But what is heart failure?
An attempt at an explainer for the curious layman.
Hello and welcome back to another edition of medically minded! I’m keeping to my promise of a change of pace this week with a relatively shallow deep dive into a common condition that conjures no explicit framework in the mind’s eye of the layman but affects nearly all of us as we age…
“They’ve got COPD”, a relative will often tell me with a knowing look while I’m rushing through a patient’s medical history in the emergency department.1 And this term clearly means something to them at this point. I’m sure it was gibberish the first time they heard it, but with the help of Dr Google, COPD expands into chronic (long-term) obstructive (blocked) pulmonary (lungs) disease. So the lungs are blocked, and there’s not enough oxygen, and the treatments help to open the airways, which all makes sense. Don’t get me wrong, this is still grossly oversimplified to the point of being wrong, but the entry-level concept makes sense.
Heart failure is as common, if not more so, than COPD. Yet, the term failure invokes no real conceptual framework for our patient to understand anything beyond the implied dysfunction. Which bit is failing exactly? Isn’t this just a heart attack? Ask your doctor, and they’ll typically explain something along the lines of the heart being a pump and it not working so well, leading to a buildup of ‘fluid’ where it’s not wanted. We simply give some medicines to remove the extra fluid and all is (eventually) well.
Listening to that explanation, you could be forgiven for thinking medicine was still guided by the philosophy of the four humours: an imbalance of too much fluid doesn’t sound too out of place with an excess of blood, phlegm, yellow bile or black bile. Doctors are well practiced at explaining medical concepts in medical terms, but every now and then a question highlights a gulf in understanding that can be difficult to bridge - in this case: “doesn’t the heart pump blood, not fluid?”
So in the first of a series of medical explainers, let’s look into bridging this gap as best we can, using some basic concepts of anatomy and physiology to build a model of heart failure.
Core concepts
An 84 year-old man is rushed into resus2, a tight fitting face mask hissing as it funnels life-prolonging oxygen from the pressurised tank into his sodden lungs. His legs are completely swollen and leave a deep thumb print when pressed, and he is coughing up pink frothy phlegm in-between rattling gasps for breath. I take a brief history from the paramedics and get to work with my assessment. A chest x-ray highlights the graveness of the situation - what is usually mostly black with streaks of white for the ribs and heart is now almost completely white, like an overexposed polaroid.
Eight years earlier, I’m in anatomy class holding a human heart, which is where we begin our explainer.3 The first thing to understand about the heart is that it actually pumps two separate circuits of blood. The first is a low-pressure circuit that pumps blood a short distance to the lungs and back to collect oxygen, the second is a high-pressure circuit that receives the blood from the lungs and pumps it into a large network of arteries that feed the rest of the body. This blood eventually making its way back to the heart via some large veins, ready to begin its journey back to the lungs once more. To maintain some level of separation between these low- and high-pressure circuits, the heart needs an area to receive blood from each circuit, and an area to pump to each circuit. Thus, we end up with our classic heart diagram, four areas or ‘chambers’ that feed blood in two separate circuits.
The left heart (which is on the right as we look at it in the diagram, confusingly), pumps blood to the body under high pressure, while the right heart (on the left, you’ll get used to it I promise) pumps blood at a much lower pressure to the lungs.
The blood itself is much more than a mass of red blood cells. The vast majority of it is water (~90%) and the rest is a smorgasbord of proteins, red and white blood cells, electrolytes, nutrients (including waste), and dissolved gases. So what we think of as blood, is really less like a bunch of red blood cells and more like… a fluid. Gasp!
The heartbeat and cardiac output
Okay, still with me so far? Now let’s zoom in on what the heart is actually doing. As a pump, the heart is an engineering marvel. The heart is built with carefully layered muscle fibres which can contract in one direction only, yet they form a complex pattern that allows the heart to not only squeeze into a small ball when ejecting blood but also twist like a spiral. After contracting, it simply relaxes back to full size. This relaxation process is actually very important: the heart can only pump out what it can fill, and the heart relaxing sufficiently causes a big sucking action4 which is important for drawing blood in. The two top chambers of the heart, the atria, separately receive blood from the lungs (on the left heart) and the body (the right) before then pumping it into the bottom two chambers, the ventricles.
To make the whole process efficient, the heart’s four chambers each have an associated valve that is designed to gatekeep blood from both exiting too early and also from back flowing once it has been pumped out, ensuring all the blood flows in one direction.5 The valves allow pressure to build, ensuring the blood is able to push past the forces of gravity to make it to important places, like your brain. The final result of this process is that the heart pumps a given amount of blood per beat, and beats a number of times each minute. Multiple those two numbers together and we have a measure of cardiac output, which is an important measure of heart function.
What determines how much blood the heart can squeeze per beat? This amount is called the stroke volume, and is the last bit to cover before we get into how it all goes wrong. Stroke volume is predominantly determined by three factors. First of all there is the preload, meaning the amount of blood we can fill the ventricles with before the valves slam shut and eject the blood out to the rest of the body.6 A famous law in medicine is that the more the heart stretches as it fills with blood, the stronger the heart can contract. This is a bit like how the more you wind your arm back, the more distance you can achieve on a throw. However, in both of these cases, there is the same caveat: an excess level of stretch can weaken the eventual ejection/throw. There is a sweet spot where the ventricle gets stretched just enough to produce a maximal contraction.
Preload’s older brother is afterload, which is the force the heart has to push against from trying to pump the blood down a series of arteries that are just a bit bigger than a drinking straw. More afterload equals more resistance that the heart has to push against, and a lower stroke volume - no messing about with sweet spots here. People with high blood pressure and stiff arteries full of cholesterol have a much higher afterload, which can cause problems for an older, weaker heart.
The third and final factor influencing stroke volume is the contractility of the heart itself, referring to how forcefully the heart contracts when it pumps blood during a heartbeat. A weaker heart can fill to the same preload as a stronger one, but less of the blood will make it out of the heart due to the ventricle generating insufficient force, and will simply wash back into the chamber instead, increasing the filling pressure in the ventricle compared to the more contractile heart’s emptier ventricle.
When things go wrong
Right, so we’re finally ready to ask what happens when the heart is no longer up to the task? Perhaps the valves are no longer working, causing blood to flow backwards as well as forwards. Or instead, maybe the heart muscle has been ravaged by a heart attack and can no longer pump with the same strength it used to. With age, the heart can struggle to fill properly, because like the other tissues in the body, it too can become a bit old and stiff over time, and no longer able to spring back to full size with the same elasticity it once had.
Now we’re into the realms of heart failure, which can present in different forms depending on exactly how the heart is struggling. If the left side of the heart is unable to pump enough blood to the body with each beat, or is unable to fill at the same pace that blood is returning from the large veins, the blood will begin to back up into the circuit like a traffic jam. Where does the left heart receive blood from again? Well remembered, the lungs. So the pressure in the blood vessels in the lungs begins to increase as the heart simply cannot clear it fast enough (insufficient cardiac output). After enough time, the pressure becomes overwhelming and the watery component of the blood is able to pass through the vessels into the lung itself. Large molecules like red blood cells and proteins don’t pass through, but the water content passes through fairly easily. The patient is beginning to drown in their own fluid. The pressure can burst tiny vessels called capillaries which allows small amounts of blood to leak out, giving a pink tinge to the patient’s frothy, watery phlegm.
Why does the heart not beat faster? Well it can, but there’s a catch! The heart can only fill with blood while it is relaxing, and a faster heart rate means less time to relax, meaning less time to fill. As we mentioned earlier, if the heart has less time to fill (a lower preload), then the resulting contraction is nearly always weaker. So speeding up the heart rate to try and chuck more blood out can paradoxically lower the amount of blood pumped over a given time period.
The left side of the heart feeds back into the lungs, which then increases the pressure the right heart has to work against as it tries pump blood into the lung vessels. The right side of the heart is far weaker than the left as it only needs to be strong enough to pump blood the short journey to the lungs. It actually relies on the much stronger left side to help it generate this force, meaning once the left side begins to struggle, so does the right. Except now, blood is backing up into the whole body, not just the lungs.
Fluid typically reveals itself in the feet first. The fluid that is squeezed out from the blood vessels under too much pressure accumulates under the skin, among other places, and tends to follow gravity. So patients will notice swollen ankles if they stand or sit, or will become breathless when they lie flat as the fluid essentially washes into the lungs. An early presentation of heart failure typically involves ankle swelling and waking up multiple times per night short of breath. Asking how many pillows a person sleeps with is genuinely an essential part of a heart failure history!
Other organs are also affected. The intestines become swollen, making absorption of nutrients more difficult. The liver also struggles as it is a major confluence of the circulation around the intestines themselves. The kidneys, often the first to cause further trouble when something else has gone wrong in the body, sense that the cardiac output has fallen and release hormones that increase blood pressure (worsening afterload) and increasing the circulating volume (which can help preload but can also push it past the sweet spot into destructive territory).
A vicious cycle begins, where the failing ability of the heart to pump a sufficient quantity of blood causes the body to panic that the heart is failing, so the kidneys attempt to increase the circulating volume even further, causing the heart’s struggles to only worsen. Now, without intervention, we have a runaway reaction, often finally precipitated into crisis by the development of a chest or urine infection, which heart failure sufferers tend to be more vulnerable to. And so we end up with our poor 84 year-old man, legs like balloons, lungs bathed in fluid, gasping for breath.
So what are we to do?
Buying time and long-term remodelling
The mainstay of early treatment for heart failure is the use of diuretics, medications that force the kidneys to offload fluid by making a patient urinate it out. The logic is fairly straightforward: an excess of fluid causes congestion, this congestion is relieved by removing fluid. However, removing fluid in and of itself does little to fix the long-term issue. A range of medications are prescribed that encourage the kidneys to stop trying to increase blood pressure and circulating volume, and to also slow the heart down to allow it to spend more time filling and contract more forcefully. These are crucial to give the heart enough of a breather to successfully remodel into a stronger, more efficient heart once again. Of course, the treatments very much rely on what the cause of heart failure is underneath, e.g., if a valve is failing, having surgery to fix the valve is going to be necessary to allow successful heart remodelling.
In the emergency setting, there are more options than diuretics alone to treat the failing heart if needed. Often, excessive diuretics can begin to dehydrate the patient, causing harm to the kidneys and worsening blood supply to the tissues. We can use a pressurised face mask which helps open the blood vessels in the lung, allowing more fluid to reabsorb, or start an infusion of nitrates that achieve a similar effect. Some patients are in extremely dire straits and require medication that stimulates the heart to beat with more force, and at the extreme end, we can install mechanical devices that physically help shoot the blood out of the ventricle or the main artery leaving the heart.
Conclusion
If you’ve stuck with this, congratulations! You can now blag your way through a conversation with a group of medical students if nobody looks too closely and asks you only about this one topic7.
Heart failure is a topic that is extremely simple to describe in a sentence, but once you look into any of the mechanisms underpinning the pumping action of the heart, you quickly become mired in ‘A affects B affects C which can affect A” type logic, as any change to part of the heart’s double circuit is bound to have ripple effects to the other areas in that circuit. While the principles of fluid overload in the lungs and body downstream from increased pressure in the ventricle are relatively universal to heart failure, the pattern of how patients present can vary considerably. I’ve tried to avoid getting too into the weeds here, but the relationships between the pressures in the heart as it relaxes, the volume the ventricle expands to while filling (preload), the force the heart contracts with (contractility), and the resistance the heart has to pump against (afterload) are extremely context dependent in terms of their interplay. Furthermore, whether the buildup of pressure in the ventricle is due to a failure of the heart to relax sufficiently or to pump sufficiently (or both!) affects the therapy options and the patient presentation.
But hey, now you have an understanding of what this mysterious excess fluid is, where it comes from, why we get rid of it, and hopefully some reassurance that we have moved beyond Ancient Greece in our understanding of disease.
Thank you for reading! I hope you enjoyed something a bit different for this post. I have been really grateful for the comments I have received from those of you who have read along so far and I’m always keen for ideas for other topics you would like covered. MM.
Nb: this post does not constitute medical advice.
No such thing as an ER in the UK, please and thank you.
Resus, or the resuscitation area, is a subsection of the emergency department where the sickest patients are rushed straight in by ambulance. It has more doctors, nurses, and resources to stabilise the critically ill patients.
A time jump which would make Christopher Nolan proud.
Shockingly, this is not actually medical terminology. Also, grow up.
The timing of all this is organised by a network of natural pacemaker cells transmitting signals to nerves that run inside the heart to ensure it all syncs up like clockwork, but this is a subject for another day.
The sound of the valves slamming shut in sequence is what produces the lub-dub noise of a single heartbeat.
Or doctors’ strikes, or the state of medicine, if you’re an avid reader, which of course you are.