Chapter 8: Chest Pain Assessment & Diagnosis

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You know, in the world of primary care, there's a specific look that washes over a waiting room when a patient walks in, clutches their sternum, and says those two magic words, chest pain.

Oh, absolutely.

It is the ultimate high stakes complaint.

It just sucks the air right out of the room.

It really does.

Because when you hear that, your brain immediately has to span this massive, terrifying spectrum.

It could be that they ate a really spicy burrito for lunch and have some reflux, or it could mean they're minutes away from cardiac arrest.

And that isn't hyperbole.

Not at all.

That is the clinical reality we live in.

You are standing on a knife's edge between take an antacid and call the paramedics.

And that anxiety isn't just felt by the patient.

Oh, absolutely not.

I mean, it is felt just as acutely by the provider because you have to be right.

And you have to be right fast.

You just, you cannot miss the big one.

So today we are doing something a little special.

We are doing a dedicated last minute lecture deep dive.

We are taking a very structured, rigorous look at the framework for this.

Specifically, we are looking at chapter eight of advanced health assessment and clinical diagnosis in primary care.

This is the blueprint.

It really is.

For the students listening, nursing, medical, PA, or even seasoned clinicians who want to tighten up their game, this is the methodology.

We are going to walk through the text's exact method for evaluating chest pain, moving from that broad panic -inducing symptom analysis right down to the precise differential diagnosis.

And the text makes it very, very clear where we start.

We don't start with how long have you had it or does it hurt when you poke it.

We start with a much simpler, darker question.

Right.

Step one is survival.

The immediate priority is determining if the condition is life -threatening.

Before you do anything else, you have to answer, is this patient dying right now?

The text groups the most immediate threats under the umbrella of acute coronary syndrome, or ACS.

Which is really a spectrum.

It covers myocardial ischemia, where the heart is basically starved of oxygen, and it goes all the way to myocardial infarction, or MI, where the tissue is actually dying.

But it's not just heart attacks we are worried about.

The text highlights a big four of immediate threats.

These are the conditions that you must assess rapidly.

Because, as the source material puts it, speed is survival.

Exactly.

The big four, you have the MI, obviously.

That's the one everyone thinks of.

Then you have aortic dissection.

Terrifying.

Just, yeah, one of the worst.

Then pulmonary embolism, or PE.

And you have pneumothorax, a collapsed lung.

And the text is pretty blunt about this.

It essentially says that rapid assessment here is completely non -negotiable.

It is.

Think about the stakes.

A quick diagnosis of an acute MI drastically increases survival chances.

Because we can intervene, we can get them to a cath lab.

But something like an aortic dissection.

That is catastrophic.

If you miss that, if you send that patient home thinking it's muscle pain, the outcome is, I mean, it's often fatal.

So before you get into the nuance of, is it heartburn?

You have to rule out the killers.

But here's the problem.

And I think this is why chest pain is so tricky for us as humans to process and for clinicians to diagnose.

The body's wiring is, let's call it messy.

Messy is a very polite way of putting it.

It's a labyrinth.

It's a complete mess.

So let's talk about the anatomy of pain.

Why is it that heartburn can feel exactly like a heart attack?

The text breaks this down to a neurological level.

And it's just fascinating.

It all comes down to the spinal cord segments.

Specifically T1 through T5.

Okay, so let's unpack that.

T1 through T5.

Why are these segments the villains in our diagnostic story?

Think of the spinal cord at that T1 to T5 level as a very busy understaffed switchboard.

You have pain fibers coming in from all over the place.

You have signals from the cardiac system, the respiratory system, the musculoskeletal system, and the gastrointestinal system.

They all use the same phone line.

Pretty much.

They all transmit to these exact same dorsal root ganglia.

So the brain is up there waiting for information.

It gets a signal from T3.

But because that line is shared, the brain doesn't necessarily know if that call is coming from the esophagus, the heart muscle, the pleura of the lung, or a muscle in the chest wall.

So the brain essentially just guesses.

It interprets.

And often it interprets poorly.

That is why we have referred pain.

That is why identifying the specific origin based on location alone is, well, it's notoriously difficult.

The text lists skin, muscles, ribs, cartilage, pleura, lungs, mediastinum.

They all dump their data into the same T1, T5 funnel.

So when a patient points to their chest and says, it hurts here, you absolutely cannot just rely on that GRB.

If you do not, you have to look at the whole picture.

The location is just one pixel in a very, very large image.

Now, before we get into the heavy diagnostics for adults, the text has a really interesting specific note on pediatrics.

And there's this one visual that really stuck with me because it feels so, I don't know, cinematic.

You're thinking of the infant with the sweaty forehead.

Yes.

It seems so specific.

Why does the text highlight that particular image?

It's a massive red flag.

In an infant, sweat on the forehead is a sign of decreased cardiac output.

The heart isn't pumping enough blood, so the body tries to compensate by kicking the sympathetic nervous system into overdrive.

So it's a cold sweat, not from being hot.

Exactly, it's a diphorasis born of stress, not heat.

It's the body's alarm system going off.

If you see a baby with a sweaty brow during feeding, or even just at rest, you have to worry about the heart.

But generally speaking, the text is pretty reassuring about older kids, right?

Very reassuring.

In children and adolescents, chest pain is rarely serious organic disease.

It's almost never a heart attack in the adult sense.

It's usually costochondritis, which is just inflammation of the rib cartilage or trauma from play,

a muscle strain, or maybe a really bad cough.

Rheumatic heart disease is thankfully rare these days.

But the anxiety level in the room is totally different with kids.

It is sky high, because parents hear chest pain and they immediately think sudden death in young athletes.

They've seen the news stories.

So while the pathology is usually benign, the fear is very real and needs to be managed with just as much care as the physical symptoms.

Okay, so let's say we have ruled out the immediate patient is dying right now scenario.

They aren't in severe oxygen deprivation.

Their airway is patent.

Now we move to the next phase, which the text calls the focused history.

This is where you put away the crash cart and you become a detective.

You need to get the patient to describe the pain.

And the text gives us some classic descriptions, almost like scripts to listen for.

Let's run through these because the adjectives, the words the patient chooses, they really matter here.

They can be the key to the lock.

Let's start with the classic one, Anjana.

Anjana is the classic cardiac pain.

It is typically described as a sub -sternal heaviness, a pressure, or a squeezing sensation.

Patients often clinch their fist over their chest.

That's called Levine's sign.

Importantly, it is not usually described as sharp or stabbing.

It's a weight.

And where does it go?

Does it stay put?

No, and the radiation is key.

Class gangina radiates to the left shoulder, down the inner aspect of the left arm, or up to the neck and jaw, sometimes even the teeth.

Okay, now contrast that with aortic dissection.

This is one of our big four killers.

Dissection is visceral and violent.

It is abrupt.

The text uses the words tearing or ripping.

Patients will say, it feels like something just tore open inside me.

That is a terrifying description.

It is.

And the location can be in the anterior chest or the back.

And here is a terrifying detail.

This pain can migrate.

It moves.

Why does it move?

Because the dissection, the tear in the artery wall, is physically extending.

As that tear zippers down the aorta, the pain literally moves with it.

It can migrate to the arms, the abdomen, the back, or even the legs.

And there is a specific syndrome mentioned here too, regarding risk.

Marfan syndrome, yes.

If you have a patient with Marfans, they're often tall, thin, with long fingers and limbs.

Their connective tissue is fragile.

Their risk for dissection is significantly higher.

Got it.

Now what about a pulmonary embolism or PE?

How does that feel?

A PE is different again.

This is often a gripping, stabbing pain.

And here is a key difference from angina.

The patient can often point with one finger to a specific area over the lung.

It is pleuritic, which means it hurts worse when they breathe in.

It's usually moderate to severe and is almost always accompanied by sudden dyspnea shortness of breath.

And newothorax, the collapsed lung.

Sudden onset, severe, sharp or tearing.

It's located in the lateral thorax, the side of the chest.

And it radiates to the shoulder on that same side, the ipsilateral shoulder.

And finally, good old pneumonia.

Pneumonia is distinct.

It's a burning or stabbing quality, but it is located right over the area of infiltration where the infection actually is.

It does not radiate.

And obviously it's associated with a cough, fever, that sort of thing.

Now the text adds a caveat here that I think is important for everyone to remember, especially when we're asking patients to rate their pain on that scale.

Pain is subjective.

Right, it's so subjective.

We use the zero to 10 scale, but that is heavily influenced by culture, personal attitude and prior experience.

A 10 for a stoic farmer who's never been to a doctor might be a four for someone else.

You have to calibrate the patient's report against their behavior.

Are they writhing in pain or are they calmly answering your questions?

Let's talk about timing.

Onset and timing seem to be huge clues in this chapter.

The when and how it started.

They are critical.

For angina, the trigger is the diagnostic key.

It comes on with exercise, exertion or strong emotion and the relief is just as key.

Rest or nitroglycerin.

It follows a predictable pattern.

Versus an MI.

An MI can happen anytime, even at rest.

And the text makes a really sharp distinction.

That classic story of pain being relieved by rest in two to five minutes, that stable angina.

MI pain might not fully resolve with rest or it takes much, much longer.

But for PE and pneumothorax, the keyword is sudden.

Those hit you like a truck.

And pneumonia is gradual.

Right, hours to days.

It sort of builds up as the infection takes hold.

Okay, I have to bring up this statistic because it is just one of those weird medical facts that sticks in your brain.

The Monday morning phenomenon.

It is fascinating, isn't it?

The text specifically notes that most MIs occur in the morning hours with a significant statistical peak on Mondays.

Why Mondays?

Is the universe just cruel?

The text doesn't explicitly speculate on the mechanism but physiologically, we generally attribute this to the circadian rhythm of cortisol and catecholamines, your stress hormones.

They surge when you wake up to get you going.

Okay, that makes sense.

So you add that physiological surge on top of the psychological stress of starting the work week and that Monday morning blues can literally be hard on your heart.

It's a surge in blood pressure and heart rate that a vulnerable plaque just can't handle.

That is wild.

And for the pediatric side of timing, what are we asking there?

You have to play detective differently.

You ask about choking episodes.

Did they swallow a foreign body?

Does it hurt to swallow?

Or if they have pain lying down after eating, you have to think about GERD or reflux.

Moving on to duration.

The text gives us a rule of thumb regarding how long the pain lasts.

Generally, yes.

The rule is that acute onset usually equals more life -threatening.

Chronic or gradual usually equals less emergent.

But we need to get more specific than that.

We need to look at minutes.

There's a specific time cutoff for the angina types, right?

Yes.

This is a crucial distinction that can change everything.

Stable angina, the kind that is predictable and generally manageable,

lasts two to five minutes and is relieved by rest.

Unstable angina.

That lasts around 20 to 30 minutes and is not necessarily related to activity.

So if you have chest pain lingering for 30 minutes while you're sitting on the couch, that is a whole other level of emergency.

That is a massive red flag for unstable angina or an impending MI.

That is not something you wait on.

Let's layer in the associated symptoms.

What comes along for the ride with these conditions?

Because chest pain rarely travels alone.

Right.

With an MI, look for the autonomic symptoms.

The body's freaking out.

You'll see nausea, vomiting, diaphoresis, that cold, clammy sweating, shortness of breath, and sometimes even syncope or fainting.

And with a PE.

Amopticis, coughing up blood.

That's a scary one, though it doesn't happen every time.

Plus a profound sense of apprehension.

The patient just feels like something is terribly wrong.

A sense of impending doom.

And pneumonia.

That's more straightforward.

Usually, yes.

Yes.

Fever, cough, the sputum, the classic signs of infection.

Okay, so we have the history of the pain itself.

Now we need to look at who the patient is.

The risk factors.

The text cites the National Cholesterol Education Program.

This is your mental checklist.

As soon as that patient says chest pain, you are running this list in your head.

You are looking for smoking, that's a huge factor.

Hypertension, low HDL, that's the good cholesterol.

Specifically, less than 40 milligDL.

Family history of premature heart disease.

What's premature in this context?

Good question.

It's a first degree male relative under 55 or a female relative under 65 who had a major cardiac event.

Got it.

What else is on the list?

Age is a big one.

Men over 45, women over 55, and of course diabetes.

Diabetes is a really big one, right?

Because it changes how people feel pain.

It does, it's a huge confounder, we will get to that.

But diabetics often have silent MIs.

They don't feel the classic crushing pain because of neuropathy.

And the text makes a point about age and gender regarding CAD, coronary artery disease.

Right, it says that clinically significant CAD is uncommon in men under 40 and premenopausal women.

Estrogen is thought to have a protective effect on the arteries, but once that protective effect has gone postmenopause or as age increases for everyone, the risk line goes up steeply.

Let's go deeper.

We talked about broad descriptions, but segment three of the text really drills down into detailed symptom analysis.

Specifically, location and character related to specific nerves.

This section is great because it explains the weird pains, the ones that don't fit the classic heart attack mold, for example, intercostal neuritis.

What does that feel like?

Stabbing or burning.

And the text mentions three maximal pain points.

This is a great physical exam trick.

If you press adjacent to the vertebrae in the axillary lines, which is under the arm, or along the parasternal lines right next to the sternum and the patient jumps, that's likely neuritis.

You've reproduced the nerve pain.

And then there is shingles or herpes zoster.

This is a tricky one because the pain often comes before the rash.

So for a few days, you just have this intense, burning, knife -like pain along a dermatome.

A specific stripe of skin fed by one nerve root.

It can restrict trunk movement because it simply hurts too much to move.

Then a few days later, the vesicles pop up and you go, ah, that's what it was.

What about bone pain?

Bone pain is intense and well localized.

This comes from irritation of the periosteum, the covering of the bone.

And the text notes something important here.

The ribs are common sites for metastatic malignant deposits cancer spread because they are so vascular.

That is a grim but important detail to keep in mind.

It is.

And then you have mediastinal tumors.

These can cause a dull, deep, sub -sternal ache just from the pressure of the tumor pushing against the spine or ribs.

It's a space -occupying problem.

Now this part blew my mind a little.

The text talks about silent zones in the lungs.

This is crucial anatomy for understanding why lung diseases are often caught so late.

The trachea and the large bronchi have innervation from the vagus nerve so they feel pain.

If you get a crumb in your windpipe, you know it immediately.

But the finer bronchioles and the lung parenchyma, the actual spongy tissue of the lung where the gas exchange happens, have no pain innervation.

So you could have a disease process happening deep in the lung.

And feel absolutely nothing.

You could have a tumor growing in the parenchyma and until it grows large enough to hit the pleura, which is the lining or the larger bronchi, it is completely silent.

That is why lung pathology can be silent for so long.

And speaking of the pleura, the lining.

Pleuritis, this is inflammation of that lining.

Normally the two layers of the pleura, one on the lung and one on the chest wall, glide smoothly against each other with a little fluid.

But when it's inflamed, you lose that lubrication.

So every time you breathe, those inflamed surfaces rub together like sandpaper.

It waxes and wanes with respiration.

It's a sharp pain with every breath.

The text also distinguishes between awakening with pain versus awakening from pain.

Yes, it's a subtle but vital distinction.

Awakening because of pain, meaning the pain was strong enough to literally pull you out of sleep.

That suggests an organic cause like cardiac ischemia.

Your body is waking you up to say something is seriously wrong.

Versus just waking up and then noticing you have some pain.

Exactly, awakening naturally and then noticing pain is much less specific.

And the text notes that in adolescence, psychogenic pain often links to sleep disturbances in general.

Moving on to the things that happen alongside the pain.

Coughs, dizziness, and palpitations.

The text gets specific on sputum colors.

It does.

I mean, if you are coughing up stuff, what does it look like?

Dark green, rust -colored or frankly red with blood in it usually points to pneumonia.

And fever.

A fever indicates infection or inflammation.

So pneumonia, myocarditis, pericarditis, or even a PE, which can cause inflammation.

But, and this is a huge but, older or immunosuppressed patients might not mound a fever even if they have a raging bacterial infection.

Why is that?

Their immune system is just too tired or too weak to heat up the body.

So you cannot rely on the thermometer alone in the elderly or immunocompromised.

The absence of a fever does not mean there's no infection.

Let's talk about syncope fainting and dizziness.

When is it scary?

Context is everything.

In adults, syncope is often cardiac in origin arrhythmias or structural disease.

The pump stops momentarily, the brain loses blood and lights out.

In children, it is usually benign breath -holding spells, vasovagal responses.

But, and this is the big red flag, if a child or adolescent faints during exercise, that is non -benign until proven otherwise.

Why is exercise syncope so bad?

Because during exercise, your heart should be pumping its hardest.

If it fails then, when demand is highest, it usually means there is a structural obstruction like hypertrophic cardiomyopathy or a fatal arrhythmia that's being provoked by the exertion.

That is a massive red flag.

And palpitations, that fluttery feeling.

Well, it's often just caffeine or stress.

We have all had that.

But it can be a sign of something like mitral valve prolapse, MVP, or, the text points out, medications.

It specifically lists theophylline, used for asthma, and levothyroxine, thyroid meds, as common triggers.

Okay, let's talk about activities.

What were you doing when it hurt?

Right, if you were weightlifting or, as the text says, engaging in horse play, you should be thinking about muscle strain pectoral or torpesius muscles.

And drugs.

Cocaine and amphetamines.

We will get into the mechanism later, but they are major causes of ischemia and MI, especially in younger people without other risk factors.

The text mentions something interesting about pediatric anomalies here.

Yes, congenital coronary anomalies.

Sometimes, a coronary arteries are just plumbed wrong from birth.

There can be fistulas or they take abnormal courses, getting squeezed between other vessels.

This can cause exertional pain in kids because when the heart works hard, those kinky vessels can't deliver the blood flow.

And trauma.

Obviously, if you get hit, it hurts, but there is a delayed effect mentioned that's really interesting.

Post -traumatic pericardial effusion.

This can appear one to three months after the trauma, so a patient comes in with chest pain, and you need to ask about car accidents or significant sports hits from months ago.

It's not always top of mind for them.

And the ruptured spleen connection.

That seems random.

It's a classic medical school trick question.

A ruptured spleen is in the abdomen, right?

But it can irritate the phrenic nerve.

And where does the phrenic nerve send pain signals?

Up to the shoulder.

So abdominal trauma can present as left shoulder pain.

That is called carosine.

Let's talk about the GI mimics again, specifically the food association.

Yeah.

This seems to be the most common confusion point for patients and clinicians.

It is.

It's a huge diagnostic challenge.

Esophageal pain mimics cardiac pain almost perfectly.

And here's the kicker.

The thing that tricks even experienced doctors.

Nitroglycerin can relieve both.

Wait, really?

I thought nitro was the magic bullet test for heart pain.

If you give nitro and the pain stocks, it's the heart.

No, that is a dangerous myth.

Nitro is a smooth muscle relaxant.

The coronary arteries have a smooth muscle, yes, so it dilates them.

But you know what else is a giant tube of smooth muscle?

The esophagus.

The esophagus.

So if you give nitro and the pain goes away, it could be angina or it could be an esophageal spasm.

That makes things incredibly complicated.

It does.

It completely ruins the diagnostic utility of the drug as a standalone test.

You have to ask other questions.

Is the pain worse when you lie down after meals?

That's more likely G or D.

Is it a colicky pain that comes on after a high fat meal?

That's cholecystitis or gallbladder pain.

And what about pancreatitis?

That's usually a severe constant epigastric pain that radiates straight through to the back.

Think pancreatitis.

Segment six looks at systemic conditions.

We mentioned shingles or hopes zoster earlier.

Right, and the key there is that it's unilateral pruritic, so itchy or burning pain.

And the rash appears days later, which makes the early diagnosis really hard.

What about connective tissue diseases?

Things like lupus, fibromyalgia, polymyositis.

These can all cause chest muscle pain due to systemic inflammation.

It's not the heart, but the muscles around it are inflamed.

And sickle cell disease.

That causes something called acute chest syndrome.

The sickling cells cause occlusion, like a traffic jam in the lung vessels.

Patient gets fever, dyspnea, a cough.

It's a major life -threatening emergency in sickle cell patients.

We touched on Marfan syndrome earlier regarding the risk for dissection.

Yes, and the statistic in the text is staggering.

It says cardiovascular involvement happens in more than 50 % of Marfan patients by age 21.

That is, that's a huge number.

Now family history.

The text throws some math at us.

It does, genetics play a huge role.

If one child has congenital heart disease, CHD, the sibling risk increases by one third.

That is very significant.

It is, and for hypertrophic cardiomyopathy, which is a leading cause of sudden death in athletes, it has an autosomal dominant transmission in one third of cases.

That means a 50 % chance of passing it on to your kids.

You also have to look for families with hypercholesterolemia, where you see CAD happening before age 20.

If dad had a heart attack at 35, you have to worry about the son at 25.

Finally, in the history taking, the text brings up psychogenic causes, specifically panic disorder.

How do we screen for that without sounding dismissive of their pain?

That's key.

The text suggests using direct validated screening questions.

In the past six months, have you had a spell of feeling frightened or anxious?

Did your heart race or feel faint?

You're not saying it's all in your head.

You're screaming for a real treatable condition, and the symptoms are different.

Patients often describe a chest heaviness that lasts for days, which is way too long for angina, or difficulty taking a deep breath that isn't related to exertion.

Okay, we have talked to the patient.

We have the history.

Now we have to touch them.

The focused physical exam.

Right.

You start with general appearance, just looking at them from the doorway.

Are they grimacing?

Are they sweating, that dipheresis?

Are they pale or cyanotic with a blue tinge?

Those are all signs of the autonomic system failing.

You see that in a big MI or PE.

What is splinting?

The text mentions that.

Splinting is when a patient takes very shallow breaths or holds their chest rigid to avoid pain.

You see this often with rib fractures or severe pleuritis.

They are terrified to take a deep breath because they know it's gonna hurt.

Moving to vital signs.

Blood pressure is key.

In an MI, it is often elevated due to the pain and stress response.

But in cardiogenic shock, where the pump is failing, or in a dissection, you might see profound hypotension.

In pulse pressure, that is the difference between the top and bottom number, right?

Exactly, and in heart failure, it often decreases or narrows.

Why does it narrow?

Because the heart pump is failing, so this systolic pressure, the top number, drops.

To compensate, the body clamps down on the blood vessel's vasoconstriction to try and keep pressure up, which raises the diastolic or bottom number, so the two numbers get closer together.

And there's a term here, paradoxical pulse.

Pulsus paradoxus.

This is a classic finding in things like myocarditis and pericarditis with effusion.

It's an exaggerated drop in blood pressure, more than 10 millimilli -8 -Hg during inspiration.

Basically, the heart is being constricted by the inflamed pericardium and can't fill properly when the lungs expand and push on it.

Palpation.

We are feeling the chest.

What are we looking for?

Tracheal shift.

This is a big one for attention pneumothorax.

Which way does it shift?

It's all about physics.

In attention pneumothorax, air builds up in the pleural space and pushes everything away from it.

So the trachea deviates to the opposite side.

But in atelectasis, which is just a simple lung collapse without pressure, the trachea deviates toward the affected lung because the lung is shrinking and pulling things toward it.

You can actually feel air under the skin.

Subcutaneous emphysema, yes.

It feels like bubble wrap or rice krispies under the skin.

It's a bizarre sensation.

It means air has leaked from the lung into the surrounding tissue.

Now let's get into auscultation.

Listening to the heart and lungs.

This is segment eight.

The text has a specific table.

Table 8 .1, breaking down breath sounds.

This is fundamental for students.

You absolutely have to know normal to be able to hear abnormal.

So vesicular sounds, where are those?

That's the normal sound.

It's soft, low pitch.

You hear it over the peripheral lung fields.

The key feature to remember is that inspiration is longer than expiration.

And bronchial sounds.

Those are loud and high pitched.

You normally hear them over the sternum and the trachea.

Here, the opposite is true.

Expiration is longer than inspiration.

If you hear bronchial sounds where you should hear vesicular sounds, that's abnormal.

It suggests consolidation, like in pneumonia.

And if you just hear silence.

Big problem.

That means pneumothorax or a very severe airway obstruction.

No air movement equals no sound.

A silent chest in a severe asthma attack is actually a sign of imminent respiratory failure.

Now, the extra sounds,

the adventitious sounds.

Let's break down crackles versus wheezing.

Crackles, which we used to call rails, are discontinuous popping sounds.

The best analogy is Velcro being pulled apart.

This is the sound of fluid or mucus in the small airways popping open with each breath.

And wheezing.

Wheezing is that classic whistling musical sound.

This usually indicates narrowing.

It could be fluid in the larger airways like you hear in heart failure or bronchospasm like in asthma.

The outline explicitly asks us to explain the mechanism of wheezing.

Why does it happen specifically on exhalation?

It's simple physics, really.

During inhalation, the negative pressure in your chest actually pulls the airways open wider.

But during exhalation, there's positive pressure from the chest wall and diaphragm pushing in on the small airways.

This naturally makes them a bit narrower.

So if they are already narrowed by asthma or fluid, that extra pressure during exhalation can collapse them.

The air has to force its way through that tiny collapsed gap and that creates the whistling sound.

That makes perfect sense.

What about raunchy?

Raunchy are deep, continuous rumbling sounds.

It sounds like snoring coming from the chest.

It's caused by turbulent air going through secretions in the large airways.

They often clear up after a good cough.

Moving to heart sounds.

What is a paradoxical S2?

Normally the second heart sound, S2, is composed of the aortic and pulmonic valves closing.

It splits slightly on inspiration.

A paradoxical S2 is when that split is reversed.

It's often a sign of coronary ischemia or a left bundle branch block.

It's a subtle but important finding.

And the gallops, S3 and S4.

They always confuse people.

S3 is the ventricular gallop.

The cadence sounds like Kentucky.

It usually means heart failure or significant mitral regurgitation.

It's the sound of blood sloshing into an overfilled, compliant ventricle.

S4 is the atrial gallop with a Tennessee cadence.

It occurs right before S1.

It indicates the atria contracting hard against a stiff, non -compliant, stressed ventricle, often from long -standing hypertension or an acute MI.

Okay, we have listened, we have felt.

Now we need hard data.

Segment nine, laboratory and diagnostic studies.

The ECG is your first line for acute chest pain.

No question.

You are looking for ST elevation or depression, which suggests injury, T wave inversion, which suggests ischemia, or Q waves, which indicate old damage, muscle that's already lost.

But again, a major caveat from the text that we have to repeat.

Yes, a normal ECG does not rule out ischemia if the chest pain is ongoing.

You cannot send a patient home just because the first ECG looks okay if they were still hurting.

You need serial ECGs and biomarkers.

What about stress testing?

If the resting ECG is normal, but they have intermittent pain that sounds suspicious, you do a treadmill test.

We stress the heart to see if we can provoke the ischemia and see it on the EKG.

And for a PE?

The VQ scan is used to see if ventilation matches perfusion, if the air is going where the blood is.

But the text calls pulmonary angiography the gold standard.

Angiography, that sounds invasive.

It is, it involves injecting dye directly into the pulmonary arteries to visualize them.

It's expensive and invasive, so it's not the first test, but the text lists it as the definitive test if other imaging is unclear.

Let's talk blood work, biomarkers.

CK and CKMB were the old standard.

They peak at 24 hours, but troponin is the preferred marker today by far.

Why is troponin so much better?

Two reasons.

First, it's much more specific to cardiac muscle.

Second, it has a great timeline.

It starts to be released two to six hours after damage, peaks at 12 to 26 hours, and stays elevated for seven to 10 days.

So it catches both the early presenters and the people who waited a few days to come in.

And D -dimer, I hear that a lot with PE.

D -dimer is a degradation product of blood clots.

It is extremely useful for what it rules out.

If the D -dimer is normal, it rules out thrombosis, a PE or DVT with a very high certainty.

It has a high negative predictive value.

But it's high.

If it's high, it doesn't prove a clot.

It could be high from inflammation, recent surgery, pregnancy, anything.

So a positive D -dimer means you need to do more tests, but a negative one often means you can stop looking for a clot.

All right.

We have gathered all our evidence.

Now we have to put it into buckets, the differential diagnosis.

Let's start with the scariest bucket, emergent conditions.

Right.

Top of the list, acute MI,

sudden pain, often at rest, deep, central, with that feeling of impending doom, typically not responsive to nitroglycerin.

Then aortic dissection.

The ripping, tearing pain.

You'll often see a widened, meaty stenom on the chest x -ray.

And the mortality is just.

It's incredibly high.

The text says 96 % if witnessed in hospital.

Wow.

Okay, what's acute coronary insufficiency?

This is severe pain that lasts over 30 minutes, but, and here's the key difference.

There's no infarct evidence.

The cardiac enzymes, the troponins, are normal, but the ischemia is very real.

It's a huge warning shot that an MI is imminent.

And pulmonary embolus.

Sedent, crushing pain if it's a big central clot, or pleuritic pain if it's smaller near the lung surface.

And you have to look for the risk factors.

Immobility, cancer, birth control, pills, recent surgery.

Okay, bucket number two.

Non -emergent cardiac and respiratory.

Less immediately deadly, but still serious.

Stable angina.

That's the one that's gradual, exertional, and goes away with rest or nitro.

Then there's pericarditis.

The friction rub is pathognomonic, meaning if you hear it, that's the diagnosis.

And the key historical clue is that the pain is relieved by sitting upright and leaning forward.

And finally, bucket number three.

GI, musculoskeletal, and other.

The great mimics.

Right, you've got your cholecystitis, that colicky pain after a fatty meal.

You can check for a positive Murphy sign.

You press on the gallbladder while they breathe in and they'll stop because of the pain.

Then acute pancreatitis, severe, constant epigastric pain radiating to the back.

And costochondritis, probably the most common benign cause.

For sure, and the diagnosis is simple.

Pain when you press on the costable cartilage.

If there is visible swelling with the pain, the text notes it's called Tietzi syndrome.

So we've traveled from the terrifying big four all the way to the benign, precordial catch.

We have looked at Monday morning heart attacks, silent lung zones, and why babies have sweaty foreheads.

It's a really comprehensive framework.

If you follow it, you can be systematic.

You start with life threats, you get the focused history, you listen to the descriptions, you check the risks, and you use the physical exam to narrow it down.

But before we go, I wanna leave everyone with a final provocative thought that comes straight from the text.

In the evidence -based practice section, there was a statistic about silent MI.

Yes, the text notes that 25 % of myocardial infarctions go unrecognized.

25%, one in four.

One in four, either because the patient had no pain at all or they had atypical symptoms like profound fatigue or shortness of breath without pain.

And this is especially true in diabetics and the elderly.

So if one in four heart attacks doesn't follow the rules we just spent this whole deep dive discussing,

how much reliance should we actually place on the classic narrative of crushing chest pain?

It raises a huge question.

I mean, does this mean we should lower our threshold for testing?

Should we be quicker to order the ECG or the troponin in an elderly patient who just comes in feeling off or unusually tired?

It definitely suggests that chest pain isn't the only signal we should be listening for.

The absence of pain does not mean the absence of disease.

Absolutely, a very sobering thought to end on.

Thank you for joining us on this deep dive into chapter eight.

Always a pleasure to unpack the details.

Keep learning, keep questioning and we will see you next time on The Deep Dive.