What is preload in the context of cardiac function?

From the Guidelines

Preload is the degree of myocardial fiber stretch at the end of diastole, just before ventricular contraction begins, and it represents the volume of blood in the ventricles at the end of filling. In the context of cardiac function, preload is a critical determinant of cardiac output, as it influences the force of contraction and stroke volume according to the Frank-Starling mechanism 1.

Key Points About Preload

• Preload is primarily determined by venous return to the heart and can be affected by blood volume, body position, intrathoracic pressure, and venous tone.
• Clinically, preload is often measured as end-diastolic volume or pressure.
• An increase in preload leads to increased force of contraction and stroke volume, up to a physiological limit, as greater stretching of cardiac muscle fibers allows for optimal overlap of actin and myosin filaments, resulting in stronger contractions.
• Understanding preload is essential for managing conditions like heart failure, shock, and hypertension, as it directly influences cardiac output and overall cardiovascular function.
• In clinical settings, preload can be manipulated through interventions like fluid administration to increase it (in hypovolemia) or diuretics to decrease it (in heart failure with volume overload), as noted in studies on heart failure management 1.

Clinical Implications of Preload

• The management of preload is crucial in conditions where cardiac output is compromised, such as heart failure, where the ability to increase cardiac output in response to increased preload may be impaired 1.
• In valvular heart disease, such as aortic regurgitation, the ventricle may adapt to increased preload through hypertrophy and dilation, but eventually, this compensation may fail, leading to systolic dysfunction 1.
• Therefore, accurate assessment and management of preload are vital for optimizing cardiac function and improving outcomes in patients with cardiovascular diseases.

From the FDA Drug Label

The principal pharmacological action of Nitroglycerin Injection is relaxation of vascular smooth muscle and consequent dilatation of peripheral arteries and veins, especially the latter Dilatation of the veins promotes peripheral pooling of blood and decreases venous return to the heart, thereby reducing left ventricular end-diastolic pressure and pulmonary capillary wedge pressure (preload).

Preload refers to the initial stretching of the cardiac myocytes prior to contraction, which is influenced by the volume of blood in the ventricles at the end of diastole. In the context of cardiac function, preload is reduced by nitroglycerin due to its effect on dilating veins, promoting peripheral pooling of blood, and decreasing venous return to the heart, thereby reducing left ventricular end-diastolic pressure and pulmonary capillary wedge pressure 2 2.

• Key points:
  • Preload reduction is a result of decreased venous return to the heart
  • Nitroglycerin causes dilatation of veins, leading to peripheral pooling of blood
  • Reduced preload decreases left ventricular end-diastolic pressure and pulmonary capillary wedge pressure

From the Research

Definition of Preload

• Preload is defined as the initial stretching of the cardiac myocytes prior to contraction, which directly reflects myocardial stretch 3.
• It is the degree to which the cardiac muscle is stretched at the end of diastole, just before contraction.

Relationship with Frank-Starling Mechanism

• The Frank-Starling mechanism is activated during any stretch of a cardiac chamber beyond its resting size, which is present immediately before contraction 3.
• Every left ventricle has an intrinsic and limited range of possible volumes at end diastole, and the left ventricular end-diastolic volume (LVEDV) will be determined by the extent of filling.
• Any change in LVEDV will result in changed activity of the Frank-Starling mechanism, and change in LVEDV might, therefore, be considered to represent change in preload.

Clinical Relevance

• The difference between the current and the maximal possible LVEDV (or the preload reserve) may be of the most clinical relevance 3.
• Minor or absent left ventricular preload reserve indicates that there will be either minimal or no increase in stroke volume following intravenous fluid administration.
• Left ventricular end-diastolic pressure (LVEDP) provides the most reliable guide to preload reserve in an individual at a specific period in time, rather than left atrial pressure 3.

Preload Reduction Therapy

• Preload reduction therapy using diuretics or vasodilators may produce a considerable decrease in cardiac output, particularly in hypertensive patients with diastolic dysfunction 4.
• Analysis of mitral flow velocity patterns may be useful in estimating the change in cardiac output following preload reduction in patients with hypertensive heart failure due to diastolic dysfunction 4.
• Intravenous vasodilators, such as nitroglycerin, may improve short-term symptoms and appear safe to administer in patients with acute heart failure, but there are no data suggesting that they impact mortality 5.