Acute heart failure and pulmonary oedema
- In the acute phase of heart failure treatment consists as necessary of oxygen therapy and CPAP therapy, vasodilatation with nitrates, and furosemide which is given initially as intravenous bolus doses followed by a continuous infusion (if necessary). Opioids can be administered according to the symptoms.
- In the presence of low filling pressures, intravenous rehydration may be needed. A fluid challenge using a small amount of fluid must be carried out before rehydration is commenced.
- If severe congestion or organ hypoperfusion are not corrected in systolic heart failure, the cardiac pumping function is improved by inotropic medication (levosimendan).
- The correction of the underlying cause and aggravating factors is crucial for a favourable outcome.
- Intensive care treatment and interventional therapies should only be considered if the patient can be thought to have a chance of recovery or the dysfunction of the heart can be considered to be reversible.
- In severe chronic heart failure, the patient's wishes regarding further medical care (living will) should be explored in good time.
- Acute heart failure (AHF) is a cardiovascular disease that uses a considerable amount of medical resources.
- The patient presents either with new, previously undiagnosed heart failure or with a worsening of chronic pre-existing heart failure.
- Heart failure can be either diastolic or systolic. In elderly patients, diastolic dysfunction is more common and is often exacerbated by tachycardia.
- AHF must be diagnosed and treated immediately.
- Heart failure is a multifaceted disorder. The most common causes of heart failure are coronary heart disease and hypertension, which are both present in more than half of the patients. Valvular diseases are the third most common cause of heart failure.
- AHF can be divided into different categories according to its clinical presentation. The most serious cases include cardiogenic shock, pulmonary oedema and right heart failure. Milder forms are decompensated congestive heart failure and hypertensive heart failure. About one third of cases are related to acute coronary syndrome (ACS).
Assessment of clinical status
- Does the patient have signs of congestion and organ hypoperfusion (see table T1)?
- Signs of pulmonary congestion include coarse and fine crackles which may be associated with airway obstruction, early diastolic ventricular gallop (S3), increased jugular venous pressure, pitting oedema, hepatomegaly and hepatojugular reflux.
- Signs of hypoperfusion include decreased level of consciousness, drowsiness, confusion, cool peripheries, cyanosis and decreased diuresis. All these signs need urgent management. The point where the extremities start to feel cool should be recorded and any changes noted. An increase in the plasma lactate concentration to over 2 mmol/l and metabolic acidosis are signs of hypoperfusion.
Table 1. Clinical assessment of congestion and hypoperfusion
|Assessment of congestion||Assessment of hypoperfusion|
|Jugular venous pressure||Skin temperature, cyanosis|
|Palpation of the liver||Alertness, consciousness|
|Pitting oedema||Urine output|
|Lung auscultation||Acid-base balance, lactate|
Laboratory test and imaging studies
- An ECG is recorded immediately in order to diagnose ischaemia and verify the rhythm.
- First line laboratory tests include blood counts, plasma potassium, sodium and creatinine as well as CRP.
- If an 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 related to severe heart failure. Increased left ventricular end diastolic pressure may also lead to subendocardial ischaemia and, moreover, advanced heart disease may be associated with silent myocardial injury.
- In advanced cases, metabolic acidosis in an arterial blood gas analysis and an increased lactate level are indicative of severe hypoperfusion.
- Plasma NT-proBNP (N-terminal probrain natriuretic peptide) and BNP (brain natriuretic peptide) provide a useful additional tool for differentiating heart failure from other aetiologies of dyspnoea. However, other factors such as age, fast arrhythmias, renal failure and pulmonary embolism may also increase the values.
- A chest x-ray permits assessment of pulmonary congestion, pleural fluid accumulation and extravasation of fluid from the intravascular to the interstitial space. A moderately increased pulmonary capillary pressure will gradually lead to fluid infiltration into the interstitium of the lungs and to the appearance of Kerley B lines (interstitial extravasation i.e. pulmonary oedema). A greatly increased pulmonary capillary pressure will lead to an accumulation of fluid in the alveoli (alveolar pulmonary oedema) which in turn will cause acute severe dyspnoea and hypoxaemia, which equates to clinical acute pulmonary oedema.
- If hypoxaemia and dyspnoea can be explained by pulmonary oedema, there is no need to proceed with unnecessary procedures, such as medical imaging studies for 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 also be avoided as it is well known that the clinical condition will improve before the x-rays!
- An echocardiogram should be obtained without delay if the patient is in cardiogenic shock, and within a couple of days unless up to date information is available. Echocardiogram is also a tool for quick estimation of cardiac filling pressures.
- Pulmonary ultrasound may be used to establish heart failure: fluid retention in the interlobular space causes so-called B-line echoes. Additionally, it can quickly establish the presence of pleural effusion.
- Pulmonary embolism
- Acute coronary syndrome
- Exacerbation of asthma or COPD
- Parenchymal lung diseases
- Pneumothorax, pleural effusion
Triggering and aggravating factors
- Atrial fibrillation
- Febrile infection
- Physical or mental stress
- Excessive fluid therapy
- Unsuitable drug therapy (e.g. NSAIDs)
- Inadequate adherence to treatment
Starting treatment and treatment of congestive heart failure
- Insert an i.v. line after the initial examination.
- Monitor the patient’s heart rhythm, blood pressure and oxygen saturation.
- Consider the need for direct arterial blood pressure measurements in patients whose haemodynamic status is unstable.
- A half-sitting position is best if the patient has severe dyspnoea.
- Relieve dyspnoea and anxiety in the initial phase of treatment and also provide vasodilatation.
- Should be used carefully, as they low down the heart rate, which should be taken into account in patients with bradycardia. May induce nausea.
- Initially a bolus dose of 2–4 mg intravenously, followed as necessary by repeat doses every 10 minutes.
- If the patient is hypoxaemic (oxygen saturation < 90%), oxygen should be administered initially via a venturi mask (8 l/min). In severe pulmonary oedema, CPAP (continuous positive airway pressure) therapy 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.
- Prolonged use of CPAP mask ventilation should be avoided as the therapy may increase the risk of aspiration. When dyspnoea and hypoxaemia have improved, the patient is weaned off the CPAP therapy by gradually reducing the amount of PEEP.
- High PEEP may cause hypotension if cardiac filling pressures are low.
- Noninvasive positive pressure ventilation via a ventilator is beneficial especially for hypoventilating patients.
- 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.
- The patient should be given nitrates, unless blood pressure is very low (systolic BP < 90 mmHg).
- In the initial phase, nitroglycerine spray or sublingual tablets can be administered.
- A nitrate infusion should be commenced with a low starting dose (e.g. 12 ml/hour with the concentration of 0.1 mg/ml) in order to prevent abrupt hypotension. The dose should, however, be actively increased while monitoring the blood pressure and the treatment response. A large drop in blood pressure at the beginning of the therapy is suggestive of hypovolaemia.
- Hypertension should be promptly and effectively treated.
- Sodium nitroprusside acts mainly by dilating the arteries, and its specific indication is hypertensive heart failure.
- It should be borne in mind that the initial treatment of oliguria is not always a diuretic; in hypovolaemia rehydration is the treatment of choice. Patients with a recent-onset or hypertensive heart failure are not necessarily overloaded, and diuretics are not indicated for them.
- In advanced heart failure, oral medication may not be well absorbed. If the patient has clinical signs of congestion, furosemide 20–40 mg (or at least at a dose that corresponds to the medication used at home) should be administered intravenously.
- In the acute phase, an administration of intravenous furosemide 3–4 times per 24 hours will usually produce the desired effect, but administration twice daily may be sufficient.
- In more serious cases, hourly urine measurements and a fluid balance chart are required. Daily weighing and monitoring of plasma creatinine, potassium and sodium is recommended.
- An infusion of furosemide guarantees an even treatment response and is an option in patients who require frequent bolus doses. The infusion is usually started at 10 mg/hour and increased in increments, up to 40 mg/hour, but in some patients doses as low as 2–4 mg/hour may produce the desired effect.
- The response to diuretics takes longer to become apparent than the response to nitrates or CPAP therapy.
- 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 is suggestive of hepatic dysfunction due to hypoperfusion and/or congestion. It is therefore recommended that, whilst severe heart failure is treated in a hospital, warfarin is temporarily changed to heparin.
- The management of the haemodynamic status of a hypotensive and shocked patient is started with a fluid challenge: about 200 ml of crystalloids are administered over 20–30 minutes and the patient is observed for the improvement of the clinical status and also for the possible worsening of congestive symptoms.
- The combination of shock and pulmonary oedema often requires intubation and mechanical ventilation.
- Disturbed organ perfusion is an alarm sign that requires immediate intervention even if the patient remains normotensive. Metabolic acidosis and lactaemia indicate severe perfusion deficit.
- More intensive treatment should only be undertaken if the patient can be considered to have a chance of recovery.
- Angiography and balloon dilatation procedure should be carried out without delay if the patient is in cardiogenic shock due to myocardial infarction. It is usually not possible to reverse this condition unless revascularisation is an option.
- If rehydration does not reverse the shock, the perfusion of vital organs must be ensured with medication that increases blood pressure. Mean arterial pressure should be brought to a level that ensures diuresis and an adequate level of consciousness, usually to above 65 mmHg.
- It is safer to use noradrenaline than dopamine to increase blood pressure.
- If severe congestion or organ hypoperfusion are not corrected in systolic heart failure, the cardiac pumping function is improved by inotropic medication (levosimendan).
- In a severe shock, extracorporeal oxygenation (ECMO) or mechanical circulatory assist devices may be used.
- Positive pressure airway support for cardiogenic pulmonary oedema
- CPAP and BiPAP non-invasive ventilation in patients with acute cardiogenic pulmonary oedema
- Nitrates for acute heart failure syndromes
- Administration of loop diuretics in acutely decompensated heart failure
- Levosimendan vs dobutamine for patients with acute decompensated heart failure
Beta-blockers, ACE inhibitors and ATR blockers
- The use of beta-blockers, ACE inhibitors and ATR blockers should be continued using the highest dose that the patient is able to tolerate haemodynamically, and their discontinuation is rarely needed except in the presence of shock.
- In new patients, the use of these drugs should be started slowly after the acute phase 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 to stop treatment.
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.
- It is worth combining differently acting diuretics rather than prescribing large doses of one agent. If renal function is satisfactory a thiazide diuretic may be added. In most cases the best combination is furosemide and spironolactone.
- Caution should be exercised in the administration of aldosterone antagonists if the patient has moderate renal insufficiency (creatinine clearance 30–59 ml/min). The treatment is contraindicated in severe renal insufficiency (creatinine clearance less than 30 ml/min).
- Treatment-resistant hypokalaemia may be caused by coexistent hypomagnesaemia, even if plasma magnesium concentrations were normal. Hypomagnesaemia may be corrected, for example with oral magnesium hydroxide 250 mg one to three times daily, or with 40–60 mmol of intravenous MgSO4 administered during the acute phase.
- Hydrochlorothiazide 25 mg combined with furosemide may improve diuresis in a diuretic-resistant patient. An alternative to hydrochlorothiazide is metolazone (on special licence only), which may be sufficient as a single dose (2.5–5 mg).
- If it is not possible to remove a sufficient amount of fluid with drug therapy, ultrafiltration may be used to remove several litres of fluid.
Treatment of the underlying cause
- The factors and underlying morbidities that precipitated AHF must always be identified. An ACS is the underlying cause in as many as one in three cases of AHF, and it always warrants further invasive investigations.
- Other causes requiring acute treatment include arrhythmias, hypertension and, as the cause of acute insufficiency of the right side of the heart, pulmonary embolism.
- Causes requiring surgical management should also be investigated during the acute treatment phase.
- Echocardiography is the most useful investigation when structural abnormalities of the heart are suspected.
- Infections are common precipitating factors of AHF. The most common sites of infection should be investigated and all infections treated as efficiently as possible.
- The prevalence of anaemia increases with the severity of heart failure. The majority of heart failure patients are taking either warfarin or aspirin, and anaemia due to bleeding or iron deficiency should be ruled out.
- A red cell transfusion to correct anaemia should only be considered in patients with acute ischaemia. The transfusion must be administered slowly to prevent the worsening of heart failure. In these cases, the haemoglobin target level should be 100 g/l.
Monitoring on the ward
- A continuous monitoring of the effects of the treatment, on a high dependency unit or a general ward, is the cornerstone of a favourable treatment outcome. The monitoring consists of regular recordings of the blood pressure, temperature, heart rate and respiration rate. The patient should also be weighed daily. Telemetry monitoring is warranted in selected patients.
- Patients with heart failure are usually elderly. Unnecessary prolongation of bed rest will hinder the restoration of the patient’s physical capacity and postpone the discharge home.
- If no treatment response is achieved, the treatment should be intensified during the first few days. If the response to treatment is good, it should be considered whether treatment could be continued at the patient’s home. Rehabilitation and assessment of the functional capacity can be carried out by a physiotherapist.
- It is worth dedicating some of the in-patient time to patient education.
- The need for home care services should be evaluated before discharge.
Post-discharge instructions and follow-up care
- On discharge, comprehensive treatment instructions must be given both to the patient and the physician in charge of the follow-up care.
- 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 possible restrictions to the care, for example, regarding resuscitation.
- The patient should be given instructions about self-care management, for example how to regulate the dose of diuretics.
- Ideally the patient is given a phone number to use should the instructions given not improve his/her condition.
Advance decisions (living will)
- Whilst end-stage heart failure remains stable and before an acute exacerbation, advance decisions regarding further care should be discussed with the patient.
- The seriousness of the condition and, for example, the decision not to resuscitate, should be broached with the patient and/or his/her relatives. A decision regarding limitations to care must be clearly recorded in the patient’s notes. The patient’s own wishes must always be taken into account.
- A general ward of a district hospital can be used to treat an acute worsening of heart failure when the cause of the heart failure is known and if it has been agreed that intensive care treatment and invasive therapies are not an option.
1. Ponikowski P, Voors AA, Anker SD 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. Eur J Heart Fail 2016;18(8):891-975. [PMID:27207191]
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