Chapter 20: Heart and Neck Vessels

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Welcome to the Deep Dive.

If you are listening to this right now, chances are you were a college nursing student.

And you're probably staring down an absolute mountain of for the very first time.

And, well, it probably feels incredibly overwhelming.

It always does.

But take a deep breath.

You are exactly where you need to be right now.

Think of this as your personalized one -on -one tutoring session.

Our mission today is total step -by -step mastery of the heart and neck vessels assessment.

We're going to get you completely ready for your exams and those upcoming clinical rotations.

We really are.

And, you know, the best way to tackle a complex system like the cardiovascular system is to follow a strict logical flow.

Right.

You can't just jump around.

Exactly.

We are going to start with the foundational blueprint, the anatomy and physiology.

We'll use that blueprint to build your subjective interview skills so you know exactly what questions to ask.

Which is huge.

Right.

Then we transition into the hands -on objective examination techniques.

We will analyze normal findings, break down the abnormal ones, and finally lock it all in with proper clinical documentation.

Because in clinical practice,

everything builds directly on the step before it.

It really does.

Okay.

Well, let's unpack this blueprint, starting with the structure and location of the heart.

The best way to visualize this is to picture the heart as an upside -down triangle.

That's a great visual.

Yeah.

It sits right in the middle third of the thoracic cage in an area called the mediastinum, just nestled right there between the second and fifth intercostal spaces.

Now, because it's an upside -down triangle, that broader flatter part at the top is actually called the base.

Which throws a lot of people off.

It totally does.

The base is at the top.

And the pointy part at the bottom is the apex.

That apex points down and to the left, which is exactly where you can feel the apical impulse beating against the chest wall during contraction.

And keeping that mental image of the upside -down triangle is vital for knowing where to place your stethoscope later.

When we look closer at that triangle, it's essentially a muscular pump encased in layers.

On the outside, you have the pericardium.

That's the tough double -walled sac, right?

Yes.

It protects the heart.

Between its layers, there are just a few milliliters of serous pericardial fluid.

It acts almost like motor oil.

Oh, to stop friction.

Exactly.

Ensuring the heart muscle can move smoothly without any friction every single time it beats.

Inside that is the myocardium, the thick muscular wall doing the actual pumping.

And finally, lining the inner surface is a thin layer called the endocardium.

But the heart isn't just one big pump.

It's really a dual pump system.

Two pumps side by side.

Yeah, the right side is pumping blood into the pulmonary circulation, so pushing it to the lungs to get oxygenated, while the left side is simultaneously pumping that newly oxygenated blood into the systemic circulation out to the rest of the body.

Imperfect synchronization.

And to keep all that blood moving strictly in one direction, the heart relies on four valves, which function like unidirectional swinging doors.

Right.

The AV valves and the SL valves.

Exactly.

You have the atrioventricular or AB valves, which separate the atria from the ventricles.

That's the tricuspid valve on the right and the mitral valve on the left.

And then the semilunar ones.

Yep.

The semilunar valve sitting between the ventricles and the major arteries.

The pulmonic valve on the right and the aortic valve on the left.

And these valves don't have their own motors.

They open and close completely passively, just pushed open and slammed shut by the pressure gradients of the moving blood.

I want to pause here for a second because there's a massive anatomical secret that feels like a trap for new nursing students.

Oh, the lack of valves.

Yes.

There are no valves between the vena cava and the right atrium.

And there are no valves between the pulmonary veins and the left atrium.

None at all.

So if there are no doors there to stop backflow, wouldn't gravity or pressure just push the blood backward?

That is one of the most important concepts you can grasp because that exact lack of valves explains so much of the pathology you're going to see at the bedside.

So it does just back up.

You're exactly right.

There is nothing to stop backflow.

So if a patient has abnormally high pressure on the left side of their heart, for instance, if their left ventricle is failing and cannot pump effectively, that blood has nowhere to go but backward.

Right into the lungs.

It backs up directly into the pulmonary veins, leading to fluid in the lungs, which gives the patient severe symptoms of pulmonary congestion.

Wow.

Okay.

So the lungs basically get flooded because the left side of the heart is backed up.

And I assume the exact same principle applies to the right side.

It absolutely does.

If the right side of the heart is failing, that pressure backs up into the vena cava.

And since there are no valves, you will literally see that back up as distended neck veins and a swollen enlarged abdomen.

Precisely.

The anatomy dictates the clinical presentation.

And this ties directly into the cardiac cycle, which has two phases.

Diastole is the resting and filling phase, taking up about two -thirds of the cycle.

Cystally is the active pumping phase.

And we measure cardiac output to see how well that cycle is working.

Yes.

Cardiac output is simply the stroke volume, the amount of blood pumped with every single beat multiplied by the heart rate.

And we can actually observe the efficiency of that cardiac output just by looking at the patient's neck vessels.

That's fun.

We carotid artery is located so close to the heart that its pulse closely coincides with ventricular systole.

You feel the pulse exactly as the left ventricle pumps.

Then you have the jugular veins, which empty directly into the superior vena cava.

And because of that lack of valves we just talked about?

The jugular veins show us a backward moving waveform.

They act like a direct pressure gauge for the right side of the heart.

The beauty of this is that once you understand the plumbing,

you know exactly what clues to look for when you talk to your patient.

Which brings us perfectly to the subjective interview.

Here's where it gets really interesting.

When you walk into a patient's room and they report chest pain,

you cannot just ask, does it hurt?

No, you have to act like a detective.

Exactly.

When exactly did it start?

Where is this specific location?

Does the pain radiate down the arm or up to the jaw?

Is the character of the pain crushing, stabbing, or burning?

You also have to figure out if this is actually a cardiac issue or if it's pleuritic pain from the lungs.

Differentiating those two is critical.

Pleuritic pain is often tied directly to respiration.

If the pain sharply increases when the patient takes a deep breath, or if you can reproduce the exact pain just by pressing a finger against their chest wall, it's much less likely to be a myocardial infarction.

But if it's cardiac?

If it's cardiac, you have to immediately consider how that compromised heart function is affecting the rest of the body's oxygen supply.

That leads right into assessing dyspnea, or shortness of breath.

And there are very specific terms you need to master here.

First is dyspnea on exertion, or DOE.

You need to quantify this.

Don't just ask if they get winded.

Right.

Ask them how many level blocks they can walk before they have to stop and catch their breath.

Yes.

Then there is orthopnea, which is the need to assume a more upright position just to breathe.

And you document orthopnea in a very practical way.

You ask the patient exactly how many pillows they use to sleep.

Though you definitely need to clarify why they are using them.

If a patient says they sleep with six pillows, you have to ask if it's because they physically cannot catch their breath lying flat, or if they just really love a giant pile of decorative pillows.

That's a very good point.

You're looking for the physiological need to be upright.

And speaking of sleeping, we have to talk about paroxysmal nocturnal dyspnea, or PND.

PND is a classic red flag symptom of heart failure.

Here is the mechanism.

When a person is walking around during the day, fluid tends to pool in their legs.

Thanks to gravity.

Right.

When they lie down to sleep, all that fluid shifts back into the central circulation, increasing the volume of intra -thoracic blood.

A weakened, failing heart simply cannot accommodate that increased volume.

So what happens?

Typically, after about two hours of sleep, the patient will wake up in a panic, feeling like they are suffocating and desperately needing fresh air.

That sounds absolutely terrifying for the patient.

And you can see how that constant cardiovascular strain leads to severe fatigue.

But the timing of the fatigue is a major clue, isn't it?

It is.

If a patient tells you their fatigue gets progressively worse in the evening, that strongly suggests their cardiac output is decreasing over the course of the day.

On the flip side, if they say they are exhausted all day, or the fatigue is actually worse first thing in the morning, that pattern leans much more toward anxiety or depression.

The exact same temporal logic applies to assessing edema, or swelling.

Cardiac edema is typically bilateral.

It happens in both legs.

And it is worse in the evening after they have been upright all day.

It often improves by morning because they have spent the night with their legs elevated in bed.

Which perfectly explains another major symptom, nocturia.

The urgent need to urinate at night.

Going back to that fluid pooling in the dependent areas during the day when the patient finally lies down at night,

that recumbency promotes the resorption of that fluid back into the bloodstream.

The heart finally pushes it to the kidneys.

Right, the kidneys process it, and suddenly the patient has to wake up multiple times a night to use the bathroom.

Beyond these symptoms, your interview must also cover past medical history, family cardiac history, and lifestyle risk factors.

Nutrition, smoking, alcohol.

Yeah, what is their daily nutrition like?

Do they smoke?

How much alcohol do they consume?

And a massive environmental safety question, do they have stairs in their home?

Asking about stairs is essential for safe discharge planning.

If a patient with severe heart failure lives in a third -floor walk -up apartment, sending them home without a support plan is a setup for immediate readmission.

Totally.

Once you've gathered all these subjective clues, you have a solid hypothesis.

Now you transition to the physical examination to gather your objective data.

And setting the scene for the physical exam is crucial for getting accurate results.

When you assess the carotid arteries in the neck, the patient can be sitting comfortably.

But when you move to the jugular veins and the percordium, which is the area of the chest wall directly overlying the heart,

the patient needs to be supine with their head and chest elevated at an exact 30 -45 degree angle.

And remember the golden rule for the order of your cardiovascular assessment?

Always move peripherally to centrally.

You start with a pulse and blood pressure, move to the extremities, then evaluate the neck vessels, and finally you auscultate the percordium.

Let's focus on the neck vessels first, specifically the carotid artery, because there is a massive safety warning here.

Very important.

You must palpate the carotid arteries gently and you must palpate only one at a time.

If you press both simultaneously, you risk compromising the arterial blood flow to the brain.

You could pass them right out.

Yes.

Furthermore, if you massage or apply excessive pressure over the carotid sinus, which is high in the neck, you can trigger carotid sinus hypersensitivity.

What actually happens if you trigger that?

It violently simulates the vagus nerve.

The patient's heart rate and blood pressure will plummet suddenly and they could easily pass out right there on the exam table.

Yikes.

So gentle pressure, one side at a time.

After you safely palpate, you need to auscultate the carotids,

you keep the patient's neck in a neutral position,

and lightly apply the bell of your stethoscope at three specific locations,

the angle of the jaw, the mid -cervical area, and the base of the neck.

And you ask the patient to take a breath, exhale, and briefly hold it.

Why do they have to hold it?

Because normal breath sounds traveling up the trachea can easily mask the vascular sounds you are trying to hear.

What you are listening for is a brute.

Right, a brute.

A brute is a blowing, swooshing sound.

It indicates turbulent blood flow from a local vascular cause, most commonly atherosclerosis, which is plaque narrowing the artery.

If the artery is partially blocked, the blood flow becomes turbulent, creating that swooshing brute.

Next, you inspect the jugular venous pulse.

Remember, you have the patient leaning back at a 30 to 45 degree angle.

You are looking at the external jugular veins overlying the sternomastoid muscle in the neck.

Normally, as you raise a person from a flat supine position up to a sitting position,

those veins could flatten out and disappear completely by the time they hit 45 degrees.

But if they don't?

Right, if those veins stay fully distended and bulging above 45 degrees, it signifies increased central venous pressure.

That is a glaring sign of right -sided heart failure.

And if you suspect heart failure, you can confirm it with the abdominal jugular test.

You position the patient's supine and press firmly on their mid -abdomen for a sustained period.

This is a wild test.

It is.

Think of the venous system like a highway and the splanschnik vessels, which are the major blood vessels supplying the abdominal organs, as a massive on -ramp.

By pressing on the abdomen, you're displacing venous blood out of those splanschnik vessels and forcing it up toward the heart.

Like diverting a bunch of extra cars onto the highway all at once.

Exactly.

A normal healthy heart can easily pump that extra volume forward.

The jugular veins might rise for a few seconds as the blood hits the heart, but they will quickly recede.

But if it's failing?

If the right side of the heart is failing, it cannot handle that sudden extra volume.

It's a traffic jam.

The jugular veins will elevate more than 4 centimeters, and they will stay elevated for as long as you are pushing on the abdomen.

That is a positive abdominal jugular test.

Fascinating.

So once the neck vessels are cleared, you move essentially to the chest, the pecordium, for heart auscultation.

You don't just put the stethoscope down randomly.

You listen in a rough Z pattern across the valve areas, focusing first on systole, then on diastole.

And you always start with the diaphragm of the stethoscope.

Which is best for hearing higher -pitched sounds.

And then you switch over to the bell, which is designed for lower -pitched sounds.

Your first goal is to identify the normal S1 and S2 heart sounds that classic lubbed up.

S1 is the sound of the AV valves closing, which signals the very beginning of systole, the pumping phase.

S2 is the sound of the semilinear valves closing, signaling the end of systole.

But a thorough nurse is also actively listening for extra heart sounds, specifically S3 and S4, which occur during diastole, the filling phase.

Yes.

What exactly causes an S3 or an S4?

It comes down to the condition of the heart muscle itself.

An S3, often called a ventricular gallop, happens early in diastole.

Imagine water sloshing into a bucket that is already completely full.

Okay, great visual.

When the ventricles are overfilled and resistant to more volume during the early rapid filling phase, it creates that S3 vibration.

Clinically, a pathologic S3 is a classic hallmark of heart failure and volume overload.

And an S4 is the opposite mechanism, right?

An S4, or an atrial gallop, occurs at the very end of diastole.

Instead of sloshing into an overfilled chamber, the atria are contracting and trying to push blood into a non -compliant, incredibly stiff ventricle.

Stiff from what?

Usually from coronary artery disease or chronic hypertension, it's like trying to inflate a balloon made of thick leather.

That vibration is the S4.

You also need to listen carefully for murmurs.

A murmur sounds like a gentle, blowing, swooshing noise right on the chest wall, caused by turbulent blood flow through the valves themselves.

If you hear one, you have to grade its loudness on a very specific six -point scale.

The grading scale is key.

Grade 1 is barely audible, even in a perfectly quiet room.

Grade 2 is clearly audible but faint.

Grade 3 is moderately loud.

Grade 4 is loud.

And this is where it gets interesting.

Grade 4 murmur is associated with a palpable thrill on the chest wall.

A thrill feels exactly like the throat of a purring cat.

It is a palpable vibration signifying extremely turbulent blood flow.

Moving up the scale, grade 5 is very loud, and you can hear it with just the edge of the stethoscope touching the chest.

Finally, grade 6 is so incredibly loud that you can hear it with the stethoscope lifted entirely off the chest wall.

But we should note, does this grading scale and baseline apply to everyone?

That's a good question.

Like, what if you're listening to a newborn's chest?

That is a critical point.

If we connect this to the bigger picture, the normal baseline changes significantly, depending on the patient's developmental stage.

In the immediate newborn period, the infant's circulation is transitioning from fetal pathways to normal pulmonic circulation.

Right, because of the shunts.

Yes, fetal shunts, primarily the ductus arteriosus, normally close within 10 to 15 hours after birth.

And because an infant's chest wall is so remarkably thin, you should expect their normal heart sounds to be much louder and harsher than an adult's.

And as they grow into childhood, innocent or functional heart murmurs are incredibly common.

A great example is Still's murmur, which is a soft vibratory murmur heard in early or mid -systil.

It has no underlying pathology.

Children also frequently present with a venous hum, which is a continuous low -pitched hum caused by normal turbulence in the jugular veins.

Conversely, when you assess aging adults, the baseline shifts again.

The anteroposterior diameter of the chest often increases with age.

That barrel chest effect.

Exactly.

That makes it much harder to palpate the apical impulse or clearly hear the splitting of the S2 sound.

While an S4 and certain systolic murmurs become much more common in the elderly and can sometimes occur without overt cardiac disease, an S3 sound is a different story.

An S3 is always a red flag, right?

Always.

An S3 sound in anyone over the age of 35 is considered abnormal and strongly points to congestive heart failure.

The assessment chapter also breaks down several specific abnormal clinical presentations that you absolutely must be able to recognize.

Let's look at congenital defects first.

A patent ductus arteriosus, or PDA,

occurs when that fetal shunt fails to close.

Because blood is continuously flowing from the high -pressure aorta back into the lower pressure pulmonary artery, it creates a very distinct continuous machinery murmur, which literally sounds like a whirring machine.

Then there is tetralogy of phallate, a complex defect that shunts unoxygenated venous blood directly into the aorta, completely bypassing the lungs.

This leads to severe cyanosis.

And they do that squatting thing.

Yes.

You'll often see a child with this condition instinctively adopt a squatting posture during play.

Squatting kinks the femoral arteries, which suddenly increases the systemic vascular resistance.

This pressure shift forces more blood back into the pulmonary artery to finally get oxygenated, providing the child with temporary relief.

Correctation of the aorta is another major one.

It's a severe narrowing of the descending aorta.

It acts almost like a tourniquet.

Because the blood flow is obstructed, you will find incredibly high blood pressure and bounding pulses in the upper extremities, but very low blood pressure and faint, weak pulses in the lower extremities.

And for acquired valvular defects, aortic stenosis is the textbook example.

Over time, the aortic valve cusps, calcify, and stiffen, which severely restricts forward blood flow out of the left ventricle.

So it's squeezing through a tiny space.

Exactly.

Because the blood is struggling so hard to squeeze through that narrow opening, you will find a slow, diminished radial pulse.

When you auscultate, you will hear a loud, harsh crescendo de crescendo murmur during systole.

Crescendo de crescendo, meaning the swooshing sound gets progressively louder as the ventricle pushes its hardest, and then softer as the contraction finishes, like a passing siren.

Exactly.

The sound mimics the pressure curve of the struggling ventricle.

So what does this all mean for your charting?

We've gathered the subjective history, performed the physical exam, and analyzed all these complex findings.

The final step is documentation.

The principles here are precision and proving your clinical reasoning.

Charting is your proof.

Right.

For the subjective portion, a perfect chart from the text might read, No chest pain, dyspnea, orthopnea, cough, fatigue, or edema.

Diet balanced, runs two miles, three to four times a week.

Notice how it explicitly lists the absence of those specific red flag symptoms we discussed.

Those are called pertinent negatives, and they prove you specifically asked about them.

The objective charting must be just as precise.

You'd write something like carotid upstrokes brisk and equal bilaterally, no brute.

Internal jugular vein pulsations disappear at 45 degrees.

Apical impulse in fifth intercostal space at left midclavicular line, S1, S2, crisp, no S3, S4, or murmurs.

So thorough.

That meticulous documentation is non -negotiable.

It is the definitive proof that you, the nurse, have successfully synthesized the patient's history, the underlying anatomy, and your physical findings to ensure safe, effective patient care.

We have covered a massive amount of ground today.

We started with the foundational anatomy, visualizing the heart as an upside -down triangle in the chest, tracing the pathways of the dual pumps, and understanding exactly why the lack of valves in the veins causes fluid to back up into the lungs or the neck.

We really untapped that blueprint.

We did.

We translated that anatomy into targeted interview questions about orthopnea and paroxysmal nocturnal dyspnea.

We walked through the physical exam and safely checking for carotid brutes to diverting the abdominal traffic jam and the abdominal jugular test, to feeling the purring thrill of a grade 4 murmur.

And finally, we looked at how age alters the baseline and how to perfectly document your findings.

Before we sign off, I want to leave you with one final thought to mull over as you study.

We discussed how the heart is technically two separate pumps, the right and the left working in perfect synchronization, separated by just a thin muscular septum.

Right, right.

Yet a failure in just one of those sides completely rewrites the pressure gradients in the rest of the body.

Picture yourself walking into your patient's room on a Tuesday morning.

How might your ability to instantly recognize the difference between right -sided symptoms like distended neck veins and left -sided symptoms like pulmonary congestion entirely change the way you plan a life -saving emergency response for that patient?

Knowing the difference changes everything.

It's exactly why mastering this assessment is so critical.

Thank you for joining us on this deep dive.

Keep reviewing those anatomical pathways, practice those auscultation points, and trust your training.

From all of us here on the Last Minute Lecture team, we wish you the absolute best of luck on your upcoming exams and out there on your clinical rotations.

You've got this.