Acute Left Ventricular Failure: Recognition and Emergency Management

Introduction

Acute left ventricular failure (LVF) is the sudden failure of the left ventricle to maintain an adequate cardiac output, causing blood to back up into the pulmonary circulation and fluid to accumulate in the lungs. The result is cardiogenic pulmonary oedema, and it is a medical emergency.¹

It presents either as a first episode, or as decompensation in someone with known chronic heart failure - the second is far more common. Acute heart failure accounts for a large share of emergency medical admissions in the UK, and in-hospital mortality remains around 10%.²

The distinction from chronic heart failure matters. Chronic heart failure is a syndrome managed over months with drugs that improve survival. Acute LVF is a presentation managed over hours with drugs that relieve congestion - and the two use largely different treatments.

Pathophysiology

The sequence is worth understanding because every sign and every treatment follows from it:

1. The left ventricle cannot eject its volume, so left ventricular end-diastolic pressure rises
2. That pressure is transmitted backwards to the left atrium, and then to the pulmonary veins and capillaries
3. Once pulmonary capillary hydrostatic pressure exceeds plasma oncotic pressure, fluid moves into the interstitium - this is interstitial oedema, and it is what produces Kerley B lines
4. As pressure rises further, fluid floods the alveoli, and gas exchange fails - producing hypoxia and the classic frothy sputum

Fluid in the alveoli increases the diffusion distance for oxygen, so patients characteristically have type 1 respiratory failure: low oxygen with a normal or low carbon dioxide, because they are hyperventilating. A rising carbon dioxide is an ominous sign of exhaustion.

Lying flat redistributes blood from the legs into the central circulation and raises pulmonary capillary pressure further. This is why patients are orthopnoeic, why they describe waking at night gasping (paroxysmal nocturnal dyspnoea), and why sitting them upright is the first thing you do.

Causes and precipitants

In a patient with known heart failure, always look for the precipitant. Treating the pulmonary oedema without addressing what caused it means the patient returns within days.

Clinical features

The patient is typically acutely breathless, distressed, sweaty and unable to lie flat. Onset is over minutes to hours.

• Breathlessness at rest, of sudden onset
• Orthopnoea - ask concretely how many pillows they sleep on, and whether that has changed
• Paroxysmal nocturnal dyspnoea - waking suddenly gasping for breath and having to sit up or open a window
• Cough, sometimes productive of pink frothy sputum in severe cases
• Fatigue, and a sense of drowning or suffocation
• Ankle swelling if there is coexistent right heart failure

Ask directly about chest pain and palpitations, since ACS and arrhythmia are the two precipitants that change immediate management most. Also establish the drug history, recent fluid administration, and whether the patient has been taking their usual diuretic.

Clinical examination

This is a diagnosis made largely at the bedside, and the examination should be quick and focused because treatment is time-critical.

• General: sitting upright, distressed, sweaty, pale, using accessory muscles
• Observations: tachypnoea, tachycardia, low oxygen saturations, and blood pressure - which may be high (hypertensive pulmonary oedema) or low (cardiogenic shock)
• Respiratory: bibasal fine inspiratory crackles; expiratory wheeze from peribronchial oedema, sometimes called cardiac asthma and easily mistaken for an asthma or COPD exacerbation
• Cardiovascular: raised JVP, displaced apex beat, a third heart sound (S3, gallop rhythm), and any murmur - a new pansystolic murmur suggests acute mitral regurgitation
• Peripheries: cool and clammy if output is low; peripheral oedema if there is chronic right-sided involvement

The Killip classification grades severity in the context of myocardial infarction and is a useful shorthand: I - no crackles; II - crackles in less than half the lung fields or an S3; III - frank pulmonary oedema; IV - cardiogenic shock. Mortality rises steeply with class.

Differential diagnosis

Acute breathlessness has a short but critical differential, and several of these are treated in opposite ways:

• Pneumonia - fever, focal crackles and consolidation rather than bibasal changes; the two frequently coexist
• Exacerbation of asthma or COPD - wheeze predominates, and the history distinguishes; giving a fluid bolus here, or a beta-blocker, would be harmful
• Pulmonary embolism - pleuritic pain, clear lung fields, hypoxia out of proportion to the examination
• Acute respiratory distress syndrome - bilateral infiltrates but a non-cardiogenic cause, with a normal JVP and no cardiomegaly
• Anaphylaxis - urticaria, angioedema, stridor and an obvious trigger
• Anxiety and hyperventilation - a diagnosis of exclusion, never made in the presence of hypoxia

Investigations

Investigations run alongside treatment, not before it. A patient in frank pulmonary oedema needs sitting up and a diuretic before anyone waits for a blood result.

Bedside

• ECG - looking for acute coronary syndrome, atrial fibrillation and other arrhythmias, and left ventricular hypertrophy. It is rarely completely normal in acute heart failure.
• Arterial blood gas - typically type 1 respiratory failure. A rising CO₂ or a metabolic acidosis indicates exhaustion or poor perfusion and warrants urgent escalation.
• Observations and continuous monitoring, plus a fluid balance chart and daily weights

Bloods

• BNP or NT-proBNP - released by ventricular myocytes in response to stretch. Their value is in ruling out: an NT-proBNP below 300 ng/L (or BNP below 100 ng/L) makes acute heart failure very unlikely.¹
• Troponin - to identify ACS as the precipitant, though it may be mildly raised by the strain of heart failure itself
• U&Es - baseline renal function before diuresis, and potassium, which diuretics will lower
• FBC - anaemia both precipitates and worsens heart failure
• TFTs, LFTs, glucose - thyrotoxicosis as a precipitant, hepatic congestion, and comorbidity

Imaging

A chest X-ray is the classic investigation, and the pattern is a reliable exam question. Remember it as ABCDE:

Transthoracic echocardiography identifies the cause and assesses left ventricular function, valve disease and pericardial effusion. NICE recommends echocardiography within 48 hours of admission for anyone with new suspected acute heart failure.¹ Point-of-care lung ultrasound showing B-lines is increasingly used at the bedside and is more sensitive than the chest X-ray.

Management

Treatment is simpler than students expect, and much of the traditional teaching has been withdrawn. The evidence-based core is sit up, oxygen if hypoxic, intravenous loop diuretic, treat the cause.

Immediate measures

1. Sit the patient upright. This reduces venous return and redistributes fluid away from the upper lobes. It is free, immediate and effective.
2. Oxygen, but only if hypoxic. Target saturations of 94-98%, or 88-92% in those at risk of hypercapnic respiratory failure.
3. Intravenous loop diuretic - furosemide 40-80 mg IV, with the dose guided by previous exposure. Someone already on a large oral dose needs more.
4. Continuous monitoring, strict fluid balance and daily weights - weight is the most reliable measure of whether diuresis is working.
5. Identify and treat the precipitant - PCI for ACS, rate or rhythm control for fast AF, antibiotics for sepsis.

If the patient does not improve

• Non-invasive ventilation (CPAP) - consider in cardiogenic pulmonary oedema with severe breathlessness and acidaemia. Positive pressure forces fluid out of the alveoli and reduces the work of breathing.
• Invasive ventilation - for exhaustion, a falling conscious level, or persisting hypoxia and acidosis
• Inotropes and vasopressors - only in cardiogenic shock, and only in a critical care setting with haemodynamic monitoring
• Ultrafiltration - considered where there is diuretic resistance
• Mechanical support or surgery - for mechanical complications such as papillary muscle rupture or a ventricular septal defect

Once stabilised

The transition to chronic heart failure therapy begins before discharge, and one point is frequently examined:

Before discharge: confirm the diagnosis with echocardiography, start or optimise disease-modifying therapy for chronic heart failure, arrange specialist heart failure team follow-up within two weeks, and refer to cardiac rehabilitation.

Complications

• Cardiogenic shock - hypotension with organ hypoperfusion; mortality remains high
• Acute kidney injury - from poor forward flow, venous congestion of the kidneys, and aggressive diuresis. Cardiorenal syndrome is the difficult balance between relieving congestion and preserving renal function.
• Electrolyte disturbance - loop diuretics cause hypokalaemia, hyponatraemia and hypomagnesaemia, each of which is arrhythmogenic
• Arrhythmia - both a cause and a consequence
• Respiratory failure requiring ventilatory support
• Recurrent admission - each decompensation is associated with a stepwise worsening of long-term prognosis

Red flags

Prognosis

Acute heart failure carries a serious prognosis. In-hospital mortality is around 10%, and roughly a quarter of patients are readmitted within three months.² Mortality at one year after an admission approaches 30%, which is worse than many common cancers.

Outcome is determined largely by the underlying cause and by whether it is reversible. Pulmonary oedema caused by a treatable precipitant - fast atrial fibrillation, an anaemia, a hypertensive crisis - may resolve completely. Decompensation of established severe left ventricular impairment carries a much poorer outlook.

The most modifiable factor is what happens after the acute episode. Specialist heart failure follow-up, optimisation of disease-modifying drugs, and cardiac rehabilitation all reduce readmission and mortality, and an admission should be treated as the opportunity to get those started.