Acute left ventricular failure occurs when an acute event results in the left ventricle being unable to move blood efficiently through the left side of the heart and into the systemic circulation.
Cardiac output is the volume of blood ejected by the heart per minute. Stroke volume is the volume of blood ejected during each beat. Cardiac output is the product of stroke volume x heart rate.
When blood cannot flow efficiently through the left side of the heart, there is a backlog of blood waiting in the left atrium, pulmonary veins and lungs. As these areas experience an increased volume and pressure of blood, they start to leak fluid and cannot reabsorb excess fluid from the surrounding tissues, resulting in pulmonary oedema.
Pulmonary oedema is where the lung tissue and alveoli are filled with interstitial fluid. This interferes with normal gas exchange in the lungs, causing shortness of breath and reduced oxygen saturation.
Triggers
Acute left ventricular failure is often the result of decompensated chronic heart failure.
The potential triggers are:
- Iatrogenic (e.g., aggressive IV fluids in a frail elderly patient with impaired left ventricular function)
- Myocardial infarction
- Arrhythmias
- Sepsis
- Hypertensive emergency (acute, severe increase in blood pressure)
TOM TIP: Acute left ventricular failure and pulmonary oedema are common in the acute hospital setting. When a nurse asks you to review a breathless and desaturating patient, ask yourself how much fluid that patient has been given and whether they will be able to cope with that amount. For example, an 85 year old patient with chronic kidney disease and aortic stenosis is prescribed 2 litres of fluid over 4 hours and then starts to drop her oxygen saturation. This is a common scenario, and a dose of IV furosemide can work like magic to clear the excess fluid and resolve the symptoms.
Presentation
Acute LVF typically presents with acute shortness of breath. This is exacerbated by lying flat and improves on sitting up.
Acute LVF causes a type 1 respiratory failure (low oxygen without an increased carbon dioxide).
Symptoms include:
- Shortness of breath
- Looking and feeling unwell
- Cough with frothy white or pink sputum
Signs on examination include:
- Raised respiratory rate
- Reduced oxygen saturations
- Tachycardia (fast heart rate)
- 3rd heart sound
- Bilateral basal crackles (sounding “wet”) on auscultation of the lungs
- Hypotension in severe cases (cardiogenic shock)
There may also be signs and symptoms related to the underlying cause, for example:
- Chest pain in acute coronary syndrome
- Fever in sepsis
- Palpitations with arrhythmias
If they also have right-sided heart failure, you could find:
- Raised jugular venous pressure (JVP), caused by a backlog on the right side of the heart, leading to an engorged internal jugular vein in the neck
- Peripheral oedema of the ankles, legs and sacrum
Assessment
Assessment in patients with acute left ventricular failure includes:
- Clinical assessment (history and examination, starting with an ABCDE approach in any acutely unwell patient)
- ECG to look for ischaemia and arrhythmias
- Bloods for anaemia, infection, kidney function, BNP, and consider troponin if suspecting myocardial infarction
- Arterial blood gas (ABG)
- Chest x-ray
- Echocardiogram
B-type Natriuretic Peptide
B-type natriuretic peptide (BNP) is a hormone released from the heart ventricles when the cardiac muscle (myocardium) is stretched beyond the normal range. A raised BNP blood result indicates the heart is overloaded beyond its normal capacity to pump effectively.
The action of BNP is to relax the smooth muscle in blood vessels. This reduces systemic vascular resistance, making it easier for the heart to pump blood through the system. BNP also acts on the kidneys as a diuretic to promote water excretion in the urine. This reduces the circulating volume, helping to improve the function of the heart in someone that is fluid-overloaded.
BNP is sensitive but not specific. This means that when the result is negative, it helps rule out heart failure, but it can be positive due to other causes. Other causes of a raised BNP include:
- Tachycardia
- Sepsis
- Pulmonary embolism
- Renal impairment
- COPD
Echocardiogram
Echocardiography is helpful in assessing the function of the left ventricle and any structural abnormalities in the heart. A key measure of the left ventricular function is the ejection fraction. This is the percentage of blood in the left ventricle that is squeezed out with each ventricular contraction. An ejection fraction above 50% is considered normal.
Chest X-ray Findings
Cardiomegaly on a chest x-ray is classified as a cardiothoracic ratio of more than 0.5. This is when the diameter of the widest part of the heart (the widest part of the cardiac silhouette) is more than half the diameter of the widest part of the lung fields.
Upper lobe venous diversion may also be seen. Usually, when standing erect, the lower lobe veins contain more blood, and the upper lobe veins remain relatively small. In acute LVF, there is such a back-pressure that the upper lobe veins also fill with blood and become engorged. This is referred to as upper lobe diversion. This is visible as increased prominence and diameter of the upper lobe vessels on a chest x-ray.
Fluid leaking from oedematous lung tissue causes additional x-ray findings of:
- Bilateral pleural effusions
- Fluid in interlobar fissures (between the lung lobes)
- Fluid in the septal lines (Kerley lines)
Management
Patients with acute left ventricular failure require hospital admission. Patients with severe pulmonary oedema or cardiogenic shock may require admission to the high dependency unit or intensive care unit. Get experienced seniors involved early.
The “sodium” mnemonic can be used for remembering the basic management of acute LVF:
- S – Sit up
- O – Oxygen
- D – Diuretics
- I – Intravenous fluids should be stopped
- U – Underlying causes need to be identified and treated (e.g., myocardial infarction)
- M – Monitor fluid balance
Sitting the patient up helps oxygenate the lungs. When lying flat, the fluid in the lungs spreads to a larger area. When upright, gravity takes it to the lung bases, leaving the middle and upper areas clear for better gas exchange.
Oxygen should be given for reduced oxygen saturation (below 95%). As always, be cautious with patients who have COPD, where the target saturations may be 88-92%. An arterial blood gas can help guide oxygen therapy when in doubt.
Diuretics (e.g., IV furosemide) increase the urine output of the kidneys, reducing the volume of fluid in the circulation. Reducing the circulating volume in a fluid-overloaded patient allows the heart to pump blood more effectively.
Fluid balance monitoring involves monitoring the fluid intake (oral and IV), urine output, U&Es and body weight.
Severe cases may require (guided by an experienced specialist):
- Intravenous opiates, such as morphine, which act as vasodilators
- Intravenous nitrates act as vasodilators, and may be considered in severe hypertension or acute coronary syndrome
- Inotropes, such as dobutamine, to improve cardiac output
- Vasopressors, such as noradrenalin, to improve blood pressure
- Non‑invasive ventilation
- Invasive ventilation (involving intubation and sedation)
Inotropes are medications that alter the contractility of the heart. Positive inotropes act to increase the contractility of the heart. This increases cardiac output (CO) and mean arterial pressure (MAP). They are used in patients with a low cardiac output, for example, due to acute heart failure, recent myocardial infarction or following heart surgery.
Vasopressors are medications that cause vasoconstriction (narrowing of blood vessels). This increases the systemic vascular resistance and, consequently, mean arterial pressure (MAP). Vasopressors are commonly used by anaesthetists as a bolus dose or in ICU as an infusion to improve patient’s blood pressure and, therefore, tissue perfusion.
Last updated March 2023
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