SOB at rest, orthopnea, edema, JVD, rales, warm extremities, BP 150/80, and EF 30%. What subset and triggers?

Warm and wet (Subset II). Possible triggers: ibuprofen use and new-onset AFib. Discontinue ibuprofen and address AFib.

CASE CD: CD has SCr 0.9, no home loop diuretic, and warm/wet ADHF. Give the exact initial treatment and next steps.

Furosemide 40 mg IV bolus once; check urine output after 2 hours (goal >500 mL). If at goal, 40 mg IV Q8–12H. If below goal, 80 mg IV bolus once; continue until euvolemic. Monitor daily I&O, weight, K/Mg/Na, BUN/SCr; BP Q6H.

CASE CD: CD is stable and switched to furosemide 40 mg PO daily. What chronic medication changes are recommended?

Discontinue metoprolol tartrate 25 mg BID; initiate metoprolol succinate 25 mg PO daily and Entresto 24/26 mg PO BID. Discontinue ibuprofen and use acetaminophen 325 mg PO Q6H PRN pain. Monitor BP, HR, SCr, K in 1 week.

CASE CD: Why change metoprolol tartrate to metoprolol succinate?

Metoprolol succinate (extended release) is an evidence-based beta blocker for HFrEF mortality benefit; metoprolol tartrate is not one of the guideline-supported HFrEF beta-blocker formulations.

CASE COMPARISON: BJ is cold/wet and hypotensive; DM is warm/wet and hypertensive; CD is warm/wet and hypertensive. What is the key treatment difference?

All require IV loop diuresis for congestion. BJ additionally needs inotropic support (dobutamine) for hypoperfusion and temporarily holds losartan. DM and CD do not routinely need inotropes because perfusion is adequate.