What is preload in the context of cardiac function?

What is Preload in Cardiac Function?

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

Physiological Definition

At the cellular level, preload is the passive ventricular wall stress (or tension) at end-diastole that establishes the starting length of myocardial fibers. 1, 2 This initial fiber length is the critical determinant of how forcefully the heart will contract—longer fibers (within physiologic limits) generate stronger contractions. 1

• Preload is most accurately measured as left ventricular end-diastolic volume (LVEDV), which reflects the degree of myocardial fiber stretch before systole. 1
• The relationship between preload and cardiac output follows the Frank-Starling curve: in healthy hearts, small increases in preload produce large increases in stroke volume due to the steep slope of this relationship. 3

Clinical Measurement Approaches

Static pressure measurements like central venous pressure (CVP) and pulmonary capillary wedge pressure are generally insensitive indicators of true preload status. 1 Low values may suggest hypovolemia, but elevated values do not reliably indicate volume overload. 1

Preferred Assessment Methods:

• Echocardiography provides direct visualization of end-diastolic volume, making it the gold standard for preload assessment. 1
• Inferior vena cava (IVC) assessment offers rapid bedside estimation: 50-99% respiratory collapse indicates normal preload, complete collapse suggests volume depletion, and <50% collapse indicates potential volume overload. 1
• Dynamic indicators like stroke volume variation during mechanical ventilation are superior to static measurements for predicting fluid responsiveness in critically ill patients. 1

Preload in Disease States

Chronic Aortic Regurgitation:

The left ventricle compensates for volume overload by increasing end-diastolic volume and developing eccentric hypertrophy with addition of new sarcomeres, which maintains preload at the sarcomere level near normal despite chamber enlargement. 4 This "preload reserve" allows the heart to maintain normal ejection performance for years or even decades. 4

• As disease progresses, preload reserve becomes exhausted, and the compensatory mechanisms fail, leading to symptomatic heart failure. 4

Heart Failure:

In heart failure, preload augmentation that would normally increase cardiac output instead precipitates decompensation because the flattened Frank-Starling curve means additional volume produces minimal increases in stroke volume but significant increases in filling pressures. 5, 6

• The splanchnic vascular compartment serves as the primary venous reservoir for preload recruitment—sympathetic stimulation shifts blood from splanchnic to thoracic compartments to increase cardiac filling. 6
• In heart failure patients, this mechanism becomes maladaptive, causing congestion rather than improved output. 6

High-Output States

Beta-thalassemia major creates a chronic high-output state with volume-loaded ventricles (high preload) due to severe anemia, requiring increased end-diastolic volume, stroke volume, and heart rate to maintain tissue oxygen delivery. 4 The body compensates by lowering systemic vascular resistance through peripheral vasodilation. 4

Perioperative Considerations

In patients with mitral stenosis undergoing noncardiac surgery, preload must be maintained high enough to allow adequate forward flow across the stenotic valve but low enough to avoid pulmonary edema—this requires invasive hemodynamic monitoring with measurement of cardiac output and pulmonary wedge pressure. 4

• In aortic stenosis, avoid hypotension and tachycardia perioperatively, as decreased coronary perfusion pressure combined with inadequate preload can precipitate myocardial ischemia, arrhythmias, or circulatory collapse. 4
• For regurgitant lesions like mitral regurgitation, maintain adequate preload while avoiding increased afterload and bradycardia. 4

Ventricular Interdependence

Right ventricular dilation from volume overload can compress the left ventricular cavity through ventricular interdependence, directly impairing left ventricular filling (preload) and reducing overall cardiac output. 1 This occurs through forces transmitted between ventricles via the shared myocardium and pericardial constraint. 1

Exercise Physiology

During high-intensity dynamic exercise, stroke volume increases primarily through elevation of end-diastolic volume (the Frank-Starling mechanism), making increased preload the most important factor for athletes. 4 This contrasts with static exercise, where preload changes minimally while afterload increases substantially. 4