Acute heart failure, or AHF, describes a sudden onset or rapid worsening of heart failure symptoms, occurring when the heart cannot pump enough blood to meet the body’s demands. This condition is distinct from a heart attack, which is a circulation problem where blood flow to the heart muscle is blocked. AHF also differs from chronic heart failure, which is a long-term condition managed over time. An acute episode represents a sudden, severe failure in the heart’s pumping action.
Precipitating Factors and Underlying Conditions
An episode of acute heart failure is often triggered by a specific event that places an overwhelming demand on the heart. A common trigger is an acute coronary syndrome, such as a heart attack, which damages the heart muscle and abruptly impairs its ability to pump. Similarly, a hypertensive emergency, where blood pressure rises to dangerous levels, can place an immense strain on the heart, forcing it to work against extreme resistance.
Other events can also initiate AHF by disrupting the heart’s normal operation. Rapid or abnormal heart rhythms, known as arrhythmias, can prevent the heart’s chambers from filling and pumping effectively, leading to a sharp drop in output. Infections throughout the body, like pneumonia or sepsis, increase the body’s demand for oxygen and blood flow that the heart may not be able to meet. For individuals with pre-existing chronic heart failure, failing to adhere to prescribed medications or consuming excess salt and fluid can be enough to disrupt a fragile balance, leading to acute decompensation.
The Vicious Cycle of Compensatory Mechanisms
When the heart’s output falls, the body activates compensatory systems to restore blood flow. The sympathetic nervous system (SNS) releases hormones like norepinephrine to increase heart rate and the force of the heart’s contractions, while also constricting blood vessels to maintain blood pressure.
A second system, the renin-angiotensin-aldosterone system (RAAS), is activated by reduced blood flow to the kidneys. The kidneys release an enzyme called renin, which initiates a chemical cascade that produces angiotensin II, a constrictor of blood vessels. Angiotensin II also stimulates the adrenal glands to release aldosterone, a hormone that causes the body to retain sodium and water to increase blood volume.
In AHF, these normally helpful responses become harmful. The increased heart rate and contractility driven by the SNS raise the heart muscle’s need for oxygen, which the struggling heart cannot afford. This increased demand can starve the heart muscle, worsening its function. The vasoconstriction caused by both the SNS and RAAS increases the resistance the heart must pump against, adding to its workload. The fluid and salt retention prompted by aldosterone expands the volume of blood returning to the heart, stretching its chambers beyond their capacity.
Hemodynamic Consequences and Fluid Shifts
These compensatory mechanisms directly alter the heart’s mechanical function, described by hemodynamic principles like preload and afterload. Preload refers to the stretching of the heart muscle fibers by the volume of blood in the ventricles at the end of the filling phase. Afterload is the resistance the heart must overcome to eject that blood into circulation.
In acute heart failure, the resulting salt and water retention increases the total blood volume. This fluid overload raises the amount of blood returning to the heart, resulting in a high preload. The ventricles become overstretched with blood they cannot effectively pump out. At the same time, widespread vasoconstriction increases systemic vascular resistance, leading to a high afterload. The heart must now push harder to eject blood into these narrowed, high-pressure vessels.
This combination of high preload and high afterload has direct consequences. When the left ventricle fails against high pressures, blood and fluid back up into the lungs. This pulmonary congestion leads to pulmonary edema, or fluid in the air sacs, causing shortness of breath. If the right ventricle fails, fluid backs up in the systemic circulation, causing peripheral edema, which is visible as swelling in the legs and ankles, and congestion in the abdominal organs.
Impact on Organ Systems
The effects of acute heart failure extend beyond the heart and lungs, causing damage to other organs through reduced forward blood flow and backward fluid congestion. The kidneys are vulnerable to these insults, and the combination of poor perfusion and high venous pressure from systemic congestion impairs kidney function, a condition known as cardiorenal syndrome. Declining kidney function leads to less sodium and water excretion, which worsens fluid overload and creates a harmful cycle that further strains the heart.
The liver is also affected by AHF. Elevated pressure in the right side of the heart leads to systemic congestion, causing blood to back up in the liver in a condition called congestive hepatopathy. This can impair liver function. In severe cases of AHF where cardiac output is extremely low, the liver can suffer from a lack of oxygenated blood, leading to acute cardiogenic liver injury.
The brain is also susceptible to reduced blood flow and oxygen, which can manifest as confusion or delirium, particularly in older patients. This multi-organ impact highlights how an acute failure of the heart’s pumping ability rapidly evolves into a systemic crisis.