Heart failure is a clinical syndrome where the heart cannot pump enough blood to meet the body’s needs. This condition arises from structural or functional impairments in the heart’s ability to fill or eject blood. The heart’s diminished pumping action means that organs and tissues may not receive adequate oxygen and nutrients, leading to symptoms. While “heart failure” might sound like the heart has stopped working, it refers to a weakened state where the heart struggles to keep up with its workload.
How the Heart Fails to Pump Effectively
The heart’s inability to pump blood effectively stems from two main types of dysfunction: issues with contraction (systolic dysfunction) or issues with relaxation and filling (diastolic dysfunction). Both types of problems can occur together.
Systolic dysfunction, also known as heart failure with reduced ejection fraction (HFrEF), occurs when the heart muscle weakens and cannot contract forcefully enough to pump blood out. The left ventricle, the heart’s main pumping chamber, struggles to eject sufficient blood with each beat. This reduced contractility means the ejection fraction falls below typical levels, often 40% or less. Increased afterload, the resistance the heart must overcome to pump blood, can further strain the weakened muscle, diminishing its ability to pump effectively.
Diastolic dysfunction, or heart failure with preserved ejection fraction (HFpEF), involves the heart muscle becoming stiff and unable to relax properly between beats. This stiffness impairs the ventricle’s ability to fill adequately, even though its pumping strength (ejection fraction) may remain within a normal range, above 50%. Impaired relaxation and increased ventricular stiffness mean higher pressures are needed to fill the heart, leading to a reduced volume of blood being ejected. This can lead to symptoms when the heart cannot increase its filling during physical activity.
The Body’s Compensatory Responses
When the heart begins to fail, the body activates compensatory mechanisms to maintain adequate blood flow and pressure. These responses are initially beneficial, but over time, they can worsen the heart’s condition.
One response is the activation of neurohormonal systems, including the Renin-Angiotensin-Aldosterone System (RAAS) and the Sympathetic Nervous System (SNS). When cardiac output decreases, the kidneys perceive a reduction in blood flow, triggering renin release. Renin initiates a cascade that leads to the production of angiotensin II, a potent vasoconstrictor that narrows blood vessels, and aldosterone, which causes the kidneys to retain salt and water. This fluid retention increases blood volume, aiming to boost cardiac output, while vasoconstriction helps maintain blood pressure.
The Sympathetic Nervous System also becomes overactive, releasing catecholamines like norepinephrine. This causes the heart rate to increase and the heart muscle to contract more forcefully, initially helping to maintain cardiac output. It also leads to peripheral vasoconstriction, diverting blood to the brain and other vital organs. While these neurohormonal responses provide immediate support, their long-term activation places increased strain on the heart, leading to further cardiac damage, fluid overload, and irregular heart rhythms.
Another compensatory change within the heart is ventricular remodeling. This refers to alterations in the heart’s size, shape, and structure in response to injury or increased workload. The heart muscle may thicken (hypertrophy) or the chambers may enlarge (dilation) to initially cope with increased stress and maintain pumping efficiency. However, this remodeling process, driven by neurohormonal activation and increased wall stress, ultimately leads to a less efficient heart and increased fibrosis, or scarring, within the muscle. These structural changes further impair the heart’s ability to contract and relax, contributing to the progression of heart failure.
Impact on Other Organ Systems
Heart failure is a systemic condition that impacts various other organ systems due to reduced blood flow and increased venous pressure. These consequences contribute to the symptoms experienced by individuals with heart failure.
The lungs are affected, as the heart’s inability to pump blood forward causes blood to back up into the pulmonary vessels. This leads to increased pressure in the lung’s blood vessels, pushing fluid into the air sacs (alveoli) and surrounding tissues, a condition known as pulmonary congestion or pulmonary edema. This fluid buildup impairs oxygen movement into the bloodstream, resulting in symptoms like shortness of breath, especially with activity or when lying down, and sometimes a cough that may produce frothy or bloody mucus. Chronic congestion can also lead to changes in lung mechanics and gas exchange capacity.
Kidney function declines in heart failure, a phenomenon termed cardiorenal syndrome. Reduced blood flow to the kidneys, along with increased venous pressure, can impair their ability to filter waste and excess fluid from the blood. This can lead to fluid retention, exacerbating congestion throughout the body. The complex interplay between the heart and kidneys creates a cycle where dysfunction in one organ can worsen the other.
The liver can also suffer from the effects of heart failure, primarily due to venous congestion. When the right side of the heart struggles to pump blood effectively, blood can back up into the veins that drain the liver, causing it to become enlarged and congested. This sustained pressure can lead to liver dysfunction, sometimes referred to as congestive hepatopathy.
Beyond these, the brain can experience cognitive impairment, affecting memory, attention, and executive functions. This is thought to be due to reduced cerebral blood flow, chronic inflammation, and neurohormonal activation, all stemming from the heart’s diminished pumping ability. Even skeletal muscles can weaken and atrophy, leading to fatigue and reduced exercise tolerance. This muscle dysfunction contributes to the overall physical limitations experienced by patients with heart failure.