Heart failure occurs when the heart’s pumping becomes impaired, resulting in inability to meet the body’s oxygen demands. The most common type of heart failure, left-sided failure, occurs when the left ventricle cannot contract sufficiently.
Afterload is the amount of resistance the ventricle pumps against. In order to pump effectively, the ventricle must generate sufficient pressure to overcome this resistance.
Left heart failure occurs when arteries downstream constrict, resulting in increased afterload: resistance too high for the ventricle to pump against.
A heart attack can also cause left heart failure.
In a failing heart, blood accumulates in the left ventricle causing pressure. This pressure, called preload, causes the ventricle to expand.
Increased preload worsens the ventricle’s ability to pump. Accumulating blood stretches the cardiac muscle fibers, pulling myosin and actin filaments farther apart. When over-stretched, myosin molecules cannot connect with actin, the myosin–actin crossbridges cannot swivel.
The inability of the crossbridges to swivel causes makes contraction weaker, reducing the likelihood that sufficient blood will be pumped. The progression of heart failure continues as blood accumulates.
Built-up blood in the left ventricle causes a backup of blood throughout the pulmonary circuit, leading to pulmonary congestion. This associated congestion is responsible for left heart failure, also known as “congestive heart failure.”
Blood build up in the lungs causes difficulty breathing, especially when a person is reclining. Pulmonary congestion also reduces the ability to oxygenate the blood, worsening systemic hypoxia.
The progressive nature of congestive heart failure, if untreated, ultimately causes death.
