Acute Heart Failure: Emergency Management and Differentiation

Acute heart failure is one of the most common emergency diagnoses in clinical practice and carries significant mortality. Whether the presentation is hypertensive pulmonary edema, acutely decompensated chronic heart failure, or cardiogenic shock – the first minutes of management determine prognosis and survival. It's not just about rapidly recognizing the diagnosis, but above all about hemodynamic classification: Is the patient "warm" or "cold"? "Dry" or "wet"? The answers to these questions determine first-line therapy and prevent a well-intentioned therapeutic reflex – such as reflexive administration of furosemide – from pushing the patient into hemodynamic catastrophe.

Definition and Differentiation

Acute heart failure is defined as the rapid onset or rapid worsening of symptoms and signs of heart failure requiring urgent initiation of therapy. The distinction between the following scenarios is clinically relevant:

• De novo heart failure: First manifestation without previously known cardiac disease – frequently in the setting of an acute coronary syndrome, a hypertensive crisis, or acute myocarditis.
• Acutely decompensated chronic heart failure (ADHF): Worsening of pre-existing heart failure, often triggered by non-compliance, infections, atrial fibrillation, or anemia.
• Cardiogenic shock: The most severe form with hypotension (systolic blood pressure < 90 mmHg), signs of end-organ hypoperfusion, and need for vasoactive substances.

These entities require fundamentally different therapeutic approaches – a fact that is frequently underappreciated in the emergency setting.

Clinical Classification: Warm-Cold-Wet-Dry

The hemodynamic classification according to Stevenson forms the backbone of initial therapeutic decision-making. It is based on two clinical axes:

Signs of Congestion (wet vs. dry)

• Orthopnea, jugular venous distension, peripheral edema, hepatomegaly, pulmonary crackles, pleural effusion
• Pulmonary congestion is the strongest predictor of symptom burden

Signs of Perfusion (warm vs. cold)

• Cool extremities, prolonged capillary refill time, oliguria, confusion, narrow pulse pressure, elevated lactate
• "Cold" indicates significant forward failure with reduced cardiac output

This yields four clinical profiles:

Profile	Congestion	Perfusion	Frequency	Therapeutic Focus
Warm-dry (A)	No	Adequate	~5%	Search for underlying cause, acute therapy may not be necessary
Warm-wet (B)	Yes	Adequate	~65%	Vasodilation, diuretics
Cold-dry (L)	No	Inadequate	~5%	Volume administration, possibly inotropes
Cold-wet (C)	Yes	Inadequate	~25%	Inotropes, vasopressors, cautious diuresis

By far the most common type in the emergency setting is the "warm-wet" patient – typically presenting with hypertensive crisis, pulmonary edema, and preserved perfusion. The "cold-wet" patient, on the other hand, has the worst prognosis and represents the greatest therapeutic challenge.

Initial Diagnostics in the Emergency Department

Diagnostics should run in parallel with therapy and follow a structured approach:

Basic Diagnostics

• 12-lead ECG: Rule out acute coronary syndrome, arrhythmia assessment (atrial fibrillation with rapid ventricular response as a frequent trigger)
• Pulse oximetry and blood gas analysis: Assessment of oxygenation and acid-base status; a lactate > 2 mmol/L indicates significant hypoperfusion
• Chest X-ray: Signs of congestion, pleural effusion, cardiomegaly – caveat: up to 20% of patients with elevated filling pressures have an unremarkable X-ray
• Point-of-care ultrasound (POCUS): B-lines as a correlate of interstitial edema, assessment of left ventricular function, pericardial effusion, inferior vena cava collapsibility

Laboratory Diagnostics

• BNP / NT-proBNP: An NT-proBNP < 300 pg/mL makes acute heart failure unlikely. Values > 900–1800 pg/mL (age-dependent) suggest acute decompensation. Limitations: obesity lowers values, renal insufficiency elevates them.
• High-sensitivity troponin: Rule out or confirm myocardial ischemia as a trigger
• Renal function parameters, electrolytes, liver function tests: Assessment of end-organ function
• TSH: Hyperthyroidism as a reversible trigger

Echocardiography

A focused echocardiogram should be performed within the first 60 minutes. Relevant questions:

• Left ventricular ejection fraction (reduced vs. preserved?)
• Regional wall motion abnormalities (suggestive of ACS?)
• Valvular pathology (acute mitral regurgitation?)
• Pericardial effusion with signs of tamponade?
• Right ventricular dilation (pulmonary embolism?)

Therapy by Hemodynamic Profile

The Warm-Wet Patient: Nitrates and Diuretics

This most common phenotype benefits primarily from aggressive afterload reduction – not primarily from diuresis. This is a crucial point that is frequently misjudged in clinical practice.

Nitrates as first-line therapy:

Nitroglycerin acts as a venodilator (preload reduction) and at higher doses as an arteriodilator (afterload reduction). Especially in hypertensive pulmonary edema, high-dose nitrate therapy is the most effective immediate intervention:

• Sublingual nitroglycerin: 0.4–0.8 mg as a bolus, repeatable every 3–5 minutes
• Intravenous nitroglycerin: Start at 10–20 µg/min, titrate in increments of 10–20 µg/min every 3–5 minutes; target dose often 100–200 µg/min; there is no fixed upper limit – guide yourself by clinical response and blood pressure
• Alternatively sodium nitroprusside: 0.3–5 µg/kg/min – particularly effective in severe afterload elevation, but requires invasive blood pressure monitoring and is limited by cyanide toxicity with prolonged use

Contraindications for nitrates: systolic blood pressure < 90 mmHg, use of PDE-5 inhibitors within the last 24–48 hours, severe aortic stenosis, right ventricular infarction.

Diuretics:

Loop diuretics are indicated for volume overload but are not the first-choice agent for every pulmonary edema. Many patients with hypertensive pulmonary edema have fluid redistribution, not true volume overload.

• Furosemide IV: 20–40 mg in diuretic-naive patients; in patients on pre-existing diuretic therapy: initial dose equivalent to the oral daily dose (1:1 to 2.5:1)
• Goal: urine output > 100–150 mL/h in the first 2 hours; if response is inadequate, double the dose or combine with a thiazide diuretic (sequential nephron blockade)

Oxygen and Airway Management:

• Oxygen administration only if SpO₂ < 90% – hyperoxia worsens outcomes
• NIV (non-invasive ventilation): CPAP or BiPAP is a Class I recommendation in cardiogenic pulmonary edema. CPAP at 5–10 cmH₂O reduces preload, improves oxygenation, and significantly reduces the intubation rate. Use it early – don't consider it a last resort
• Intubation only if NIV fails, consciousness is impaired, or respiratory exhaustion occurs – then with a hemodynamically stable induction (ketamine-based, avoid propofol monoinduction)

The Cold-Wet Patient: Inotropes and Vasopressors

This patient has the worst profile: congested and simultaneously hypoperfused. Therapy is a balancing act between decongestion and circulatory stabilization.

Vasopressors in cardiogenic shock:

• Norepinephrine: First-line vasopressor in cardiogenic shock with hypotension. Dosing: 0.1–1 µg/kg/min. Target: MAP ≥ 65 mmHg. Norepinephrine is superior to dopamine – dopamine is associated with a higher rate of arrhythmias.

Inotropes:

• Dobutamine: 2–20 µg/kg/min – first-line inotrope. Increases contractility and reduces peripheral vascular resistance. Caveat: tachycardia, proarrhythmic potential, blood pressure drop in hypovolemia.
• Milrinone (PDE-3 inhibitor): 0.125–0.75 µg/kg/min – has inotropic and vasodilatory effects. Advantage: effective even in patients on beta-blocker therapy. Disadvantage: vasodilation can worsen hypotension; often requires combination with norepinephrine.
• Levosimendan: 0.05–0.2 µg/kg/min over 24 hours – a calcium sensitizer with an inotropic-vasodilatory profile. Particularly discussed in beta-blocker-induced decompensation. The loading bolus is frequently omitted due to the risk of hypotension.

Mechanical Circulatory Support:

In refractory cardiogenic shock despite optimized pharmacological therapy, mechanical support devices must be considered early:

• Intra-aortic balloon pump (IABP) – based on current evidence, no mortality benefit in infarction-related cardiogenic shock, but still used in certain scenarios
• Impella® (percutaneous microaxial pump) – increasingly used in high-risk PCI and refractory shock
• VA-ECMO – as bridge-to-recovery or bridge-to-decision in the most severe circulatory failure

The decision for mechanical support requires interdisciplinary coordination and should not be made too late.

The Cold-Dry Patient: Volume Administration and Caution

This rare but deceptive phenotype presents with forward failure without signs of congestion – typically in the setting of excessive diuresis or dehydration of a heart failure patient. Therapy consists of a cautious volume challenge (250 mL crystalloid solution over 15–20 minutes) with close reassessment. If perfusion remains poor, inotropes are initiated.

Identifying Reversible Causes and Triggers

In parallel with symptomatic therapy, treatable triggers must always be sought. A useful mnemonic for this is CHAMP:

• C – Coronary (acute coronary syndrome)
• H – Hypertensive Emergency
• A – Arrhythmia (tachycardic or bradycardic)
• M – Mechanical (acute valvular regurgitation, ventricular septal rupture, pericardial tamponade)
• P – Pulmonary Embolism

Each of these triggers requires specific, causal therapy – and their identification takes priority.

Common Errors in Emergency Management

• Reflexive high-dose furosemide administration without prior hemodynamic classification: In vasoconstrictive pulmonary edema with normal total volume, aggressive diuresis worsens perfusion
• Overly hesitant use of nitrates: Nitrates are frequently underdosed. In hypertensive pulmonary edema, aggressive titration is both appropriate and recommended
• Delayed NIV initiation: CPAP/BiPAP must be understood as a first-line intervention, not as an escalation step before intubation
• Beta-blocker administration in the acute setting: In decompensated heart failure, beta-blockers should not be newly initiated and should be paused if hemodynamic instability is present
• Omission of echocardiography: Failing to perform a timely echo leads to missed mechanical complications and reversible causes

Summary of First-Line Therapy

Clinical Profile	Blood Pressure	First-Line Therapy
Warm-wet, hypertensive	> 140 mmHg systolic	Nitrates (high-dose), NIV, diuretics
Warm-wet, normotensive	90–140 mmHg systolic	Nitrates (moderate), diuretics, NIV
Cold-wet	< 90 mmHg systolic	Norepinephrine + dobutamine/milrinone, cautious diuresis
Cold-dry	Variable	Volume challenge, possibly inotropes

Practical Training

Acute heart failure requires not only theoretical knowledge but confident handling under time pressure: rapid hemodynamic classification, correct dosing of vasoactive substances, management of NIV, and structured team communication. In the ACLS courses by Simulation Tirol, you train exactly these scenarios using realistic simulation cases – with direct feedback and according to current AHA guidelines. This is how theoretical knowledge becomes the practical competence that makes the difference in a real emergency.