PRELOAD, AFTERLOAD AND CONTRACTILITY
Preload is the initial stretching of the cardiac myocytes (muscle cells) prior to contraction. It is related to ventricular filling.
Afterloadis the force or load against which the heart has to contract to eject the blood.
Contractilityis the intrinsic strength of the cardiac muscle independent of preload, but a change in preload will affect the force of contraction.
Afterload is the ‘load’ to which the heart must pump against. Afterload goes down when aortic pressure and systemic vascular resistance decreases through vasodilation.
Decreasing afterload will affect the Doppler numbers in a number of ways. Peak velocity (PV) may increase as the heart finds it easier to pump against decreasing pressures. This will also affect corrected flow times (FTc), as the duration of aortic blood flow will increase as afterload decreases.
Poor Left Ventricular Function
The waveform below demonstrates the response to apositiveinotrope. In the first (left) screenshot, the patient had a ‘rounded’ flow waveform, with a low Peak velocity (PV) and stroke volume (SV), possibly indicating left ventricular failure. The patient was not fluid responsive and following administration of apositive inotrope, both PV andSVincrease (right screenshot).
Systemic Vascular Resistance
Systemic vascular resistance (SVR) is the resistance to blood flow offered by all of the systemic vasculature [2]. An increase in SVR depends on the degree of sympathetic stimulation which itself depends on the degree of sympathetic activation, responsiveness of the vasculature, the number of vascular beds involved and the relative series and parallel arrangement of these beds to each other. Changes in blood viscosity also affect SVR.
SVR is an unreliable indicator of left ventricular afterload [2] since it reflects only peripheral vasomotor tone and not left ventricular systolic wall force. Discordant changes in left ventricular afterload and SVR can occur during pharmacological interventions as shown by Lang et al. They conclude “In the clinical setting, changes in SVR do not necessarily reflect left ventricular loading conditions since the true measure of ventricular afterload must consider the interaction of factors internal and external to the myocardium.”
References
1. Klabunde, R.E., Cardiovascular Physiology Concepts. 2005.Philadelphia. Lippincott Williams & Wilkins
2. Lang et al 1986. Systemic vascular resistance: an unreliable index of left ventricular afterload. Circulation 74:1114-1123
FAQs
Contractility is the intrinsic strength of the cardiac muscle independent of preload, but a change in preload will affect the force of contraction. Afterload is the 'load' to which the heart must pump against. Afterload goes down when aortic pressure and systemic vascular resistance decreases through vasodilation.
What are the three factors influencing stroke volume preload afterload or contractility and what factors might impact them? ›
Stroke volume index is determined by three factors: Preload: The filling pressure of the heart at the end of diastole. Contractility: The inherent vigor of contraction of the heart muscles during systole. Afterload: The pressure against which the heart must work to eject blood during systole.
What happens to preload contractility and afterload during exercise? ›
Cardiac output is enhanced by (1) greater preload, (2) increased heart rate, (3) increased myocardial contractility, and (4) reduced afterload during exercise, and both ventricles need to generate the same stroke volume.
What is the cardiac output made easy? ›
Cardiac output is the product of heart rate (HR) and stroke volume (SV) and is measured in liters per minute. HR is most commonly defined as the number of times the heart beats in one minute. SV is the volume of blood ejected during ventricular contraction or for each stroke of the heart.
How does problems with contractility preload and afterload affect the heart? ›
If you have too much preload and not enough afterload, then your ventricles will fill up faster than they can pump out all that blood — which can cause a stroke or even death.
How does preload contractility and afterload affect stroke volume? ›
An increase in afterload, for example, in individuals with long-standing high blood pressure, generally causes a decrease in stroke volume. [2] In summary, stroke volume may be increased by increasing the contractility or preload or decreasing the afterload.
What are the 3 major factors affecting cardiac output? ›
Cardiac output is the amount of blood the heart pumps in 1 minute, and it is dependent on the heart rate, contractility, preload, and afterload. Understanding of the applicability and practical relevance of each of these four components is important when interpreting cardiac output values.
Can increases in preload and contractility increase stroke volume? ›
This relationship, known as the Frank-Starling law after famous researchers from the early 1900s, basically states that an increase in preload leads to an increase in contractility and, therefore, stroke volume. The relationship between tension and length (i.e. stretch) is shown in Figure 1.
What are the three main factors that affect the stroke volume? ›
The three primary factors that regulate SV are preload, afterload and contractility. Heart rate (HR) also affects SV. Changes in HR alone inversely affects SV.
Why do you want to decrease preload in heart failure? ›
A doctor may prescribe medications that decrease preload to treat heart failure. While this may seem like an unusual approach, decreasing preload helps to reduce the amount of blood the heart has to pump. Reducing preload gives the heart a more reasonable workload.
Cardiac contractility of the ventricle increases during catecholamine stimulation, as occurs during exercise and emotional stresses.
Why does contractility increase afterload? ›
The increased afterload causes an increased end-systolic volume. This increases the sarcomere stretch. That leads to an increase in the force of contraction.
What best describes a preload? ›
Preload is defined as the stretch of myocardium or end-diastolic volume of the ventricles and most frequently refers to the volume in a ventricle just before the start of systole.
What does contractility mean in the heart? ›
A focused group of molecular physiologists stated that, “Cardiac contractility can be defined as the tension developed and velocity of shortening (i.e., the “strength” of contraction) of myocardial fibers at a given preload and afterload.
What are the two factors that cause cardiac output to increase during exercise? ›
The cardiac output increase is due to a large increase in heart rate and a small increase in stroke volume.
Is contractility independent of preload and afterload? ›
Contractility is the intrinsic contractile function of the ventricle, independent of preload and afterload. Alterations in contractility are shown on the ventricular function curve in Figure 1-8.
Does increasing preload increase contractility? ›
Increasing preload increases the force of contraction. The rate of increase in force of contraction per any given change in preload increases with higher contractility. This is expressed as a change in the slope of the end-systolic pressure volume relationship (ESPVR)
Does increased afterload decrease contractility? ›
During this same period, extensive research demonstrated an inverse relationship between afterload and systolic performance, which is accepted today. This means that cardiac output decreases as the afterload on the heart increases and vice versa.
Does afterload change contractility? ›
Conclusions: This study in newborn lambs demonstrates that stepwise increases in afterload increase contractility considerably and that this enables the heart to maintain stroke volume at different levels of afterload.
