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So one of the clinical signs of Cardiac insufficiency is a low blood pressure, and to treat cardiac insufficiency we try to decrease the Afterload. what I don't get is that the Afterload is defined as being the force that opposes cardiac ejection and is represented by the blood pressure, and during Cardiac insufficiency we have a low blood pressure doesn't that mean the Afterload is already low ??

Thanks in advance!

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Short answer: When treating cardiac insufficiency the key focus is increasing stroke volume. To do this we don't just decrease afterload but we also lower preload and sometimes increase contractility.

Long answer

So cardiac insufficiency is all about cardiac output (CO) and CO = stroke volume(SV)* heart rate (HR). The key problem in cardiac insufficiency is the lowered stroke volume, i.e. the amount of blood that is ejected from the heart on each heartbeat. HR can sometimes be relevant but let's focus on the SV for now.

SV is mostly dictated by three factors afterload, preload and contractility. The Frank-Starling mechanism regulates the relationship between these factors.

There is an inverse relationship between afterload, the pressure the left ventricle has to overcome to eject blood, and stroke volume that is represented by the force/tension curve. So in the setting of cardiac insufficiency and high blood pressure the lowering of afterload is key.

There is however a more complex relationship between preload and stroke volume. Stroke volume increases with increased preload up until a certain threshold where the preload pulls the sarcomeres of the cardiac muscles to wide. At this point increased preload decreases the stroke volume even further. This is sometimes referred to as the Starling mechanism (see fig 1). In the setting of fluid overload as we see in cardiac insufficiency blood backs up in the pulmonary blood stream leading to increased preload to the point where it is so high as to decrease the stroke volume. This is where decreasing preload is helpful in increasing stroke volume.

Figure 2 The Starling mechanism (note that Ventricular end-diastolic volume is

The Sterling Mechanism

The relationship between preload and stroke volume is even further determined by the hearts contractility. An increased contractility leads to a greater increase in stroke volume with each unit of preload (see fig 2). In cardiac insufficiency contractility is usually decreased leading to lower stroke volume in relation to preload. Sometimes, especially in a critical care environment contractility is increased by giving inotropic medication.

Figure 3 (LV EDP: Left ventricular end-diastolic volume (i.e. preload))

Contractility affecting the starling mechanism

So when we treat cardiac insufficiency we can manipulate all those factors to alleviate the key problem of a low stroke volume.

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