National JCS Heart Failure Protocols – (2025)
National JCS Heart Failure Protocols – (2025)
Acute Heart Failure – Emergency and Early In-Hospital Management
“Developed by the Jordan Cardiac Society (JCS) Heart Failure National Task Force”
(Adapted from ESC 2021–2024 / 2023 updates, AHA–ACC–HFSA 2022–2025, NICE 2025, AHA–ACLS 2025)
1. Rapid Recognition and Initial Assessment
* Initial assessment must be clinical and concurrent with vital signs stabilization (airway, breathing, circulation).
* Any patient presenting with acute dyspnea, orthopnea, or pulmonary rales should be considered as possible AHF or acute pulmonary edema until proven otherwise.
Key bedside findings:
* Agitation and shortness of breath (SOB)
* Diaphoresis (sweating and distress)
* Tachypnea and tachycardia
* Blood pressure (BP): may be elevated in hypertensive AHF, normal in most cases, or low in cardiogenic shock
Immediate actions:
* Ensure ABCs and start continuous SpO₂ and BP monitoring.
* Perform ECG, chest X-ray, and bedside echocardiography (PoCUS/focused echo).
* Order BNP or NT-proBNP, troponin, creatinine/electrolytes, and CBC.
Interpretation:
* NT-proBNP < 300 pg/mL → AHF unlikely.
* Elevated troponin suggests myocardial strain or ischemia but is not diagnostic alone.
* Always integrate lab results with clinical and imaging findings.
Diagnostic support tool :
PRIDE Score: combines NT-proBNP (2 points if above age-adjusted cutoff) with clinical and radiographic findings (1 point each for history of HF/CAD, orthopnea, rales, edema, and chest congestion).
* High probability: ≥ 6 points → supports acute HF.
* Low probability: < 4 points → HF unlikely.
2. Early Clinical Presentation for Initial Management in the Emergency Department
* The clinical presentation reflects the initial hemodynamic profile — congested (wet), hypoperfused (cold), or both.
* Identifying the profile early directs therapy:
– Wet/warm: diuretics ± vasodilators.
– Cold/wet: inotropes or vasopressors; avoid vasodilators.
– Dry/warm: compensated; review chronic therapy.
* In most cases, congestion predominates, similar to acute pulmonary edema, where SBP dictates treatment sequence:
– High BP : vasodilator first, diuretic after oxygenation improves.
– Normal BP (100–140 mmHg): diuretic first, add vasodilator if BP stable and congestion persists.
– Low BP (< 100 mmHg): avoid vasodilators; initiate inotropes/pressors.
* Common presentations:
– Acute on chronic HF (ADHF) – 60–70 % of admissions.
– Flash pulmonary edema – rapid onset, high BP, severe dyspnea.
– Isolated RV failure – JVP distension, ascites, hepatomegaly.
– Cardiogenic shock – “cold & wet”: hypotension, congestion, end-organ hypoperfusion.
3. Hemodynamic Management in AHF
Refers to adjusting therapy according to blood pressure and congestion, using diuretics, vasodilators, inotropes, or vasopressors as indicated.
The management of congestion follows the same principles as acute pulmonary edema, where SBP determines therapy priority.
A. Timing, Monitoring, and Sequential Use of Diuretics and Vasodilators
* Loop diuretics are the first-line therapy for congested, normotensive AHF.
* Onset: 5–15 min; peak effect: ≈ 2 h.
* Monitor and guide therapy from the start and throughout the first 2 hours:
– Begin immediate clinical and hemodynamic observation once IV loop diuretics are given.
Track symptoms, respiratory effort, and overall clinical progression continuously, along with vital signs (BP, HR, SpO₂, urine output) and physical findings (dyspnea, crackles, jugular venous pressure, peripheral edema, mental status).
– Adjust treatment dynamically according to the patient’s condition:
* If marked pulmonary congestion or severe respiratory distress persists and SBP ≥ 110 mmHg, initiate a vasodilator concurrently with the loop diuretic for faster relief.
* If IV nitroglycerin is not yet available, a sublingual nitrate (Isojey SL 5 mg) may be given as an emergency bridge, provided SBP ≥ 110 mmHg and no evidence of RV infarction or hypotension.
* Once possible, switch to IV nitroglycerin 5–10 µg/min, titrating every 3–5 minutes while checking BP frequently.
– Continue close reassessment during the first two hours, noting changes in dyspnea, oxygenation, urine output, and blood pressure to decide whether to intensify diuretics, continue combination therapy, or withhold vasodilators if SBP falls below 100 mmHg or perfusion worsens.
* Avoid vasodilators early or if SBP < 100 mmHg.
B. Vasodilator Therapy (SBP ≥ 90 mmHg)
* Use only if congestion present and BP allows safe reduction (preferably > 100 mmHg).
* Add after or with diuretics if symptoms persist and BP stable.
* IV nitroglycerin: start 5–10 µg/min → titrate every 3–5 min up to 200 µg/min.
* • In hypertensive AHF or acute pulmonary edema, initiate intravenous nitroglycerin at 5–10 µg/min and titrate rapidly every 3–5 minutes by 5–20 µg/min increments (or by doubling the rate if tolerated) until clinical improvement and a 20–25 % reduction in systolic BP are achieved, while maintaining SBP > 100 mmHg.
* Continuous monitoring required.
* Avoid: SBP < 100 mmHg, cardiogenic shock, or RV infarction.
C. Hypoperfusion or “Cold” States
* Norepinephrine: start at 0.05 µg/kg/min, titrate to maintain MAP ≥ 65 mmHg (≈ SBP ≥ 90–100 mmHg).
* If signs of hypoperfusion persist despite achieving adequate MAP — such as cold extremities, oliguria, altered mentation, narrow pulse pressure, or elevated lactate — add one inotrope (dobutamine or milrinone) to improve contractility and systemic perfusion.
• Dobutamine:
– Start: 2–5 µg/kg/min.
– Titrate: gradually up to 10 µg/kg/min (may reach 20 µg/kg/min in ICU with invasive monitoring).
– Effective range for most patients: 2–10 µg/kg/min.
Titration goals and monitoring:
* Increase cardiac output and systemic perfusion (target MAP ≥ 65 mmHg).
* Monitor for tachycardia or arrhythmia — reduce the dose if HR > 120–130 bpm or ectopy develops.
* Continuous ECG and BP monitoring are recommended.
* Dopamine only if hypotension with bradycardia, under invasive monitoring.
4. Supportive and Preventive Measures
* Oxygen: only if SpO₂ < 90 % (target > 92 %; in known COPD, target 88–92 %).
* Non-Invasive Ventilation (NIV) (CPAP/BiPAP): for persistent hypoxemia or RR > 25/min; decreases preload and afterload.
5. Venous Thromboembolism (VTE) Prophylaxis
* Hospitalized AHF patients are at high risk due to immobility and venous congestion.
* Balance VTE risk (IMPROVE-VTE) vs bleeding risk (IMPROVE-Bleed).
IMPROVE-VTE (Thrombosis Risk):
* HF/respiratory failure, cancer, immobility > 7 days (3 pts), previous VTE (3 pts), age ≥ 60, elevated D-dimer.
* ≥ 4 = high risk → LMWH 40 mg SC daily or UFH 5000 U SC q8–12 h.
IMPROVE-Bleed (Bleeding Risk):
* Prior major bleed (4), platelets < 50 000 (4), CrCl < 30 (2.5), liver failure (2.5), active cancer (2), age ≥ 85 (3.5), central line/ICU/rheumatic disease (1–2).
* ≥ 7 = high risk → avoid or shorten pharmacologic prophylaxis.
Combined Approach:
* VTE ≥ 4 & Bleed < 7 → start pharmacologic prophylaxis.
* VTE < 4 or Bleed ≥ 7 → mechanical methods only.
* Reassess both scores every 48–72 h or when clinical status changes.
6. Pre-Discharge and Transition of Care
* Confirm complete decongestion, stable weight, optimized oral diuretics.
* SBP > 100 mmHg, SaO₂ > 92 %.
* Review renal/electrolyte balance.
* Arrange follow-up within 7–14 days with GDMT titration plan and rehab referral.
7. Discharge Readiness and Risk Tools
* Safe discharge: improved symptoms, SBP > 100, HR < 90, RR < 20, stable biomarkers, no ischemia/arrhythmia, adequate social support, and early follow-up.
HEARTRISK6 – Tool for ED Disposition
(final ED decision – admit ,or discharge) from ER:
* Determines need for admission vs safe discharge.
* Components:
– H: valvular heart disease
– E: elevated HR after stabilization
– A: early need for NIV (CPAP/BiPAP)
– R: raised creatinine (↑Cr)
– T: troponin elevation
– “6”: abnormal post-treatment vitals (tachycardia, hypotension, desaturation)
* Score ≥ 3 → admit; < 3 → consider discharge if stable and follow-up secured.
8. Advanced and Rescue Therapies
* Cardiogenic shock unresponsive to drugs → escalate to MCS (IABP, Impella, or VA-ECMO).
* Apply Door-to-ECMO concept – each minute saved improves neurologic survival in ECPR.
* Proposal: establish a national CPR-ECMO Center (JCS + MoH) for standardized simulation and training.
National JCS Heart Failure Protocols – Framework (2025)
Developed by the Jordan Cardiac Society (JCS) Heart Failure National Task Force
(Adapted from ESC 2021–2024 / 2023 updates, AHA/ACC/HFSA 2022–2025, NICE 2025, AHA/ACLS 2025)
A) Acute Heart Failure – Emergency and Early In-Hospital Management
1. Rapid Recognition and Initial Assessment
• Treat any patient with sudden severe dyspnea, crackles, orthopnea, or pink frothy sputum as acute HF or pulmonary edema until proven otherwise.
• Key bedside observations: upright sitting posture, agitation, tachypnea, tachycardia, elevated BP, history of HF, CAD, or hypertension.
• Early differential includes bronchospasm (asthma/COPD), PE, pneumonia, tamponade, and acute valvular failure.
• Immediate investigations:
• ECG, chest X-ray, echocardiography (PoCUS or full echo), BNP / NT-proBNP, troponin, creatinine/electrolytes, CBC.
• BNP rule-out thresholds: NT-proBNP < 300 pg/mL (acute) → HF unlikely.
• Use PRIDE score or similar when diagnosis uncertain.
2. Clinical Phenotyping (ED Profiles)
1. Acute on top of chronic HF
(Acute Decompensated Heart Failure)
= acute worsening of chronic heart failure, accounting for about 60–70% of HF hospital admissions.
Common triggers include volume or sodium overload, uncontrolled hypertension, myocardial ischemia, arrhythmia, infection, renal dysfunction or acute kidney injury, thyroid disorders, anemia, pulmonary embolism, and poor medication adherence.
2. Flash Pulmonary Edema – rapid hypoxemia, often hypertensive.
3. Isolated Right-Ventricular Failure – jugular distension, ascites, hepatic congestion, often without lung crackles.
4. Cardiogenic Shock – The most severe form of acute heart failure — marked by pulmonary congestion (wet) and poor perfusion (cold) due to low cardiac output hypotension + hypoperfusion (cold/clammy, oliguria, confusion).
3. Hemodynamic Management
A. Congested or “Wet” States
• IV loop diuretics: first-line; if on oral, give 1–2× home dose IV.
• Check response at 2 h: urine > 100–150 mL/h or urine Na⁺ > 50–70 mmol/L.
• If poor response → double dose or add thiazide/acetazolamide.
• For refractory cases → consider ultrafiltration.
B. Vasodilators (SBP ≥ 90 mmHg)
• IV nitroglycerin: start 5–10 µg/min → titrate q3–5 min (up to 200 µg/min).
• High-dose strategy beneficial in hypertensive flash pulmonary edema : Titrate every 3–5 minutes by 10–20 µg/min increments until symptoms improve or SBP decreases by about 25 %, keeping SBP > 100 mmHg.
• Avoid vasodilators in hypotension or suspected RV infarction.
C. Hypoperfusion or “Cold” States
• Norepinephrine 0.05 µg/kg/min → titrate to MAP ≥ 65 ( mmHg(MAP ≥ 65 mmHg roughly corresponds to SBP ≥ 90–100 mmHg, which serves as a quick clinical reference for adequate organ perfusion in emergency settings.)
• If low output persists (cold skin, low urine, confusion) despite adequate MAP, combine norepinephrine with one inotrope (dobutamine or milrinone) — but never use two inotropes together routinely.: give one inotrope — dobutamine (2–10 µg/kg/min).
Dopamine is no longer recommended as a routine inotrope for cardiogenic shock or low-output heart failure.
It should be used only in patients with hypotension accompanied by bradycardia, and always under close hemodynamic monitoring (AHA / ESC / SCAI 2023–2025).
• Continuous arterial and central venous monitoring recommended if available.
• Do not combine two inotropes except in refractory ICU cases.
4. Supportive & Preventive Measures
• Oxygen: only if SpO₂ < 90 % (target > 92 %).
• Non-invasive ventilation (CPAP/BiPAP): for persistent hypoxemia or RR > 25 /min; improves preload & afterload.
* VTE prophylaxis: guided by IMPROVE-VTE (≥ 4 = high risk) and IMPROVE-Bleed (≥ 7 = high bleeding risk).
• IMPROVE-VTE (for clot risk) – each 1 pt unless noted:
• Heart or respiratory failure
• Cancer
• Immobility > 7 days (3 pts)
• Previous VTE (3 pts)
• Age ≥ 60 y
• Elevated D-dimer
→ ≥ 4 pts = high VTE risk → give prophylaxis.
• IMPROVE-Bleed (for bleeding risk):
• Prior major bleed (4 pts)
• Platelets < 50 000 (4)
• Severe renal failure (CrCl < 30 mL/min) (2.5)
• Liver failure (2.5)
• Active cancer (2)
• Age ≥ 85 (3.5)
• Central line, ICU stay, or rheumatic disease (1–2)
→ ≥ 7 pts = high bleeding risk → avoid or shorten prophylaxis.
If VTE ≥ 4 and Bleed < 7: use LMWH 40 mg SC daily or UFH 5000 U SC every 8–12 h until mobility is restored.
• Re-initiate GDMT early once hemodynamically stable — SGLT2 inhibitors and MRAs can start during hospitalization due to mild BP effect.
• Identify and treat triggers early (CHAMPIT mnemonic: Coronary syndrome, Hypertension, Arrhythmia, Mechanical cause, PE, Infection, Tamponade).
5. Pre-Discharge & Transition of Care
• Confirm complete decongestion, stable weight, and optimized oral diuretics.
• Review renal function / electrolytes, ensure SBP > 100 mmHg, SaO₂ > 92 %.
• Arrange early follow-up within 7–14 days, with clear GDMT titration plan and rehabilitation referral.
6. Discharge Readiness & Risk Tools
• Safe discharge criteria: improved symptoms, SBP > 100, HR < 90, RR < 20, stable biomarkers, no ischemia/arrhythmia, adequate social support, and early follow-up arranged.
• HEARTRISK6 score: used after initial stabilization in the emergency department (ED) to decide if a patient with acute heart failure (AHF) can be safely discharged or should be admitted.
Includes valvular disease, high HR, early NIV (Non-Invasive Ventilation), elevated creatinine (↑Cr), elevated troponin, and abnormal post-treatment vitals.
→ Score ≥ 3 = moderate/high risk → admit; Score < 3 = low risk → consider discharge if stable.
7. Advanced & Rescue Therapies
• Cardiogenic shock unresponsive to pharmacotherapy:
• Escalate to mechanical circulatory support (MCS) — IABP, Impella, or VA-ECMO.
• Door-to-ECMO concept: each minute saved improves neurologic survival in ECPR.
• National proposal: create a CPR-ECMO Center under JCS + MoH for standardized ECPR and simulation training.
