Cardiovascular

Acute decompensated heart failure: CCS-style inpatient management

Clinical Overview and When to Suspect Acute Decompensated Heart Failure

— >1 million US hospitalizations/year; 30-day readmission ~20%, 1-year mortality ~30% post-discharge.

— Most admissions are acute-on-chronic decompensations of known HF (HFrEF or HFpEF), not de novo HF.

— Progressive dyspnea on exertion → orthopnea → paroxysmal nocturnal dyspnea

— Rapid weight gain (>2 kg/3 days), worsening lower-extremity edema, abdominal fullness/early satiety

— Known HF patient with medication nonadherence, dietary indiscretion (high Na), new arrhythmia (especially AF with RVR), recent NSAID use, or ischemic event

— Warm & Wet (~70%): congested, perfused → diuresis ± vasodilator

— Cold & Wet (~20%): congested + hypoperfused → inotrope + diuresis ± mechanical support

— Cold & Dry (~5%): hypoperfused, euvolemic → cautious fluid or inotrope

— Warm & Dry: compensated, not ADHF

— Forgot meds, Arrhythmia/anemia, Ischemia/infection, Lifestyle (Na, fluid), Upregulation (pregnancy, hyperthyroid), Renal failure, Embolus (PE), Stenosis (valvular/RAS)

Acute decompensated heart failure (ADHF) = new or worsening signs/symptoms of heart failure requiring urgent therapy, most often presenting with congestion (volume overload) rather than low output.

Epidemiology and burden:

When to suspect ADHF in the ED or clinic:

Forrester/Stevenson profile (warm/cold × wet/dry) frames everything that follows:

Triggers to identify on admission (FAILURES mnemonic):

CCS pearl: On a CCS case opening with dyspnea + leg swelling + JVD, your first three orders should be continuous pulse oximetry, IV access, and 12-lead ECG while you simultaneously order BNP, troponin, BMP, CBC, and CXR. Do not delay IV loop diuretic waiting on labs if the diagnosis is clinically clear — advance the clock only after initial stabilization orders are placed. Identifying and treating the trigger is as important as treating congestion itself for the exam.

Presentation Patterns and Key History

— Gradual volume overload (days–weeks): weight gain, edema, orthopnea, fatigue — most common; usually HFrEF or HFpEF acute-on-chronic

— Flash pulmonary edema (minutes–hours): sudden severe dyspnea, hypertensive crisis (SBP often >180), diffuse rales, pink frothy sputum — think HFpEF with hypertensive surge or acute MR/AS

— Cardiogenic shock: hypotension, cool extremities, oliguria, altered mentation, lactic acidosis — usually post-MI, fulminant myocarditis, or end-stage HFrEF

— Baseline NYHA class and EF (if known); dry weight; home diuretic dose

— Medication adherence and recent changes (stopped beta-blocker? new NSAID, glitazone, dronedarone?)

— Dietary Na and fluid intake; recent IV contrast or fluid administration

— Infectious symptoms, chest pain, palpitations, syncope

— Substance use: cocaine, methamphetamine, alcohol (alcoholic cardiomyopathy), chemo exposure (anthracyclines, trastuzumab, 5-FU), radiation

— Sleep apnea symptoms (OSA worsens RV function and triggers AF)

— Orthopnea/PND → elevated LV filling pressure

— Bendopnea (dyspnea bending forward) → very high filling pressures, poor prognosis

— RUQ pain, anorexia, ascites → right-sided congestion / hepatic congestion

— Exertional fatigue without dyspnea → low cardiac output

Three classic ADHF presentation phenotypes (recognize on the stem):

History essentials to extract on the CCS:

Symptom-to-pathophysiology mapping:

Key distinction: HFpEF patients are typically older women with HTN, AF, obesity, CKD, and DM; they decompensate with hypertensive surges and AF with RVR. HFrEF patients are more often men with CAD or prior MI; they decompensate with ischemia, arrhythmia, or med nonadherence. Both get IV loop diuretics acutely, but HFpEF responds dramatically to BP control while HFrEF needs neurohormonal blockade restored before discharge.

Board pearl: A normal BNP (<100 pg/mL) in an untreated, non-obese patient makes ADHF very unlikely (NPV >90%). Obesity lowers BNP; AF, PE, sepsis, and CKD raise it.

Physical Exam Findings and Hemodynamic Assessment

— Elevated JVP (>8 cm H₂O, or visible above clavicle at 45°) — best bedside marker of elevated RA pressure

— Hepatojugular reflux: sustained JVP rise >3 cm with 10 sec RUQ pressure — sensitive for RV/LV dysfunction

— S3 gallop: highly specific for elevated LV filling pressure and HFrEF; LR+ ~11 for ADHF

— Pulmonary rales (bibasilar, wet) — insensitive (often absent in chronic HF due to lymphatic compensation)

— Lower extremity pitting edema, ascites, hepatomegaly with pulsatile liver (TR)

— Narrow pulse pressure (<25% of SBP) — surrogate for low cardiac output

— Cool/mottled extremities, delayed capillary refill, weak thready pulses

— Altered mentation, oliguria (<0.5 mL/kg/hr), lactate >2

— Pulsus alternans — severe LV dysfunction

— Loud P2, RV heave, TR murmur — pulmonary HTN from chronic LV failure

— New murmur → acute MR (papillary muscle rupture), VSD post-MI, endocarditis

— Irregularly irregular pulse → AF as trigger

— B-lines (>3/zone in ≥2 zones bilaterally) — sensitive/specific for pulmonary edema

— IVC >2.1 cm with <50% collapse — elevated RA pressure

— Reduced LV systolic function on parasternal view

Bedside congestion ("wet") signs — sensitivity varies, specificity reasonable:

Bedside perfusion ("cold") signs:

Other targeted findings:

POCUS at bedside (increasingly board-relevant):

Step 3 management: Use the 2×2 hemodynamic profile at the bedside to drive initial therapy before any lab returns: if warm & wet → IV furosemide ± nitroglycerin; if cold & wet with SBP <90 → add dobutamine or milrinone and call cardiology/ICU. Document profile in the admission note — it's the most efficient handoff tool and frames downstream orders on CCS cases.

Board pearl: Absence of rales does not rule out ADHF — up to 80% of chronic HF decompensations lack rales. JVP and S3 are more reliable.

Diagnostic Workup — Initial Labs, Imaging, ECG, Biomarkers

— CBC (anemia as trigger), BMP (Na, K, BUN/Cr, baseline renal), Mg, phosphate

— LFTs (congestive hepatopathy: ↑AST/ALT, ↑bili; "shock liver" if AST in thousands)

— Troponin (rule out ACS trigger; mild elevation common in ADHF from demand)

— BNP or NT-proBNP: BNP >400 or NT-proBNP age-adjusted (>450 if <50, >900 if 50–75, >1800 if >75) supports HF

— TSH (new HF or AF), HbA1c, iron studies (ferritin, TSAT — IV iron indication)

— Lactate, ABG if shock or severe respiratory distress

— UA, urine Na (pre-renal vs ATN; spot urine Na <20 suggests effective hypovolemia despite total-body overload)

— STEMI/NSTEMI as trigger → emergent cath

— AF with RVR (rate control + anticoagulation decisions)

— LBBB, QRS >150 ms → future CRT candidate

— LVH, prior MI Q-waves, low voltage (amyloid, effusion)

— Cardiomegaly, cephalization, Kerley B lines, peribronchial cuffing, perihilar "bat-wing" edema, pleural effusions (R > L typical)

— Normal CXR does not exclude ADHF, especially flash edema

— Lower in obesity (BMI >35)

— Higher in CKD, advanced age, AF, sepsis, PE, RV strain

— Sacubitril/valsartan raises BNP (blocks neprilysin) but lowers NT-proBNP — use NT-proBNP for trending in ARNI patients

Initial bundle on every suspected ADHF admission (order simultaneously on CCS):

ECG — get within 10 minutes:

CXR findings (often lag clinically by hours):

Natriuretic peptides — pitfalls:

Key distinction: BNP <100 has high NPV; BNP >400 has high PPV; the 100–400 "gray zone" requires clinical judgment + echo. Don't reflexively diurese a gray-zone BNP without confirming congestion.

CCS pearl: On the CCS interface, order "daily weights, strict I&Os, 2 g Na diet, 1.5–2 L fluid restriction" as standing orders on admission — these are graded actions and frequently scored.

Diagnostic Workup — Advanced and Confirmatory Studies

— Obtain in all new HF presentations and in acute-on-chronic if no recent echo (within 6–12 months) or if clinical change suggests new pathology

— Assess LVEF (categorize as HFrEF ≤40%, HFmrEF 41–49%, HFpEF ≥50%), wall motion (regional → ischemic), valvular function, RV size/function, pericardial effusion, estimated PASP

— Inpatient echo within 24–48 hr is appropriate for new HF

— Coronary angiography if troponin-positive, regional wall motion abnormality, angina, or high pretest probability CAD

— Functional stress imaging (stress echo, nuclear, CMR) if intermediate risk and stable

— Coronary CTA acceptable in low-to-intermediate risk

— Indicated when hemodynamics are unclear, cardiogenic shock not responding to therapy, evaluation for advanced therapies (LVAD, transplant), or suspected pulmonary HTN of unclear etiology

— Not routine for ADHF (ESCAPE trial showed no mortality benefit, more complications)

— Targets: CI >2.2, PCWP <18, SVR 800–1200, RAP <8

— Iron studies/ferritin (hemochromatosis), HIV, TSH, SPEP/free light chains/pyrophosphate scan (amyloid), ANA (lupus myocarditis), alcohol/cocaine history, family history (genetic cardiomyopathy panel if early onset or family Hx)

— Sleep study if OSA suspected

Transthoracic echocardiogram (TTE) — the single most important confirmatory test:

Ischemic workup — critical to decide before discharge:

Cardiac MRI: gold standard for myocarditis (LGE pattern), infiltrative disease (amyloid, sarcoid, hemochromatosis), arrhythmogenic cardiomyopathy

Right heart catheterization (PAC/Swan-Ganz) — selective use:

Etiology workup for new HFrEF (don't miss reversible causes):

Endomyocardial biopsy: reserved for suspected giant cell myocarditis, eosinophilic myocarditis, or unexplained rapidly progressive HF

Board pearl: A TTAS ("transferrin sat") >45% with ferritin >300 in new cardiomyopathy → screen for hereditary hemochromatosis (HFE C282Y). Reversible cardiomyopathy with phlebotomy.

Step 3 management: Before discharge for new HFrEF, document EF, ischemic workup completed, and trigger identified — these three items drive the entire long-term plan including ICD candidacy at 90 days.

Risk Stratification and First-Line Management Logic

— OPTIMIZE-HF / ADHERE risk trees: highest in-hospital mortality with BUN ≥43, SBP <115, Cr ≥2.75

— GWTG-HF score: validated for in-hospital mortality

— Seattle Heart Failure Model: outpatient/long-term prognosis

— ICU/CCU: cardiogenic shock, respiratory failure requiring NIV/intubation, hemodynamically significant arrhythmia, ongoing ischemia, need for inotropes or mechanical circulatory support

— Step-down/telemetry: most ADHF admissions — need IV diuresis, monitoring of K/Mg/Cr, arrhythmia surveillance

— Observation unit: select low-risk patients (no troponin elevation, preserved renal function, responsive to initial diuresis, BP stable)

— 1) Airway/oxygenation — supplemental O₂ to SpO₂ ≥90%; NIV (BiPAP) for respiratory distress, hypercapnia, or pulmonary edema → reduces intubation and mortality

— 2) Decongest — IV loop diuretic dosed to effect

— 3) Address trigger — ischemia, arrhythmia, infection, BP control

— 4) Continue/restart GDMT when stable — do NOT routinely stop beta-blockers unless cardiogenic shock

— 5) Prevent VTE — DVT prophylaxis (heparin SQ or enoxaparin) unless contraindicated

— Warm & Wet: IV loop diuretic; add IV nitroglycerin or nitroprusside if SBP elevated/flash edema

— Cold & Wet, SBP <90: dobutamine or milrinone + diuretic when perfusion improves; consider MCS

— Cold & Dry: cautious fluid challenge 250 mL, then reassess; inotrope if no response

Risk stratification tools (useful for triage and prognosis):

Disposition triage:

Core management priorities, in order:

Hemodynamic-guided therapy:

CCS pearl: Always order telemetry, continuous pulse ox, daily weights, strict I&Os, fluid restriction 1.5–2 L/day, 2 g Na diet, DVT prophylaxis, and a cardiology consult on admission. Forgetting DVT prophylaxis is a classic scored omission.

Board pearl: Beta-blocker continuation during ADHF (unless overt shock) is associated with lower mortality and rehospitalization (B-CONVINCED trial). Halve the dose if borderline; stop only if shock.

Pharmacotherapy — First-Line Drug Regimen

— Furosemide IV is first-line. Dose = 2.5× the home oral dose given IV (DOSE trial); diuretic-naïve start 40 mg IV

— Bolus q12h vs continuous infusion: equivalent in DOSE trial; high-dose strategy → more rapid symptom relief, transient ↑Cr without long-term harm

— Alternatives if sulfa concern or refractory: bumetanide (1 mg ≈ 40 mg furosemide), torsemide (better PO bioavailability — preferred for discharge in poor responders, TRANSFORM-HF trial neutral on mortality but improved QoL)

— Goal urine output: 3–5 L/day net negative until euvolemic

— Spot urine Na at 2 hr >50–70 mmol/L and/or urine output >150 mL/hr in first 6 hr = adequate response

— If inadequate → double the dose, not the frequency; reassess in 2 hr

— Add thiazide-type: metolazone 2.5–10 mg PO or chlorothiazide 500 mg IV 30 min before loop

— Add acetazolamide 500 mg IV daily (ADVOR trial — improved decongestion when added to loop)

— Add SGLT2 inhibitor early (empagliflozin/dapagliflozin) — EMPULSE showed benefit started in-hospital

— Consider tolvaptan for severe hyponatremia with congestion (short-term)

— Ultrafiltration if truly refractory

— IV nitroglycerin 10–200 mcg/min — preload reduction, ideal for flash pulmonary edema

— IV nitroprusside 0.3–5 mcg/kg/min — afterload + preload; watch cyanide toxicity in renal failure

— Avoid nesiritide (no mortality benefit, ↑hypotension)

— Dobutamine 2.5–10 mcg/kg/min (β1 agonist; tachyarrhythmia risk; avoid if on beta-blocker — use milrinone)

— Milrinone 0.125–0.5 mcg/kg/min (PDE3 inhibitor; vasodilates → can drop BP; renally cleared)

— Norepinephrine added if MAP <65 in cardiogenic shock

IV loop diuretics — the cornerstone:

Assessing diuretic response:

Diuretic resistance strategy (sequential nephron blockade):

Vasodilators (warm & wet with elevated BP):

Inotropes (cold & wet):

Step 3 management: Monitor K, Mg, Cr daily; replete K to >4.0 and Mg to >2.0 to prevent diuretic-induced arrhythmia. A rise in Cr up to 0.3 mg/dL during effective diuresis is acceptable and does not mandate stopping diuretics.

Expanded Pharmacology — Initiating GDMT During Hospitalization

— 1) ARNI (sacubitril/valsartan) preferred over ACEi/ARB (PARADIGM-HF, PIONEER-HF)

— Start 24/26 mg or 49/51 mg BID; hold 36 hr after last ACEi dose (angioedema risk)

— Avoid if SBP <100, eGFR <30, K >5.2, pregnancy, history of angioedema

— 2) Beta-blocker — only carvedilol, metoprolol succinate, or bisoprolol have mortality benefit

— Continue if already on; initiate when euvolemic and off inotropes ≥24 hr

— 3) MRA (spironolactone or eplerenone) — start if K <5.0 and eGFR >30

— Spironolactone 12.5–25 mg daily; monitor K and Cr at 1 week

— 4) SGLT2 inhibitor (dapagliflozin or empagliflozin) — benefit across HFrEF, HFmrEF, HFpEF (DAPA-HF, EMPEROR-Reduced/Preserved)

— Start regardless of diabetes status; hold if eGFR <20, type 1 DM, or DKA risk

— SGLT2 inhibitor — class I recommendation

— MRA — class IIb (TOPCAT subgroup benefit)

— ARNI — class IIb (PARAGON-HF — benefit in EF 45–57% and women)

— Aggressive BP control and AF rate/rhythm control are central

— Hydralazine + isosorbide dinitrate: add to GDMT in self-identified Black patients with NYHA III–IV HFrEF (A-HeFT)

— Ivabradine: HFrEF, sinus rhythm, HR ≥70 on max beta-blocker

— Vericiguat: worsening HFrEF after recent decompensation (VICTORIA)

— Digoxin: symptom relief in HFrEF with AF; narrow therapeutic window, level 0.5–0.9

— IV iron (ferric carboxymaltose): if ferritin <100 or 100–300 with TSAT <20% — improves symptoms (AFFIRM-AHF)

Why initiate GDMT in-hospital: STRONG-HF trial showed rapid up-titration of GDMT before discharge with close follow-up reduces 180-day death/readmission. Inpatient initiation captures a teachable, monitored window.

The "four pillars" of HFrEF (EF ≤40%) — start all four before discharge if hemodynamically tolerated:

HFpEF (EF ≥50%) pharmacology:

Adjuncts and disease-specific therapies:

CCS pearl: Before "end case," verify the discharge med list includes ARNI/ACEi, beta-blocker, MRA, SGLT2i, loop diuretic at lowest effective dose, and statin/antiplatelet if CAD. Missing pillars are commonly scored.

Board pearl: Never combine ACEi + ARB + MRA (renal failure, hyperkalemia); never combine ACEi + ARNI (angioedema).

Special Populations — Elderly and Renal/Hepatic Impairment

— Higher prevalence of HFpEF, AF, CKD, polypharmacy, frailty

— Increased sensitivity to diuretics → orthostasis, falls, AKI; monitor standing BP

— Cognitive impairment affects medication adherence — engage caregivers, consider pillboxes/blister packs

— NT-proBNP age-adjusted cutoffs (>1800 if >75) avoid false positives

— Goal SBP often 130–140 (not <120) to avoid orthostasis

— Deprescribe nonessential meds; reassess statin if life expectancy <5 yr and primary prevention

— Types 1 (acute cardiac → AKI) and 2 (chronic cardiac → CKD) most relevant in ADHF

— A rise in Cr up to 0.3–0.5 mg/dL during effective decongestion is acceptable; persistent oliguria or rise >0.5 with worsening congestion suggests inadequate diuresis, not over-diuresis

— Diuretic dosing in CKD: higher doses needed (eGFR <30 often requires furosemide 80–200 mg IV); add thiazide for synergy

— ARNI/ACEi/ARB: continue if eGFR ≥30 and K <5.0; tolerate Cr rise up to 30% with restart

— MRA: avoid if eGFR <30 or K >5.0

— SGLT2i: dapagliflozin OK to eGFR ≥20, empagliflozin ≥20; continue even as eGFR drops

— Avoid NSAIDs, metformin in AKI, gadolinium if eGFR <30

— Mild ↑AST/ALT/bili from passive congestion is common — improves with decongestion

— Cardiac cirrhosis in long-standing right HF (constrictive pericarditis, severe TR) — coagulopathy, ascites

— Avoid hepatotoxic drugs; adjust amiodarone, statins, warfarin dosing

— Spironolactone is preferred diuretic in cirrhosis-associated ascites (ratio 100:40 with furosemide)

Elderly patients (>75):

CKD and the cardiorenal syndrome:

Hepatic dysfunction / congestive hepatopathy:

Key distinction: Pre-renal AKI from over-diuresis (BUN/Cr >20, FENa <1%, urine Na <20, responsive to fluid) vs cardiorenal physiology from under-diuresis (persistent congestion, JVP elevated, weight not falling — needs MORE diuretic). Do not reflexively give fluids to a congested ADHF patient with rising Cr.

Step 3 management: Order orthostatic vitals before discharge in elderly diuresed patients — symptomatic orthostasis is a leading cause of 30-day readmission and falls.

Special Populations — Pregnancy, Peripartum, and Other Demographics

— New HFrEF (EF <45%) in last month of pregnancy through 5 months postpartum, no other cause

— Risk factors: African ancestry, age >30, multiparity, preeclampsia, multiple gestation

— Diagnosis: TTE; rule out PE, MI, valvular disease

— Treatment: standard HF therapy with pregnancy modifications

— Safe in pregnancy: hydralazine + nitrates, beta-blockers (metoprolol, labetalol — avoid atenolol), loop diuretics (cautious — placental perfusion)

— Contraindicated in pregnancy: ACEi, ARB, ARNI, MRA (spironolactone), SGLT2i, ivabradine, warfarin (first trimester)

— Postpartum: switch to full GDMT; safe with breastfeeding: enalapril, captopril, metoprolol, warfarin

— Bromocriptine — adjunct in PPCM (suppresses prolactin); controversial but used

— Anticoagulation if EF <35% (high LV thrombus risk)

— ~50% recover EF; avoid subsequent pregnancy if EF does not normalize (high recurrence and mortality)

— Congenital heart disease, myocarditis, cardiomyopathies most common

— Symptoms: poor feeding, failure to thrive, tachypnea, diaphoresis with feeds

— Manage at pediatric cardiology center; principles similar but dosing weight-based

— Suspect: HFpEF + low voltage on ECG + thick walls on echo + bilateral carpal tunnel/spinal stenosis history

— ATTR-CM: confirm with pyrophosphate (PYP) scan (grade 2–3) after ruling out monoclonal gammopathy (SPEP, UPEP, free light chains)

— AL amyloidosis: tissue biopsy; refer to hematology urgently

— Specific therapy: tafamidis for ATTR-CM

— Avoid digoxin, CCBs, ACEi/ARB high doses (sensitive, hypotensive)

— Transgender patients on estrogen therapy have increased VTE risk — important for HF + AF anticoagulation decisions

Peripartum cardiomyopathy (PPCM):

Pediatric HF (less commonly tested on Step 3):

Patients with cardiac amyloidosis (increasingly recognized in HFpEF):

LGBTQ+ and gender considerations:

Board pearl: PPCM with persistent EF <35% beyond 6 months → contraception counseling and pregnancy avoidance; subsequent pregnancy mortality ~16%.

Step 3 management: Refer all PPCM patients to a specialized cardio-obstetric clinic before discharge; arrange repeat echo at 6 weeks, 3 months, 6 months postpartum.

Complications and Adverse Outcomes

— Acute kidney injury (cardiorenal syndrome) — 25–30% of admissions

— Hyponatremia (Na <135) — marker of high neurohormonal activation, poor prognosis; severe (<125) → consider tolvaptan, fluid restriction

— Electrolyte derangements: hypokalemia, hypomagnesemia from diuresis → arrhythmia substrate

— Arrhythmias: new AF (20%), VT/VF (especially with hypokalemia or ischemia)

— Worsening renal function and diuretic resistance

— Hypotension from over-diuresis, vasodilators, or initiating GDMT too aggressively

— Drug toxicity: digoxin (visual changes, bradyarrhythmia), ARNI angioedema, hyperkalemia from MRA + ACEi

— Acute MR (papillary muscle rupture) — new holosystolic murmur, flash pulmonary edema 2–7 days post-MI

— Ventricular septal rupture — harsh holosystolic murmur with thrill, RV failure

— Free wall rupture — tamponade, sudden death

— All require emergent surgical consult and mechanical circulatory support

— LV thrombus (especially EF <30%, apical akinesis post-MI) → systemic embolism, stroke

— DVT/PE from immobility — always order prophylaxis

— 30-day readmission ~20% — the single most measured HF quality metric

— 1-year mortality ~30% post-hospitalization

— Progressive functional decline, cachexia, frailty

— Depression (40% prevalence) — independent predictor of readmission/death

— SCAI shock stages A–E (At risk → Beginning → Classic → Deteriorating → Extremis)

— Escalation: vasopressor → inotrope → IABP → Impella → VA-ECMO → durable LVAD/transplant

In-hospital complications:

Mechanical complications (especially post-MI ADHF):

Thromboembolic complications:

Long-term adverse outcomes:

Cardiogenic shock progression:

Key distinction: Worsening renal function (WRF) during diuresis in a patient who is decongesting (losing weight, improving symptoms) has a benign prognosis and should not stop diuretic. WRF in a patient not decongesting is true cardiorenal failure with poor prognosis — needs hemodynamic reassessment, possibly RHC.

Board pearl: New murmur + sudden decompensation 3–5 days post-MI = papillary muscle rupture → emergent TEE, IABP, surgical mitral valve replacement. Do not waste time on medical management alone.

When to Escalate Care — ICU, Consults, Mechanical Support

— Cardiogenic shock (SBP <90, lactate >2, end-organ hypoperfusion)

— Respiratory failure requiring NIV or intubation

— Hemodynamically unstable arrhythmia (VT, complete heart block)

— Acute MI with HF, mechanical complication

— Need for IV inotropes, vasopressors, or mechanical circulatory support

— Severe hyponatremia (Na <125) requiring close monitoring

— Massive PE with RV dysfunction

— Cardiology — virtually all ADHF admissions; mandatory for new HFrEF

— Cardiothoracic surgery — mechanical complications, valvular emergencies, LVAD/transplant evaluation

— Interventional cardiology — STEMI, NSTEMI with hemodynamic instability

— Advanced HF/transplant cardiology — recurrent admissions, EF <25%, inotrope-dependent, peak VO₂ <14

— Nephrology — refractory cardiorenal syndrome, ultrafiltration candidate, eGFR <30 with HF

— Palliative care — NYHA IV, recurrent admissions, advanced age, declining functional status (parallel to disease-directed therapy, not replacing it)

— Intra-aortic balloon pump (IABP) — modest support, easy insertion; afterload reduction, coronary perfusion. IABP-SHOCK II showed no mortality benefit in MI-CS but still used

— Impella (2.5, CP, 5.0/5.5) — axial flow LV unloading; up to 5 L/min support

— VA-ECMO — biventricular and respiratory support for refractory shock; complications: limb ischemia, bleeding, Harlequin syndrome

— Durable LVAD (HeartMate 3) — destination therapy or bridge to transplant; INTERMACS profile 1–3

— Heart transplant — definitive therapy; UNOS allocation by status

ICU/CCU admission criteria:

Consults to order on CCS:

Mechanical circulatory support escalation pathway:

CCS pearl: When you "transfer to ICU" in a CCS case, the location change resets some monitoring; remember to re-order continuous telemetry, arterial line, central line, hourly I&Os, and bedside echo in the new location.

Step 3 management: Early palliative care consult in advanced HF improves symptom control, QoL, and goals-of-care clarity without shortening life — increasingly emphasized on boards. Don't equate palliative care with hospice.

Key Differentials — Same-Category (Cardiac) Causes of Acute Dyspnea

— Can present as pure ADHF without chest pain (silent MI in diabetics, elderly, women)

— ECG + serial troponins; emergent cath if STEMI or hemodynamic instability

— Acute MI is a top trigger of ADHF — always rule out

— Acute severe MR: papillary muscle rupture (post-MI), endocarditis, chordal rupture (myxomatous) → flash pulmonary edema, often quiet/absent murmur because of rapid LA pressure equalization

— Acute severe AR: aortic dissection (type A), endocarditis, prosthetic dysfunction → low diastolic BP, soft S1, no time for LV dilation → flash edema

— Critical AS: angina, syncope, HF triad; HF onset → median survival 2 years untreated → urgent TAVR/SAVR

— Prosthetic valve thrombosis/dysfunction: fluoroscopy, TEE

— Persistent AF with RVR, atrial flutter, frequent PVCs (>20% burden) → LV dysfunction reversible with rate/rhythm control

— SBP often >200; flash pulmonary edema; treat with IV nitroglycerin/nitroprusside + loop diuretic

— Beck's triad (hypotension, muffled heart sounds, JVD), pulsus paradoxus >10 mmHg, electrical alternans, equalization of diastolic pressures

— Bedside echo → emergent pericardiocentesis

— Right HF predominance, Kussmaul's sign, pericardial knock, calcified pericardium on imaging

— Mimics restrictive cardiomyopathy — distinguish with CMR, simultaneous LV/RV cath

— Viral prodrome → rapid HFrEF; CMR with LGE in epicardial/midmyocardial pattern

— Giant cell myocarditis → endomyocardial biopsy; very high mortality without transplant

— Anemia, hyperthyroidism, AV fistula, beriberi (thiamine deficiency), Paget's, sepsis

— Warm extremities, bounding pulses, wide pulse pressure, elevated CO on echo

Acute coronary syndrome (STEMI/NSTEMI):

Acute valvular emergencies:

Tachyarrhythmia-induced cardiomyopathy:

Hypertensive emergency with HF:

Cardiac tamponade:

Constrictive pericarditis:

Myocarditis (especially fulminant):

High-output HF (often overlooked):

Key distinction: Flash pulmonary edema with hypertensive BP and preserved EF on echo → think HFpEF crisis or acute mitral/aortic regurgitation or renal artery stenosis (recurrent flash edema with HTN crisis = bilateral RAS until proven otherwise — Pickering syndrome).

Board pearl: Recurrent flash pulmonary edema episodes in a patient with HTN, abdominal bruit, and asymmetric kidneys → renal artery duplex → revascularization can be curative.

Key Differentials — Non-Cardiac Causes of Acute Dyspnea

— Can mimic ADHF: dyspnea, hypoxia, elevated BNP and troponin, RV dysfunction on echo

— Distinguishing features: pleuritic chest pain, unilateral leg swelling, recent immobilization/surgery, CXR often clear

— Wells score → D-dimer or CTPA

— Massive PE with RV failure can cause cardiogenic shock — thrombolysis indicated

— Fever, productive cough, leukocytosis, focal infiltrate

— Common ADHF trigger — coexists rather than excludes HF

— Cautious fluids in HF patient with sepsis: small boluses (250–500 mL), reassess JVP/lung POCUS

— Wheezing, prolonged expiration, smoking history, prior PFTs

— "Cardiac asthma" (wheezing from pulmonary edema) can mimic — BNP, CXR, echo help

— Both can coexist; treat both

— Diffuse bilateral infiltrates, PaO₂/FiO₂ <300, no evidence of cardiogenic origin (PCWP <18, normal LV function)

— Berlin criteria; managed with low tidal volume ventilation

— High-output failure or precipitates ADHF in fixed-output cardiomyopathy

— Hb < 7 (or <8 with cardiac disease) → transfuse

— ESRD missing dialysis → uremic pulmonary edema; treat with emergent HD, not just diuretics

— Thyroid storm → high-output HF, AF; myxedema → pericardial effusion, low-output state

— Acute respiratory distress with urticaria, angioedema, hypotension

— Right-sided failure predominant; loud P2, RV heave, TR

— Group 2 (left heart disease) — most common cause; treat underlying LV dysfunction

Pulmonary embolism:

Pneumonia / sepsis:

COPD/asthma exacerbation:

ARDS:

Anemia/blood loss:

Acute renal failure with volume overload:

Thyroid storm or severe hypothyroidism:

Anaphylaxis / drug reaction:

Pulmonary hypertension (Group 1–5):

Key distinction: BNP elevation is not specific to HF — PE, sepsis, CKD, AF, and right heart strain all elevate it. The presence of elevated BNP in PE actually carries worse prognosis (RV strain marker) and helps risk-stratify for thrombolysis.

Step 3 management: When dyspnea workup is ambiguous, POCUS (lung B-lines, IVC, LV function, RV size, pleural effusion, DVT screen) in <10 minutes can simultaneously suggest ADHF, PE, pneumothorax, or COPD — increasingly the standard bedside approach.

Secondary Prevention, Discharge Medications, and Long-Term Plan

— ARNI (sacubitril/valsartan) or ACEi/ARB if ARNI not tolerated

— Beta-blocker (carvedilol, metoprolol succinate, bisoprolol) at tolerated dose, plan for up-titration

— MRA (spironolactone or eplerenone) if K <5 and eGFR >30

— SGLT2 inhibitor (dapagliflozin or empagliflozin)

— Loop diuretic at lowest effective dose to maintain euvolemia — often torsemide preferred for outpatient PO

— Statin if ASCVD or LDL-driven indication

— Aspirin + P2Y12 if recent ACS or PCI

— Anticoagulation if AF (CHA₂DS₂-VASc ≥2 men, ≥3 women) or LV thrombus

— Hydralazine + isosorbide dinitrate add-on in self-identified Black patients NYHA III–IV

— IV iron if iron-deficient

— Vaccinations: annual influenza, pneumococcal (PCV20 or PCV15+PPSV23), COVID-19, RSV (≥60 yr)

— SGLT2 inhibitor (class I), MRA (IIb), ARNI (IIb)

— Aggressive BP <130/80, AF rhythm/rate control, OSA treatment, weight loss

— Diuretic for congestion symptom relief

— ICD for primary prevention if EF ≤35% after 3 months of GDMT (90-day waiting period; ischemic CM after 40 days post-MI)

— CRT if EF ≤35%, LBBB with QRS ≥150 ms, NYHA II–IV on GDMT

— Defer device decisions until GDMT-optimized EF reassessed

— Na restriction <2–3 g/day, fluid restriction 1.5–2 L/day (especially if hyponatremic)

— Daily weights; call clinic if weight up >2 lb/day or >5 lb/week

— Smoking cessation, alcohol cessation (avoid if cardiomyopathy related)

— Cardiac rehab — class I for HFrEF, improves QoL and reduces readmissions

— Sleep apnea screening and CPAP if OSA

Discharge medication checklist for HFrEF (verify ALL before "end case"):

For HFpEF:

Device therapy — plan but typically NOT inpatient:

Lifestyle counseling (document and order dietary consult on CCS):

Step 3 management: Use structured discharge with medication reconciliation, teach-back education, follow-up appointment within 7–14 days, and a 48–72-hour phone call — this bundle reduces 30-day readmissions by ~30% (BOOST/Project RED).

Board pearl: Sacubitril/valsartan + ACEi = absolute contraindication (angioedema). Wash out ACEi 36 hours before starting ARNI.

Follow-Up, Monitoring Parameters, and Rehab/Counseling

— 48–72 hours: telephone or telehealth check-in by RN/pharmacist (med adherence, weight, symptoms)

— 7–14 days: in-person clinic visit with HF specialist or PCP — reassess volume status, BMP, titrate GDMT

— 2–4 weeks: BMP recheck after MRA, ARNI, or diuretic dose changes

— 30 days: comprehensive visit — readmission risk highest in this window

— 3 months: TTE to reassess EF and determine ICD candidacy in new HFrEF

— Weight daily — patient-reported; call if >2 lb/day or 5 lb/week

— BP and HR — target SBP 110–130, HR 60–70 (HFrEF); avoid SBP <90 symptomatic

— BMP — K, BUN, Cr — at 1–2 weeks after med change, then every 3–6 months when stable

— NT-proBNP — trending controversial but can guide therapy in select patients (GUIDE-IT was neutral)

— Echo — repeat at 3 months after GDMT optimization, then PRN clinical change

— Aim to double doses every 2 weeks as tolerated until target or maximally tolerated dose

— Target doses: carvedilol 25 mg BID (50 mg BID if >85 kg), metoprolol succinate 200 mg daily, sacubitril/valsartan 97/103 mg BID, spironolactone 25–50 mg daily

— STRONG-HF strategy: rapid in-hospital initiation + intensive 6-week up-titration with biweekly visits

— Class I for HFrEF (HF-ACTION trial)

— 36 sessions over 12 weeks; improves QoL, exercise capacity, reduces readmissions

— Covered by Medicare for systolic HF (EF ≤35%, NYHA II–IV on GDMT ≥6 weeks)

— Recognize symptoms of decompensation; have rescue diuretic dose plan

— Medication purpose and side effects

— Na/fluid restriction practical tips (read labels, avoid soups/processed foods)

— Vaccination schedule

— Advance directives and goals of care

— CardioMEMS (implantable PA pressure sensor) — CHAMPION/MONITOR-HF — reduces HF hospitalizations in NYHA III with recent admission

— Multidisciplinary HF clinics and disease management programs reduce mortality

Post-discharge follow-up cadence:

Monitoring parameters:

GDMT up-titration schedule:

Cardiac rehabilitation:

Self-care education (teach-back required):

Remote monitoring:

Board pearl: Early post-discharge follow-up within 7 days is associated with lower 30-day readmission — this is the single most testable transitions-of-care intervention on Step 3.

Ethical, Legal, and Patient Safety Considerations

— Advanced HF (NYHA IV, recurrent admissions, EF <20%, inotrope-dependent) has prognosis comparable to or worse than many cancers

— Initiate goals-of-care conversations early, not at end of life — document advance directive, healthcare proxy, code status, preferences for LVAD/transplant/hospice

— Surprise question: "Would you be surprised if this patient died in the next 12 months?" — if no, trigger palliative care consult

— ICD shocks at end of life cause significant distress; deactivation is ethical and not euthanasia

— Discuss deactivation when hospice enrollment, comfort-focused care, or DNR decided

— Requires informed consent; nurses/EP techs can deactivate with order; magnet over device temporarily disables shocks

— Pre-implant: discuss device complications (stroke, bleeding, infection, pump thrombosis), caregiver burden, deactivation circumstances

— Withdrawal of LVAD is legally and ethically permissible if patient (or surrogate) decides; equivalent to withdrawal of any life-sustaining therapy

— Cardiogenic shock patients may be obtunded — use surrogate (spouse > adult child > parent > sibling in most states); emergency exception for immediate life-saving intervention

— Jehovah's Witness with ADHF needing cardiac surgery — document refusal of blood, use blood conservation, EPO, IV iron

— Medication reconciliation at admission and discharge — high-risk medication class

— Hand-off communication (SBAR, I-PASS) — failure here is leading cause of post-discharge adverse events

— Avoid prescribing nephrotoxic NSAIDs at discharge; review OTC and herbal use

— Pillbox/blister-pack strategies for elderly or cognitively impaired

— CMS Hospital Readmissions Reduction Program penalizes hospitals for excess 30-day HF readmissions

— HF is a publicly reported core measure (LVEF assessment, ACEi/ARB at discharge, smoking cessation counseling, discharge instructions)

— Patients with syncope or recent ICD shock may have driving restrictions (varies by state — typically 6 months private, longer commercial after ICD for secondary prevention)

Goals of care and advance care planning:

ICD deactivation at end of life:

LVAD-specific ethics:

Informed consent edge cases:

Patient safety and transitions of care:

Quality reporting and value-based care:

Reportable conditions and driving:

Step 3 management: When a hospitalized HF patient enters hospice, order ICD deactivation, discontinue non-comfort meds (statins, anticoagulants if no symptomatic benefit), continue diuretics and opioids/benzodiazepines for symptom control, and arrange home hospice.

Board pearl: Concurrent palliative care + disease-directed therapy in advanced HF (PAL-HF trial) improves QoL without shortening survival — palliative care is not synonymous with hospice.

High-Yield Associations and Rapid-Fire Clinical Facts

— PARADIGM-HF: sacubitril/valsartan > enalapril in HFrEF

— DAPA-HF / EMPEROR-Reduced: SGLT2i benefit in HFrEF regardless of DM

— EMPEROR-Preserved / DELIVER: SGLT2i benefit in HFpEF

— RALES / EPHESUS / EMPHASIS-HF: MRA mortality benefit

— SHIFT: ivabradine in HFrEF with HR ≥70 on max beta-blocker

— A-HeFT: hydralazine/ISDN in Black HFrEF patients

— HF-ACTION: cardiac rehab benefit in HFrEF

— DOSE: high vs low, bolus vs infusion furosemide — equivalent

— ADVOR: acetazolamide adjunct to loop improves decongestion

— CHAMPION: CardioMEMS reduces HF hospitalizations

— STRONG-HF: rapid in-hospital GDMT initiation + close follow-up

— Verapamil/diltiazem in HFrEF (negative inotrope)

— Thiazolidinediones (pioglitazone, rosiglitazone) — fluid retention

— NSAIDs — Na retention, renal injury, blunt diuretic

— Dronedarone in NYHA IV or decompensated HF (PALLAS trial — ↑ mortality)

— Class I antiarrhythmics (flecainide, propafenone) in structural heart disease

— Metformin in cardiogenic shock or acute renal injury

— Saxagliptin/alogliptin — increased HF hospitalization (SAVOR-TIMI 53)

— Low voltage + thick walls on echo → amyloid

— Diffuse PR depression → pericarditis

— Electrical alternans → tamponade

— LBBB with QRS ≥150 ms → CRT candidate

— Apical sparing ("cherry on top") on strain echo → cardiac amyloid

— Apical ballooning with preserved base → Takotsubo (apical hypokinesis after emotional stressor)

— Ground-glass + Kerley B + pleural effusions → cardiogenic pulmonary edema

— BNP <100 → ADHF unlikely

— BNP very high in renal failure even without HF

— ARNI raises BNP, lowers NT-proBNP → use NT-proBNP for monitoring

— Troponin frequently mildly elevated in ADHF (demand); marked elevation → think ACS

Trial-pearl pairs:

Drug-disease landmines (Do Not Use):

ECG associations:

Imaging clues:

Biomarker pearls:

Board pearl: AF with RVR is both a cause and a consequence of ADHF — rate control with IV diltiazem is contraindicated in HFrEF; use IV digoxin or amiodarone acutely; beta-blocker when stable.

Key distinction: HFmrEF (EF 41–49%) behaves more like HFrEF — give all four pillars of GDMT.

Board Question Stem Patterns

— 65-year-old man with known EF 25%, presents with 1-week worsening DOE, orthopnea, 4 kg weight gain, BP 140/85, JVP 14 cm, bibasilar rales, 2+ pitting edema. BNP 1800. Best next step?

— Answer: IV furosemide at 2.5× home dose; continue beta-blocker, restart/optimize GDMT, order TTE if no recent

— 78-year-old woman with HTN, DM, AF. Acute severe dyspnea at home. BP 220/110, SpO₂ 82%, diffuse rales, EF on prior echo 55%. Most appropriate immediate therapy?

— Answer: NIV (BiPAP) + IV nitroglycerin infusion + IV furosemide; suspect HFpEF with hypertensive surge

— 58-year-old man, 3 days post-anterior STEMI s/p PCI, develops hypotension (SBP 78), cool extremities, lactate 5, new harsh holosystolic murmur. Most likely diagnosis and next step?

— Answer: Ventricular septal rupture; emergent echo, IABP/Impella, CT surgery consult

— Patient on IV furosemide infusion, urine output drops, Cr rises from 1.4 to 1.9, weight unchanged, JVP still 12, lungs still wet. Best next step?

— Answer: Increase furosemide dose and/or add thiazide for sequential nephron blockade — patient is under-diuresed, not over-diuresed

— Hospitalized HFrEF patient, euvolemic on hospital day 3, off inotropes 48 hours, BP 110/70, K 4.2, Cr 1.1. Currently on furosemide and carvedilol. What to add before discharge?

— Answer: ARNI (after 36-hr ACEi washout if applicable) + spironolactone + dapagliflozin

— 70-year-old woman with HTN, recurrent flash pulmonary edema 3 times in 6 months, abdominal bruit, asymmetric kidneys. Diagnostic test?

— Answer: Renal artery duplex → bilateral RAS (Pickering syndrome)

— HF patient discharged after 5-day admission. When is the best time for first follow-up?

— Answer: Within 7–14 days, with phone check at 48–72 hours

— Advanced HF patient enrolling in hospice has ICD. Family asks about device. Best action?

— Answer: Discuss and offer ICD deactivation to prevent end-of-life shocks

Stem 1 — Classic warm & wet HFrEF:

Stem 2 — Flash pulmonary edema with HTN:

Stem 3 — Cardiogenic shock post-MI:

Stem 4 — Cardiorenal syndrome decision:

Stem 5 — GDMT initiation timing:

Stem 6 — Recurrent flash edema:

Stem 7 — Post-discharge follow-up:

Stem 8 — End-of-life ICD:

Step 3 management: When the stem mentions "recently started on sacubitril/valsartan" plus swollen tongue/lips → angioedema; stop drug, support airway, never rechallenge

Board pearl: "Most likely to reduce 30-day readmission" → early follow-up + medication reconciliation; "most likely to reduce mortality in HFrEF" → ARNI/SGLT2i/MRA/beta-blocker (the four pillars).

One-Line Recap

ADHF management is a structured loop: assess hemodynamic profile → decongest with IV loop diuretics → identify and treat the trigger → restart and optimize the four-pillar GDMT before discharge → arrange tight 7–14-day follow-up to prevent the readmission spiral.

Acute care: warm & wet → IV loop diuretic ± nitro; cold & wet → inotrope + diuretic + consider MCS; NIV for respiratory distress; continue beta-blocker unless shock; address triggers (ischemia, arrhythmia, infection, nonadherence).

In-hospital GDMT (HFrEF): initiate all four pillars — ARNI (or ACEi/ARB), evidence-based beta-blocker, MRA, SGLT2 inhibitor — once euvolemic and hemodynamically stable; add hydralazine/ISDN in Black NYHA III–IV; IV iron if deficient.

HFpEF: SGLT2 inhibitor is class I; aggressive BP control, AF management, weight loss, OSA treatment; diuretic for symptoms.

Transitions and prevention: medication reconciliation, teach-back education, 48–72-hour phone call, 7–14-day clinic visit, cardiac rehab referral, vaccinations, advance care planning, and palliative care for advanced disease — together these define exam-quality HF care and the modern value-based metric set on which Step 3 increasingly tests you, with ICD reassessment at 3 months of optimized GDMT closing the longitudinal loop.