When dealing with patients who have left ventricular systolic dysfunction, I believe afterload is the most important hemodynamic component to focus on. In this blog, I am going to give a simplified explanation for afterload. Then building on that will discuss afterload and its effects on preload and ventricular function. Ending part A, I will discuss how to measure afterload.
Part B will discuss the physiology and equations behind afterload and how it correlates clinically.
Breaking down cardiac output in terms of the Left heart.
Let’s relook at the breakdown of cardiac output into its four core components (Figure 1). I have added in the preload and contractility components that were filled out in parts 1 and 2.
Figure 1: Cardiac output breakdown
Part 3: Afterload
Definition: Afterload is defined as the load or resistance the heart must overcome during systole. This is the simplified definition. It is more accurately defined as the forces opposing the shortening of the myocardia during systole (1).
A Simplified look at afterload:
Afterload is often visualized as a dam the ventricle must overcome that can be raised or lowered. The amount of fluid let out is the stroke volume. If the dam is raised, the amount of water released is decreased and there will be limited forward flow and the water will back up. If the dam is lowered, the amount of water released will increase and the release of water will decrease the amount of water behind the dam.
Figure 2: Afterload as a Dam
How does afterload affect other hemodynamics markers?
For a better understanding of afterload, it can help to look at how afterload changes the Starling Curve and the Cardiac Pressure-Volume Loop.
Afterload vs. Stroke Volume:
Stroke volume has an inverse relationship to afterload. When afterload decreases, the LV has less to push against, and stroke volume increases. The same is true when afterload increases, it is significantly harder to push against and stroke volume decreases.
Figure 3: How Afterload Affects Stroke Volume
Afterload vs. Ventricular Function:
As described in part 2, contractility is independent of preload and afterload, but ventricular function can change with changes in afterload. Ejection fraction (EF) is the most common measurement of LV function. When afterload decreases, stroke volume increases for the same end-diastolic volume (EDV) which leads to a lower end-systolic volume (ESV). So the graph is identical to Figure 3, decreasing afterload increases EF and increasing afterload decreases EF.
SV = EDV-ESV
EF = SV/EDV x 100
Figure 4: How Afterload Affects Ejection Fraction
Afterload vs Preload:
To say that afterload affects preload is an oversimplification, but when the LV unloads more volume during the systole, there will be less left-over volume in the ventricle. This means a lower LVEDV or LVEDP, which correlates to a lower preload. Increases in afterload increase preload, and decreases in afterload decrease preload.
Afterload and the Pressure-Volume Loop:
Changes in afterload will slide the pressure-volume loop to the left or the right. When it shifts to the right, the loop extends vertically and contracts inward which means there will be higher pressures and smaller stroke volume. When it shifts to the left the loop shortens and widens, so the pressures drop and the stroke volume increases.
Figure 5: Afterload and the Pressure-Volume Loop
Measuring Afterload:
1. Systemic Vascular Resistance (SVR):
The most common way to measure afterload is SVR. The SVR is the resistance the LV must push against. Calculating SVR is based on a derivation of Ohm’s law, V = IR. This becomes the formula the resistance (R) equals the pressure at the beginning of the system minus the pressure at the end of the system (△P) divided by the flow (F).
R = △P/F
or
SVR = (MAP-CVP)/CO x 80
*Multiplying the equation by 80 changes the units from Woods Units (WU) to Dynes.
Normal Range: 800-1200 dynes⋅sec⋅cm-5
This can be measured completely non-invasively using transthoracic echo to get the cardiac output, and carotid tonometry to get the change in pressure. However, it is usually calculated with some type of invasive device, using a combination of a central line, arterial line, or pulmonary artery catheter.
2. Wall stress:
This has been looked at and can be calculated using echo, but does not correlate with SVR and is not used currently (4).
There are no other markers currently used for afterload measurement.
Summary:
Afterload is the most important component in cardiac output because of how it affects the other components. Let’s look at heart failure, optimizing afterload, by decreasing it, will decrease preload and increase EF, both of which will help heart failure patients. This is beneficial because there are many PO options for afterload reduction and no real options for PO inotropy. You could argue Digoxin, but it has minimal inotropy. Visualizing the lowering or raising of a dam will help in understanding how afterload affects hemodynamics. Lowering the dam increases forward flow (Increases stroke volume) and lowers the amount of volume behind the dam (Decreases preload).
Table 1: Afterload Assessment
Figure 6: LV Afterload Measurements
Figure 7: Cardiac Output Breakdown Complete
References:
1. Crystal GJ, Assaad SI, Heerdt PM. 24 - Cardiovascular Physiology: Integrative Function. In: Hemmings HC, Egan TD, eds. Pharmacology and Physiology for Anesthesia (Second Edition). Philadelphia: Elsevier; 2019:473-519.
2. Klabunde, R., 2017. CV Physiology | Cardiac Afterload. [online] Cvphysiology.com. Available at: <https://cvphysiology.com/Cardiac%20Function/CF008> [Accessed 16 January 2022].
3. Yartsef A. Determinants of afterload | Deranged Physiology. Derangedphysiology.com. https://derangedphysiology.com/cicm-primary-exam/required-reading/cardiovascular-system/Chapter%20025/determinants-afterload. Accessed January 16, 2022.
4. Greim C, Roewer N, Meissner C, Bause H, Schulte am Esch J. Abschätzung akuter linksventrikulärer Nachlaständerungen. Untersuchung mit der transösophagealen Echokardiographie bei beatmeten Patienten [Estimation of acute left ventricular afterload alterations. Transesophageal echocardiography in artificially respirated patients]. Anaesthesist. 1995;44(2):108-115. doi:10.1007/s001010050137