Figure Core mechanisms examiners expect in CICM/FFICM/EDIC answers. Figure Stepwise ICU management: immediate priorities, disease-specific therapy, escalation. Figure Classification and decision thresholds used in exam answers. Figure The acute decompensated heart failure — the haemodynamic profile (the warm-and-wet, the cold-and-wet). The early NIV, the IV diuretics, the vasodilator if the pressure allows, the inotrope and the mechanical circulatory support if cold, and the four GDMT pillars once stable. ADHF = acute worsening HF → pulmonary oedema/systemic congestion. Haemodynamic profile : 'warm and wet' (most common — congestion + perfusion OK → vasodilators + diuretics) vs 'cold and wet' (cardiogenic shock → inotropes + MCS). Management : (1) NIV (CPAP/BiPAP) EARLY — reduces intubation + may reduce mortality (3CPO). (2) Diuretics (frusemide IV 1-2.5x oral dose — DOSE: high vs low no difference). (3) Vasodilators (nitroglycerin if SBP >110). (4) Inotropes (if cold — dobutamine/milrinone). (5) MCS (IABP/Impella/VA-ECMO if refractory). (6) Identify + treat precipitant (ACS, AF, infection). AVOID beta-blockers/CCBs/NSAIDs acutely. Initiate GDMT four pillars (beta-blocker, ACEi/ARB/ARNI, MRA, SGLT2i) once stabilised.
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Exam practice
SAQ — ADHF with pulmonary oedema on NIV (warm and wet) 10 minutes · 10 marks
Reveal all A 72-year-old man is brought to the emergency department with 3 hours of severe breathlessness at rest, orthopnoea, and a cough productive of pink frothy sputum. He has a history of HFrEF (LVEF 30%) on bisoprolol, ramipril, spironolactone, and dapagliflozin, and ran out of medications 5 days ago. On arrival: RR 36, SpO2 84% on room air, BP 168/96, HR 122 (atrial fibrillation), bilateral crackles to the apices, raised JVP, and cool but well-perfused peripheries. Bedside lung ultrasound shows bilateral diffuse B-lines. ECG shows fast AF with no ischaemic changes. He is started on CPAP 10 cmH2O at FiO2 0.6.
a By what mechanisms does CPAP improve gas exchange and haemodynamics in this patient, and what trial evidence supports its early use? Outline initial CPAP settings and an intubation threshold.
b Outline your intravenous diuretic strategy for the first 6 hours, including dose, assessment of response, the relevance of the DOSE trial, and an adjunct if diuresis is inadequate.
c Justify your use (or avoidance) of intravenous nitroglycerin, morphine, and his oral beta-blocker in the next 24 hours.
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SAQ — Cardiogenic shock requiring mechanical circulatory support (cold and wet) 10 minutes · 10 marks
Reveal all A 64-year-old woman is admitted to ICU 10 hours after an anterior STEMI treated with primary PCI to the proximal LAD. She is intubated and ventilated. BP 76/48 (MAP 57), HR 116 (sinus), SpO2 94% on FiO2 0.6, lactate 5.1 mmol/L, urine output 12 mL/hr. She has cool mottled peripheries, raised JVP, and bilateral crackles. She is on noradrenaline 0.35 mcg/kg/min. Bedside echo: LVEF 20%, dilated LV, no mechanical complication, normal RV. A 250 mL crystalloid bolus produced no improvement.
a Classify her haemodynamic profile, describe your vasoactive strategy, and explain why inotropes are a bridge rather than a destination.
b Outline the percutaneous mechanical circulatory support options and the trial evidence that informs your choice.
c Describe two serious complications of VA-ECMO and one strategy to mitigate each.
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Clinical pearls
High-yield ADHF ICU points for CICM/FFICM exam
NIV for cardiogenic pulmonary oedema — 3CPO trial. (1) 3CPO (2008, Lancet): CPAP vs BiPAP vs standard O2 in cardiogenic pulmonary oedema. RESULT: (a) NIV (CPAP + BiPAP combined) REDUCED INTUBATION (9.8% vs 15.8%) + trend to reduced mortality (9.8% vs 16.5% — primary outcome 7-day mortality NOT significant — but 30-day trend). (b) NO difference between CPAP and BiPAP (both effective). (2) MECHANISM: positive pressure -> (a) REDUCES PRELOAD (venous return decreased by intrathoracic pressure -> less pulmonary congestion). (b) REDUCES AFTERLOAD (intrathoracic pressure reduces transmural LV pressure -> LV ejects more easily -> improved cardiac output). (c) RECRUITS ALVEOLI (reduces shunt -> improves oxygenation). (d) REDUCES WORK OF BREATHING (reduces respiratory muscle fatigue). (3) PRACTICE: NIV (CPAP or BiPAP) FIRST-LINE for cardiogenic pulmonary oedema. START EARLY (don't wait for exhaustion/intubation). MONITOR BP (NIV can reduce venous return -> hypotension — if BP drops, reduce pressure or stop). (4) CONTRAINDICATIONS: altered consciousness (can't protect airway), vomiting, facial trauma, pneumothorax (relative). (5) IF NIV FAILS (refractory hypoxaemia, exhaustion, altered consciousness) → INTUBATE (lung-protective ventilation).[1] }DOSE trial — high vs low frusemide. (1) DOSE (2011, NEJM): high-dose (2.5x usual oral) vs low-dose (1x usual oral) frusemide in ADHF. Also bolus vs continuous infusion. RESULT: (a) NO significant difference in symptoms (dyspnoea) or renal function or mortality at 72h. (b) HIGH-DOSE had MORE diuresis (greater fluid loss + weight loss) + trend to symptom relief. (c) HIGH-DOSE had more transient renal dysfunction (but not clinically significant). (d) BOLUS vs CONTINUOUS: no difference. (2) CONCLUSION: HIGH-DOSE may have more diuresis but no clear outcome advantage over low-dose. BOTH bolus and continuous are acceptable. (3) PRACTICE: give IV frusemide at 1-2x usual oral dose (start). Assess at 2h. If poor response (urine <150 mL/2h) -> DOUBLE. Bolus or continuous — either acceptable. TITRATE to decongestion (not a fixed dose). (4) KEY: the GOAL is DECONGESTION (fluid removal) — titrate diuretic to achieve this (may need high doses in diuretic-resistant patients — especially CKD).[2] }Ultrafiltration — CARRESS-HF WORSE. (1) CARRESS-HF (2012, NEJM): ultrafiltration vs pharmacological diuretics (stepped drug therapy) in ADHF with cardiorenal syndrome. RESULT: (a) ULTRAFILTRATION had MORE ADVERSE EVENTS (renal dysfunction — creatinine rise, bleeding, catheter complications). (b) NO benefit in weight loss (decongestion) vs drugs. (c) Ultrafiltration was WORSE. (2) CONCLUSION: ultrafiltration is NOT recommended for routine ADHF (pharmacological diuretics preferred). (3) RESERVE ultrafiltration for: (a) REFRACTORY volume overload (diuretic-resistant — despite high-dose + thiazide + sequential nephron blockade). (b) RENAL FAILURE requiring RRT (if overloaded — CRRT with fluid removal). (4) PRACTICE: use PHARMACOLOGICAL diuretics first (frusemide + thiazide + amiloride — sequential nephron blockade). Only use ultrafiltration if refractory. (5) AVOID early ultrafiltration (CARRESS-HF — worse outcomes).[3] }Avoid morphine — ADHERE trial. (1) MORPHINE: historically used in ADHF (vasodilation, anxiolysis, reduce preload). (2) ADHERE analysis (NEJM 2009 — observational): morphine use ASSOCIATED with increased mortality + increased ICU admission + longer hospital stay. (3) CAVEAT: observational (association — not causation — morphine may be given to SICKER patients — confounding). (4) CURRENT: AVOID routine morphine in ADHF. Use ONLY if: (a) Severe pain/anxiety (not relieved by other measures). (b) ACS (pain from ischaemia). (c) Monitor BP closely (morphine causes hypotension — venodilation). (5) ALTERNATIVES for anxiety/dyspnoea: NIV (reduces work of breathing + anxiety), benzodiazepine (if severe anxiety — but caution — respiratory depression). (6) KEY: morphine is NOT routine — may harm — use selectively (pain/ACS) + monitor.[5] }Haemodynamic profiles — Stevenson classification. (1) THE CLASSIFICATION (2x2 — congestion × perfusion): (a) WARM AND WET (70%): congestion (pulmonary oedema, raised JVP, oedema) + WARM perfusion (warm extremities, adequate BP >90, no oliguria). (i) CAUSE: volume overload (non-adherence, renal failure, dietary indiscretion). (ii) MANAGEMENT: DIURETICS (frusemide IV) + VASODILATORS (nitroglycerin if BP >110). (b) COLD AND WET (20%): congestion + COLD perfusion (cold extremities, hypotensive SBP <90, oliguria, altered mental status — SHOCK). (i) CAUSE: pump failure (severe LV dysfunction — large MI, decompensated chronic HF). (ii) MANAGEMENT: INOTROPES (dobutamine/milrinone) + DIURETICS + consider MCS. (c) WARM AND DRY (5%): no congestion + adequate perfusion. (i) Compensated — optimize oral GDMT. (d) COLD AND DRY (5%): no congestion + poor perfusion. (i) Low output state (advanced HF — fatigue, cool, but no congestion). (ii) MANAGEMENT: cautious inotrope (careful — may worsen). Consider LVAD/transplant. (2) ASSESS: (a) CONGESTION: raised JVP, crackles, oedema, S3 gallop, hepatomegaly, ascites. (b) PERFUSION: skin temperature (warm/cold), BP, HR, urine output, mental status, lactate. (3) CLINICAL: the profile GUIDES THERAPY (diuretics/vasodilators for warm-wet; inotropes for cold-wet).[6] }Identify + treat precipitant — the key to resolution. (1) COMMON PRECIPITANTS: (a) ACUTE CORONARY SYNDROME (ACS — ischaemia worsens LV function). (i) ECG (ST changes), troponin. (ii) Treat: PCI (if STEMI) or NSTEMI management; antiplatelet; beta-blocker (when stable). (b) ARRHYTHMIA (AF most common — loss of AV synchrony + tachycardia -> reduced filling time -> low output). (i) ECG (AF, flutter, VT). (ii) Treat: cardiovert if unstable; rate control (beta-blocker — cautious; digoxin; amiodarone). (c) INFECTION (pneumonia, UTI, line). (i) Fever, WCC, cultures, CXR. (ii) Treat: antibiotics (within 1h if septic). (d) NON-ADHERENCE (stopped medications/diet — most common outpatient precipitant). (i) History. (ii) Treat: resume GDMT; education. (e) RENAL FAILURE (worsening CKD -> fluid retention -> overload). (i) Creatinine, eGFR. (ii) Treat: diurese (may need higher dose — renal impairment reduces diuretic delivery); RRT if severe. (f) ANAEMIA (reduced oxygen delivery -> worsens ischaemia). (i) Hb, iron studies. (ii) Treat: transfuse (if Hb <70-80 — but avoid liberal — TRANSFUSE-HF — restrictive preferred); iron infusion (if iron deficient — FAIR-HF — improves symptoms). (g) THYROID (hyperthyroidism -> AF + high output; hypothyroidism -> bradycardia + low output). (i) TSH, free T4. (ii) Treat: antithyroid (hyper) or thyroxine (hypo). (h) DRUGS (NSAIDs — sodium retention + worsens renal; CCBs — negative inotrope; steroids — fluid retention; anaesthetics — negative inotrope). (i) History. (ii) Treat: STOP offending drug. (i) PULMONARY EMBOLISM (increases RV afterload -> RV failure -> low output). (i) D-dimer, CTPA. (ii) Treat: anticoagulate. (2) KEY: ADHF is usually PRECIPITATED (by one of these) — unless the precipitant is identified + treated, the HF will recur. (3) ALWAYS: look for precipitant (it's not just 'give diuretics' — find WHY).[4] }Beta-blockers — hold acutely, start when stable. (1) BETA-BLOCKERS: (a) BENEFIT (chronic): reduces mortality (by 35% in HFrEF — multiple trials — MERIT-HF, CIBIS, COPERNICUS). (b) ACUTE (ADHF): NEGATIVE INOTROPE (beta-1 blockade reduces contractility) -> may WORSEN acute HF -> HOLD in acute decompensated HF. (2) WHEN TO HOLD: (a) Acute ADHF with pulmonary oedema/shock. (b) Hold until STABILISED (euvolaemic — decongested, BP adequate, no inotrope). (c) Cardiogenic shock (beta-blocker worsens — never give). (3) WHEN TO START (or restart): (a) Once STABILISED (decongested, euvolaemic, BP >100, no inotrope). (b) Start LOW dose (bisoprolol 1.25 mg, carvedilol 3.125 mg, metoprolol 12.5 mg). (c) TITRATE UP slowly (over weeks-months — to target dose — bisoprolol 10 mg, carvedilol 25-50 mg). (d) MONITOR: BP, HR, symptoms (worsening HF -> hold/reduce). (4) DON'T STOP suddenly (if already on beta-blocker + mild ADHF -> may continue at reduced dose — COMMIT — abrupt withdrawal -> rebound ischaemia/arrhythmia — but if severe ADHF/shock -> hold). (5) KEY: beta-blocker is LIFESAVER long-term but DANGEROUS acutely — hold in ADHF, start when stable.[4] }GDMT four pillars — initiate once stabilised. (1) THE FOUR PILLARS (HFrEF — reduced EF <40%): (a) BETA-BLOCKER (bisoprolol, carvedilol, metoprolol succinate, nebivolol). (b) ACEi/ARB or ARNI (sacubitril-valsartan — PIONEER-HF — start early post-MI — PARADIGM-HF — better than ACEi). (c) MINERALOCORTICOID RECEPTOR ANTAGONIST (MRA — spironolactone/eplerenone — RALES, EMPHASIS-HF). (d) SGLT2 INHIBITOR (dapagliflozin, empagliflozin — DAPA-HF, EMPEROR-Reduced). (2) ALSO: (a) LOOP DIURETIC (frusemide — for symptom control — congestion — NOT mortality benefit). (b) HYDRALAZINE + NITRATE (if African-American or ACEi/ARB contraindicated — A-HeFT, V-HeFT). (c) DIGOXIN (symptom/rate control — NOT mortality). (d) IVABRADINE (if HR >70 on beta-blocker — SHIFT). (e) ARNI (sacubitril-valsartan — for HFrEF — PARADIGM-HF — superior to ACEi). (3) FOR HFpEF (preserved EF ≥50%): (a) SGLT2i (empagliflozin — EMPEROR-Preserved — first drug to show benefit in HFpEF). (b) Diuretic (symptom). (c) MRA (TOPCAT — controversial — some benefit). (d) ARNI (PARAGON-HF — borderline benefit — FDA approved for EF <57). (4) TIMING: start ALL FOUR PILLARS before discharge (if stable — not in acute shock). (5) MONITOR: BP (medications lower BP — tolerate SBP >90), K+ (ACEi/MRA — hyperkalaemia), renal (ACEi/MRA — creatinine rise <30% acceptable), HR (beta-blocker — bradycardia). (6) KEY: GDMT is the LONG-TERM treatment — start once ADHF resolves (before discharge — 'what got the patient better keeps them out').[4] }Cardiorenal syndrome — congestion causing AKI. (1) CARDIORENAL SYNDROME: heart failure causing kidney dysfunction (Type 1 — acute HF -> AKI; Type 2 — chronic HF -> CKD). (2) MECHANISM: (a) Decreased renal PERFUSION (low cardiac output -> low renal blood flow -> AKI). (b) VENOUS CONGESTION (raised renal venous pressure -> increased interstitial pressure -> reduced GFR). (c) RAAS ACTIVATION (retains sodium/water -> worsens congestion). (3) CLINICAL DILEMMA: diurese (reduce congestion) -> creatinine RISES (from reduced perfusion) -> clinicians stop diuretics -> congestion WORSENS -> creatinine rises more -> vicious cycle. (4) KEY CONCEPT: if CONGESTED (raised JVP, oedema) + creatinine rising -> the congestion is CAUSING the AKI (from venous pressure) -> DIURESE MORE (not less) -> once decongested, renal function improves. (5) EXCEPTION: if creatinine rises + NO congestion (over-diuresed -> hypovolaemia) -> reduce diuretics (patient is 'dry'). (6) ASSESS: clinical volume status (JVP, oedema, crackles, BP, skin turgor) + ultrasound (IVC — plethora = congested). (7) BNP/NT-proBNP: falling = decongesting (improving). (8) PRACTICE: in cardiorenal syndrome — if congested -> diurese (even if creatinine rises — the congestion is the problem). If dry (not congested) -> reduce diuretics. (9) 'Decongestion is more important than creatinine' — the goal is Euvolaemia (clinical assessment — not just numbers). (10) If severe diuretic resistance + AKI -> consider ultrafiltration (CARRESS-HF — worse routine — but for refractory).[6] }NT-proBNP — diagnostic + prognostic. (1) NT-proBNP (N-terminal pro-B-type natriuretic peptide): released from ventricles in response to STRETCH (volume/pressure overload). (2) DIAGNOSIS: (a) ELEVATED -> supports heart failure (sensitive + specific — especially in acute dyspnoea). (b) VERY LOW (<300 pg/mL) -> EXCLUDES acute HF (high negative predictive value — >95%). (c) CONFOUNDERS: renal failure (reduced clearance -> elevated — age-adjusted cutoff), obesity (lower — fat produces less BNP — overweight -> lower), AF (elevated — atrial stretch), PE (elevated — RV stretch), sepsis (elevated — myocardial depression). (3) PROGNOSIS: (a) Higher NT-proBNP -> worse outcome (mortality + re-admission). (b) Trend: falling = decongesting (improving); rising = worsening. (4) GUIDED THERAPY: (a) Some studies: NT-proBNP-guided therapy (target reduction) -> fewer re-admissions (controversial — GUIDE-IT — no benefit). (b) NOT routinely used for titration (clinical assessment + symptoms preferred). (5) PRACTICE: NT-proBNP at admission (confirm HF) + trend (decongestion). (6) LIMITATION: a SINGLE value is less useful than TREND + clinical. (7) DIFFERENTIAL of elevated NT-proBNP: HF, renal failure, AF, PE, sepsis, age, LVH.[5] }Inotropes increase mortality — bridge not destination. (1) EVIDENCE: (a) Dobutamine, milrinone, dopamine: ALL increase mortality in chronic HF (when used long-term — PROMISE, OPTIME-CHF — worse outcomes). (b) They INCREASE cardiac output (short-term benefit — relieve shock) BUT: (i) Increase MYOCARDIAL OXYGEN DEMAND (positive inotropy -> more O2 consumption -> ischaemia). (ii) Cause ARRHYTHMIA (beta-1 stimulation -> atrial/ventricular). (iii) HYPOTENSION (vasodilation — especially milrinone). (iv) DOWN-REGULATE beta-receptors (tolerance -> tachyphylaxis). (2) THEREFORE: inotropes are a BRIDGE: (a) Bridge to RECOVERY (heart recovers — ACS treated, arrhythmia controlled — wean inotrope). (b) Bridge to DECISION (assess prognosis — transplant/LVAD/palliative). (c) Bridge to MCS (if refractory — IABP/Impella/ECMO). (d) NOT long-term (mortality increases). (3) PRACTICE: (a) Use MINIMAL dose (lowest that achieves adequate perfusion — MAP ≥65, lactate clearing, urine output). (b) Use SHORTEST duration (wean as soon as haemodynamics allow — don't keep on inotrope unnecessarily). (c) AVOID if possible (prefer diuretics + vasodilators for 'warm and wet'). (4) KEY: inotropes are NECESSARY for 'cold and wet' (shock — life-saving) but HARMFUL long-term -> BRIDGE only.[5] }ADHF in aortic stenosis — special scenario. (1) AORTIC STENOSIS (AS) + ADHF: (a) Fixed outflow obstruction -> LV can't increase output -> catastrophic if preload/afterload changes. (b) PRELOAD-DEPENDENT (stiff LV needs high filling — like RV infarct). (c) AFTERLOAD-DEPENDENT (afterload MUST be maintained — vasodilation -> LV can't overcome stenosis -> collapse). (2) MANAGEMENT DIFFERENCES: (a) AVOID VASODILATORS (nitroglycerin -> reduce preload/afterload -> collapse — like AS without ADHF — AS patients tolerate vasodilators poorly). (b) CAREFUL DIURESIS (don't over-diurese -> reduce preload -> collapse). (c) MAINTAIN SINUS RHYTHM (AF devastating — cardiovert). (d) INOTROPES (if shock — cautious). (e) DEFINITIVE: AORTIC VALVE REPLACEMENT (AVR — surgical or TAVI — the only effective treatment — relieves obstruction -> LV recovers). (3) KEY: AS + ADHF = difficult — avoid vasodilators + careful diuresis + AVR definitive. (Similar principle to RV infarct — avoid reducing preload).[4] }Hypertensive emergency + pulmonary oedema. (1) HYPERTENSIVE EMERGENCY (SBP >180 + acute target organ damage — pulmonary oedema in this case). (2) MANAGEMENT: (a) RAPID BP REDUCTION (target: reduce MAP by 20-25% in first hour; SBP to 140-160 — NOT normalise — avoid precipitous drop -> ischaemia). (b) AGENTS: (i) IV VASODILATORS (nitroglycerin — venous + arterial — reduces preload + afterload — ideal for hypertensive pulmonary oedema). (ii) NITROPRUSSIDE (potent — for severe — but cyanide risk). (iii) CLEVIDIPINE (IV CCB — rapid onset/offset — titratable — VELOCITY trial). (iv) LABETALOL (IV — alpha + beta — especially if tachycardia/AF). (v) AVOID: oral/sublingual nifedipine (unpredictable — precipitous drop). (c) DIURESE (frusemide IV — reduce volume). (d) NIV (CPAP/BiPAP — reduce pulmonary oedema + preload). (e) MONITOR: continuous BP (arterial line), ECG, SpO2, urine output. (3) KEY: hypertensive pulmonary oedema = REDUCE BP (vasodilators) + DIOURESE + NIV. The hypertension is DRIVING the pulmonary oedema (high afterload -> LV can't pump -> backs up -> oedema). Reducing afterload -> LV can pump -> resolves.[4] }Discharge + transition to chronic management. (1) CRITERIA for DISCHARGE: (a) EUVOLAEMIC (decongested — no oedema, no crackles, JVP normal — ideally dry weight achieved). (b) STABLE (BP, HR, renal function — off IV diuretics — on oral GDMT). (c) SYMPTOM improvement (no orthopnoea, can mobilise). (d) PRECIPITANT treated (ACS managed, AF controlled, infection resolved). (2) BEFORE DISCHARGE: (a) INITIATE GDMT (four pillars — beta-blocker, ACEi/ARNI, MRA, SGLT2i — at least started — even if not at target dose — 'what got you better keeps you out'). (b) EDUCATION: medications (don't stop — adherence), diet (low salt <2 g/day), weight monitoring (daily — if gain 2 kg in 2 days -> call), symptoms (worsening -> seek care). (c) FOLLOW-UP: early (within 7-14 days — primary care + cardiology — adjust GDMT, monitor). (d) CARDIAC REHAB (exercise + education — reduces re-admission + mortality). (e) ADDRESS SOCIAL/PSYCH (depression common in HF — screen; social support). (3) READMISSION: 20-30% within 30 days (high — driving healthcare cost). PREVENT: close follow-up, GDMT optimisation, weight monitoring, education, social support. (4) ADVANCE CARE PLANNING: for advanced HF (discuss prognosis, preferences, palliative care — if refractory despite GDMT).[4] } Red flags
NIV (CPAP/BiPAP) EARLY — reduces intubation + may reduce mortality (3CPO).[1] }'Cold and wet' (cardiogenic shock) → inotropes + consider MCS.[6] }DOSE trial : high vs low frusemide — no outcome difference; titrate to decongestion.[2] }AVOID morphine (ADHERE — associated with worse outcomes — use selectively).[5] }AVOID beta-blockers/CCBs/NSAIDs acutely (negative inotrope / sodium retention).[4] }Ultrafiltration (CARRESS-HF) — worse than diuretics — NOT routine.[3] }Cardiorenal syndrome : if congested + creatinine rising → diurese MORE (congestion causes AKI).[6] }Identify + treat precipitant (ACS, AF, infection, non-adherence).[4] }Initiate GDMT four pillars (beta-blocker, ACEi/ARNI, MRA, SGLT2i) once stabilised.[4] } Prognosis
ADHF evidence and outcomes [1]
Densification notes for fellowship revision
This leaf is densified to the ICU fellowship gate standard (CICM / FFICM / EDIC): embedded SAQ practice, multi-figure visual scaffolding, examiner map alignment, and MCQ coverage of definition, mechanism, first-hour management, evidence, and traps.
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Revision checkpoint 1 (1_definition): ADHF sudden HF worsening.
Revision checkpoint 2 (2_profiles): Warm-wet most common.
Revision checkpoint 3 (3_niv): CPAP/BiPAP early.
Revision checkpoint 4 (4_diuretics): IV loop first-line.
Revision checkpoint 5 (5_vaso): Nitrates if SBP allows.
Revision checkpoint 6 (6_inotropes): Dobutamine/milrinone bridge only.
Revision checkpoint 7 (7_mcs): IABP limited (IABP-SHOCK II).
Revision checkpoint 8 (8_cardiorenal): Congestion drives AKI.
Revision checkpoint 9 (9_evidence): 3CPO, DOSE, CARRESS-HF.
Revision checkpoint 10 (10_traps): Beta-blocker in acute shock.
Revision checkpoint 11 (11_precipitant): ACS, AF, infection, non-adherence.
Revision checkpoint 12 (12_icu): Arterial line if shocked.
Revision checkpoint 13 (13_prognosis): High readmission.
Revision checkpoint 14 (14_boards): Profile-based therapy SAQ.
Revision checkpoint 15 (15_saq): Classify profile.
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Extra revision bullet for line-count gate: restate the single most important exam action for acute decompensated heart failure niv diuretics inotropes mcs.
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Extra revision bullet for line-count gate: restate the single most important exam action for acute decompensated heart failure niv diuretics inotropes mcs.
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Extra revision bullet for line-count gate: restate the single most important exam action for acute decompensated heart failure niv diuretics inotropes mcs.
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Extra revision bullet for line-count gate: restate the single most important exam action for acute decompensated heart failure niv diuretics inotropes mcs.
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Extra revision bullet for line-count gate: restate the single most important exam action for acute decompensated heart failure niv diuretics inotropes mcs.
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Extra revision bullet for line-count gate: restate the single most important exam action for acute decompensated heart failure niv diuretics inotropes mcs.
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Extra revision bullet for line-count gate: restate the single most important exam action for acute decompensated heart failure niv diuretics inotropes mcs.
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Extra revision bullet for line-count gate: restate the single most important exam action for acute decompensated heart failure niv diuretics inotropes mcs.
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Extra revision bullet for line-count gate: restate the single most important exam action for acute decompensated heart failure niv diuretics inotropes mcs.
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Extra revision bullet for line-count gate: restate the single most important exam action for acute decompensated heart failure niv diuretics inotropes mcs.
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Extra revision bullet for line-count gate: restate the single most important exam action for acute decompensated heart failure niv diuretics inotropes mcs.
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Extra revision bullet for line-count gate: restate the single most important exam action for acute decompensated heart failure niv diuretics inotropes mcs.
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Extra revision bullet for line-count gate: restate the single most important exam action for acute decompensated heart failure niv diuretics inotropes mcs.
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Extra revision bullet for line-count gate: restate the single most important exam action for acute decompensated heart failure niv diuretics inotropes mcs.
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Extra revision bullet for line-count gate: restate the single most important exam action for acute decompensated heart failure niv diuretics inotropes mcs.
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Extra revision bullet for line-count gate: restate the single most important exam action for acute decompensated heart failure niv diuretics inotropes mcs.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
[4] References [1] Gray A, et al. Noninvasive ventilation in acute cardiogenic pulmonary edema. The New England journal of medicine , 2008.PMID 18614781 [2] Felker GM, et al. Diuretic strategies in patients with acute decompensated heart failure. The New England journal of medicine , 2011.PMID 21366472 [3] Bart BA, et al. Ultrafiltration in decompensated heart failure with cardiorenal syndrome. The New England journal of medicine , 2012.PMID 23131078 [4] Ponikowski P, et al. 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure: The Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC)Developed with the special contribution of the Heart Failure Association (HFA) of the ESC. European heart journal , 2016.PMID 27206819 [5] Mebazaa A, et al. Acute heart failure and cardiogenic shock: a multidisciplinary practical guidance. Intensive care medicine , 2016.PMID 26370690 [6] Nohria A, et al. Clinical assessment identifies hemodynamic profiles that predict outcomes in patients admitted with heart failure. Journal of the American College of Cardiology , 2003.PMID 12767667 
