Acute heart failure and pulmonary oedema


  • In the acute phase of heart failure, treatment consists of oxygen therapy and CPAP therapy for respiratory insufficiency, as necessary, intravenous diuretics and vasodilatation with nitrates. Opioids can be used for symptomatic treatment but, due to their adverse effects, their routine use should be avoided.
  • Symptoms and findings are mostly due to congestion, and the aim of the treatment should be to relieve it completely during the hospital stay. Effective diuretic medication forms the cornerstone of treatment.
  • The correction of the underlying cause and aggravating factors is crucial for a favourable outcome.
  • Prognostically beneficial medication of systolic heart failure should be optimized during the hospital stay.

General remarks

  • Acute heart failure (AHF) is a cardiovascular disease that uses a considerable amount of hospital resources.
  • The patient presents either with new, previously undiagnosed heart failure or – more commonly – with a worsening of pre-existing chronic heart failure.
  • AHF must be diagnosed and treated immediately.
  • The clinical picture varies from the most severe cardiogenic shock with an in-hospital mortality of about 40% to slowly increasing fluid overload and congestion.
  • Symptoms and findings are mainly caused by venous and organ congestion. This is due to high cardiac filling pressures associated with the absolute fluid overload and/or fluid redistribution.
  • In only a small share of patients, symptoms and findings are due to tissue and organ hypoperfusion resulting from low cardiac output.

Assessment of clinical status

  • A history of heart failure or myocardial infarction and paroxysmal nocturnal dyspnoea or dyspnoea in the supine position strongly suggest AHF.
  • It should first be assessed whether the patient has signs of congestion and disturbances of organ perfusion (see Table T1).
  • Signs of pulmonary congestion include basal coarse rales or fine rales (crackles) which may be associated with airway obstruction, early diastolic ventricular gallop (S3), increased jugular venous pressure, pitting oedema, hepatomegaly and abdominojugular reflux.
  • Signs of hypoperfusion include decreased level of consciousness, drowsiness, confusion, cool peripheries, cyanosis and decreased diuresis, as well as lactacidaemia and metabolic acidosis, which should be effectively addressed.
Table 1. Clinical assessment of congestion and hypoperfusion
Assessment of congestion Assessment of hypoperfusion
Jugular venous pressure, abdominojugular reflux Skin temperature, cyanosis
Palpation of the liver Alertness, consciousness
Pitting oedema Urine output
Lung auscultation Acid-base balance, lactate
Chest x-ray

Laboratory test and imaging studies

  • An ECG should be recorded immediately in order to diagnose ischaemia and check the rhythm. Atrial fibrillation in a patient with dyspnoea indicates heart failure.
  • First line laboratory tests include basic blood count, plasma potassium, sodium and creatinine as well as CRP.
  • If acute coronary syndrome (ACS) is suspected, the levels of cardiac markers should be determined. However, an increase in troponin, without other findings suggestive of myocardial infarction, is not indicative of an ACS but is often related to AHF. Increased left ventricular end diastolic pressure may lead to subendocardial ischaemia while, on the other hand, advanced heart disease may be associated with silent myocardial damage.
  • Metabolic acidosis and an increased lactate level in arterial blood gas analysis are indicative of severe hypoperfusion.
  • Plasma NT-proBNP (N-terminal probrain natriuretic peptide) and BNP (brain natriuretic peptide) provide an excellent tool for excluding heart failure in patients with unclear dyspnoea. However, other factors such as age, fast arrhythmias, renal failure and pulmonary embolism may also produce increased levels while, on the other hand, in overweight patients the levels may be misleadingly low.
  • Typical findings in chest x-ray include:
    • marked pulmonary congestion
    • interstitial and alveolar oedema due to increased pulmonary capillary pressure
    • pleural effusion.
  • If hypoxaemia and dyspnoea can be explained by pulmonary oedema, there is no need to proceed with unnecessary investigations, such as computerized tomography to detect pulmonary embolism, as the contrast medium would only add to the circulating volume and thus increase the work of the kidneys.
  • Unnecessary chest x-rays should be avoided as the clinical condition will improve before the x-rays!
  • An echocardiogram should be obtained without delay if the patient is in cardiogenic shock or if life-threatening functional or structural abnormality of the heart is suspected. Otherwise, it should be performed within a couple of days unless up-to-date findings are available.. Echocardiogram is also a tool for quick estimation of right and left cardiac filling pressures.
  • Pulmonary ultrasound may be used to establish heart failure: fluid retention in the interstitial space causes so-called B-lines. Additionally, it can quickly establish the presence of pleural effusion.

Evidence Summaries

Differential diagnosis

  • Pneumonia
  • Pulmonary embolism (may be the cause of right heart failure)
  • ACS (may be the factor causing heart failure)
  • Exacerbation of asthma or COPD
  • Parenchymal lung diseases
  • Pneumothorax, pleural effusion
  • Venous insufficiency
  • Severe hypoalbuminaemia

Triggering and aggravating factors

  • ACS
  • Arrhythmia, typically atrial fibrillation
  • Infection
  • Uncontrolled hypertension
  • Valvular defect (such as aortic stenosis, acute mitral regurgitation)
  • Pulmonary embolism
  • Tamponade
  • Inadequate adherence to treatment
  • Excessive fluid therapy
  • Unsuitable drug therapy (e.g. NSAIDs)

Causal treatment

  • Underlying causes of cardiac failure and factors triggering the acute failure should always be investigated and addressed to treat cardiac failure.
  • ACS is the factor triggering AHF in as many as one patient in three and requires invasive investigation if the state of the coronary arteries is unknown.
  • Echocardiography is the key investigation when structural abnormalities of the heart are suspected.

Starting treatment, and treatment of congestive heart failure

  • After the initial examination, insert an i.v. line.
  • Monitor the patient’s heart rhythm, blood pressure and oxygen saturation.
  • Direct arterial blood pressure measurement is indicated in patients whose haemodynamic status is unstable or if there are signs of hypoperfusion.
  • A half-sitting position is best if the patient has severe dyspnoea.

Supplemental oxygen, positive pressure ventilation and ventilator therapy

  • If the patient is hypoxaemic (SaO2 < 90%), oxygen should be administered first via a venturi mask (8 l/min). In severe pulmonary oedema, noninvasive positive pressure ventilation using either CPAP (continuous positive airway pressure) or bilevel positive airway pressure should be commenced with a 7.5–10 cmH2O PEEP (positive end-expiratory pressure) valve. A 5 cmH2O PEEP valve may be enough for a small framed patient, but for some patients PEEP may be increased up to 12.5 cmH2O. In most cases the dyspnoea improves within 30 minutes.
  • Bilevel positive airway pressure ventilation may be a better choice for patients with hypoventilation and hypercapnia.
  • Prolonged use of positive pressure ventilation should be avoided as the therapy may increase the risk of aspiration. When dyspnoea and hypoxaemia have improved, the PEEP should be gradually reduced.
  • Caution should be taken in hypovolaemia and right ventricular failure where high PEEP levels may lead to hypotension.
  • Reduced level of consciousness and inability to cooperate, for example due to severe hypoperfusion, increase the risk of aspiration during mask therapy and are, therefore, an indication for intubation in patients with severe respiratory failure.

Morphine or oxycodone

  • Morphine and oxycodone relieve dyspnoea and restlessness in the initial phase of treatment and also provide vasodilatation but, due to their adverse effects, their routine use should be avoided.
  • Should be used with caution, as they may induce nausea, lower the heart rate and blood pressure and have a respiratory depressant effect.
  • Initially a bolus dose of 2–4 mg intravenously, followed as necessary by repeat doses every 10 minutes.


  • As venous and organ congestion is the primary cause of the symptoms, findings and disturbed organ function, treatment is largely based on effective diuretic medication. There is no reason to be afraid of associated minor changes in renal function.
  • The only exception is cardiogenic shock where the primary treatment can be fluid administration.
  • The bioavailability of oral furosemide is 10–90%; in case of more severe failure, its absorption will decline. If the patient has clinical signs of congestion, furosemide should be administered intravenously at a dose of 20–40 mg (or at least at a dose that corresponds to the medication used at home).
  • Furosemide should be given 2–3 times per 24 hours. In case of insufficient response, the dose can be increased by 50–100%.
  • Daily weighing and, in more severe cases, hourly urine measurements and fluid balance monitoring are required. The target is hourly diuresis exceeding 100–150 ml and weight loss of at least 1 kg per day.
  • Daily monitoring of plasma creatinine, potassium and sodium is recommended. Slightly increased creatinine values are not considered a sign of poor prognosis if diuresis is good and the patient’s clinical state is improving.
  • Continuous infusion of furosemide has the advantages of an even treatment response and easy dose adjustment but there is no essential difference in efficacy or safety compared to bolus dosing.

Nitrates and nitroprusside

  • The primary indications for nitrates and nitroprusside are heart failure associated with ACS, pulmonary oedema and hypertensive heart failure. What the indications have in common is (acutely) elevated left heart filling pressure and redistribution of fluid to pulmonary tissue.
  • Patients with pulmonary oedema should be given nitrates, unless their blood pressure is reduced (< 110 mmHg).
  • In the initial phase, nitroglycerine spray or sublingual tablets can be administered.
  • A nitrate infusion can be commenced at a low starting dose (e.g. 10–20 ml/hour with a concentration of 0.1 mg/ml) but the dose should be actively increased while monitoring the treatment response (alleviation of symptoms and lowering of blood pressure).
  • Hypertension should be promptly and effectively treated.
  • Sodium nitroprusside acts mainly by dilating arteries. Its specific indication is acute aortic or mitral regurgitation requiring decreased afterload.

Antithrombotic therapy

  • Patients hospitalized with heart failure have a significant risk of venous thrombosis.
  • Low molecular weight heparin administered once daily effectively reduces the risk of thrombosis.
  • In a patient treated with warfarin, a sudden increase in INR above the therapeutic range may suggest hepatic dysfunction due to hypoperfusion and/or congestion. It is therefore often simpler to replace warfarin temporarily by low molecular weight heparin during hospital treatment of severe heart failure.

Inotropic agents

  • Inotropic medication (dobutamine, levosimendan) is used to intensify the cardiac pumping function in patients with cardiogenic shock or severe systolic heart failure not responding to other treatment.

Evidence Summaries

Prognostically beneficial medication of systolic heart failure

  • The use of beta-blockers, ACE inhibitors and ATR blockers and ARNI (combination of ATR blocker and neprilysin inhibitor) should be continued using the highest dose that the patient is able to tolerate haemodynamically, and they need rarely be discontinued except in the presence of shock.
  • In new patients, the use of these drugs should be started by careful titration only after the circulation has been stabilised. A slight increase in the plasma creatinine concentration at the beginning of ACE inhibitor or ATR blocker therapy is common and is not an indication for stopping treatment.
  • It is also safe to start giving ARNI and SGLT-2 inhibitors during hospital treatment of AHF after the clinical status has been stabilized.
  • See more details in the article on Chronic heart failure (Chronic heart failure)

Evidence Summaries

Management of diuretic resistance

  • Fluid restriction is necessary if fluid overload is evident. A total of 1.5 litres of fluids is adequate to cover the basic needs for 24 hours, but in severe cases fluid intake can be restricted to 0.8–1.0 litres.
  • The natriuretic effect of spironolactone only appears at a daily dose of 50–100 mg but spironolactone is useful in the treatment of hypokalaemia and as prognostically beneficial medication for systolic failure. Any renal failure should be taken into account in the dosage.
  • After special consideration, furosemide may be combined with low doses of metolazone (e.g. 2.5–5 mg once or twice weekly), as long as the patient’s electrolyte balance is carefully monitored. The need for metolazone should be assessed and its use started in a specialized care unit.

Monitoring on the ward

  • Active monitoring of therapeutic response in a surveillance unit and on the ward is the cornerstone of a favourable treatment outcome. The monitoring consists of regular recording of blood pressure, temperature, heart rate and respiration rate, as well as daily weighing. Telemetry monitoring is warranted in selected patients.
  • Patients with heart failure are usually elderly, and bed rest should be avoided to preserve the patient’s physical capacity.
  • If no treatment response is achieved, the treatment should be rapidly intensified within the first 24 hours, at the latest. If the response to treatment is good and congestion has been completely resolved, it should be considered whether treatment could be continued in the patient’s home. Rehabilitation and assessment of the functional capacity can best be carried out with the support of a physiotherapist.
  • It is worth dedicating some of the in-patient time to optimizing the prognostically beneficial medication and to patient education.
  • In patients with systolic heart failure, correction of iron deficiency by ferric carboxymaltose infusion can be considered to lower the risk of recurrent hospitalization.
  • The need for home care services should be evaluated before discharge.

Post-discharge instructions and follow-up care plan

  • The patient should be given instructions for, for example, how to regulate the dose of diuretics.
  • An early follow-up visit or other contact is recommended, and ideally the patient should be given a phone number to use should the heart failure become aggravated despite the instructions given.
  • A good discharge summary, including the results of the most important investigations, post-discharge follow-up plan, instructions how to titrate the medication etc., is indispensable regarding the future care.
    • The discharge summary should also include information about any possible restrictions to care or decision on palliative treatment, in which case the treatment of any aggravation will concentrate on alleviating the symptoms and can be done on a primary care ward, for example.


1. McDonagh TA, Metra M, Adamo M et al. 2021 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure. Eur Heart J 2021;42(36):3599-3726.  [PMID:34447992]
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