Treatment of acute heart failure

At a glance

1. Treatment moves through three phases: first save life and relieve breathlessness, then remove the congestion and find the cause, then start the long-term drugs before discharge and see the patient often over the next 6 weeks, first within 1 to 2 weeks.
2. Look at once for the seven causes that need their own urgent treatment: an acute coronary syndrome, a hypertensive emergency, an arrhythmia, a mechanical cause, pulmonary embolism, infection and tamponade.
3. Oxygen is for hypoxaemia, non-invasive ventilation for respiratory distress, and intravenous loop diuretics for congestion, at twice the usual oral dose, with the response checked by urinary sodium and urine output.
4. Vasodilators such as nitrates help when the blood pressure is high, and are avoided when it is low. Routine morphine is no longer used.
5. Inotropes and vasopressors are only for cardiogenic shock, with mechanical support for selected patients in a specialist centre.
6. Patients go home free of congestion and on the long-term heart failure drugs, which are increased quickly in the weeks after discharge.

01Definition and overview

The treatment of acute heart failure has short-term aims (keeping the patient alive, relieving breathlessness, restoring oxygenation and perfusion, removing congestion) and long-term aims (preventing readmission and death). European guidance arranges it in three phases:

The first treatment depends on the patient's profile: congested or not (wet or dry) and perfused or not (warm or cold). Most patients are warm and wet and need diuretics, with vasodilators if the blood pressure is high. Cold and wet patients, in cardiogenic shock, need support of the circulation as well.

02Etiology and pathophysiology

What the treatment targets

• Congestion, the main problem in nearly all patients: a raised filling pressure, fluid in the lungs and the tissues, and venous congestion of the kidneys and the liver. Diuretics remove the fluid; vasodilators lower the filling pressure quickly by moving blood into the veins and lowering the afterload.
• Hypoperfusion, in a minority: low output and organ failure. Inotropes and vasopressors raise the output and the pressure, at the cost of oxygen use and arrhythmias, and mechanical devices take over the work of the heart.
• The cause and the trigger, without whose treatment the patient will not improve or will return.

How the main drugs work

• Loop diuretics (furosemide, bumetanide, torasemide) block the Na-K-2Cl cotransporter in the thick ascending limb of the loop of Henle. Intravenous furosemide also dilates the veins within minutes, before the diuresis begins. Their effect is limited by poor gut absorption in a congested bowel, by reduced delivery to the kidney, by a rebound sodium retention once each dose wears off, and by the distal tubule growing and taking up more sodium in chronic use. This is why intravenous doses, higher doses, repeated doses and a second diuretic that acts elsewhere in the nephron are needed.
• Thiazides (and metolazone) block sodium uptake in the distal tubule, and acetazolamide blocks it in the proximal tubule; added to a loop diuretic, each blocks a site of compensation (sequential nephron blockade).
• Nitrates dilate the veins at low doses, lowering the preload, and the arteries at higher doses, lowering the afterload. Nitroprusside is a strong arterial and venous dilator.
• Inotropes raise contractility: dobutamine through β1-receptors, milrinone by inhibiting phosphodiesterase 3, and levosimendan by sensitising troponin C to calcium. Vasopressors (noradrenaline) raise the pressure through α-receptors.

03Clinical features

Judging severity

At arrival, the bedside signs place the patient:

• respiratory distress: a respiratory rate above 25 a minute, an oxygen saturation below 90 per cent, use of the accessory muscles;
• congestion: crackles, a raised JVP, oedema, hepatomegaly;
• perfusion: cold, clammy skin, confusion, oliguria, a narrow pulse pressure, a raised lactate;
• blood pressure: high (hypertensive pulmonary oedema), normal, or low (shock).

Judging response

The patient is weighed every day, with fluid balance charted. Breathlessness, the respiratory rate, the oxygen need and the signs of congestion are reviewed daily. Creatinine and electrolytes are checked every day while on intravenous diuretics. In the first hours, the urinary sodium and the urine output show whether the diuretic dose is enough. A small rise in creatinine during effective decongestion is expected and is not a reason to stop. A patient who leaves hospital still congested is likely to come back.

04Diagnosis and management

Breathing

• Oxygen when the saturation is below 90 per cent or the arterial oxygen is below 8 kPa, not routinely, because hyperoxia constricts vessels.
• Non-invasive ventilation (CPAP or bilevel) for respiratory distress: it reduces the work of breathing, recruits flooded alveoli, lowers the preload and the afterload of the left ventricle, and relieves breathlessness faster. It is used with care when the blood pressure is low.
• Intubation and mechanical ventilation when hypoxaemia, hypercapnia and exhaustion progress despite this.

Diuretics

• Intravenous furosemide at once for congestion: 40 mg in a patient not taking diuretics, or twice the usual daily oral dose (more in chronic kidney disease), as boluses or an infusion.
• The response is checked early: a spot urinary sodium of at least 70 mmol/L after 2 hours, or a urine output of at least 100 mL an hour over the first 6 hours. If the response is inadequate, the dose is doubled or, in a patient already on loop diuretics, a second diuretic is added: acetazolamide, which in a large trial increased successful decongestion, or a thiazide. If congestion persists with less than 3 litres of urine in the first day, the loop dose is raised towards the maximum and other diuretics are added. Potassium, magnesium and sodium are watched closely.
• When even maximal diuretics fail, ultrafiltration may be considered in selected patients, though its benefit is unproven.
• Diuresis continues until all signs of congestion have gone, and the patient goes home on the lowest oral dose that keeps them dry.

Vasodilators and other drugs

• Intravenous nitrates (glyceryl trinitrate) can be given when the systolic pressure is above about 110 mmHg, and they are the main treatment of hypertensive pulmonary oedema, with nitroprusside as an alternative. The pressure is monitored closely. Nitrates are avoided in hypotension, and in severe aortic stenosis and obstructive cardiomyopathy.
• Morphine is no longer given routinely: it eases distress, but it causes nausea, depresses breathing and was linked to worse outcomes in observational studies. It is kept for severe pain or anxiety.
• Thromboprophylaxis with low-molecular-weight heparin, unless the patient is already anticoagulated.
• Long-term drugs: beta-blockers are continued unless the patient is in shock or has severe bradycardia, and ACE inhibitors, ARNI and mineralocorticoid antagonists are reduced or paused only for hypotension, hyperkalaemia or severe kidney injury. SGLT2 inhibitors are started in hospital once the patient is stable.
• Fast atrial fibrillation: beta-blockers if the patient is stable; digoxin or intravenous amiodarone if not; electrical cardioversion if the arrhythmia is driving the instability.

Cardiogenic shock

Cardiogenic shock needs a team (heart failure cardiology, interventional cardiology, cardiac surgery and intensive care) and transfer to a centre that can provide mechanical support.

• An ECG and echocardiography at once. Immediate coronary angiography and revascularisation of the culprit artery when shock follows an acute coronary syndrome.
• Fluids only if the filling is low, as in right ventricular infarction.
• Inotropes (dobutamine, or milrinone or levosimendan, which act beyond the β-receptor and are preferred in a patient on beta-blockers) for low output with hypoperfusion, at the lowest dose for the shortest time.
• A vasopressor, preferably noradrenaline, to restore perfusion pressure when it is too low.
• Temporary mechanical circulatory support for selected patients: a microaxial flow pump in selected patients with shock from an ST-elevation infarction, which in a trial reduced death at six months from about 59 to 46 per cent. It is not used in every patient with infarct-related shock, because it causes bleeding and vascular injury. Extracorporeal membrane oxygenation did not reduce deaths when used routinely in infarct-related shock, and it is kept for selected patients as a bridge to recovery, a decision or transplantation. The intra-aortic balloon pump did not reduce mortality in infarct-related shock and is no longer used routinely, though it still has a role in mechanical complications such as a ruptured septum or acute mitral regurgitation, as a bridge to surgery.
• Patients who do not recover go on to a durable ventricular assist device or transplantation, or to palliative care.

Particular presentations

• Hypertensive acute pulmonary oedema: sit the patient up; intravenous nitrates and non-invasive ventilation, with diuretics. The fluid has mostly moved into the lungs rather than accumulated, so vasodilators matter more than large doses of diuretic. The pressure is brought down promptly (European hypertension guidance aims for a systolic below 140 mmHg) while avoiding hypotension, and the patient often improves dramatically.
• Acute coronary syndrome: treated as an emergency with reperfusion, as in STEMI.
• Mechanical causes, such as acute mitral regurgitation, a ruptured septum, aortic dissection or tamponade, need urgent surgery or drainage.
• Isolated right ventricular failure: diuretics for the systemic congestion, which is the usual picture; fluids only when the filling is low, as in right ventricular infarction; treatment of the cause (reperfusion of a right ventricular infarction, or of a pulmonary embolism); vasopressors and inotropes for shock; non-invasive ventilation with caution, because it can lower the output.

Before and after discharge

• No signs of congestion, a stable dose of oral diuretic for at least a day, and stable kidney function.
• The long-term heart failure drugs started or restarted before discharge, and increased quickly afterwards: in a large trial, reaching full doses within about two weeks with close follow-up reduced death or readmission at six months from about 23 to 15 per cent.
• A clinic visit within 1 to 2 weeks of discharge, then frequent visits over the first 6 weeks while the drugs are increased, education about daily weights and symptoms, a heart failure nurse, and cardiac rehabilitation.
• Intravenous iron before discharge for patients with iron deficiency.

05Epidemiology

About 8 to 9 in 10 patients admitted with acute heart failure receive intravenous diuretics, most within the first hour or two. Vasodilators are used in about 1 in 5 in European practice, mostly in hypertensive presentations, and inotropes in about 1 in 8, mostly in shock. Non-invasive ventilation is needed by roughly 1 in 10. Readmission is common: about 1 in 4 patients returns within a month or two, most often with congestion, and many leave hospital on fewer or lower doses of the long-term drugs than they should.

06Prognosis

Most patients improve within days with diuretics and treatment of the trigger. No drug given in the acute phase, other than treatment of the cause, has been shown to lower mortality, and inotropes may raise it in patients who are not in shock. What changes the outlook is what happens afterwards: leaving hospital free of congestion, on the long-term drugs at rising doses, with early follow-up. About 1 in 4 patients dies within a year of an admission, and cardiogenic shock still kills about 4 in 10 in hospital despite modern treatment.

Check yourselfAnswer, then say how sure you were: a lucky guess still counts as a weak point.

1When should oxygen be given to a patient with acute heart failure?

To every patient, at 15 litres a minuteOnly when there is chest painNever in a patient who also has COPDWhen the oxygen saturation is below 90 per cent or the arterial oxygen below 8 kPa

2A man who takes oral furosemide 80 mg a day is admitted with worsening breathlessness and oedema. What is a suitable first intravenous dose?

20 mg160 mg1000 mgNone; a nitrate infusion alone is enough

3How is the response to the first dose of an intravenous loop diuretic judged early?

A urinary sodium of at least 70 mmol/L after 2 hours, or a urine output of at least 100 mL an hour over the first 6 hoursA fall in the serum creatinine by the next morningDisappearance of the ankle oedema within an hourA weight loss of 5 kg on the first day

4Which patient with acute heart failure needs an inotrope?

A congested patient with a blood pressure of 170/100 mmHgA congested patient with a blood pressure of 120/70 mmHg and warm handsA congested patient with a blood pressure of 80/50 mmHg, cold peripheries, confusion and a rising lactateAny patient with an ejection fraction below 30 per cent

5After an admission for acute heart failure with a reduced ejection fraction, what has been shown to reduce death and readmission?

Rapid up-titration of the heart failure drugs, with close follow-up in the weeks after dischargeRegular morphine for breathlessnessContinuing an inotrope infusion at homeAn intra-aortic balloon pump before discharge