Instead of memorizing guidelines and treatments, if someone can understand the physiology behind the disease process it is easier to remember. The body can make acute changes to afterload in response to systemic changes. There are also chronic diseases that make permanent changes that contribute to afterload.
For Part B, I will first look at diseases that acutely alter afterload, then will look at the physiological definition and physiological equations that show how afterload is determined. Finally, I will look at how chronic diseases affect afterload at a physiological level.
Acute changes to afterload:
Increased afterload due to acute systemic changes (Clamped down):
Most of this response is due to the renin-angiotensin-aldosterone system (RAAS). When there is low blood flow to the kidneys the RAAS system is activated. This can be due to decreased volume in the vasculature, like hypovolemia or hemorrhage, or it can be due to diseases causing a decrease in flow to the kidney despite a normal vascular volume, like heart failure, cardiogenic shock, and cirrhotic shock. Either way, there is an increase in angiotensin II which leads to vasoconstriction and increased afterload. This is often described as someone being "clamped down" and patients present with cool extremities.
Figure 1: RAAS System Physiology
https://www.verywellhealth.com/what-is-the-renin-angiotensin-system-1763941
Decreased afterload due to acute systemic changes (Vasoplegia):
The classic example of systemic changes leading to decreased afterload is sepsis and septic shock. When an infection enters the body, it causes a release of inflammatory markers or cytokines. This inflammatory response causes an increase in inducible nitric oxide (iNO) which dilates the vascular system. This dilation can dramatically decrease afterload and is often referred to as vasoplegia
Figure 2: Cytokines leading to inducible Nitric Oxide and Vasoplegia
https://www.quora.com/Why-is-there-hypoperfusion-in-septic-shock-when-there-is-vasodilation
This phenomenon is seen in other disease processes like acute pancreatitis and burns. Also, it can be seen in patients with acute cardiac dysfunction like post-myocardial infarction (MI), post-cardiac bypass, and post ECMO cannulation. The infarcted myocardium or exposure to the cannulas and circuits causes an inflammatory response and the release of cytokines.
When it occurs in cardiac patients it is often called cardiogenic vasoplegia and it is underdiagnosed. Patients can be in cardiogenic shock but still have vasoplegia, giving them a more mixed picture of cardiogenic + distributive.
Table 1: Acute Systemic Changes in Afterload
The Physiology of Afterload
Physiological Definition: The ventricular wall stress that occurs during systole
Physiology:
Laplace’s law shows that wall stress (T) is determined by the pressure across the ventricle during systole, or transmural pressure (P), multiplied by the cavitary radius (r) of the ventricle and then divided by double the wall thickness (H)(2).
Laplace’s law:
T = (P x r)/2H
This means that afterload is directly proportional to the pressure and the radius of the ventricle, and inversely proportional to the wall thickness.
How does this help?
It is now easier to see how chronic systolic cardiomyopathy (HFrEF) has problems with increased afterload. In chronic HFrEF the heart dilates and walls thin, this decreases wall thickness and increases the ventricular radius. Both of these will increase wall tension (afterload).
Looking back at part A, when there is a higher dam (more afterload), there is more water behind the dam, which also means more pressure. The same is true with the ventricle, more afterload means more pressure.
How Chronic Diseases Affect Afterload?
The LV radius and LV wall thickness are more easily visualized. The transmural pressure (P) is the pressure across the ventricular wall.
Figure 3: Left Ventricular Transmural Pressure
The ventricular pressure is dependent on the structures distal to the ventricle. Think of these structures as the tube the ventricle must push the blood through. The intrathoracic pressure is the pressure outside the ventricle, but in the thorax. This pressure changes with breathing and other processes like mechanical ventilation.
Determinants Affecting Transmural Pressure:
Group A: Outflow Pressure
1. Left ventricular outflow tract (LVOT)
2. Aortic valve (AV)
3. Aorta
4. Arterial vasculature
5. Blood
Group B: Intrathoracic Pressure
6. Intrapleural pressure
Understanding the different components resisting flow out of the ventricle
How group A determines ventricular pressure can be explained with Poiseuille’s Law and the formula for compliance.
Poiseuille’s Law:
Compliance:
In Poiseuille’s Law, the flow rate (Q) through a tube is directly proportional to the radius (r) and the change in pressure (P). This means that the larger the tube and the larger the pressure gradient across the tube the faster the flow rate, and since the radius is to the 4th power, small changes in radius can make large differences in flow.
The flow rate (Q) is inversely proportional to the length of the tube (l) and the viscosity of the fluid (n). In other terms, the longer the tube the slower the flow, and the thicker the fluid the slower the flow rate.
The change in pressure in Poiseuille’s Law is affected by compliance. A decrease in compliance will increase the pressure in the tube. The increased pressure in the tube will decrease the pressure gradient within the tube and so the change in pressure (P) will decrease which decreases flow.
A. How diseases alter ventricular outflow:
Using Poiseuille’s Law, the LVOT and AV contribution depends on their radius. When there is an LVOT obstruction or AV stenosis the blood must go through a much smaller space which decreases flow rate, puts more back pressure on the LV, which increases afterload.
The aorta is based on its compliance. Usually, it will allow increases in volume without large increases in pressure, but it can become less compliant. Looking again at Poiseuille’s Law, less compliance will decrease the pressure gradient between the LV and aorta which will decrease the blood flow rate.
The vasculature also has a compliance that can be decreased and added to afterload. The length of the vasculature also affects afterload.
The blood determines afterload depending on its viscosity. The thinner the blood, the lower the afterload and vice versa.
B. How disease alter intrathoracic pressure:
Intrathoracic pressure and how it affects afterload is better explained by going back to Laplace’s law and transmural pressure (P). Significant negative pressure will add to the transmural pressure and make the afterload higher. This is seen in diseases that cause decreased lung compliance requiring more negative pressure to achieve the same tidal volumes. Increased intrathoracic pressure will decrease afterload since it reduces transmural pressure (Figure 4). This is very well described at Deranged Physiology(5).
Figure 4: Positive Intrathoracic Pressure Decreases Afterload(5)
What Diseases Affect Afterload?
There are different medical conditions that can lead to afterload issues. Afterload can be increased and decreased. These are very different disease processes and why afterload is one of the markers used to differentiate types of shock.
Table 2: Chronic Diseases that Increase Afterload
Summary:
This is obviously a much more in-depth look at afterload compared to Part A, but hopefully, it helped show why certain disease processes are associated with changes in afterload. Additionally, by understanding how afterload is affected, therapeutics can be used to target the underlying cause and hopefully return the afterload to normal.
Left Ventricular Heart Failure Series:
Part 1a: Introducing Preload
Part 1b: Measuring Preload
Part 2a: Physiological Contractility
Part 2b: Clinical Contractility
Part 3a: Simplifying Afterload
Part 3b: The Physiology of Afterload
Part 4: Managing LV dysfunction
Other Left-Sided Heart Failure:
Part 1: Valvular disease
Part 2: LVOT obstruction/SAM
Cardiogenic Shock:
Part 1: Why a Protocol is Needed
Part 2: Cardiogenic Shock Protocols
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. Mahmood SS, Pinsky MR. Heart-lung interactions during mechanical ventilation: the basics. Ann Transl Med. 2018;6(18):349. doi:10.21037/atm.2018.04.29
5. Yartsef A. Effects of Positive Pressure Ventilation on Cardiovascular Physiology| Deranged Physiology. Derangedphysiology.com. https://derangedphysiology.com/cicm-primary-exam/required-reading/respiratory-system/Chapter%20523/effects-positive-pressure-ventilation-cardiovascular-physiology. Accessed January 16, 2022.
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