From the FDA Drug Label
Dilation of postcapillary vessels, including large veins, promotes peripheral pooling of blood, decreases venous return to the heart, and reduces left ventricular end-diastolic pressure (preload)
- Preload refers to the initial stretching of the cardiac myocytes prior to contraction, which is directly related to the left ventricular end-diastolic pressure.
- The reduction of preload is achieved through the dilation of postcapillary vessels, including large veins, which promotes peripheral pooling of blood and decreases venous return to the heart.
- This effect is a result of the vasodilatory action of nitroglycerin, which leads to a decrease in left ventricular end-diastolic pressure 1.
From the Research
Preload refers to the volume of blood in the ventricles at the end of diastole, just before contraction begins, and is a key determinant of cardiac output, as increased preload stretches the heart muscle fibers, allowing them to contract more forcefully according to the Frank-Starling mechanism. This concept is crucial in managing various cardiac conditions, including heart failure and hypovolemic shock. According to the study by 2, preload must directly reflect myocardial stretch, and the Frank-Starling mechanism is activated during any stretch of a cardiac chamber beyond its resting size.
Factors Influencing Preload
Preload is influenced by several factors, including:
- Blood volume
- Venous tone
- Atrial contraction
- Ventricular compliance
Manipulating Preload
To increase preload, interventions include:
- Intravenous fluid administration (typically crystalloids like normal saline at 500-1000mL boluses)
- Passive leg raising (elevating legs 45 degrees for 1-2 minutes)
- The use of venous constrictors like phenylephrine (50-200 mcg/min IV) To decrease preload, options include:
- Diuretics like furosemide (20-40mg IV)
- Venodilators such as nitroglycerin (5-200 mcg/min IV)
- Proper positioning with head elevation
Clinical Relevance
Understanding preload is essential for managing conditions like heart failure, where excessive preload causes pulmonary congestion, or hypovolemic shock, where insufficient preload reduces cardiac output and tissue perfusion. The study by 3 highlights the feasibility, safety, and efficacy of outpatient intravenous diuretic treatment for decompensated heart failure, demonstrating a significant reduction in 30-day mortality compared to standard inpatient care.
Preload Reserve
The concept of preload reserve, as discussed in 2, is also crucial, as it represents the difference between the current and maximal possible left ventricular end-diastolic volume. A minor or absent left ventricular preload reserve indicates that there will be either minimal or no increase in stroke volume following intravenous fluid administration. This highlights the importance of considering preload reserve in clinical decision-making, particularly in patients with heart failure or other conditions where fluid management is critical.