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Left-Sided Heart Failure: Pathophysiology Explained
Introduction
Left-sided heart failure (LSHF) is a condition in which the left ventricle of the heart cannot pump blood effectively to the body. This leads to a backlog of blood in the pulmonary circulation and causes symptoms such as shortness of breath and fatigue. Understanding the pathophysiology of LSHF helps in early detection and management.
Causes of Left-Sided Heart Failure
Left-sided heart failure results from various cardiovascular disorders, including: - Coronary artery disease (CAD) – Reduced blood flow weakens heart muscle. - Hypertension (high blood pressure) – Left ventricular hypertrophy increases the heart's workload. - Valvular heart disease – Aortic or mitral valve dysfunction leads to inefficient pumping. - Cardiomyopathies – Structural changes impair the heart's function. - Myocardial infarction (heart attack) – Damage to the myocardium reduces contractility.
Pathophysiology of Left-Sided Heart Failure
The failure of the left ventricle to pump blood efficiently leads to a series of physiological changes:
1. Systolic vs Diastolic Dysfunction
- Systolic heart failure (HFrEF – heart failure with reduced ejection fraction): The left ventricle weakens and cannot contract properly, leading to a reduced ejection fraction (<40%).
- Diastolic heart failure (HFpEF – heart failure with preserved ejection fraction): The left ventricle struggles to relax and fill properly, maintaining a near-normal ejection fraction but reduced cardiac output.
2. Increased Pulmonary Pressure & Congestion
With an impaired left ventricle, blood starts backing up into the left atrium and further into the pulmonary veins. This leads to pulmonary congestion and symptoms such as: - Dyspnea (shortness of breath) - Orthopnea (difficulty breathing while lying down) - Paroxysmal nocturnal dyspnea (sudden nighttime breathlessness)
3. Neurohormonal Activation and Compensatory Mechanisms
In response to reduced cardiac output, the body activates compensatory mechanisms: - Sympathetic Nervous System (SNS) Activation: Increases heart rate and vasoconstriction to maintain blood pressure, but over time worsens heart failure. - Renin-Angiotensin-Aldosterone System (RAAS) Activation: Leads to fluid retention and vasoconstriction, increasing preload but exacerbating congestion. - Ventricular Remodeling: The ventricle undergoes hypertrophy or dilation to compensate, worsening heart function long term.
Conclusion
Left-sided heart failure significantly impacts circulation, leading to pulmonary congestion and systemic compensation. Understanding this process aids in targeted therapies such as ACE inhibitors, beta-blockers, and diuretics to manage symptoms and improve cardiac function.
Source recommendations
1. American College of Cardiology/American Heart Association Heart Failure Guidelines
- https://www.ahajournals.org/doi/10.1161/CIR.0000000000001063
- https://www.acc.org/Guidelines
- https://www.jacc.org/doi/10.1016/j.jacc.2023.12.024
- https://www.acc.org/education-and-meetings/products-and-resources/features/global-cv-institute/heart-failure-guidelines
- https://professional.heart.org/en/science-news/-/media/832EA0F4E73948848612F228F7FA2D35.ashx
2. European Society of Cardiology Heart Failure Guidelines
- https://www.escardio.org/Guidelines/Clinical-Practice-Guidelines/Acute-and-Chronic-Heart-Failure
- https://academic.oup.com/eurheartj/article/42/36/3599/6358045
- https://www.escardio.org/Guidelines/Clinical-Practice-Guidelines/Focused-Update-on-Heart-Failure-Guidelines
- https://academic.oup.com/eurheartj/article/44/37/3627/7246292
- https://www.escardio.org/Guidelines/Clinical-Practice-Guidelines
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