What is Preload
Preload represents the initial stretching of cardiac myocytes before contraction, which is clinically measured as left ventricular end-diastolic volume (LVEDV) and determines the force of contraction through the Frank-Starling mechanism. 1
Physiological Definition and Mechanism
At the cellular level, preload determines the initial length of myocardial sarcomeres, which directly influences the force of subsequent contraction 1. This relationship forms the basis of the Frank-Starling mechanism, where increased ventricular filling leads to greater myocardial fiber stretch and consequently stronger contraction 1.
Preload is fundamentally the volume of blood in the ventricle at end-diastole, which establishes the starting volume from which the ventricle ejects blood during systole. 1 This makes it a key determinant of stroke volume 1.
Clinical Measurement Approaches
Static Measurements
- Left ventricular end-diastolic pressure (LVEDP) provides the most reliable guide to preload at a specific point in time, though it has limitations 2
- Pulmonary capillary wedge pressure and central venous pressure are generally insensitive indicators—low values may reflect hypovolemia, but high values don't necessarily indicate volume overload 1
- Echocardiography provides direct visualization of ventricular dimensions, allowing assessment of end-diastolic volume as the most accurate measure of preload 1
- Inferior vena cava (IVC) assessment can provide qualitative estimates: collapse of 50-99% during respiration is normal, complete collapse may indicate volume depletion, and <50% collapse may suggest volume overload 1
Dynamic Measurements
Dynamic indicators of preload responsiveness (such as stroke volume variation and arterial pulse pressure variation) are more reliable than static parameters for predicting fluid responsiveness in critically ill patients. 1 This represents a paradigm shift from traditional static pressure measurements 3.
Preload in Pathological States
Heart Failure Context
In heart failure, the ventricle may develop eccentric hypertrophy with addition of new sarcomeres to maintain preload reserve despite chamber dilation 1. However, preload augmentation in established heart failure may precipitate decompensation rather than improve cardiac output 4.
Preload reserve represents the heart's ability to increase stroke volume in response to increased venous return, which becomes exhausted in advanced heart failure. 1 The difference between current and maximal possible LVEDV (the preload reserve) has the most clinical relevance—minimal or absent preload reserve indicates that there will be either minimal or no increase in stroke volume following intravenous fluid administration 2.
High-Output States
In conditions like β-thalassemia major, chronic anemia creates a high-output state with volume-loaded ventricles (high preload) 5. The increased preload combined with decreased afterload from peripheral vasodilation leads to increased ejection fraction 5.
Pharmacological Manipulation
Nitroglycerin reduces preload by causing dilation of postcapillary vessels and large veins, which promotes peripheral pooling of blood, decreases venous return to the heart, and reduces left ventricular end-diastolic pressure. 6 This mechanism makes it effective for acute heart failure management by reducing the volume load on the failing ventricle 6.
Clinical Implications for Assessment
In hypovolemic shock, echocardiography can rapidly document a small hyperdynamic unloaded ventricle with reduced left ventricular end-diastolic area, indicating decreased preload 1. Conversely, optimal preload management is crucial in perioperative cardiac surgery, as heart failure cannot be properly assessed unless volume loading is optimal 1.
Common Pitfalls
- Do not rely solely on filling pressures (CVP or PCWP) to assess preload status, as they correlate poorly with actual ventricular volumes 1
- Left atrial pressure can remain within normal range even when LVEDP is elevated, making LVEDP the more reliable indicator 2
- Static measurements fail to predict fluid responsiveness in mechanically ventilated patients—use dynamic parameters instead 1, 3