Chapter 26: Palpitations Assessment & Diagnosis

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Welcome back to the Deep Dive.

Today is a bit of a special one.

We're putting on our clinical hats, or maybe more accurately, our nursing student hats, because we're doing a dedicated walkthrough for the Last Minute Lecture Series.

That's right.

So if you're a college student or maybe an advanced practice nursing student, and you're scaring down a pretty scary exam or a clinical rotation,

and you've got Chapter 26 of Advanced Health Assessment and Clinical Diagnosis in Primary Care, sixth edition open in front of you, well, you are in exactly the right place.

It's good to be here.

And yes, this is a very focused mission today.

We are not chatting vaguely about heart issues.

We're going to guide you step by step through Chapter 26, specifically on the topic of palpitations.

And we're going to do it in the exact order the text presents it.

That is the game plan.

We're going to try and translate that really dense clinical assessment material into knowledge that's clear, that's accessible.

You want to make sure you really get the why behind the what.

So let's just jump right in.

We're starting at the very top of the chapter with the definition itself.

You know, your heart is usually this silent partner.

It just works.

Completely silent.

It beats, what, something like 100 ,000 times a day.

And for almost all of those, you are just blissfully unaware that it's even happening.

It's just background noise, autonomic.

Exactly.

But then all of a sudden it isn't.

You're lying in bed or maybe you're just sitting at your desk and you feel it, a thud, a flutter.

Sometimes it feels like a kick in the chest.

That moment,

that transition from silence to sensation, that's what we're breaking down today.

It's the unpleasant awareness.

That is the clinical definition that the chapter gives us to work with.

Unpleasant awareness.

I like that.

It really captures it.

And that's where we're doing this deep dive on Chapter 26, because let's be honest, if you're a student, this chapter can feel like a minefield.

Oh, absolutely.

It's dense.

It's incredibly high stakes and it really requires you to be a detective.

A detective, yeah.

Because when a patient comes in and their chief complaint is palpitations, your job is to filter through a massive amount of, well, noise to find a potentially lethal signal.

And most of the time it is just noise.

Most of the time, yes.

Most of the time palpitations are completely benign.

But sometimes, and this is the terrifying part for any clinician, they are the first and only warning sign of sudden cardiac death.

Wow.

Okay, so that is the tension of this whole deep dive, isn't it?

We're going to walk through the chapter from that initial definition all the way to the final diagnostic synthesis where to decode the patient's sometimes really vague descriptions.

It feels like a fish flopping around.

Exactly.

And we'll explain the physics behind the weird symptoms, like why would your neck suddenly start pounding.

And we'll figure out how to separate what we might call the anxious heart from the failing heart.

The mission then is to build a safety net.

A mental safety net, yes.

We want you to understand the physiology so well that when you hear a patient describe their symptoms, you're not just checking a box on a form, you're visualizing the actual electrical pathways in their chest.

Okay, so let's start with that definition again.

The text says palpitations are an unpleasant awareness of the forceful, rapid, or irregular beating of the heart.

I think that word unpleasant is doing a lot of heavy lifting there.

It really is.

It implies a violation of the norm.

It's something that shouldn't be happening.

Patients don't usually come in and say, I feel my heart beating.

They use these visceral words.

Like what?

They'll say it's thumping, it's pounding, it's fluttering or, and this is a classic one you'll hear, it feels like a bird is trapped in their chest.

A trapped bird.

That's so specific.

And the text makes a really interesting point about when they notice it.

It's often when they're quietly resting.

It seems kind of counterintuitive, doesn't it?

You'd think you'd feel your heart when you're sprinting up a hill, not when you're trying to fall asleep.

It's actually a signal to noise ratio issue.

Okay, break that down.

Think about your day.

You're running around, you're stressed, you're on your phone, you're talking to people.

Your brain is just bombarded with sensory input.

It filters out a lot of the internal autonomic signals, like your heartbeat.

It has to, or you'd go crazy.

Precisely.

But then you lay down, you turn off the lights, you silence the world.

The external noise drops to zero and suddenly that internal thumping, which might've been happening all day long, becomes the loudest thing in the room.

So when the patient says it only happens at night,

what you're hearing as a clinician is that it might be happening all the time.

They just only perceive it at night.

Exactly.

That's a critical distinction to make in your head.

And that brings us to the first major fork in the road in the chapter.

The first big decision point, we have to categorize the cause.

The text gives us two massive buckets to sort things into, cardiac causes and non -cardiac causes.

The cardiac bucket is the scary one.

It is.

That's the heart itself, the plumbing and the wiring.

Right.

You're looking at structural problems or electrical problems.

We're talking about arrhythmias, valvular disease, cardiomyopathy, the things that can actually kill you.

And the non -cardiac bucket, what's in there?

That's everything else.

And it's a surprisingly deep bucket.

It includes the psychological triggers like anxiety or panic attacks.

It includes the whole metabolic system, thyroid issues, fever, hypoglycemia, anemia, and it includes exogenous substances.

What we eat, what we drink, what we smoke, what drugs we take.

The text specifically mentions that anything causing just plain old sinus tachycardia, things like pain,

dehydration, even menopause, can trigger this complaint.

Absolutely.

So we essentially have to be these holistic detectives.

Is the heart the criminal or is the heart just the victim reacting to a really bad environment?

I like that analogy.

So to figure that out, we have to start where all good assessments start, the focused history.

The text has a section on key questions, which I kind of use the red flag, huh?

That's a great way to put it.

We are hunting for reasons to send this person to the emergency room right now.

This is the do not pass go, do not collect $200 section of the assessment.

The very first thing the text highlights is coronary artery disease,

CAD.

Why is that number one?

Why is that the very first question?

Because of the scar tissue.

It all comes down to scar tissue.

If a patient has a history of CAD, or more specifically, a history of a myocardial infarction, a heart attack, it means part of their heart muscle has died.

And that dead muscle gets replaced by scar tissue.

And scar tissue is different.

It's electrically inert.

It doesn't conduct the signal smoothly.

It forces the electricity to detour to find a new path.

Like a roadblock on a highway or a fallen tree on a path.

Exactly.

And those detours are what create these dangerous re -entry circuits.

The electricity can get trapped spinning around and around the scar tissue.

And that can trigger life -threatening ventricular arrhythmias.

So if a patient has a history of a heart attack and now they have new palpitations, the likelihood that this is a dangerous ventricular rhythm just skyrockets.

You have to take that very seriously.

So that's why we ask about smoking, hypertension, diabetes, the standard vascular risks.

But the text also emphasizes family history with a very specific age cutoff,

death, or a heart attack happening before age 60.

Why that number?

The before 60 part is the genetic marker.

It's the clue that this isn't just about lifestyle.

If your grandfather died of a heart attack at 90, that's sad, but it's probably just life.

But if your father died of a heart attack at 45, or your sister had a stroke at 30, that screams genetic predisposition.

To what though?

To things like familial hypercholesterolemia or inherited clotting disorders.

It completely changes your risk calculus for that patient sitting in front of you.

Okay, that makes sense.

The next red flag is hemodynamic compromise.

This sounds very technical, but when you translate it for the patient, it's basically, are you passing out?

Do you fall down?

Right.

The clinical term is syncope, or presyncope, which is that feeling of nearly blacking out, you know, the vision goes gray, you get dizzy.

If a patient says to you, my heart starts fluttering and then the room goes dark, you need to stop everything and pay very close attention.

Because that means the pump has failed.

It means the arrhythmia is so fast or so chaotic that the heart isn't actually pushing enough blood up to the brain to keep consciousness online.

That is a life -threatening sign until you have proven otherwise.

What about chest pain?

That's always a scary symptom to hear.

It is, but context is key here.

The details matter.

If the palpitations come with that classic angina, that pressure, that squeezing like an elephant on the chest, we're thinking ischemia.

The heart muscle isn't getting enough oxygen.

Okay.

But there's a specific nuance that the text brings up regarding pericardial disease.

Right.

This is the leaning forward sign.

Yes.

If they say, I have chest pain and palpitations, but it gets a lot better when I sit up and lean forward, that is classic for pericarditis.

Which is what exactly?

Inflammation of the sac around the heart.

The leaning forward creates a bit more space and reduces the friction, which eases the pain.

It's a great diagnostic clue.

Got it.

And then we have the athletes.

The chapter puts a big bold warning label on exertional palpitations in athletes.

This is the tragedy we all see in the news from time to time.

A young, seemingly perfectly healthy basketball player drops dead on the court.

It's horrifying.

It is.

And it's often preventable if we listen.

If an athlete complains of chest pain or lightheadedness that happens while they are exercising, we have to suspect something serious.

Like what?

What are we worried about?

The big ones are hypertrophic cardiomyopathy, a thickened heart muscle, or anomalous coronary arteries, where the plumbing is just wired wrong from birth.

The bottom line is you cannot dismiss a 20 -year -old athlete's palpitations as just stress or being out of shape.

And dyspnea, shortness of breath.

Yeah, shortness of breath.

If the heart is beating way too fast, a sustained tachyarrhythmia, it can't fill properly between beats.

It can't pump efficiently.

So fluid starts to back up into the lungs, oxygen exchange suffers, and the patient gets breathless.

It's another sign that the heart is really struggling to keep up with the demand.

Exactly.

The section on history also brings up sudden cardiac death or SCD.

We touched on family history, but this is a bit more specific.

It is.

You need to ask the question very directly.

Did anyone in your family die suddenly and unexpectedly from a heart problem, especially at a young age?

This points toward inherited electrical problems like Long QT syndrome or structural problems like hypertrophic cardiomyopathy.

These things run in families.

And the last red flag in this section is cardiac surgery.

Is that because scar tissue from surgery is basically the same as scar tissue from a heart attack?

Precisely.

It doesn't matter to the electricity why the scar is there.

Whether they are children who had a congenital defect repaired or adults who had bypass surgery, anyone who has had their heart cut into is at a lifelong increased risk for arrhythmias.

Those surgical scars can disrupt the normal electrical pathways.

Okay.

So we've covered the really dangerous stuff, the red flags.

We know who is potentially in immediate danger.

Now we can move on to part two of the history,

descriptions and occurrences.

This is where we have to become like interpreters.

We have to decode the weird things that patients say.

And patients are very creative with their descriptions.

You'll hear all sorts of things, but usually they fall into one of three physiological patterns.

Let's start with the most common one, the skipped beat.

A patient says, my heart stopped for a second and then it kicked me in the chest.

That description is almost pathognomonic.

It's almost a diagnosis in itself for a premature contraction.

A PVC or a PAC?

A PVC, a premature ventricular contraction or a PAC, a premature atrial contraction.

So can you explain the mechanics of that kick?

Why does a skipped beat feel like a punch?

It's just basic fluid dynamics.

It's actually really cool.

So the heart's electrical system fires early.

That's the premature beat.

It's usually a pretty weak contraction because the ventricle hasn't had time to fill up with blood.

The patient usually doesn't even feel that little premature beat.

Okay, so they don't feel the skip.

No, but after that early beat, the electrical system has to reset itself.

So there's what we call a compensatory pause.

The heart waits just a little bit longer than usual for the next normal beat to come.

And while it's waiting, it's filling with blood.

Exactly.

It's overfilling.

The ventricle fills with more blood than it normally would.

So when that next normal beat finally fires, the heart muscle is stretched out more than usual, and it snaps back with extra force, what we call increased contractility, to eject that extra volume of blood.

That's the kick.

That massive forceful squeeze is what the patient feels.

They don't feel the skip.

They feel the powerful recovery beat.

That is a fantastic explanation.

It's like a super beat to make up for the pause.

Now, what about the description, rapid fluttering?

That one's a lot less specific, unfortunately.

It just means fast.

It could be a simple sinus tachycardia, because they're nervous sitting in your office, or it could be something more serious, like atrial fibrillation or SVT.

It tells us the rate is the issue, but it doesn't really tell us much about the underlying rhythm.

Okay, so it's a starting point, but not a destination.

Right.

Now we get to my favorite one.

The coolest, weirdest sign in the whole chapter, pounding in the neck.

The text calls this a high -yield diagnostic clue.

Oh, it is.

This is the frog sign.

Yes, and to understand it, you have to visualize the heart's chambers and valves.

So normally, the top chamber, the atrium, squeezes blood down into the bottom chamber, the ventricle, through an open valve, the tricuspid valve on the right side.

Then that valve closes, and the ventricle squeezes the blood out to the lungs.

It's all in harmony,

a perfect synchronization.

Right, but in certain arrhythmias, specifically, AV nodal reentry tachycardia, or in some cases, a ventricular tachycardia, that synchronization is completely broken.

The atrium and the ventricle contract at the exact same time.

So the atrium is trying to push blood down, but the ventricle is squeezing up, which means the valve between them is slammed shut.

Exactly, it's like trying to open a door that someone is kicking shut from the other side at the same instant.

The blood in the atrium has nowhere to go forward, so it bounces off that closed tricuspid valve and shoots backward.

Up into the veins.

Up into the great veins.

The superior vena cava and the jugular veins in the neck.

It creates this massive, visible pressure wave, what we call a cannon wave.

And the patient feels that as a pounding in their neck.

Yes, and if you're looking at the patient, you can sometimes see their neck pulsing, almost like a frog's throat.

That's the frog sign.

It's a dead giveaway for AV dissociation.

That is such a vivid, incredible physical sign.

The frog sign.

I will never forget that.

Okay, let's talk about triggers.

The text mentions sleep, and the post -exercise window is being significant.

This brings the vagus nerve into the conversation.

The vagus nerve is the brake pedal for the heart.

It slows things down.

Its job is to promote rest and digest.

So when you go to sleep or right after you finish a hard run, your body slams on the brakes.

Your vagal tone goes way up.

And that's usually a good thing, slowing the heart down.

Usually, yes.

But for some people, that sudden surge in vagal tone, that powerful braking signal, can actually trigger specific electrical misfires in the atria.

There's a condition called vagal mediated atrial fibrillation.

It literally happens when the patient is most relaxed.

Which must be so frustrating and confusing for the patient.

I was just lying there doing nothing.

It feels like a betrayal, doesn't it?

I'm finally relaxing, and now my heart is going crazy.

Yeah.

What about the light switch onset?

The really abrupt start and stop.

This is a fantastic clue for differentiating a true arrhythmia from a normal physiological response.

Think about it.

If you get scared or you go for a run, your heart rate ramps up smoothly.

And when you stop, it ramps down smoothly.

It's a curve.

But supraventricular tachycardia, SVT, isn't a curve.

No.

SVT is a switch.

The patient is just walking down the street and snap.

Their heart rate is instantly 180.

Ten minutes later, snap, it's back to 80.

That instantaneous change is a hallmark of a reentrant arrhythmia.

It's an electrical short circuit turning on and off.

And the text says you can sometimes turn that switch off yourself with something called the Valsalva maneuver.

Yeah, which is basically bearing down like you're having a bowel movement.

So how on earth does straining on the toilet stop a heart arrhythmia?

It's a brilliant little biohack.

When you bear down, you increase the pressure inside your chest.

When you release that strain, all the blood that was held back rushes back to the heart.

This triggers special pressure sensors called baroreceptors in your major arteries.

And they sense that sudden rush of pressure.

They sense it and they scream at the brain, whoa, pressure is way too high.

The brain's immediate response is to fire the vagus nerve, our brake pedal to slow the heart down.

That powerful vagal blast can be enough to interrupt and terminate the short circuit of SVT.

That is incredible.

A physical maneuver to reset an electrical problem.

And what about exercise as a trigger?

It depends.

If it's a rapid chaotic rhythm during exercise, it could be VT, sinus tach, or AFib.

But if it's regular palpitations with exertion, we start to worry more about structural issues like hypertrophic cardiomyopathy or coronary artery disease.

And here's an interesting one.

If they have palpitations at rest that get worse with exercise, you should think about anemia.

Why is that?

Because the heart is already struggling to deliver enough oxygen at rest.

Exercise just increases the demand to an impossible level, so the heart has to beat even faster to try and compensate.

And one last odd one, positional changes.

Yeah, if a patient says rolling over in bed is what triggers it, you have to at least consider an atrial mixoma.

That's a tumor in the heart, right?

Yes, usually a benign tumor that grows on a little stalk, often in the left atrium.

When you change position, it can swing and plop into the mitral valve opening, like a ball in a funnel.

It obstructs blood flow and can cause both palpitations and fainting.

Wow.

Or it could just be a mediastinal mass, something outside the heart pressing on it.

Exactly.

It's rare, but it's on the list.

Okay, let's pivot now.

Let's talk about the mind, psychological causes.

We have to tread very, very carefully here.

The text is extremely explicit about this, and it's a critical point for any student.

You must, must rule out clinically significant arrhythmias before you label something as anxiety.

This is the cardinal, don't gaslight your patient rule.

Absolutely, because here's the trap that clinicians can fall into.

Arrhythmias cause anxiety.

I mean, think about it.

If your heart suddenly started beating 200 times a minute for no reason, would you be anxious?

I'd be utterly terrified.

I think I was dying.

Right, so anxiety is very often a symptom of the arrhythmia, not the cause of it.

That being said, panic disorder is a real cause of palpitations.

The mechanism is simple, adrenaline.

The fight or flight response going haywire.

Exactly.

A panic attack dumps a huge amount of catecholamines into the blood.

The heart just responds to that chemical signal by racing.

The key differentiator, often, is duration.

A true panic attack usually lasts longer than a few minutes, often 15 to 30 minutes, and it comes with a whole constellation of other symptoms.

The intense fear of dying, tingling in the hands and around the mouth, shortness of breath from hyperventilation.

But the text mentions there's a mimic lurking in the shadows here.

Pheochromozytoma.

The great mimic, yes.

This is a tumor on the adrenal gland.

It's very rare, but you do not want to miss it.

It sits there on the gland and sporadically squeezes out massive doses of adrenaline and norepinephrine into the bloodstream.

So it chemically induces a panic attack.

Basically, yes.

But the symptoms tend to be a bit more physical and extreme.

We look for the classic triad, a severe pounding headache, profuse sweating and tachycardia.

And these patients often have episodic flushing.

They'll just turn bright red for no reason.

So if a patient says, I have these panic attacks where my head feels like it's going to explode and I soak through my shirt with sweat.

You need to stop thinking about Xanax and start thinking about checking your urine for metanoferins.

You might be missing a tumor.

That's a huge clinical pearl.

Let's talk about the evidence -based practice, sidebar in the chapter.

The Thavengeranathin study from 2009.

They asked a simple question.

Can we predict the arrhythmia just by talking to the patient?

Just from the history.

And the answer, pretty definitively, was not really.

That's both comforting and a little scary.

It's humbling, is what it is.

The study showed that history alone is just not sufficient.

We can get clues, like we discussed.

The neck pounding significantly increases the odds of it being avianotal reentry tachycardia.

But at the end of the day, you cannot diagnose a rhythm without seeing the rhythm.

So the history just gives you probabilities.

It helps you decide how aggressively to test.

That's a perfect way to put it.

A history of cardiac disease.

The likelihood of a dangerous arrhythmia goes up.

A history of panic disorder.

The likelihood goes down slightly.

But the ultimate conclusion of the study and of the chapter is that an ECG or some form of monitoring is almost always required.

You can't just talk to the patient and say, you're fine, you need objective data.

Okay, so before we get to the ECG, we have to look at the rest of the body.

The systemic causes.

The text calls this the normal heart in a metabolic mess.

I love that phrasing.

It's so descriptive.

The heart's wiring is fine.

The plumbing is fine.

The environment it's living in is toxic.

Let's run through some of the common messes.

What about just basic fluid and electrolyte issues?

Absolutely.

Dehydration, a high fever, hypoglycemia, or low blood sugar.

All of these stress the body and can cause the heart to race.

And particularly vomiting or diarrhea can lead to electrolyte imbalances, especially low potassium or low magnesium, which can make the heart muscle electrically irritable.

And then there's the thyroid.

The tech spends a good amount of time on this.

Hyperthyroidism is a classic cause of palpitations, especially new onset atrial fibrillation.

The thyroid controls your body's metabolic throttle.

If it's stuck on full, everything speeds up.

Your heart rate, your metabolism, your gut motility.

So what are the signs you'd look for?

You're looking for weight loss despite a good appetite, heat intolerance, nervousness and anxiety, thinning hair, and a fine tremor in the hands.

And anemia, how does that cause palpitations?

This is a plumbing capacity issue.

If you don't have enough red blood cells to carry oxygen, the heart has to compensate.

It has to pump the same small amount of blood around faster and faster to try and meet the body's oxygen demands.

It's a high output state.

So the patient would look pale, complain of fatigue, in shortness of breath, and maybe report heavy menstrual periods is the cause in pregnancy.

Pregnancy itself creates a hyperdynamic cardiovascular state.

Blood volume increases by almost 50%.

The heart has to work much harder.

Palpitations are very common, but again, you never just assume, you always investigate to be sure.

And then we have the things we put in our own bodies.

Let's start with medications.

This is a huge and often overlooked category.

You always, always need to get a detailed medication list, including over -the -counter stuff.

You're specifically looking for drugs that are QT prolongers.

Okay, what does that mean?

On an ECG, the QT interval represents the time it takes for the heart's electrical system to recharge after a beat.

Some drugs stretch that time out, making it dangerously long.

This makes the heart vulnerable to a chaotic, life -threatening rhythm called torsades de pointes.

What are some of the common culprits?

The list is long, but some big categories are certain antibiotics, especially macrolides like azithromycin, many psychotropic drugs, some antihistamines, antifungals, and diuretics that waste potassium.

And the text pulls out a specific statistic about acetylcholinesterase inhibitors.

Yes, these are drugs often used for dementia, like dunteazle.

The chapter states they can cause arrhythmia in about 25 % of users.

One in four.

That is a massive number.

It's huge.

So if you have an elderly patient on one of these drugs for Alzheimer's, who starts having falls or palpitations, you have to think about the medication as a possible cause.

And what about in children?

In kids, you have to watch out for over -the -counter cold medicines.

Decongestants like pseudoephedrine are stimulants.

Which brings us to other stimulants.

Caffeine, cocaine, nicotine.

Amphetamines.

And a really big one these days, especially in younger people, is fitness supplements.

Pre -workout drinks.

Exactly.

They are often just an unregulated cocktail of stimulants.

If a college student comes into your clinic with a racing heart, you have to ask them specifically about supplements.

What do you drink before you go to the gym?

Energy drinks, too.

Energy drinks, workout supplements.

They often have massive, sometimes undisclosed amounts of caffeine or other stimulant compounds.

Oh yeah, we've done a ton of talking, now we have to touch the patient.

The focused physical examination.

Right.

And the challenge here, as we mentioned, is that the patient is usually asymptomatic when they're in your office.

The palpitations happened last night.

They feel fine now.

So you're not looking for the arrhythmia itself.

You're looking for the structural evidence, the clues it might have left behind.

We start with just general appearance.

Do they look anxious?

Are they tremulous or flushed?

Making you think thyroid or pheochromocytoma?

Are they pale?

Suggesting anemia?

Then vital signs.

The text is very specific, saying to check BP and pulse in three positions.

Supine, sitting, and standing.

We call that checking for orthostatics.

We're looking for signs of volume depletion or an abnormal autonomic response.

But when you're checking the pulse, you're not just counting.

You are feeling for the rhythm.

And this is where we might find that irregularly irregular pulse.

The hallmark of atrial fibrillation, it's pure chaos.

There is no pattern whatsoever.

If you try to tap it out on a table, it's just random.

And this is also where we can find the pulse deficit.

This is a concept that I think trips a lot of students up.

It can be tricky, but it's simple once you get it.

It's a math problem.

You listen to the heart at the apex with your stethoscope.

That's the apical rate.

At the exact same time, you feel the radial pulse at the wrist.

In a normal heart, every lub -dub you hear produces a pulse you can feel.

The ratio is one to one.

But not an AFib.

Not an AFib.

In AFib, the heart is twitching so fast and chaotically that sometimes the ventricle contracts before it's had time to fill up with much blood.

It's an empty squeeze.

It makes a sound.

You hear it with your stethoscope.

But it doesn't push enough blood out to create a palpable wave at the wrist.

The heart rate you hear might be under 20, but the pulse you feel is only 80.

And that gap of 40 beats is the pulse deficit.

It's a direct measure of how inefficient the heart is being.

Got it.

The text also mentions a specific triad to watch out for.

Fever plus hypotension plus a heart murmur.

Yes.

If you see that combination, you have to worry about an infection of the heart itself, like myocarditis or even endocarditis.

That is a very sick patient who needs immediate attention.

Moving to the neck again.

Jugular venous pressure or JVP.

We talked about the history of cannon A waves, but now we're actually looking for them.

You position the patient correctly, have them turn their head, and you look at the neck veins.

If you see these large prominent pressure waves shooting up the neck, those are cannon A waves.

And the frog sign.

That's when those waves are happening rapidly and regularly.

You see the whole side of the neck bulging rhythmically.

It's a dramatic sign of AV dissociation, pointing you towards SVT or even complete heart block.

Oscultation.

Listening to the heart sounds.

First, you find the PMI, the point of maximal impulse, where the heartbeat is strongest.

If it's displaced to the left or feels enlarged, that suggests the left ventricle is big.

From hypertrophy or cardiomyopathy.

Exactly.

Then you listen carefully for murmurs.

The text highlights two really important ones.

Yes.

First, a mid -systolic click is highly suggestive of mitral valve prolapse, or MVP.

That's a floppy valve.

It's often associated with benign palpitations, but can also be linked to SVT.

And the really scary one for athletes.

A harsh, hollow systolic murmur.

If you hear it along the left sternal border, and it gets louder when the patient performs a Valsalva maneuver, that is the classic finding for hypertrophic cardiomyopathy, HCM.

Why does it get louder?

Because the Valsalva maneuver decreases the amount of blood returning to the heart.

This makes the chamber smaller and brings the thickened muscle walls closer together, making the obstruction worse and the murmur louder.

That is a critical clinical pearl.

Louder with Valsalva equals HCM.

If you hear that in a young person with exertional palpitations, you stop them from playing sports immediately and get an echocardiogram.

Head, neck, and mental status.

What are we looking for there?

We're looking for signs of substance abuse again.

A constant runny nose, rhinorrhea, nosebleeds, or even lesions on the nasal septum could suggest cocaine use.

Dilated pupils too.

And the thyroid again.

You need to actually put your hands on the neck and feel the thyroid gland, is enlarged, what we call a goiter.

Then you listen over it with your stethoscope.

Do you hear a brute?

That's the sound of turbulent blood flow in a hyperactive gland.

And don't forget to look at their eyes.

Right.

Look for exophthalmos, which is that bulging appearance of the eyes seen in Grave's disease.

Mental status.

Just observe.

Are they irritable, overly anxious, or showing signs of delusions that might be drug -induced?

And finally, the extremities.

The thyroid signs can show up here too.

The text mentions onycholysis, where the fingernail actually detaches from the nail bed.

And localized mixed edema, a strange thick waxy skin on the shins.

You check the nails for cyanosis or clubbing?

Yes, which would point towards a more chronic underlying heart or lung condition.

Okay.

We've done the complete history and the full physical exam.

Now we need the hard data.

Laboratory and diagnostic studies.

The text is crystal clear on this.

The 12 -lead ECG is the initial test.

It is completely non -negotiable.

Every patient with palpitations gets one.

What are we hoping to find on it?

We're looking for two things.

One, active electrical abnormalities, like the telltale signs of Wolf -Parkinson -White syndrome, or a long QT interval.

Or two, we're looking for structural clues, like evidence of a previous heart attack or a left ventricular hypertrophy.

If that initial ECG is abnormal, the path is clear.

You keep digging.

Right.

Further evaluations needed.

But if the palpitations are episodic,

that snapshot ECG in the office is probably going to be normal.

It usually is.

And that's why we need what I call the detectors.

The ambulatory monitors.

Okay.

We have a few options in our toolbox.

Let's start with the Holter monitor.

A Holter is a continuous recording for a short period, usually 24 to 48 hours.

The patient wears it, goes home, lives their life, and keeps a diary.

They write down, At 2 .15 p .m., I was walking up the stairs and fell to flutter.

Then we can go back and look at the tape at exactly 2 .15 p .m.

and see what the heart was doing.

So it's good for frequent symptoms, things that happen every day.

Exactly.

If their symptoms only happen once a month, a 24 -hour Holter is probably going to miss it.

So for that, we need an event monitor.

Yes.

This is for longer -term monitoring.

For weeks or even months.

It's a loop recorder.

It's constantly recording over itself.

But it saves the last few minutes of data in a buffer.

When the patient feels the symptom, they press a button and it freezes and saves that event the few minutes before and after they press the button.

The text makes a point of comparing auto -trigger versus patient -triggered monitors.

And the evidence shows that auto -triggered devices are superior.

Why is that?

It's simple.

Because if the arrhythmia is so severe that it makes you pass out, you can't press the button.

Ah.

Good point.

The device needs to be smart enough to recognize a problem on its own.

Right.

It needs to say, whoa, that heart rate is 200, or hey, there's a three -second pause, and save that clip automatically.

And for the really, really infrequent but serious symptoms.

For the person who has an unexplained syncope once every six months, we have implantable loop recorders.

It's the size of a small USB stick.

And we inject it just under the skin of the chest.

The battery lasts for up to three years.

We just sit back and wait for the arrhythmia to happen.

What about the echocardiogram?

That's our ultrasound of the heart.

We use it to look at the structure of the plumbing.

Are the valves leaking or narrowed?

Is the heart wall too thick?

Is the muscle squeezing correctly?

And finally, the lab test.

What are we ordering to figure out the why?

A CBC, a complete blood count, is essential.

We're looking at the white count for signs of infection, and the hemoglobin and hematocrit for anemia, a basic metabolic panel to check electrolytes, especially potassium and magnesium, the battery fluid of the heart.

And TSH and free T4.

Absolutely essential.

If the TSH comes back as undetectable, that's virtually diagnostic for hyperthyroidism.

You've found your cause.

And for our rare but important friend,

pheochromocytoma.

For that, you order urine or plasma metonephrons.

Usually it's a 24 -hour urine collection.

If those levels come back significantly elevated, you start looking for the tumor with imaging.

Okay, so we've gathered all the clues.

We have the history, the physical exam, the ECG, the labs.

Now comes the moment of synthesis,

the differential diagnosis.

It all comes down to a funnel, really.

The chapter provides these great boxes to help organize your thinking.

Box 26 .1 lists the main cardiac causes.

This is a recap of all the electrical villains we've discussed.

AFib, atrial flutter, SVT, VT, those premature contractions, PACs and PVCs, six sinus syndrome, and heart block.

And there's a red flag reiteration right there in the text.

If syncope or significant lightheadedness is present, a referral to a cardiologist is warranted.

Do not pass go.

Don't try to manage that yourself in primary care.

Box 26 .2 then lists the structural causes.

Valvular disease, cardiomyopathy, pericarditis, and metral valve prolapse.

The things you'd find on your physical exam and confirm with an echo.

So let's break down the non -cardiac causes one last time with the specific clues the text gives for really putting it all together.

For panic disorder.

Ask that specific screening question.

In the last month, have you experienced brief periods of terror or intense fear?

For generalized anxiety disorder or GAD, you're looking for a chronic history.

Six months or more of excessive worry, often accompanied by physical symptoms like muscle tension.

Anemia, power on exam, fatigue, and low hemoglobin hematocrit on the CBC.

Hyperthyroidism, that high output state.

Fast metabolism, fast heart, fast bowels, and a low TSH.

And don't forget that great clinical pearl about older adults.

They may present with what's called apathetic hyperthyroidism.

They don't look revved up and anxious.

They just look tired, withdrawn, and happen to be in atrial fibrillation.

That's such a great one to remember.

And pheochromocytoma, the classic spell symptoms of headache, sweating, and tachycardia.

And finally, drugs and stimulants.

The history coincides with use.

You might see physical signs of abuse, and you can confirm with a toxicology screen if needed.

We have covered a massive amount of ground.

Chapter 26 is now officially unpacked.

Let's wrap this all up with a final synthesis of the clinician's workflow.

How should a student think through this in a real world setting?

It's a funnel, a logical progression.

One, start with the history.

Ask the dangerous questions first.

Syncope,

chest pain, family history of sudden death.

Then characterize the feeling.

Is it a skip?

Is it a neck pound?

And ask about triggers.

Exercise, sleep, caffeine.

Two, the physical exam.

Look for the frog sign.

Look for thyroid eyes.

Feel the thyroid.

And listen carefully for that pulse deficit or those specific murmurs.

Three,

the ECG.

Get the snapshot.

It's mandatory.

And four, the monitor.

If the snapshot is normal but you're still concerned, you get a movie.

A holter for frequent symptoms.

An event monitor for less frequent ones.

And if it's none of those cardiac causes.

Then, and only then, after a thorough workup, do we start to consider benign premature contractions or psychiatric causes.

But we never ever start there.

We end there.

That is the discipline, isn't it?

The text wraps up by reiterating that most palpitations are benign.

Statistically, yes, that is true.

But clinically, our mindset has to be the exact opposite.

We must assume it's dangerous until we have proven that it is safe.

We don't reassure the patient based on statistics.

We reassure them based on their own personal data from the workup.

So you can finally say, I've checked the wiring.

I've checked the plumbing.

I've checked the body's chemistry.

Your heart might be a bit annoying right now, but it is not trying to kill you.

And that is the best news you can possibly give a patient who's been terrified by the symptom.

This has been a really deep walkthrough of Chapter 26.

We've covered the thump, the frog sign, the metabolic mess, and all the red flags.

Yeah.

To all the nursing students listening, when you're in that exam room, don't just count the rate.

Look at the neck.

Ask about that stopped sensation.

Be the detective.

You've absolutely got this.

Good luck out there.

Thanks for diving in with us.

We'll see you on the next rotation.

This has been a last -minute lecture from the Deep Dive.

Thanks so much for listening.