What is preload in the context of cardiac function?

Understanding Preload in Cardiac Function

Preload is defined as all factors that contribute to passive ventricular wall stress (or tension) at the end of diastole, primarily determined by the end-diastolic volume of the ventricular chamber. 1

Physiological Basis of Preload

Preload represents the initial stretching of cardiac muscle fibers before contraction begins. It is fundamentally related to:

• End-diastolic volume: The amount of blood in the ventricle at the end of filling
• Ventricular wall tension: According to LaPlace's law, wall stress is directly proportional to intracavitary pressure and internal ventricular diameter, and inversely related to ventricular wall thickness 2
• Sarcomere length: The stretching of myocardial fibers that influences contractile force via the Frank-Starling mechanism

Frank-Starling Mechanism

The Frank-Starling mechanism explains how increased preload leads to increased stroke volume:

• Greater ventricular filling (increased preload) stretches cardiac muscle fibers
• This stretching optimizes the overlap between actin and myosin filaments
• The result is more forceful contraction and increased stroke volume

Preload in Normal Cardiac Function

In healthy individuals, preload serves as a crucial mechanism to augment cardiac output:

• Increased venous return increases end-diastolic volume
• The ventricle responds with enhanced stroke volume primarily through a larger end-diastolic volume 3
• This "preload reserve" allows the heart to meet changing metabolic demands 4

Preload in Heart Failure

In heart failure, preload dynamics become significantly altered:

• The dilated left ventricle may be operating near its maximal volume, exhausting preload reserve 3
• As stated by the American Heart Association, "The reduced ability to augment LV end-diastolic volume is explained by the fact that the already dilated LV is operating near its maximal volume and has thus exhausted most of its preload reserve." 3
• In chronic aortic regurgitation, the ventricle initially compensates through increased end-diastolic volume, but eventually preload reserve may be exhausted 3

Clinical Assessment and Management of Preload

Clinically, preload is managed through several mechanisms:

• Volume status: Diuretics reduce preload by decreasing intravascular volume 2
• Venodilation: Nitrates primarily reduce preload by promoting venous pooling
• Positioning: Elevating legs can temporarily increase preload by improving venous return

Pitfalls in Preload Management

• Excessive reduction in preload (overdiuresis) can precipitate acute renal failure, especially in patients with compromised oncotic status 2
• Inadequate preload can lead to decreased cardiac output, particularly across stenotic valves 2
• Excessive preload in heart failure can worsen pulmonary congestion and edema

Preload vs. Afterload

It's important to distinguish preload from afterload:

• Preload: Factors contributing to passive ventricular wall stress at end-diastole
• Afterload: Factors contributing to total myocardial wall stress during systolic ejection 1

While preload primarily relates to filling pressures and volumes, afterload relates to the resistance against which the heart must pump, including systemic vascular resistance and arterial stiffness.

Modern Clinical Applications

Understanding preload is essential for:

• Fluid management in critical care settings
• Titration of diuretics in heart failure
• Assessment of volume responsiveness in shock states
• Optimization of cardiac function in valvular heart disease

In patients with valvular disease, continuous optimization of loading conditions is crucial, with invasive hemodynamic monitoring allowing for continuous assessment of LV filling pressures 2.