I will try my best to discuss it in layman terms. In medical language, “ secondary to” means “ as a result of an underlying disease”, so “heart failure secondary to diastolic dysfunction” indicates “heart failure as an outcome of diastolic dysfunction” or to put it simply “diastolic heart failure”.
Systole ( systolic phase) is the part of the heart cycle where the heart agreements in order to pump blood from the ideal ventricle to the lungs and from the left ventricle to the rest of the body. Diastole ( diastolic stage) is the part of the heart cycle where the heart’s ventricles are filled with blood. Cardiac arrest is a condition in which the function of the heart is inadequate to supply the body with blood, either at rest or on exertion.
The most obvious case of malfunction is when the heart does not drain throughout the systolic phase enough of the blood that it gets filled with throughout the diastolic phase. This is called systolic heart failure. Its specifying particular is a reduced “ ejection fraction“, which means that the heart pumps out less than half of the maximum volume of blood that the heart is filled with throughout the end of the diastolic stage (ejection portion less than 50%, regular is 60%or above).
A heart with an inability to drain enough blood during the systolic stage has the majority of the times likewise a problem getting filled with blood during the diastolic phase, a so called “ diastolic dysfunction“. The opposite, nevertheless, is not always true. One third of patients with signs of cardiac arrest only have an issue in the diastolic phase and apparently no issue in the systolic phase. This is what we call a “cardiac arrest secondary to diastolic dysfunction” or else a “ diastolic cardiac arrest“. It differs from “systolic heart failure” in that the ejection fraction is typical.
How can it be that a client gets signs of cardiac arrest if their heart has gets filled with difficulty however still handles to drain seemingly enough? Of all, the ejection fraction is really just a ratio of the volume of blood pumped out to the volume of blood that the heart gets filled with. It states nothing about how much blood actually leaves the heart.
- Let’s presume that the walls of the heart muscle are thickened (so called hypertrophy, as in arterial hypertension, aortic stenosis or hypertrophic cardiomyopathy). The inner volume of the ventricles (cavum) gets smaller sized, so that the heart is filled with less blood. The percentage of blood that gets drained throughout the systolic stage may be nominally enough, thus a regular ejection portion, however the volume is not actually enough to support the body’s requirements.
- The ventricles get dilated (as in severe valvular regurgitation, advanced coronary artery illness or dilatative cardiomyopathy). The volume of blood that gets drained is enough to cover the body’s needs at rest, however not at effort, where there is no “room” for further dilation of the ventricles.
In reality, it is not as basic as that. You do not require hypertrophy or dilation of the ventricles to have a diastolic dysfunction. The hallmark is an increased tension of the heart walls throughout its filling stage due to increased stiffness of the walls. Hypertrophy (once again, as in arterial high blood pressure) does make the walls stiffer, but the walls put on’ need to be thicker (hypertrophic) in order to be stiffer.
There are diseases of the heart that change the structure of its walls making them stiffer. A few of these fall into the category of so called limiting or infiltrative cardiomyopathy (as in amyloidosis), but any disease that causes systemic swelling and endothelial dysfunction (dysfunction of the inner layer of the vessels) can cause the walls of the heart to end up being stiffer: ischaemic heart disease, metabolic illness with diabetes, chronic kidney illness and, lastly, aging (even in the lack of amyloidosis, which is largely an illness of older age).
Endothelial inflammation and malfunctioning or obliteration of the small vessels (microvascular angiopathy) triggers the development of harmful arbitrators which further restrict vessels and a reduction in the bioavailability of compounds such as nitrogen monoxide (NO), which are expected to dilate vessels. Increased tightness of the veins leads to a moving of blood volume into the systemic blood circulation, increasing arterial pressure (triggering arterial hypertension). Increased stiffness of the arteries triggers arterial high blood pressure, but even without arterial high blood pressure, it increases the stiffness of both the heart muscle cells themselves and their extracellular matrix.
The increased stiffness of the walls of the ventricles increases the filling pressure inside the ventricles and this increased pressure is moved backwards into the pulmonary veins, causing fluid to come out of the veins into the lungs, and in reverse into the systemic veins, causing fluid to come out of the veins into the remainder of the body, manifesting itself typically as leg swelling.