The preload on the heart is all about venous return to the heart, or the volume that is emptying into the heart from the venous system. It is how much "load" (or blood volume), that is returning to the heart from the veins of the body that the left ventricle (LV) must then pump forward. Technically, preload is more specifically defined as the length of the myocyte muscle fibers at the end of diastole (or the stretch the myocytes experience at maximum filling). However, muscle fiber length is difficult to measure and is directly related to the volume of blood filling the heart from the venous system (as more blood fills the LV, the LV muscle fibers will experience greater stretch).

Estimating Preload

Preload on the LV can be estimated by left ventricular end-diastolic volume (LVEDV). Since LVEDV is the volume of blood in the LV at the end of diastole, or ventricular filling, it is a good approximation of preload.

Preload, Contractility, and Stroke Volume

As preload increases, contractility increases and, therefore, stroke volume (SV) increases. If more blood fills the LV during diastole, the LV will pump harder because it has more blood to eject during systole. Under normal circumstances, the heart will work to maintain its ejection fraction at 55-75%. If preload increases and a greater volume of blood is present at the start of LV contraction, then, under normal circumstances, the heart will have to pump out a greater volume blood with each heart beat (SV increases). Therefore--in a normal healthy heart--as preload increases, cardiac output will typically increase.

Increases and Decreases in Preload

Preload is affected by 1.) venous tone, and 2.) circulating blood volume.

Preload is increased whenever venous return to the heart is increased.

• Increased venous tone (eg, older age) --> decreased venous capacitance --> less blood held in venous system, more blood pushed forward to the heart --> increased venous return to the heart
• Increased circulating blood volume (eg, during pregnancy) --> increased blood volume available to return to heart --> increased venous return
• Other increases in venous return: Leg raise maneuver (blood falls back to heart with gravity)

Preload is decreased whenever venous return to the heart is decreased.

• Decreased venous tone (eg, nitroglycerin and other venous vasodilators) --> increased venous capacitance --> greater volume of blood held in venous system, less blood pushed forward to the heart --> decreased venous return to heart
• Decreased circulating blood volume (eg, acute blood loss or internal bleeding) --> decreased blood volume available to return to heart --> decreased venous return
• Other decreases in venous return: Standing up (blood rushes down to legs with gravity)

The afterload on the heart is all about arterial pressure, or the pressure of the arterial system that the left ventricle (LV) must pump against during each contraction.

Estimating Afterload

Afterload can be estimated by mean arterial pressure (MAP). Since MAP is a function of the pressure in our arterial system--determined by systolic and diastolic blood pressure--we can think of blood pressure as a reasonable proxy for estimating afterload. As someone's blood pressure increases, their afterload--or the pressure the LV must overcome to eject blood--increases. We can also think of aortic pressure as a proxy of afterload, since it is the first main artery the blood from the LV must traverse on its way to the rest of the body.

Afterload and Stroke Volume

As afterload increases, stroke volume (SV) decreases. If the LV has a greater pressure that it has to push against during systole, it will pump out less blood per heartbeat. So, as afterload increases, cardiac output will decrease unless the heart compensates in some other way. This means the heart will have to work harder--either increase heart rate or contractility--in order to maintain its cardiac output. Typically, the heart will compensate by undergoing hypertrophy; this will cause thickening of the LV walls, so they can maintain their strength and contractile force as the LV pumps against the increased afterload. This increased work (and thicker LV wall) results in increased myocardial oxygen demand, which can lead to myocardial ischemia and, ultimately, myocardial infarction.

Increases and Decreases in Afterload

Afterload is increased whenever arterial pressure is increased. For example:

• Hypertension: Hypertension, or increased blood pressure, represents a state of increased mean arterial pressure (MAP). In a person with hypertension, afterload is increased because the pressure of the arterial system is higher than normal. Their heart must work harder to pump blood against this higher pressure system in order to maintain cardiac output. Over time, this leads to LV hypertrophy as the heart compensates for this increased afterload.
• Aortic stenosis: Aortic stenosis is when the aortic valve narrows and calcifies, which restricts blood flow through the valve. Since the aortic valve is the outflow tract for the LV (the LV must eject its blood through the aortic valve in each round of systole), aortic stenosis creates higher pressures against which the LV must contract. It's functionally similar to hypertension, except the increase in pressure is localized to the aortic valve itself. So, in someone with aortic stenosis, afterload is increased and the LV must work harder and generate greater contractile force in order to maintain cardiac output.

Afterload is decreased whenever arterial pressure is decreased. For example:

• Distributive shock: Distributive shock is characterized by widespread vasodilation. This leads to a systemic decrease in vascular resistance, which decreases afterload. The causes of this vasodilation vary depending on the cause of shock. In septic and anaphylactic shock, the inflammatory response to infection or antigen exposure causes widespread vasodilation. In neurogenic shock, sympathetic nervous system dysfunction results in loss of vasular tone, due to disruption in
• Anti-hypertensive drugs: Anti-hypertensive drugs function to lower blood pressure through a variety of mechanisms. Someone taking anti-hypertensives will have a decreased afterload compared to their normally hypertensive state.