ContentsTightness in chest, first thoughts? Serious types of chest pain Heart attack - the medical process and treatment Non-life-threatening types of chest pain Risk factors for chest pain Risk factors in detail - why they are harmful
Tightness in chest, first thoughts?
Say a patient comes in with tightness in chest, what would be on your mind?
Chest tightness or pain can be caused by a really broad number of things (also see 23 Reasons Why You Have Random Chest Pain). There are a few really key characteristics that could help categorize someone's chest pain as something acute that require you to mobilize a ton of resources right away versus other things that are not life threatening even if they may be causing the patient's chest pain and discomfort.
The diagnoses that are fatal within one day
I start by thinking about the “can’t miss” diagnoses that can cause people to die within a day. They include things like an ongoing heart attack, a pulmonary embolism (blood clot in the lungs), a pneumothorax (collapse of the lungs), and an aortic dissection (a tear in the aorta which is the biggest blood vessel in the body).
There are a few key questions you could ask to figure out if someone has one of those four “can’t miss” conditions. Some of the questions are more historical and demographic. For example, if someone is very old, has smoked their whole life, has a history of high blood pressure and high cholesterol, they're automatically at a much higher likelihood of having some of those “can’t miss” conditions just by the nature of their risk factors. Afterwards, I would ask three other questions to tease out the true nature of the pain they're having:
- if the pain comes on with exertion
- if it's right under the chest under the breast-bone
- if it’s relieved by a nitroglycerin tablet.
A yes to any of the three questions would suggest that the patient’s chest pain is related to their heart not getting enough blood flow, which could indicate a heart attack.
Serious types of chest pain
Typical angina symptoms: 3 symptoms to watch out for
The ones that are concerning are if the chest pain is substernal (it’s underneath the center of your chest where the is heart located), if it’s provoked by exertion or stress, and if it’s relieved by rest or nitroglycerin tablets. If you have all three of those, we call that typical chest pain or typical angina. Those are typical angina symptoms. That by definition means that you have obstructive coronary artery disease. If you only have one of those, then we think that there's low likelihood that you have coronary artery disease. If you have 2 of them, then it's kind of in the gray zone and in between.
The big caveat to this is that all of these symptoms, these 3 characteristics of typical angina, were based on studies that were done in the past and really looked predominantly at men. This typical chest pain and typical angina syndrome were defined historically based on large studies of men. So women tend to not have typical angina. Women tend to have a lot of atypical angina or other symptoms like nausea, lightheadedness or bloating, and that can be their equivalent of angina, so a lot of people might not pick up on that.
Aortic dissection - back pain
As for the other 4 conditions we talked about. Something like an aortic dissection typically presents with chest pain that’s underneath the sternum, where your heart is located, but also very characteristic like a tearing or knife-like pain in the back. Your aorta comes in an arch forward and then goes down your back. An aortic dissection is literally a tearing of the vessel so you feel that tear or knife-like pain going down your back along with the chest pain.
Pulmonary embolism - swelling in one leg
For pulmonary embolism, it’s not as well defined in terms of features of the chest pain, but some of the things that would point towards that would be if you have a history of swelling in just one of your legs, because the most common cause of a pulmonary embolism is a blood clot travelling from the veins of the legs up to the lungs. Another sign would be that the patient has significant increase in the chest pain with deep breathing because pulmonary embolism causes inflammation around the lungs that is exacerbated by deep breathing.
Episodes of palpitation
Some of the other factors that are just concerning in general for a patient with chest pain is if they’ve had significant episodes of palpitations where they feel like their heart is racing or if they’ve had episodes where they feel like they're fainting or about to faint. That could indicate that they have a really large pulmonary embolism or they're having a heart attack that’s causing their heart to go into abnormal heart rhythms.
Penumonthorax - trouble breathing
Pneumothorax usually is a combination of having chest pain and having a really significant component of trouble breathing because part of your lung has collapsed. Another clue would be if the patient experiences the chest pain and it was a real sudden sharp pain, meaning it didn’t come and build up over the course of an hour or even thirty minutes, it just happened and stayed the same way. The pain is sudden because the lung collapsed. Usually, it's in the context of someone who has some kind of abnormal lungs to begin with– someone who might have COPD or emphysema- their lungs are predisposed to collapsing on their own or if the patient just had some kind of procedure or surgery involving the lungs or the chest. Outside of that, there's not anything really specific for pneumothorax.
Heart attack - the medical process and treatment
What is a heart attack?
A heart attack is when one of the blood vessels that typically feeds blood and oxygen to the heart muscle itself becomes blocked. That’s the colloquial meaning of a heart attack. In medicine, we call it a myocardial infarction. It usually happens in the context of a patient or person who already has small pre-existing blockages scattered throughout the arteries that feed your heart called the coronary arteries.
What happens during a heart attack?
In a heart attack, those arteries get blocked for one reason or another, usually involving some kind of worsening of their risk factors. For example, someone might have a night where they smoke a pack of cigarettes when they usually only smoke a few cigarettes. They might experience a heart attack because all the chemicals floating around in their blood already increased the likelihood of their existing blockages into rupturing. Here’s how an existing blockage ruptures. A buildup of cholesterol, fat, and inflammatory cells accumulates underneath a thin layer of protein. When this thin layer of protein is perturbed in some way, it ruptures and all the stuff beneath it are exposed. There are these factors called clotting factors in the blood that are responsible for causing clots to happen when they see something "foreign" (something that’s not supposed to be in the blood vessel). They perceive those streaks of fat, deposits of cholesterol and inflammatory cells as foreign and create a clot - kind of like the clot you get when you get a papercut; air is a foreign material to your blood so your blood will start to clot so you don’t bleed out to death. That’s what happens inside of your coronary artery when that cap ruptures and the blood is exposed to all the stuff that’s harbored inside.
After the clot happens, it blocks off your coronary arteries just like a pipe being closed. Now your blood can't go past that blockage and all of the muscles of your heart downstream from the blockage don’t get any oxygen and nutrients. That leads your heart to struggle and causes you to feel pain because the nerves on your heart are not getting enough oxygen either. You feel this sensation of pain or angina because the oxygen supply and demand is mismatched where the supply has suddenly gotten dramatically lower but the demand is the same. Your heart is still trying to beat. From there, because the electrical system of the heart is not getting oxygen either in that area, your heart can start going into an abnormal heart rhythm which is usually how people with heart attacks die - a sudden arrhythmia we call it - they stop pumping blood forward and just fall flat and die.
The other thing that can happen is that even though that one area of your heart is not getting enough blood supply, the other parts are trying to pump and will try to compensate for it. But they might not be able to fully and you can develop heart failure where instead of pumping blood out to the rest of your body, your heart's not functioning effectively and the blood starts backing up and pooling up into the veins in the lungs. Blood will then leak out into the lungs and cause you to feel like you're drowning and build up fluid throughout your lungs and sometime into your legs.
How long does it take for the heart muscle to start to die?
We can measure little leakage of enzymes called troponin that comes from the heart muscle. That usually becomes measurable 6-8 hours after the blood clot has formed in the coronary artery. Presumably for that first 6-8 hour time frame, after you have this sudden occlusion (blockage), you are going to feel sudden pain at that moment but your heart muscle is not necessarily dead yet. It's still salvageable. The real key is to get your artery open again either through medicines or stent before the heart muscle dies. Usually, that’s not possible because it takes a long time to mobilize everything and for someone to come to the hospital. You're looking at around 6-8 hours before cells start dying. That’s not necessarily a huge deal if you still get to the hospital on time, but if you, for example, had the heart attack and your cells started dying starting at 6 hours and you didn’t show up to see a physician until a week or 2 later, that heart muscle might be so dead that they wouldn't even recommend opening your artery ever again because it wouldn’t do anything. It wouldn’t serve any purpose.
Main therapy for heart attack
The main therapy right now is to give a whole cocktail of medicines that will thin your blood, prevent further clots from forming and lowering your heart rate. Usually, just those medical things could be enough to make your chest pain go away and make your heart muscle not die. But, we know that if the demand on the heart were to increase, like in the case if you were going for a walk which makes your heart rate increase, your heart muscle will start dying again. What we usually do is a cardiac catheterization, a procedure in which doctors thread a wire through the groin or wrist and follow the arteries all the way back to the heart and to the coronary arteries and, while looking at the coronary arteries from an x-ray, shoot some dye to identify the area of blockage. Then, blow up a balloon attached to the wire to smush all that plaque and blockage against the artery wall, and then put in a stent (a stiff metallic tube that holds the heart's artery open, see image above). Once that stent is in, you have a much lower chance of having a recurrent blockage in that area or causing more heart tissue to die.
Medication vs. cardiac catheterization (putting in a stent by running a wire)
Far and away, everyone should get the medicines and if you can, and on top of that, if it’s the right time frame, everyone will do much better if they get a stent if they're having a heart attack. The effectiveness of stents has been shown through years and years of clinical trials since the 80s. Prior to stenting, the only treatment for heart attacks was to give people the medicines we already mentioned and have them rest for up to 2 weeks to prevent the heart from demanding more oxygen. But during those days, almost 30-50% of people could still die if their blood vessel wasn’t opened in some way. The era of stenting really dropped that rate down significantly and that’s definitely the preferred strategy in addition to medicines to treat someone who has a fresh heart attack.
Medication that you could use to break up the clot?
Yes there is a clot-busting medicine they use on patients who had a stroke that they can use on patients having heart attacks. It's called TPA, and that medicine is a really potent blood thinner that will dissolve any clots in your body and can cause you to have unwanted bleeding. It's used now in the modern era in places where either there isn’t the resources or staff to do a stenting procedure or if there are some other major reasons against having the stent procedure. The main downside though about the clot-buster medicine is that there's about a 3% chance the patient could have a fatal, catastrophic brain bleed and die. So it’s a real big risk-benefit tradeoff. There's no way to predict who might bleed but at the end of the day. If the doctor ends up having to use it, we'll see what happens and hope for the best. Most of the times there's no problem, but there's a small chance things don’t go well and cost you your life.
Non-life-threatening types of chest pain
It's been a few days
A lot of the other diagnoses and conditions that can cause non-life-threatening chest pain typically cause chest tightness on the order of days to even weeks, and yet the patient is still alive. If you had a life-threatening cause of chest pain, by definition, you wouldn’t be alive to talk about it if it was going on for a week or even more than 3 or 4 days constantly. People who have constant chest pain that doesn’t change with exertion, that never really seems to go away—as soon as they wake up it's back— are very unlikely to be having any kind of life-threatening emergency because if they were without treatment, they probably would have died.
Only when you lie down at night
Other clues of less serious causes of chest pain or tightness would be if you really experience the chest pain only when you lie down at night or if you have chest pain after eating large meals. Those symptoms would indicate that it's reflux. If there's a burning quality to the pain along with it, that would also indicate that it's reflux.
Pain only when you're in a certain position
Also, one of the more common causes of chest pain that send people to the hospital, out of an abundance of caution, is musculoskeletal chest pain, which means, whether the patient remembers or not, he or she may have strained one of the muscles, joints, or ligaments in their chest wall. They pulled a chest muscle either by doing a new exercise, by bending over to pick up a large number of groceries, or by sleeping funny. A telling sign of chest pain on the left side, the right side or a particular location due to muscle strain is if the patients have chest pain that only happen when they are in an unusual position or at a particular location - for example, they reproduce the pain if they raise their left or right arm or if they bend over a certain way.
Usually, these are diagnosable if you physically press onto their chest. If you can reproduce the pain repeatedly this way when you press onto the chest, it would indicate that something is not wrong with your chest or lungs, but just with the chest wall itself. The last one we see a lot is anxiety related chest discomfort which is still real pain and still distressing to patients, but typically comes on in the setting of some other kind of stressor—it is an emotional stressor, social stressor, or financial stressor—some other thing typically triggers it and again, it usually comes on only when they are thinking or experiencing that thing, and then it goes away on its own after they relax or calm down. That would be really characteristic of an anxiety related chest pain.
Risk factors for chest pain
Age, smoking and high cholersterol
For cardiac risk, the top factors are age, history of smoking, and history of high cholesterol. Age increases our risk of having heart issues the most because as we age, we're more at risk to develop blockages in the arteries of the heart. Second is having a history of smoking and high cholesterol. People that have smoked for a really long time or have high cholesterol are at a much higher risk for developing serious heart conditions. Also, people with lots of relatives who've had heart attacks, especially at a young age, are also at higher cardiac risk.
Other risk factors include people who are obese or have what we call metabolic syndrome, which is a constellation of having a sedentary lifestyle, obesity, high blood pressure, diabetes, and high cholesterol. After those big buckets, there are some more nuanced smaller, niche risk factors like people who've had a history of radiation to their chest for cancer or people who have been on certain medications that could have increased their cardiovascular risk. I would say age, obesity, hypertension, high cholesterol, diabetes, and a strong family history are the really big ones.
Is it any of the above? Is it at least two?
I think if you have any of the above and you have chest pain, then it’s concerning and with each additional factor that you also have, that increases your pre-test probability—I am sure there's literature out there about how much, maybe one of the Framingham heart studies would categorize people better. I don’t know the exact number off the top of my head but that would be a place to look because they identified risk factors for coronary risk factors in general. They did a good job at explaining and quantifying how much each additional risk factor adds to people.
40 years old or older
Usually we think of people being at least 40 years old or so to be at risk. If someone's coming in with what we call typical chest pain, which is chest pain that is substernal (area in the center of your chest, also your heart location), precipitated by physical exertion, and that is relieved by rest or nitroglycerin, if they're 40 then they probably have a 2/3 chance of having obstructive coronary artery disease. On the contrary, if someone's coming in with those symptoms and is 25, there's a higher chance than not that that symptom is related to something completely different like anxiety chest pain or musculoskeletal strain or something else. That said, if you have a type 1 diabetic aged 31 whose coming in with those symptoms, then you’re automatically in a high-risk category. So you always have to take those other things into consideration.
Risk factors in detail - why they are harmful
What does obesity have to do with a higher risk of heart attack?
It's probably the one least understood exactly why being obese causes you to develop more blockages in the arteries of your heart. Outside of the fact that people who are obese tend to have some of the other risk factors already, there's a lot of emerging evidence, data, science, and literature, that the fat cells we store in our bodies are intricately involved in a lot of signaling through hormones in the body. It used to be thought that fat was just a storage of excess calories and that they laid dormant until they break down to sugar when you’re starving. We’ve found in the last two decades that fat is actually a metabolically active tissue that is involved in a lot of hormonal signaling especially related to cortisol levels. There are other specific hormones like adiponectin and others things that have been shown to play a role in the development of plaques and blockages in the arteries of the heart. The thought is that the more fat you have, and the longer you have it, the more likely you are to have higher levels of these certain hormones that promote the development of the blockage of arteries in the heart, and that over time, those blockages progress and can eventually lead to heart attack.
High cholesterol is one of the first risk factors identified as being something that can lead people to have heart attacks at a higher rate. The main reason is that cholesterol is a pretty significant component of the plaques that are present in the arteries of the heart. Like I mentioned, underneath the protein caps is a collection of cholesterol, fat, and inflammatory cells. By eating either large amounts of cholesterol as part of an unhealthy diet, or having a genetic predisposition (i.e. genetically susceptible to) having high levels of cholesterols, specifically bad cholesterol LDL, in your blood, you are providing the substrate for these plaques to develop. The discovery of statins, which are the main class of drugs used to lower cholesterol in current clinical practice, was based on people who had genetically astronomically high levels of cholesterol and basically mutations in the signaling of their liver that controlled how much good and bad cholesterol is floating around in their blood. What we found over many years, is that the more LDL or bad cholesterol you have floating around in your blood, the more likely you are to keep developing more and more plaques. The real target of the medical therapy to challenge this has been to drive that number as low as possible. The only diet which has been shown to really mitigate your risk of having a heart attack is a Mediterranean diet which is quite low in cholesterol, bad cholesterol specifically.
What about high blood pressure? Smoking?
High blood pressure is involved in the development of blockages in the arteries of the heart because it puts a lot of stress on the heart. The heart has to pump against a certain blood pressure, meaning it has to pump at a certain force into the aorta (the big vessel that the heart pumps into). The higher the pressure is in the aorta, which is measured by the blood pressure in your arm, the more work the heart has to do chronically. As that happens over decades and many years, the heart starts to remodel and try to develop strategies to overcome that high blood pressure over time. What we've seen over time is that the heart develops larger muscle size over time to compensate for the high blood pressure, and those changes are not favorable. The remodeling of blood vessels in these ways leads you to have a much higher likelihood of developing not only more plaques, but more plaques that can rupture and cause heart attacks.
Diabetes, like most people might know, is a dis-regulation of the amount of the control of insulin in sugar in the bloodstream. Chronically high levels of glucose in your blood can cause you to have heart attacks or have blockages in the arteries of your heart because the sugar alters the chemistry in the endothelial cells (cells lining the insides of the blood vessels in your entire body and in your heart). When that happens, the endothelial cells can start to recruit and bring in inflammatory cells (cells that normally fight viruses, bacteria, infections, and maybe tumors in your body) because they think they're being damaged in some way. When those inflammatory come into the endothelium and blood vessels of the heart, they'll start recruiting other components of the immune system to cause a lot of inflammation and then that inflammation can lead to more clotting because it is abnormally viewed by the clotting system. On top of that, that inflammation also couples with the cholesterol and fat floating around to develop plaques.Disclaimer: The article does not replace an evaluation by a physician. Information on this page is provided as an information resource only, and is not to be used or relied on for any diagnostic or treatment purposes.