Heart attacks and cardiac arrests (Part 1)

In the next two or three posts, I want to talk about some acute cardiac conditions that people have usually heard of but are often a bit unclear about, or even completely misunderstand. The list includes heart attacks, heart failure, shock, cardiomyopathy and cardiac arrest.

Heart attacks

There are more than 100,000 heart attacks in the UK each year. The good news is that more than 7 out of 10 victims live to tell the tale. Actually, it’s really great news because when I first embarked on my medical career, the exact same proportion of heart attack victims died. The vast improvement in the outlook during the past 30-40 years probably isn’t all down to me, but just saying. The bad news is that if you are unlucky enough to have an out-of-hospital cardiac arrest as a consequence of your heart attack, your chances of survival are less than 1 in 10.

Is a heart attack the same as a cardiac arrest?

The answer is no. Although heart attacks may present as cardiac arrests, not all heart attacks cause cardiac arrest, and there are other causes of cardiac arrest apart from heart attacks.

What is a heart attack?

A heart attack is a life-threatening, acute medical emergency that occurs when blood flow to a part of the heart is suddenly either severely reduced or completely blocked. I learnt pretty quickly after I started doctoring that, as far as the patient, their friends and relatives were concerned, there were only two types of heart attack that they needed to know about: small ones, which you survived, and massive ones, which killed you.

There is a whole lexicon of alternative terms available for heart attack, including myocardial infarction, MI, acute myocardial infarction, infarct, coronary thrombosis and the even simpler coronary (because the cause of a heart attack is usually a blocked coronary artery). Whatever you care to call it, the heart takes a dim view of not receiving the full quota of blood it was expecting, along with the oxygen and nutrients carried in the bloodstream. It responds with a hissy fit. Well, you can hardly blame it.

What causes the interruption in blood supply to part of the heart in a heart attack?

Your heart is basically a globular muscle about the size of your fist, with four one-way valves and some electrical circuitry inside. It functions as a hydraulic pump with a flow rate of 5 L/min. Like any other pump, the heart requires a source of energy to power it. To keep its engine running smoothly for the approximately 3,000,000,000 (3 billion!) beats of an average human lifespan, it must receive a steady supply of blood to deliver the oxygen and nutrients necessary to feed its energy metabolism.

Although all the blood coursing through your body passes through the four chambers of your heart, only a relatively small proportion of the total blood flow is siphoned off to supply the heart itself. A healthy heart at rest receives about 250 ml/min oxygenated blood, which is about 5% of the total cardiac output. During vigorous exercise, this figure may increase fivefold. All this blood flows through the coronary arteries, whose internal diameter is 3-5 mm. I’ll repeat that. The blood that keeps your ticker ticking flows through channels just 3-5 mm wide.

There are two main coronary arteries: the left and the right. The left main coronary artery soon divides into two branches. It does most of the heavy lifting because it supplies the left ventricle, which does a lot of work generating the high pressure needed to pump blood around the body. The right main coronary artery has a cushy number in comparison, supplying blood to the right ventricle, which only needs to pump blood around the lungs, which is a low pressure circulation. Complete occlusion of the left main coronary artery is sometimes called the ‘Widowmaker’. It more often results in massive heart attacks, cardiogenic shock (see later) and death.

By now, readers will be loudly shouting at their phones or computer screens that there are four chambers in your typical heart, and I’ve made no mention of the two atria. This isn’t an oversight, although I was being simplistic in my explanation. While atrial contraction does help to prime the ventricles with a full load of blood ready for the next contraction, the atria actually do very little work even on a good day, and you can manage reasonably well without them – as many people with atrial fibrillation will tell you.

When we are born, our coronary arteries are pristine. However, unless you are particularly fortunate in the genes you inherit and/or have parents who deny you any and all fatty, additive-laden food, force you to exercise for eight hours a day throughout your childhood, and starve you whenever your BMI rises above 18.5, your coronary arteries are already showing signs of atherosclerotic damage by the time you reach adulthood. Atherosclerosis is a progressive, degenerative arterial disease characterised by the deposition of fatty cholesterol plaques in blood vessel walls. By the time you’re forty, if you’ve not looked after yourself, you lead a sedentary lifestyle, you’re overweight or obese from too many kebabs, burgers and chicken vindaloos, you like a drink or two, and, God forbid, you smoke, those coronary arterial channels (which, remember, are only 3-5 mm wide to begin with) could well be dangerously narrowed by sticky, gloopy, fatty plaques. You’ve turned into a walking MI, and you didn’t even know it because you feel fine. You’re a ticking time bomb, and it’s only a matter of time before it goes off. Did that scare you? It certainly scared the shit out of me. The diet starts tomorrow. And I’m joining a gym.

It follows, of course, that if you do look after your heart by exercising regularly, eating a well-balanced nutritional diet and maintaining a healthy weight, by not smoking at all and drinking alcohol modestly, you are less likely to suffer a heart attack. And even if you are unlucky and the worst should happen, your heart is in much better shape to survive the insult and recover. This begs the question, though, why do some ultrafit, young, elite athletes with no history of heart disease or anything else have a heart attack?

To understand why, you have to appreciate that coronary arteries block off in one of two distinct ways. In most cases, atheromatous plaques build up gradually over the years. Disease progression is accelerated by factors such as high blood pressure, obesity, high cholesterol, diabetes and smoking. Until roughly three-quarters of the internal lumen of an artery is obstructed, blood flow along it is not significantly impeded, and the atherosclerosis is therefore asymptomatic. As the degree of obstruction progresses further, angina may develop. The person experiences chest pain on exertion because the increased metabolic demands of the exercising heart muscle cannot be met by increasing the coronary artery blood flow. Angina pain is rapidly relieved by resting.

An elite athlete, on the other hand, may only have 20% narrowing of a coronary artery. It’s inconsequential to their performance. But whilst such small plaques do not impede coronary blood flow at all, they are like dormant volcanoes. Atherosclerotic plaques are inherently unstable. At any moment, they can rupture, triggering the formation of an instantaneous blood clot that completely occludes the arterial lumen. The volcanic eruption may be triggered by the surge in blood pressure associated with intense physical exercise. Ultrafit athlete one minute, ultradead athlete the next.

What’s the moral of the story? Is there any point in looking after yourself? Yes, absolutely. Be an ultra-fit elite athlete every time. You’ll live longer, on average.

What happens after a heart attack?

The key factor is whether your heart attack is only a small one (you live) or massive (you die). After that, it’s just detail. The type you have depends on several factors, including your age, your previous level of physical fitness, which coronary artery is affected, and how quickly and well a collateral circulation develops (the area of the heart affected receives a fresh blood supply from the opening up of previously dormant, small coronary arteries originating from a non-obstructed part of the coronary circulation). Oh, and how well and quickly you are resuscitated, of course. Never forgetting the all-important wildcard, Lady Luck!

Severe chest pain

Classically, the victim of a heart attack complains of chest pain as the area of heart muscle downstream of the arterial blockage cramps up. The pain intensity is often severe and may be described as a diffuse, dull, aching tightness or as a heavy weight on the chest. Rarely is the pain sharp, stabbing or well localised. Unlike angina, it may not be precipitated by exercise, and if you are exerting yourself when the pain first comes on, it doesn’t relieve with rest. The pain may radiate down one or both arms or into the neck and jaw. To make matters more complicated diagnostically, the pain can mimic indigestion, and some people have a heart attack without experiencing much or any chest pain at all (see silent heart attacks).

Associated symptoms

Apart from chest pain, many heart attack victims feel nauseated and vomit. They may notice palpitations, an unpleasant awareness of their heart beating hard in their chest, often rapidly and irregularly. They may feel lightheaded and dizzy if their heart is not beating strongly enough to generate a decent blood pressure. Victims often report feeling a sense of impending doom. This is caused by the effect of industrial quantities of adrenaline, the fight-or-flight hormone for the body’s emergency use only, on the brain. The sense of doom is not an overreaction. Fully 10% of all people who have a heart attack present with cardiac arrest. They’re minding their own business, getting on with their day, when they drop down stone cold dead without warning. Game over. Or maybe not. Does anyone know how to perform bystander CPR?

The silent heart attack

Some heart attacks go unrecognised because the pain is not that severe or it’s blamed on a dodgy kebab, IBS or something else relatively trivial that the victim doesn’t seek medical advice for. Still other heart attack victims have no pain at all. Diabetics with sensory neuropathy (dysfunction of nerves that convey sensation) are more prone to this.

As a related aside, I examined hundreds of routine preoperative ECGs when I was a surgical house officer, a significant number of which exhibited the unmistakable pattern of a previous heart attack that hadn’t been disclosed by the patient in their medical history. When I later quizzed these patients as to when their heart attack had occurred and what had happened to them, they would deny all knowledge.

Heart failure and cardiogenic shock

This is a life-threatening problem and is more common after a Widowmaker event. Cardiac muscle cells die if they lose their blood supply for more than a few minutes. If enough left ventricular muscle mass is lost, it is unable to generate sufficient arterial blood pressure to force a normal cardiac output through all the organs and tissues of the body. This combination of low arterial blood pressure and low cardiac output is called cardiogenic shock. On top of this, the right ventricle hasn’t been perturbed one jot by the events happening on the other side and is still merrily pumping blood through the lungs to the left ventricle. A massive backlog of blood pools in the lungs, leading to fluid leaking into the alveolar air spaces of the lungs. The resulting acute pulmonary oedema is a terrifying ordeal for a patient, who becomes severely breathless. They are literally drowning in their own blood.

Powerful drugs can be administered intravenously in the coronary care unit or the ICU to patients with cardiogenic shock and offer a helping hand to the failing left ventricle while it (hopefully) weathers the storm and gets its act together as a collateral circulation is established. I used them hundreds of times during my career, and although they can’t polish a turd, they undoubtedly saved many lives.

Before we move on from talking about cardiogenic shock, I wanted to clarify what doctors mean when they say that somebody is suffering from shock. It’s a term that is often loosely banded around when a major incident or other tragic event is reported in the news. The victim is said to be ‘in shock’. I’m not certain precisely what reporters mean by this because I’ve never asked one. What I think they mean to say is that the person affected is in a state of high emotional and psychological trauma. That’s not what medical shock is. Shock is defined as life-threatening circulatory failure in which the body’s tissues and vital organs do not receive sufficient blood flow or oxygen, often, but not always, associated with low arterial blood pressure. There are other causes of shock aside from the cardiogenic shock of acute heart failure. Major blood loss or severe dehydration produces hypovolaemic shock; severe systemic infection produces septic shock; an acute allergic reaction produces anaphylactic shock.

Heart Failure

If the Widowmaker does not, in fact, make your nearest and dearest a widow by sending you to meet your maker after succumbing to the acute heart failure of cardiogenic shock, you’re not necessarily out of the woods. Your left ventricle may lose the ability to contract forcefully forevermore, and you end up with chronic heart failure. Sufferers complain of chronic fatigue, poor exercise tolerance, episodes of acute nocturnal breathlessness and swelling of legs, feet and ankles. It’s a serious life-limiting medical condition with about half of all those affected dying within five years. That’s a worse outlook than many cancer diagnoses.

Cardiac arrest

By the simplest definition, cardiac arrest occurs when the heart stops beating. Technically, of course, everyone dies of a cardiac arrest, from the person run over by a bus to the emaciated sufferer of stage four cancer to the centenarian who dies quietly of old age in their bed, asleep one night. It is, after all, how we tend to define death (unless we’re talking about brainstem death). A more useful definition in the context of acute medicine and resuscitation is that a cardiac arrest is the sudden, unexpected collapse of the heart’s mechanical pumping action that is potentially reversible. Thus, when a catastrophic injury, terminal illness or decreptitude reaches its natural end, the stopping of the heart is the result of death. In contrast, during acute resuscitation, cardiac arrest is treated as a remediable condition that may or may not lead to death.

That’s all I’m going to say on the subject of cardiac arrests for this post. It’s a big topic, and I’ll devote the next post to it.

Cardiomyopathy

Before I nip off, I just want to say a brief word about cardiomyopathies. They are a collection of cardiac conditions unrelated to heart attacks and atherosclerotic coronary artery disease that can, however, cause heart failure and cardiac arrest. They are surprisingly common, affecting about 1 in 250 people. There are inherited and acquired forms that come in a variety of flavours, including dilated cardiomyopathy, hypertrophic cardiomyopathy, restrictive cardiomyopathy and arrhythmogenic cardiomyopathy. The core symptoms are generally those of chronic heart failure. Arrhythmogenic cardiomyopathy is the cause of sudden death in some young, healthy individuals playing sport.