The Pathophysiology of Heart Failure - A biological civil war
Heart failure defined as a complex syndrome in which structural or functional impairment of ventricular filling or ejection of blood results in dyspnea, fatigue and other signs of heart failure. That is a confusing definition. Let’s try to break that down.
Heart failure, as the name tells us, is the inability of the heart to perform its function. And what is that function? Circulation of blood. In order to circulate the blood, the heart has to first receive the blood and then pump it and anything that hampers either the flow of the blood to the heart or the heart’s ability to pump blood out will ultimately lead to heart failure.
Now, heart failure can be of two types - heart failure with preserved ejection fraction or diastolic failure and heart failure with reduced ejection fraction or systolic failure.
Heart failure with preserved ejection fraction is usually because of some kind of restrictive pathology. It occurs because the heart muscles become rigid and and less flexible. Heart failure with reduced ejection fraction occurs when there is some structural damage to the heart or the heart becomes weak due to some functional insufficiency. The aetiologies for both these types of failures are given in the table below.
So now that we have understood what heart failure is, it is important to understand how exactly hear failure happens. It usually starts with an index event. The index event can be abrupt, like a myocardial infarction or it can be insidious, like chronic volume or pressure overload. This event damages the myocytes and reduces the ability of the myocardium to generate force. This results in the heart not being able to contract effectively.
However, immediately after the index event, the patients do not become symptomatic. This is because there are some compensatory mechanisms in the body that keep the circulation going even in times of stress. But when these compensatory mechanisms are also overloaded, then the patients become symptomatic.
What does the body do to compensate for the damage caused by the index event? In an acute response to the index event, three things happen.
The fall in cardiac output is sensed by the baroreceptors in the carotid body and aortic arch and and they activate the renin and angiotensin system. There is increased sodium and water absorption. This increases the circulating volume and maintains the perfusion.
There is a reflex sympathetic overdrive which results in increased myocardial contractility.
In addition, there is increased systemic vascular resistance due to reflex vasoconstriction.
These compensatory mechanisms are meant to protect the body from the acute effects of heart failure. However, what happens when these three mechanisms continue to try and rescue a failing heart.
The increases circulating volume and the increased myocardial contractility, when chronic, increase the myocardial demand many fold. The increase in after load due to the vasoconstriction also increases the load on the heart as it has to pump against higher pressures. Eventually the heart gives up and the antidote becomes the poison.
But what does it mean, really? On a cellular level, how does the heart fail? The damage to the heart occurs on three levels - the myocyte, the myocardium and the left ventricular geometry.
In the myocyte, there is damage to the cross bridge formation and there is also failure of the excitation contraction coupling.
In the myocardium, there is myocyte loss due to necrosis and apoptosis and autophagy and these cells are replaced by degeneration and fibrosis.
While these changes happen microscopically, macroscopically the left ventricle dilates, becomes more spherical and the walls become thin, making it weak.
The heart is one of the most intricate structures in the human body. However, like every structure, it too has a limit and when that limit is exceeded, it stops functioning and gives up on us sometimes.
Heart failure is a tragedy of the human body because the systems put into place to protect the heart will themselves ultimately lead to the hearts untimely demise.
Author: Narendran Sairam (Facebook)
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