In acute or acutely decompensated chronic heart failure, symptoms of heart failure develop rapidly or worsen to the extent that the patient requires unplanned medical attention or hospitalization.

 

The most common symptom and reason for seeking medical care is dyspnea, which occurs either at rest or with minimal exertion. In some patients, the predominant symptom is peripheral edema. A weight gain of several kilograms over a short period (<1–2 weeks) strongly suggests fluid retention.

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Signs of Congestion

Typical findings include:

• Inspiratory crackles, or sometimes obstructive lung sounds (“cardiac asthma”)

• Ventricular gallop (S3) at early diastole

• Elevated jugular venous pressure (JVP)

• Pitting edema

• Hepatomegaly (possibly tender)

• Hepatojugular reflux

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In severe cases, cardiogenic shock develops, representing extreme circulatory failure. Cardiogenic shock is an emergency requiring immediate treatment directed at the underlying cause.

 

Typical features of cardiogenic shock:

• Low blood pressure or a fall in blood pressure (usually systolic <90 mmHg)

• Inadequate organ perfusion (hypoperfusion), indicated by:

  • Poor peripheral circulation (mottled skin, slow capillary refill, cool extremities)

  • Reduced urine output

  • Elevated blood lactate concentration

  • Altered mental status, drowsiness, or confusion

• Metabolic acidosis, which aggravates tachypnea associated with pulmonary congestion. Acidosis and elevated lactate are signs of severe perfusion deficit.

  • Lactate elevation, considered significant at >2 mmol/L (some studies have used >2.5 mmol/L).​​

    • A lactate value >3.1 mmol/L after 8 hours of treatment predicts increased mortality.

• In cardiogenic shock, pulse pressure is often narrow, and diastolic blood pressure may appear relatively high compared to true perfusion pressure.

  • Hence, mean arterial pressure (MAP) may be less informative than systolic blood pressure in this context.

 

Classification of Acute Heart Failure

The classification of acute heart failure is based either on the clinical presentation or on the hemodynamic status of the patient.

 

The Forrester classification remains one of the most widely used clinical frameworks.

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Patients can also be categorized according to blood pressure and oxygenation parameters:

1. Acutely Worsening Chronic or Latent Heart Failure

• Gradual (over days or about a week) worsening of dyspnea (due to pulmonary congestion) and/or edema (due to fluid retention).

• Blood pressure: normal or mildly elevated.

• Respiratory effort: moderate.

• Oxygenation: arterial oxygen saturation (SpO₂) >94% on room air or with low-flow supplemental oxygen.
   

2. Pulmonary Edema

• Markedly increased respiratory effort and respiratory rate.

• Poor oxygenation: SpO₂ <90–92%.

• Tachycardia is common.

• Blood pressure: normal or slightly elevated.

• Symptoms include restlessness and a sensation of suffocation.

• Chest X-ray: interstitial or alveolar pulmonary edema.
   

3. Hypertensive Heart Failure

• High blood pressure: systolic >160–180 mmHg.

• Respiratory effort increased, oxygen saturation reduced (SpO₂ <90–92% on room air).

• Often accompanied by radiological pulmonary edema (alveolar).

• Tachycardia and peripheral vasoconstriction are common.

• Left ventricular contractility: normal or reduced.
   

4. Right-Sided Heart Failure

• Elevated venous pressure, peripheral edema, hepatomegaly, and pleural effusion.

• Insufficient organ perfusion, low or normal blood pressure, and poor peripheral circulation without pulmonary congestion.
   

5. Cardiogenic Shock

• Severe hypoperfusion, manifested by cool peripheries, decreased urine output, elevated lactate levels, reduced consciousness, or confusion.

• Usually low blood pressure, typically systolic <90 mmHg.
   

There are no widely accepted universal criteria for cardiogenic shock. The classic diagnostic criteria for Cardiogenic Shock are from the SHOCK Trial:

Clinical Criteria:

• Hypotension: systolic blood pressure <90 mmHg for ≥30 minutes, or need for supportive measures to maintain systolic pressure ≥90 mmHg.

Signs of tissue hypoperfusion (at least one of the following):

• Urine output <30 mL/hour

• Cold, clammy skin

• Mental confusion or altered alertness

• Metabolic acidosis or elevated lactate

Hemodynamic Criteria:

• Cardiac index: ≤2.2 L/min/m²

• Pulmonary capillary wedge pressure: ≥15 mmHg
   

Usually lactate >2.0 mmol/L is considered significant. Some shock studies have used lactate >2.5 mmol/L as a cutoff for defining shock severity.

Most studies use urine output of <0.5ml/kg/hour as a definition for oliguria and reduced urine output

A disturbance in organ perfusion should always be treated as a warning sign requiring rapid action, even if blood pressure is not low. Metabolic acidosis and elevated lactate indicate severe perfusion deficit.

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Diagnostic Investigations in Acute Heart Failure

In most cases, an underlying trigger or precipitating factor can be identified that worsens heart failure symptoms. Targeted treatment of this underlying cause is essential to alleviate symptoms and prevent further decompensation.

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The main laboratory tests recommended for evaluating the cause of acute heart failure are summarized in table below

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Key diagnostic markers include:

Troponins

Troponin levels are often mildly elevated in acute heart failure.
A clearly elevated concentration — TnT ≥ 52 ng/L or TnI ≥ 225 ng/L (cutoffs vary by assay) — together with ischemic symptoms (e.g., chest pain) or ischemic ECG changes, suggests acute myocardial injury or acute coronary syndrome.
 

Natriuretic Peptides (BNP, NT-proBNP)

Measurement is particularly useful when acute heart failure is suspected in a patient without a prior diagnosis of heart failure.

A proBNP <300 ng/L effectively excludes acute heart failure, regardless of age or sex.
An NT-proBNP >900 pg/mL in middle-aged patients or >1,800 pg/mL in those over 75 years strongly supports the diagnosis of heart failure.

• The higher the value, the greater the likelihood of heart failure.

 

Chest X-ray Findings

Radiographic findings vary according to the severity of heart failure:

1. Increased pulmonary vascular markings

2. Interstitial edema

   • Blurred vascular margins due to interstitial swelling

   • Moderately elevated pulmonary capillary pressure

   • Kerley B-lines present

3. Alveolar edema

   • “Cotton wool” opacities

   • Indicates markedly elevated capillary pressure

   • Often clinically corresponds to acute pulmonary edema with severe dyspnea and hypoxemia

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Pleural effusion may accompany decompensated heart failure. It might be unilateral, more commonly on the right side.

Possible explanations for this right sided tendency include:

• The right lung has a larger surface area (three lobes vs. two on the left), allowing greater fluid accumulation.

• Patients with heart failure often avoid lying on the left side, which may favor right-sided fluid accumulation

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Echocardiography

Should be performed immediately in any patient whose hemodynamic condition deteriorates despite treatment or who is in cardiogenic shock.

• Possible underlying causes include:

  • Pericardial tamponade

  • Mechanical complication of myocardial infarction

  • Chordae tendineae rupture
     

Echocardiography should be performed during the same hospitalization if not recently done, especially when left ventricular function is unknown.​
Echocardiography confirms the diagnosis of heart failure​ and differentiates between systolic and diastolic heart failure and may reveal the etiology (e.g. valve disease)

 

Treatment of Acute Heart Failure

Management of acute or decompensated heart failure focuses on rapid stabilization, symptom relief, optimization of hemodynamics, and correction of precipitating causes.

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Initial Measures

Supplemental oxygen and/or non-invasive ventilation (CPAP/BPAP) if hypoxemic or in respiratory distress.

Vasodilator therapy (e.g., nitrates) if blood pressure allows and indicated (pulmonary edema).

Loop diuretics (typically intravenous furosemide) for congestion.

Morphine may be used for symptom relief, not routinely.

Position the patient in a semi-upright (Fowler’s) position to improve oxygenation.

If signs of low filling pressure are present in hypotensive/under perfused patients, a cautious fluid challenge should be performed. If hypoperfusion or hypotension persists after adequate preload, vasopressor support is initiated.

 

Fluid Challenge

Be aware of the fact that a normal human heart is fluid responsive. Thus a fluid responsive patient will not always benefit from fluid therapy in the long run and may not get a benefit in terms of mortality. Fluid responsiveness rather indicates where the patient is positioned on the Frank-Starling curve. The benefits and risks of fluid therapy should always be considered on a case-by-case basis.

 

A fluid challenge can be done when there are no signs of severe fluid overload. If the patient appears fluid overloaded but is hypotensive, a limited trial can still be considered.

Protocols vary and there is no hard data to support a particular regimen. Typical regimens include:

• 200 mL of 0.9% NaCl or Ringer’s solution over 15–20 minutes, or

• 500 mL over 20–30 minutes.

Monitoring parameters and goals:

• Increase in MAP (≥65 mmHg is generally acceptable)

• Improved urine output (usual goal of >0.5 mL/kg/h)

• Resolution of end-organ hypoperfusion (improved mental status, decreased lactate, normalized capillary refill)

• Ultrasound and echocardiography optimal filling state (e.g. atrial pressures, IVC diameter, ventricular filling and EF)

• Cardiac output monitoring e.g. cardiac index, stroke volume, stroke volume variation

Most of these variables are surrogates for cardiac output and stroke volume, which are the true targets of preload optimization.

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Morphine

Relieves dyspnea and induces vasodilation.

Reduces heart rate — caution if bradycardic. May cause nausea or vomiting.

 

Dose: 2–4 mg IV, repeated every 10 minutes as needed.

Alternative: IV oxycodone.

Routine opioid use is not recommended.

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Oxygen, HFNC, CPAP, and BPAP

Administer oxygen only if SpO₂ <90–92% or respiratory effort is markedly increased (eg RR >25/min). Prolonged increased respiratory effort carries a high risk of patient fatigue (respiratory exhaustion) and increased respiratory rate should always act as a serious warning sign.

Oxygen is not indicated if SpO₂ >94%, as excessive oxygen can cause peripheral vasoconstriction and reduce cardiac output.

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In cases of mild congestion, oxygen can be administered via a Venturi (air entrainment) mask, nasal cannula, or high-flow nasal cannula (HFNC). If pulmonary edema is severe, or if increased respiratory effor or hypoxemia does not improve with a Venturi mask or nasal cannula/HFNC, CPAP (continuous positive airway pressure) or BPAP (bilevel positive airway pressure) therapy should be initiated.

 

High-Flow Nasal Cannula (HFNC)

Provides mild positive pressure (~1 cmH₂O per 10 L flow). Positive pressure decreases if patient breathes through their mouth.

 

Less effective than CPAP/BPAP in pulmonary edema.

 

Evidence for HFNC in acute heart failure is very limited. According to treatment guidelines, HFNC therapy cannot be recommended for acute heart failure due to a lack of evidence. However HFNC may be tried under close monitoring if CPAP/BPAP would require transfer to a higher-care unit. If no improvement within 1–2 hours, switch to CPAP/BPAP.

 

CPAP/BPAP

Reduces mortality and intubation rates in cardiogenic pulmonary edema. Reduces the need for intubation and ICU admission/length of stay compared to air entrainment masks.

 

PEEP: 7.5–10 cmH₂O most often sufficient. 5 cmH₂O may suffice for small patients. PEEP may be increased up to 12.5 cmH₂O if needed.

Dyspnea often improves rapidly — within 30 minutes.

 

High PEEP can cause hypotension if preload is low. PEEP increases intrathoracic pressure, which can reduce venous return to the heart and lower cardiac output. 

 

Prolonged CPAP mask ventilation should be avoided, as the treatment increases the risk of aspiration.

 

Wean CPAP gradually by lowering PEEP once symptoms improve.

 

BPAP treatment via ventilator is especially beneficial for hypercapnic or hypoventilating patients.

 

A decreased level of consciousness and lack of cooperation, for example due to severe hypoperfusion, increase the risk of aspiration during mask ventilation and are relative indications for intubation. A GCS score of 8 is often considered as the threshold for considering intubation, but there is some evidence supporting the use of BPAP treatment even with a GCS below 8, particularly if the low GCS is caused by hypercapnia.

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Intubation and mechanical ventilation are used if the patient becomes exhausted or if noninvasive positive pressure ventilation cannot be performed due to confusion or agitation.

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Nitrates (Glyceryl Trinitrate, Nitroprusside) in pulmonary edema

Use unless severe hypotension (<85–90 mmHg) is present.

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Start with a low-dose infusion (e.g., 10 mL/h of 0.1 mg/mL solution) to avoid sudden hypotension.

Titrate actively to blood pressure and clinical response. Rapid BP drop suggests hypovolemia.

 

Vasodilatation decreases both preload and afterload. Use with caution in RV failure as the RV is often more preload dependent.

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Glyceryl trinitrate is the drug of choice in pulmonary edema when no marked hypertension exists.

 

Hypertension should be treated rapidly. Sodium nitroprusside is primarily an arterial vasodilator, indicated for hypertensive AHF.

Target BP in acute HF is <140/80 mmHg to reduce afterload.

 

Continuous monitoring required, often by invasive BP monitoring.

 

Intravenous nitroglycerin and isosorbide dinitrate have not been shown to improve prognosis in patients with heart failure or to be more effective than diuretic- or opioid-based therapy in relieving symptoms. However, due to the limited amount of research data, no strong conclusions can be drawn.

 

In patients with severe obstructive valvular disease (aortic stenosis), treatment should be carried out with careful blood pressure monitoring because of the risk of sudden hypotension. In severe aortic stenosis, the heart is dependent on adequate preload, which is reduced by nitrates.

 

Diuretics

The oral bioavailability of furosemide varies greatly, ranging from 10% to 90% (mean 40–60%).

As a general guideline for dose equivalence, 20 mg orally corresponds to approximately 10 mg intravenously.

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In decompensated heart failure, IV furosemide is preferred; oral absorption may be unreliable especially in decompensation.

• Initial dose: 20–40 mg IV bolus. If a patient already uses furosemide, the total daily oral dose may be given as a single IV bolus (up to 180 mg).

• Assess response within 1–2 hours:

  • Good response: urine output >100–150 mL/h.

  • Alternatively measure urine sodium (U-Na) after 1–2 hours: >50–70 mmol/L suggests effective natriuresis.

• If inadequate response, double the dose (increase by 50–100%).

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​According to research evidence, IV bolus or continuous infusion are equally effective. Intravenous administration of furosemide three to four times per day often produces the desired effect.

• Infusion allows more precise titration based on hourly diuresis.

  • Typical rate: 5–10 mg/h, up to 40 mg/h. In some patients, a rate as low as 2–4 mg/h may produce the desired response.

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Combination therapy:

Add hydrochlorothiazide 25 mg or metolazone 2.5–5 mg for diuretic resistance.

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The maximal daily dose for i.v. loop diuretics is generally considered furosemide 400-600 mg. Up to 1000 mg may be considered in patients with severely impaired kidney function.

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Vasoactive and Inotropic Drugs in Acute Heart Failure

The use of vasoactive drugs in acute heart failure is mainly limited to cases of severe systolic heart failure and cardiogenic shock when cardiac output is critically reduced and end-organ perfusion is compromised.

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Vasoactive drugs are divided into vasopressors (which raise blood pressure) and inotropes (which enhance myocardial contractility). Inotropes such as dobutamine, levosimendan, and milrinone often also have vasodilatory effects. These drugs are therefore also referred to as inodilators.

 

Use of vasoactives requires continuous (often invasive) hemodynamic and rhythm monitoring, ideally in an intensive care or coronary care unit.

 

Vasopressors

Indications

• Hypotension (often MAP <65 mmHg, systolic blood pressure <90 mmHg) or hypoperfusion (e.g. oliguria, altered mental status, elevated lactate) despite adequate filling pressures.
   

Common Agents

• Norepinephrine (noradrenaline) – first-line vasopressor in cardiogenic shock.

  • Predominantly α-adrenergic vasoconstrictor with mild β₁ effects.

  • Increases systemic vascular resistance and MAP with limited rise in heart rate.

• Epinephrine (adrenaline) – may be used if norepinephrine response inadequate or in refractory shock.

  • α-adrenergic vasoconstrictor with stronger β-adrenergic effects. May increase heart rate and myocardial oxygen demand.

• Vasopressin – adjunctive therapy when catecholamine requirements are high; helps restore vascular tone.
   

Inotropes

Inotropes enhance cardiac contractility and improve stroke volume.

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Inotropic therapy is initiated if severe congestion or impaired organ perfusion does not improve despite optimization of other treatments and optimal pre- and afterload. Its use usually requires invasive blood pressure monitoring and continuous cardiac rhythm monitoring.

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Adjust doses carefully to achieve adequate perfusion while minimizing arrhythmogenic risk and oxygen consumption.

 

Dobutamine

• Synthetic catecholamine; β₁-agonist with mild β₂ and α₁ effects.

• Increases contractility by raising intracellular calcium levels.

• Enhances cardiac output but also increases myocardial oxygen consumption.

• May precipitate serious arrhythmias.
   

Levosimendan

• Calcium sensitizer with vasodilating properties.

• Increases the sensitivity of contractile proteins to Ca²⁺ without increasing intracellular calcium concentration.

• Effects are independent of catecholamines, making it suitable for patients on β-blockers.

• Improves hemodynamics without increasing cardiac oxygen demand.

• Also causes systemic and pulmonary vasodilation, reducing preload and afterload.
   

Milrinone

• Phosphodiesterase-3 (PDE3) inhibitor.

• Increases intracellular cyclic AMP, leading to enhanced contractility and vasodilation (including pulmonary arteries).

• Catecholamine-independent mechanism.

• Particularly beneficial in right ventricular failure or pulmonary hypertension.

 

Coronary Angiography

Immediate coronary angiography is indicated if the ECG shows:

1. ST-elevation myocardial infarction (STEMI) changes, or

2. Ischemic ECG changes suggesting acute myocardial ischemia with shock (at minimum, consult an interventional cardiologist)

 

Highly urgent angiography (<2 hours) is recommended if an acute coronary syndrome (ACS) is suspected as the underlying cause of acute heart failure.
In clinical practice, hemodynamic stabilization is often attempted before angiography using medications and ventilatory support.

 

Continuation of Guideline-Directed Heart Failure Therapy

Whenever possible, continue disease-modifying heart failure medications at the maximum tolerated dose:

• Spironolactone (or other mineralocorticoid receptor antagonists)

• SGLT2 inhibitors

• ACE inhibitors or ARBs (angiotensin receptor blockers)

Discontinuation should be avoided and is not usually necessary, except in cases of cardiogenic shock or severe hypotension.

Beta-blockers may be temporarily withheld if the patient is hypotensive or near-hypotensive without significant tachycardia.

 

Hemoglobin correction with blood transfusions is reserved only for acutely ischemic patients, and transfusions should be given slowly to prevent fluid overload.

• Target hemoglobin: (90–)100(-120) g/L

 

As soon as the patient’s circulatory and renal function allow, start or resume oral, heart failure medications (ACE inhibitor/ARNI, beta-blocker, MRA, SGLT2 inhibitor). Early initiation improves long-term prognosis.

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Imaging

Avoid unnecessary chest X-ray controls. Radiographic findings often resolve more slowly than clinical symptoms.

 

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Management of Cardiogenic Shock

General Principles

Prognosis-improving treatment in cardiogenic shock must target the underlying cause. Prompt recognition and correction of the precipitating mechanism are essential.

Immediate ECG and transthoracic echocardiography are the first-line diagnostic tools to identify the etiology.

In approximately 80% of cases, cardiogenic shock is caused by acute myocardial infarction (AMI).

 

All patients with AMI and cardiogenic shock should undergo immediate coronary angiography and revascularization (PCI or CABG). Early revascularization is the only intervention proven to improve survival in cardiogenic shock complicating MI.

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Pharmacological Management

Vasoactive Support

• Inotropes and vasopressors are administered intravenously to maintain perfusion in patients with:

  • Reduced cardiac output

  • Hypotension threatening organ perfusion (brain, kidneys, liver, gastrointestinal tract).
     

Hemodynamic Targets

• Maintain mean arterial pressure (MAP) at a level that ensures:

  • Adequate urine output

  • Preserved mental status

• Typically 65–70 mmHg is sufficient.

• Assess and document limb temperature and perfusion boundaries, and monitor changes frequently.
   

Fluid Resuscitation

Initial management should include a fluid challenge to ensure adequate preload.

 

Vasopressors

Norepinephrine is the first-line agent to achieve target blood pressure.

Additional vasopressors may be used as adjuncts

 

Inotropes

Used to augment contractility when low cardiac output persists despite adequate filling pressures.

However, no inotrope has been shown to improve survival in cardiogenic shock.

 

Ventilatory Support

Combined shock and pulmonary edema frequently necessitate intubation and mechanical ventilation.

 

Mechanical Circulatory Support

Mechanical circulatory support refers to systems in which blood circulation is assisted by an external or implantable device or pump.

Mechanical circulatory support may be appropriate for patients eligible for active therapy who have a refractory cardiogenic shock despite optimized medical and device therapy,

However, current evidence does not demonstrate a mortality benefit from mechanical support in cardiogenic shock.

 

Intra-Aortic Balloon Pump (IABP)

Randomized trials have shown no reduction in mortality in post-MI cardiogenic shock.

 

Extracorporeal Membrane Oxygenation (ECMO)

Immediate use of ECMO has not shown clear clinical benefit in randomized studies.

May be considered if:

• Myocardial recovery is expected, e.g., after cardiac surgery or myocarditis.
   

Other Devices

Impella microaxial flow pump

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Left ventricular assist device (LVAD) (e.g., HeartMate) for prolonged or chronic circulatory support.

• Right ventricular function must not be severely impaired to qualify for LV assist therapy.

Indications for LVAD Use

• Bridge to transplantation: for eligible patients with worsening condition and long expected wait time.

• Bridge to candidacy: to allow recovery of reversible end-organ dysfunction (e.g., due to hypoperfusion).

• Bridge to recovery: for reversible causes such as myocarditis or peripartum cardiomyopathy.

• Destination therapy: as a permanent solution when heart transplantation is not feasible.