Cardiac Failure (Heart Failure)

Medicine > Cardiovascular

Background Knowledge 🧠

Definition

A clinical syndrome where the heart is unable to pump blood at a rate commensurate with the requirements of the metabolising tissues, or can only do so with an elevated filling pressure.

Classification

Systolic: Impaired ejection (commonly reduced ejection fraction).
Diastolic: Impaired filling (normal ejection fraction but reduced compliance).
Based on presentation: Acute vs. Chronic.
Based on side of heart affected: Left, right, or biventricular failure.

Pathophysiology

Reduced cardiac output → Activation of renin-angiotensin-aldosterone system & sympathetic nervous system → Fluid retention & vasoconstriction → Worsens cardiac workload.

Aetiology/Risk Factors

Primary cardiac: Ischaemic heart disease, hypertension, valvular heart disease, cardiomyopathies.
Systemic: Thyroid disease, anaemia, high output states, chronic kidney disease.
Toxins/Drugs: Alcohol, chemotherapy, cocaine use.
Others: Infections (e.g., myocarditis), arrhythmias, constrictive pericarditis.

Clinical Features 🌡️

Clinical Features

Left-Sided Failure: Dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea, pulmonary oedema.
Right-Sided Failure: Peripheral oedema, ascites, hepatic congestion, raised jugular venous pressure (JVP).
General: Fatigue, palpitations, reduced exercise tolerance.

Investigations 🧪

Investigations

ECG: May show signs of underlying cause (e.g., ischaemia, arrhythmia).
Chest X-ray: Cardiomegaly, pulmonary congestion, pleural effusion.
Echocardiography: Assess chamber sizes, function, and valvular abnormalities.
Bloods: NT-proBNP, electrolytes, renal function, liver function, thyroid function.

Management 🥼

Management

Lifestyle: Salt & fluid restriction, smoking cessation, weight management, exercise.
Pharmacotherapy: Diuretics, ACE inhibitors/ARBs, beta-blockers, mineralocorticoid receptor antagonists, digoxin.
Devices: Implantable cardioverter-defibrillator (ICD), cardiac resynchronisation therapy (CRT).
Severe cases: Left ventricular assist device (LVAD), heart transplantation.

Prognosis

Prognosis is generally poor.
Approximately 50% of patients with heart failure die within 5 years of the diagnosis.

Complications

Cardiogenic shock
Arrhythmias
Thromboembolism (e.g., stroke)
Cardiac cachexia

Key Points

Cardiac failure is a complex clinical syndrome with various underlying causes and presentations.
Management is multifaceted and tailored to the patient’s needs and underlying aetiology.
Early diagnosis and intervention can improve the quality of life and prognosis.

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31588

Typical symptoms of cardiac failure include which one of the following?

31591

Which of these is a cause of high-output heart failure?

31547

Which of the following drugs decreases the mortality associated with heart failure?

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53.06% of users got this question correct

ACE (Angiotensin-Converting Enzyme) inhibitors decrease mortality in heart failure due to several mechanisms:

Suppression of the Renin-Angiotensin-Aldosterone System (RAAS):
- ACE inhibitors block the conversion of angiotensin I to angiotensin II, reducing the production of angiotensin II, a potent vasoconstrictor.
- Lower levels of angiotensin II result in decreased vasoconstriction, leading to vasodilation and reduced afterload on the heart.
- Suppression of angiotensin II also reduces aldosterone secretion, leading to decreased sodium and water retention, thereby reducing preload on the heart.
Anti-Remodelling Effects:
- Chronic activation of the RAAS in heart failure leads to adverse cardiac remodelling, characterized by myocardial hypertrophy, fibrosis, and dilation of the ventricles.
- ACE inhibitors attenuate cardiac remodelling by inhibiting aldosterone secretion, reducing myocardial hypertrophy, and decreasing collagen deposition in the myocardium.
Improved Hemodynamic:
- Vasodilation induced by ACE inhibitors reduces systemic vascular resistance, resulting in decreased cardiac workload and improved cardiac output.
- This leads to improved hemodynamic, including increased stroke volume and cardiac index, and decreased pulmonary capillary wedge pressure.
Decreased Neurohormonal Activation:
- ACE inhibitors reduce sympathetic nervous system activation and the release of norepinephrine, which contribute to vasoconstriction and adverse cardiac remodelling.
- By inhibiting the breakdown of bradykinin, ACE inhibitors also increase nitric oxide synthesis, promoting vasodilation and reducing vascular resistance.
Antiarrhythmic Effects:
- ACE inhibitors may have antiarrhythmic properties by reducing myocardial fibrosis and decreasing sympathetic activity, thereby reducing the risk of arrhythmias.
Renoprotective Effects:
- ACE inhibitors reduce intraglomerular pressure by dilating efferent arterioles in the kidneys, leading to decreased proteinuria and slowing the progression of renal dysfunction in heart failure patients.

29943

28211

Which of the following medications do not confer a prognostic benefit in the management of heart failure?

28188

A 55-year-old Asian man with known thalassaemia trait registers with a new GP and is found to have a mild microcytic anaemia on routine testing. He does not complain of any symptoms.

What is the most appropriate treatment?

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