Pathophysiology of Heart Failure

Those of you doing the course with me might realise that I've been posting things out of sequence. That is because I don't think I'll have time to write about everything this year, so I'm prioritising the lectures that I had a little bit more trouble with. As always, if you have any topics you want me to prioritise, let me know in the comments and I'll see what I can do :)

Define heart failure

Heart failure occurs when cardiac output is insufficient for the body's demands. This might occur because the heart isn't pumping out enough blood, or because demand for blood has been increased for some reason, or both.

Describe the aetiology, pathogenesis and pathophysiology of heart failure

Aetiology

Heart failure is largely preventable as a lot of the aetiological factors are lifestyle factors that could have been modified: coronary artery disease, obesity, hypertension, excessive alcohol consumption, diabetes, and so on. Pretty much anything that increases demand on the heart, or that damages the heart leading to impaired pumping, could lead to heart failure.

Pathogenesis and Pathophysiology

To understand the pathogenesis of heart failure, it is important to understand the factors that are important in normal cardiac output. The main variables affecting cardiac output are heart rate and stroke volume, so anything affecting either of those two variables could lead to heart failure. For example, arrhythmias affecting heart rate (as well as the ability of the heart to contract as a single unit) could lead to heart failure, as could damage to the heart affecting stroke volume.

Stroke volume can be further broken down into preload, contractility, and afterload. Factors affecting preload, such as too much or too little blood volume, could lead to a reduced stroke volume through the Frank-Starling mechanism (see here). Factors affecting contractility include coronary artery disease, which affects blood flow to the heart, as well as other diseases that affect the heart muscle directly. Finally, factors affecting afterload include blood pressure and arterial wall stiffness.

Sometimes, the body tries to compensate for insufficient cardiac output. Unfortunately, these compensatory actions can make things worse.

Firstly, the body might try and increase cardiac output by firing up the sympathetic nervous system and decreasing the parasympathetic nervous system. This is great for increasing heart rate and thus cardiac output, but it also increases cardiac work and electrical instability, thus increasing the risk of arrhythmia. Furthermore, sympathetic stimulation increases vasoconstriction, increasing resistance and by extension blood pressure, increasing the afterload on the heart.

Secondly, the body might try to use and abuse the renin-angiotensin-aldosterone system (discussed here under "salt reabsorption") to increase blood perfusion to the kidneys. Unfortunately, firing up the RAAS system can increase fluid and salt overload, which in turn increases cardiac preload and afterload.

As well as the above mechanisms, other signalling molecules, such as the natriuretic peptides (ANP and BNP), ADH, nitric oxide, endothelin, and various cytokines, might act to try and correct what the body senses is reduced blood perfusion. Unfortunately, these mechanisms can lead to increased afterload, damage to the heart, or other counter-productive effects.

When discussing the pathophysiology of heart failure, we need to consider two main types of heart failure: heart failure with reduced ejection fraction (HFrEF, a.k.a. systolic heart failure), and heart failure with preserved ejection fraction (HFpEF, a.k.a. diastolic heart failure).

In HFrEF, there is some damage to the ventricle (usually due to coronary artery disease) that affects ventricular function. HFrEF may be seen in dilated cardiomyopathy (a heart problem where the ventricles are enlarged with weak walls). In HFrEF, as the name suggests, there is reduced ejection fraction as the heart is not strong enough to pump out the usual amount of blood.

In HFpEF, the ventricles become hypertrophied (hypertrophic cardiomyopathy) and stiff, often due to hypertension. The ejection fraction remains normal or near-normal. Due to the stiffness of the ventricles, there is increased ventricular pressure, which can sometimes back up and cause increased pressure in the veins immediately preceding that side of the heart (i.e. vena cava pressures increase in right-sided heart failure and pulmonary venous pressures increase in left-sided heart failure). Furthermore, due to the increased ventricular pressure, there is less passive filling of the heart and therefore atrial contraction is more important. Therefore, tachycardia (which would decrease filling time) and atrial fibrillation (which would impair atrial contraction), are both poorly tolerated in people with HFpEF.

Understand the clinical relevance and principles of assessment in heart failure

There wasn't actually a lot on assessment in this lecture. There were some supplementary slides given with more details that we don't have to know about right now. I might look at that at a later date when I have a bit more time, but not now.

For now, it seems all we need to know are the tests used to diagnose HFpEF. B-type natriuretic peptide (BNP) greatly increases during HFpEF and can be used for diagnosis. Echocardiography to view the heart and catheterisation to measure the diastolic pressure can also be used for diagnosis.