Understanding Cardiac Preload and Afterload

The concepts of preload and afterload are very important to the understanding of cardiovascular medicine and to knowing how to care for patients with compromised hearts due to heart failure. Even so, the two terms can be confusing when it comes to understanding how the heart functions. Let’s take a look at what these terms mean, which things change these values, and which drugs can be used to affect the preload and afterload.

The preload is the amount of stretch or pressure left in the left ventricle at the end of diastole—when the heart is the most relaxed. It is also referred to as the left ventricular end-diastolic pressure or LVEDP. The greater the preload, the more pressure is available for the next cardiac contraction. The afterload is the amount of vascular resistance that must be overcome by the left ventricle to allow blood to flow out of the heart.  It is also referred to as the systemic vascular resistance or SVR.  The greater the afterload, the harder the heart has to work to push blood through the systemic vasculature.

Cardiac Preload

The preload is directly related to the stretch of the sarcomeres (or muscle fiber units) of the ventricular cardiac muscle. This, of course, is impossible to actually determine in a living person so it is indirectly measured as the left ventricular pressure during diastole or the ventricular end-diastolic volume.

Another way to look at this term is to think of it as the amount of venous return to the heart.  If this return is increased, there is more blood available for pumping and an increase in the stretch of the sarcomeres. When you look at preload this way, you can conceive of cases where the preload is too low, such as when there is hypovolemia with a lack of enough volume left over after pumping to stretch the left ventricle during diastole.  In the same way, too much venous return by the presence of excessive volume will increase the preload. This can be a problem in heart failure patients.

The Frank-Starling mechanism speaks directly to preload. According to Starling’s Law of the heart, changes in the venous return to the heart will alter the ability of the heart to change the force of contraction and will change the stroke volume of the left ventricle.  Stretching of the cardiac muscle fibers will increase the sarcomere length.  This will increase the amount of force generated by these myocytes so that the heart can more efficiently eject the excess venous return, resulting in an increased stroke volume.

So, what changes the preload of the heart?  As it turns out, there are many factors that will increase or decrease the preload.

What Increases the Preload?

Things that increase the preload include :

  • Increasing central venous pressure—this can occur through an increase in blood volume in the body so that there is increased volume in the venae cavae or through increased respiratory activity through exercise, which will increase the flow of blood through the lungs and the amount of blood going to the left side of the heart.
  • Increased ventricular compliance—the more compliant and stretchier the heart, the greater will the expansion of the left ventricular chamber be at a given left ventricular filling pressure. The greater the stretch, the greater the stroke volume.
  • Increased left atrial forces—the greater the force of the contraction of the atria, usually from increased sympathetic stimulation, the more blood will flow into the left ventricle and the greater will be the preload.
  • Decreased heart rate—the slower the heart rate, the greater is the left ventricular filling time with more blood flowing into the heart per diastolic period.
  • Increased pressure in the aorta—this increases the afterload, which will increase the amount of blood left over after contracting the left ventricle. This will increase the left ventricular end-diastolic volume and thus the preload.
  • Certain heart conditions—things like aortic stenosis and aortic regurgitation will increase the amount of blood in the left ventricle. The same is true of pulmonary valve stenosis and pulmonary valve regurgitation when it comes to the preload of the right ventricle. In addition, systolic failure of the ventricles will increase the stretch of the heart muscle fibers by decreasing the amount of blood that can be pumped out of the heart per contraction.

What Decreases the Preload?

Things that decrease the preload include :

  • Decreased central venous pressure—this can happen when standing upright; gravity will allow blood to pool in the lower extremities, leading to a decrease in central venous pressure. Low blood volume from dehydration or hemorrhage will also decrease the central venous pressure.
  • Impairment of atrial contraction—this can happen in atrial fibrillation, which will decrease the “atrial kick” so less blood fills the left ventricle prior to systole.
  • Increased heart rate—this will shorten diastole so that there will be less time to fill the heart during the shorter time period, resulting in a decreased preload.
  • Decreased afterload—anything that enhances the ejection of blood out of the heart will decrease both the end-systolic ventricular volume and the end-diastolic ventricular volume. This decreases the preload.
  • Decreased ventricular compliance—anything that makes the heart less stretchy, such as ventricular hypertrophy or impairment of the relaxation ability of the heart (the lusitropy of the ventricles), will decrease the preload.
  • Heart defects—those valvular defects that decrease ventricular inflow, such as mitral or tricuspid stenosis, will decrease the filling ability of the left ventricle and will decrease preload.

What Does Afterload Mean in Cardiac Physiology?

The afterload is directly related to the force that must be overcome by the heart in order to eject blood into the systemic or pulmonary vasculature.  More directly, it is connected to the pressure in the aorta and is expressed as the “wall stress” on the left ventricle.

According to LaPlace’s Law of the heart, wall tension in the ventricles is proportional to the pressure in the ventricle times the ventricular radius.  This is further expanded to include the definition of wall stress, which is proportional to the left ventricular pressure times the radius and divided by the wall thickness.

The pressure generated by the ventricle during systole is very near to the aortic pressure (unless the patient has aortic stenosis, resulting in a pressure gradient across the aortic valve).  A thick, hypertrophied ventricle will have less wall stress and will have a reduction in afterload. The thicker the ventricular wall, the less tension will be on each sarcomere unit in each heart muscle fiber.

What Factors Affect Afterload?

Factors that affect afterload include :

  • Increased or decreased aortic pressure—when the blood pressure is increased, there is a natural increase in the pressure the ventricle must press against and increased Similarly, when the blood pressure is reduced, there is less force to be pressed against by the ventricles and a reduction in afterload.
  • Increased or decreased systemic vascular resistance (SVR)—the systemic vascular resistance will affect the overall pressure and will change the resistance to outflow of the ventricles. Increased SVR will increase the afterload, while decreased SVR will decrease the afterload.
  • Aortic valve stenosis—this will not affect the aortic pressure but will, of course, change the force that the heart needs to push against, increasing the afterload.
  • Ventricular dilation—this will increase the afterload by increasing the radius of the heart chamber. The wall stress, as you know, is proportional to the radius of the chamber so it will increase the end-diastolic volume because the ventricle will not be able to push blood out to the extent it needs to. This decreases the stroke volume or the amount of blood that is pushed out of the ventricle with each beat.

The Relationship Between Afterload and Preload

There is a relationship between afterload and preload. Anytime the afterload is increased, the stroke volume will be decreased and the left-ventricular end-diastolic volume (the preload) will be increased.  Increased afterload will decrease the speed of myocardial muscle fiber shortening.  Because the time frame for ventricular ejection is only 200 milliseconds, a shorter velocity translates to more blood left in the ventricle and an increased preload. Conversely, a decreased afterload will increase the stroke volume and reduce preload.

This relationship between preload and afterload is used in the management of heart failure.  Drugs like vasodilators will decrease arterial pressure, which will increase stroke volume and reduce the ventricular preload. The left ventricle will be able to eject more blood volume, which leaves less blood in the ventricle after each beat.  The ventricle will be able to generate less pressure before it can open the aortic valve and the velocity of ejection will be increased; more blood can be ejected during systole.

You should know that there are certain baroreceptor reflexes that will change both the heart rate and strength of the heart (inotropy) when the afterload is altered. Both of these values will change the end-diastolic volume, the stroke volume, and the end-systolic volume.  For example, suddenly reducing the blood pressure will trigger a reflex that will increase the ventricular inotropy and the heart rate.  These will reduce the filling time, further decreasing the preload and the stroke volume.

What Drugs Affect Preload and Afterload?

In managing heart failure, attempts can be made to decrease the preload or decrease the afterload—both of which will improve the contractility of the ventricle and the cardiac output.  Preload reducers include those medications that contain nitroglycerin.  This is the drug of choice in those patients with heart failure who do not have low blood pressure. Low doses will reduce the preload, while high doses will mildly reduce the afterload.

Furosemide (Lasix) and other loop diuretics will decrease the preload by decreasing the total blood volume. These drugs do not act on the heart but cause renal diuresis within an hour of intravenous administration.  Because about half of all heart failure patients have volume overload, the administration of a loop diuretic will improve this problem, resulting in an improvement in heart function.

An afterload reducer, on the other hand, will attempt to cause afterload reduction by reducing the systemic vascular resistance. This decreases the “load” on the heart, which improves cardiac output. An added advantage to this approach is that many of these drugs will improve renal blood flow, which enhances urinary output and may reduce preload as well.

Captopril and other ACE inhibitors will prevent the conversion of angiotensin I in the blood to angiotensin II by inhibiting the action of angiotensin-converting enzyme.  This results in vasodilation, reduction in systemic blood pressure, and reduction in afterload.  Aldosterone secretion is reduced, which has an effect on renal sodium reuptake and resultant water reuptake. This will reduce preload secondarily.   Intravenous captopril will improve cardiac output within fifteen minutes of administration.

Nitroprusside directly acts on vascular smooth muscle, causing it to relax.  By relaxing arterial smooth muscle, the systemic vascular resistance will decrease and blood pressure will be reduced. The major effect of nitroprusside is on the arteries, meaning that it affects afterload more than preload.  It does, however, relax venous smooth muscle, reducing the preload to a lesser degree.  Within minutes of intravenous administration, the cardiac output will be improved and heart failure symptoms will diminish. It works best in heart failure patients that have pulmonary edema and hypertension.