Trinilos

Translation: at the beginning of heart failure the heart has to worker harder, and because it's a muscle it gets bigger, but weirdly the bigger the muscle the weaker the heart can squeeze resulting in less blood pumped - why?

Answer - at first it does pump better, but there are other changes that happen in the muscle cells which result in the size overall being bigger but the strength decreasing, meaning the heart stays large but doesn't pump well.

In medical school we're taught 2 things that didn't make intuitive sense to me:

1. Digoxin increases contractility and improves symptoms but does nothing to improve mortality. I'm presuming that mortality is associated with hypoperfusion, so why does a drug which improves cardiac output not decrease mortality?

2. AICDs are considered in heart failure patients so long as their NYHA classification is > IV. Why is this lower limit in place? It seems they'd still benefit from it, so my guess is this is a cost-benefit issue where patients aren't expected to live long enough for the surgery to be worth the risks associated with surgery?

Different places do different things. Every operation I've had I was sedated before going to the OR.

There are several kinds of adaptation depending on what's causing the change. There are fibers inside muscle cells which are built/broken down based on that cell's demand (these are sarcomeres). They can be built in parallel (issuing contraction strength and thickness) and parallel (increasing strength and stretchiness). There are also small organelles inside the cells which can increase or decrease to meet metabolic demand.

Exercise: Muscles squeeze veins returning blood to the heart, which provides some stretch. Metabolic/gas demand from the body drives an increase in heart rate and contraction strength. In total, this means the heart becomes bigger, stretchier, and more efficient in how it metabolizes fit energy. Sarcomeres are built in both parallel and series.

High blood pressure: diseased arteries become stiff and narrow requiring the heart to pump harder. There is no stimulus for increased speed nor is there increased blood return (like in exercise). This means the muscle cells become bigger, but not stretchier. Sarcomeres are built in parallel.

Heart failure: a multifactorial disease with many possible root causes (including high blood pressure) which typically causes overstretching of the heart muscle cells. They increase in stretchiness, but are limited in ability to contract (lifting heavy weights only effectively increases muscle when you lift the weight off the ground, and the heart needs to adequately pump it's volume out, which in heart failure it cannot). Sarcomeres develop on series, and less so in parallel.

This is oversimplified, but I hope it adequately answers your question. Like many diseases, heart remodeling pathology uses the multiple adaptations that would be normal in exercise in an abnormal way, causing an imbalance and thus disease.

Right, which will reduce EF. And I believe there's a similar explanation for HFpEFV wherein the diastolic dysfunction is a result of myocyte remodeling in parallel rather than series, diminishing ventricular stretch.