I will try my best to explain it in layman terms. In medical language, “ secondary to” indicates “ as a result of an underlying illness”, so “cardiac arrest secondary to diastolic dysfunction” indicates “cardiac arrest as an outcome of diastolic dysfunction” or simply put “diastolic cardiac arrest”.
Systole ( systolic stage) is the part of the heart cycle where the heart agreements in order to pump blood from the right ventricle to the lungs and from the left ventricle to the remainder of the body. Diastole ( diastolic phase) 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 not enough to supply the body with blood, either at rest or on exertion.
The most obvious case of breakdown is when the heart does not drain throughout the systolic stage enough of the blood that it gets filled with during the diastolic stage. This is called systolic cardiac arrest. Its defining particular is a reduced “ ejection portion“, which indicates that the heart pumps out less than half of the maximum volume of blood that the heart is filled with during the end of the diastolic stage (ejection portion less than 50%, regular is 60%or above).
A heart with a failure to pump out enough blood throughout the systolic phase has most of the times also an issue getting filled with blood throughout the diastolic phase, a so called “ diastolic dysfunction“. The opposite, nevertheless, is not always true. One third of patients with symptoms of cardiac arrest only have a problem in the diastolic stage and seemingly no problem in the systolic phase. This is what we call a “cardiac arrest secondary to diastolic dysfunction” otherwise a “ diastolic heart failure“. It varies from “systolic cardiac arrest” in that the ejection fraction is regular.
How can it be that a client gets signs of cardiac arrest if their heart has gets filled with problem however still manages to pump out seemingly enough? To start with, the ejection fraction is truly only a ratio of the volume of blood drained to the volume of blood that the heart gets filled with. It states absolutely nothing about how much blood in fact leaves the heart.
- Let’s presume that the walls of the heart muscle are thickened (so called hypertrophy, as in arterial high blood pressure, 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 phase might be nominally enough, thus a typical ejection portion, but the volume is not actually enough to support the body’s needs.
- The ventricles get dilated (as in extreme valvular regurgitation, advanced coronary artery disease or dilatative cardiomyopathy). The volume of blood that gets pumped out is enough to cover the body’s needs at rest, but not at effort, where there is no “space” for further dilation of the ventricles.
In truth, it is not as easy as that. You do not require hypertrophy or dilation of the ventricles to have a diastolic dysfunction. The trademark is an increased stress of the heart walls throughout its filling phase due to increased stiffness of the walls. Hypertrophy (once again, as in arterial hypertension) does make the walls stiffer, however the walls don’ require to be thicker (hypertrophic) in order to be stiffer.
There are diseases of the heart that alter the structure of its walls making them stiffer. Some of these fall into the category of so called restrictive or infiltrative cardiomyopathy (as in amyloidosis), but any illness that triggers 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 cardiovascular disease, metabolic illness with diabetes, persistent kidney illness and, finally, aging (even in the lack of amyloidosis, which is largely a disease of older age).
Endothelial swelling and malfunctioning or obliteration of the small vessels (microvascular angiopathy) causes the formation of damaging conciliators which further restrict vessels and a decrease in the bioavailability of compounds such as nitrogen monoxide (NO), which are expected to dilate vessels. Increased stiffness of the veins leads to a moving of blood volume into the systemic flow, increasing arterial pressure (causing arterial high blood pressure). Increased tightness of the arteries triggers arterial hypertension, but even without arterial hypertension, it increases the tightness of both the heart muscle cells themselves and their extracellular matrix.
The increased tightness of the walls of the ventricles increases the filling pressure inside the ventricles and this increased pressure is moved backwards into the lung veins, triggering fluid to come out of the veins into the lungs, and backwards into the systemic veins, triggering fluid to come out of the veins into the rest of the body, manifesting itself usually as leg swelling.