What is preload in the context of cardiac function?

What is Preload in Cardiac Function

Preload represents the initial stretching of cardiac myocytes (sarcomere length) at end-diastole before contraction, which directly determines the force of subsequent ventricular contraction through the Frank-Starling mechanism. 1

Physiological Definition

At the cellular level, preload establishes the starting length of myocardial fibers, which influences contractile force generation. 1 More comprehensively, preload encompasses all factors contributing to passive ventricular wall stress (or tension) at end-diastole, including chamber pressure, chamber radius, and wall thickness as described by the Law of LaPlace. 2

Preload is fundamentally a determinant of stroke volume - it establishes the initial ventricular volume from which blood is ejected during systole. 1

Clinical Measurement

Direct Volumetric Assessment

• Echocardiography provides the most reliable assessment through direct visualization of end-diastolic volume. 1
• Transpulmonary dilution techniques measuring intrathoracic blood volume or global end-diastolic volume provide superior preload assessment compared to pressure-based measurements in critically ill patients. 3

Pressure-Based Measurements (Less Reliable)

• Central venous pressure (CVP) and pulmonary capillary wedge pressure (PCWP) are generally insensitive indicators of actual preload status. 1
• Low CVP values may reflect hypovolemia, but elevated values do not necessarily indicate volume overload. 1

Dynamic Assessment

• Inferior vena cava (IVC) diameter and respiratory collapsibility can estimate preload: 50-99% collapse is normal, complete collapse suggests volume depletion, and <50% collapse may indicate volume overload. 1
• Dynamic indicators like stroke volume variation are more reliable than static parameters for predicting fluid responsiveness in mechanically ventilated patients. 1

Preload Reserve Concept

Preload reserve represents the heart's capacity to increase stroke volume in response to increased venous return. 1 In healthy individuals, recruitment of preload from the splanchnic vascular compartment increases effective circulating blood volume and cardiac output. 4, 5

In Chronic Heart Disease

• The left ventricle compensates for volume overload (such as in aortic regurgitation) through eccentric hypertrophy with addition of new sarcomeres, maintaining preload at the sarcomere level near normal despite chamber dilation. 6
• This compensation allows the ventricle to retain preload reserve for decades in many patients. 6
• Preload reserve can become exhausted in advanced heart failure, at which point further increases in venous return precipitate decompensation rather than augmenting cardiac output. 6, 4

Ventricular Interdependence

Preload of one ventricle directly affects the other through shared anatomical structures:

• Right ventricular dilation from volume overload causes the interventricular septum to shift leftward, physically impeding left ventricular filling and reducing left ventricular preload. 1
• This ventricular interdependence can equalize biventricular diastolic pressures and compromise overall cardiac output. 1
• The pericardium provides restraining forces that amplify these interdependent effects when either ventricle dilates acutely. 6

Clinical Management Implications

Right Ventricular Infarction

• Maintaining adequate right ventricular preload is critical - factors that reduce preload (diuretics, nitrates, volume depletion) or diminish atrial contraction can have profoundly adverse hemodynamic effects. 6
• Volume loading with IV normal saline is the primary treatment for hypotension in RV infarction. 6

Perioperative Management in Valvular Disease

• In mitral stenosis, preload must be maintained high enough for adequate forward output but low enough to avoid pulmonary edema - this requires invasive hemodynamic monitoring with measurement of cardiac output and pulmonary wedge pressure. 6
• In aortic stenosis, continuous optimization of loading conditions with avoidance of hypotension is essential, as decreased preload combined with fixed outflow obstruction can precipitate cardiovascular collapse. 6

Heart Failure

• In decompensated heart failure, preload augmentation exacerbates congestion rather than improving cardiac output, making preload reduction through diuretics the cornerstone of acute management. 4, 5
• Emerging therapies targeting splanchnic nerve modulation aim to prevent pathological preload recruitment that precipitates decompensation. 4, 5